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Sample records for brain edema

  1. Osmotherapy in brain edema

    DEFF Research Database (Denmark)

    Grände, Per-Olof; Romner, Bertil

    2012-01-01

    on outcome, or leads to worse outcome. Here we describe the action and potentially beneficial and adverse effects of the 2 most commonly used osmotic solutions, mannitol and hypertonic saline, and present some critical aspects of their use. There is a well-documented transient intracranial pressure (ICP......, osmotherapy can be negative for outcome, which may explain why we lack scientific support for its use. These drawbacks, and the fact that the most recent Cochrane meta-analyses of osmotherapy in brain edema and stroke could not find any beneficial effects on outcome, make routine use of osmotherapy in brain...

  2. Aquaporin-4 and traumatic brain edema

    Institute of Scientific and Technical Information of China (English)

    XU Miao; SU Wei; XU Qiu-ping

    2010-01-01

    Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortal-ity following traumatic brain injury as it increases intracra-nial pressure, impairs cerebral perfusion and oxygenation,and contributes to additional ischemic injuries.Classically,two major types of traumatic brain edema exist: "vasogenic"and "cytotoxic/cellular".However, the cellular and molecu-lar mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no ef-fective drugs can be used now.Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, pre-dominantly in astrocyte foot processes at the borders be-tween the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood.This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma.In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma.AQP4 has been proposed as a novel drug target in brain edema.These findings sug-gest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.

  3. Radiosurgery for brain metastases and cerebral edema.

    Science.gov (United States)

    Gazit, Inbal; Har-Nof, Sagi; Cohen, Zvi R; Zibly, Zion; Nissim, Uzi; Spiegelmann, Roberto

    2015-03-01

    The objective of this study was to assess reduction in cerebral edema following linear accelerator radiosurgery (LINAC) as first line therapy for brain metastasis. We reviewed the medical records of all patients who underwent LINAC radiosurgery for brain metastasis at our institution during 2010-2012, and who had not previously undergone either surgery or whole brain radiotherapy. Data were analyzed for 55 brain metastases from 46 patients (24 males), mean age 59.9 years. During the 2 months following LINAC radiosurgery, the mean steroid dose decreased from 4.8 to 2.6 mg/day, the mean metastasis volume decreased from 3.79±4.12 cc to 2.8±4.48 cc (p=0.001), and the mean edema volume decreased from 16.91±30.15 cc to 12.85±24.47 cc (p=0.23). The 17 patients with reductions of more than 50% in brain edema volume had single metastases. Edema volume in the nine patients with two brain metastases remained stable in five patients (volume change 10%, 2-14 cc). In a subanalysis of eight metastases with baseline edema volume greater than 40 cc, edema volume decreased from 77.27±37.21 cc to 24.84±35.6 cc (p=0.034). Reductions in brain edema were greater in metastases for which non-small-cell lung carcinoma and breast cancers were the primary diseases. Overall, symptoms improved in most patients. No patients who were without symptoms or who had no signs of increased intracranial pressure at baseline developed signs of intracranial pressure following LINAC radiosurgery. In this series, LINAC stereotactic radiosurgery for metastatic brain lesions resulted in early reduction in brain edema volume in single metastasis patients and those with large edema volumes, and reduced the need for steroids.

  4. Aquaporin-4 and ischemic brain edema

    Institute of Scientific and Technical Information of China (English)

    Saihong Dun; Yang Guo

    2007-01-01

    OBJECTIVE: To investigate the relationship of aquaporin 4 (AQP4) and brain edema.DATA SOURCES: Using the terms of "aquaporin-4, brain edema", we searched PubMed database to identify studies published from January 1997 to April 2006 in the English languages. Meanwhile, we also searched China National Knowledge Infrastructure (CNKI) for related studies.STUDY SELECTION: The collected data were selected firstly. Studies on AQP4 and brain edema were chosen and their full-texts were searched for, and those with repetitive or review studies were excluded.DATA EXTRACTION: Totally 146 related studies were collected, 42 of them were involved and the other 104 studies were used for reading reference data.DATA SYNTHESIS: AQP4 is a selective water permeable integral membrane protein. It is mainly expressed in astrocytes and ependymocyte, and is the important structural basis for water regulation and transportation between glial cells and cerebrospinal fluid or vessels. Phosphorylation is involved in the regulation of AQP4.AQP4 participates in the formation of brain edema caused by various factors. Studies on the structure and pathological changes of AQP4 are still in the initial stage, and the role and mechanism of AQP4 in the formation of brain edema is very unclear.CONCLUSION: AQP4 plays a critical regulating role in the formation of ischemic brain edema, but whether it is regulated by drugs lacks reliable evidence.

  5. Peritumoral brain edema in angiomatous supratentorial meningiomas

    DEFF Research Database (Denmark)

    Nassehi, Damoun; Sørensen, Lars Peter; Dyrbye, Henrik;

    2013-01-01

    The aim of this work was to study the vascular endothelial growth factor A (VEGF-A) pathway and peritumoral brain edema (PTBE) through comparison of non-angiomatous and angiomatous meningiomas. Meningiomas are common intracranial tumors, which often have PTBE. VEGF-A is an integral part of PTBE...

  6. Pathogenesis of Brain Edema and Investigation into Anti-Edema Drugs

    Directory of Open Access Journals (Sweden)

    Shotaro Michinaga

    2015-04-01

    Full Text Available Brain edema is a potentially fatal pathological state that occurs after brain injuries such as stroke and head trauma. In the edematous brain, excess accumulation of extracellular fluid results in elevation of intracranial pressure, leading to impaired nerve function. Despite the seriousness of brain edema, only symptomatic treatments to remove edema fluid are currently available. Thus, the development of novel anti-edema drugs is required. The pathogenesis of brain edema is classified as vasogenic or cytotoxic edema. Vasogenic edema is defined as extracellular accumulation of fluid resulting from disruption of the blood-brain barrier (BBB and extravasations of serum proteins, while cytotoxic edema is characterized by cell swelling caused by intracellular accumulation of fluid. Various experimental animal models are often used to investigate mechanisms underlying brain edema. Many soluble factors and functional molecules have been confirmed to induce BBB disruption or cell swelling and drugs targeted to these factors are expected to have anti-edema effects. In this review, we discuss the mechanisms and involvement of factors that induce brain edema formation, and the possibility of anti-edema drugs targeting them.

  7. Effect of AVP on brain edema following traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    XU Miao; SU Wei; HUANG Wei-dong; LU Yuan-qiang; XU Qiu-ping; CHEN Zhao-jun

    2007-01-01

    Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤ 8) and moderate traumatic brain injury group (MTBI, GCS>8).Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group)and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan.Results: plasma AVP levels (ng/L) were (mean±SD): control, 3.06±1.49; MTBI, 38.12±7.25; and STBI, 66.61±17.10.The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0.01). And the AVP level was correlated with the severity (STBI r=0.919, P<0.01; MTBI r=0.724, P<0.01) and the duration of brain edema (STBI r=0.790, P<0.01; MTBI r=0.712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.

  8. Role of ammonia in the pathogenesis of brain edema.

    Directory of Open Access Journals (Sweden)

    Fujiwara,Masachika

    1986-12-01

    Full Text Available The role of hyperammonemia in the pathogenesis of cerebral edema was investigated using mongrel dogs to develop a treatment for cerebral edema in acute hepatic failure. Intravenous infusion of ammonium acetate alone into dogs did not induce brain edema, although blood ammonia reached unphysiologically high levels. However, ammonium acetate infusion during mannitol-induced reversible (osmotic opening of the blood-brain barrier (BBB effectively induced cytotoxic brain edema. Pretreatment with a branched-chain amino acid (BCAA; valine, leucine and isoleucine solution prevented an increase in intracranial pressure (ICP and brain water content, and caused a decrease in brain ammonia content and an increase in brain BCAA and glutamic acid. The results suggest that ammonia plays an important role in the pathogenesis of cerebral edema during acute hepatic failure and that BCAAs accelerate ammonia detoxification in the brain.

  9. Mathematical modelling of blood-brain barrier failure and edema

    Science.gov (United States)

    Waters, Sarah; Lang, Georgina; Vella, Dominic; Goriely, Alain

    2015-11-01

    Injuries such as traumatic brain injury and stroke can result in increased blood-brain barrier permeability. This increase may lead to water accumulation in the brain tissue resulting in vasogenic edema. Although the initial injury may be localised, the resulting edema causes mechanical damage and compression of the vasculature beyond the original injury site. We employ a biphasic mixture model to investigate the consequences of blood-brain barrier permeability changes within a region of brain tissue and the onset of vasogenic edema. We find that such localised changes can indeed result in brain tissue swelling and that the type of damage that results (stress damage or strain damage) depends on the ability of the brain to clear edema fluid.

  10. Drowning stars: Reassessing the role of astrocytes in brain edema

    OpenAIRE

    2014-01-01

    Edema formation frequently complicates brain infarction, tumors and trauma. Despite the significant mortality of this condition, current treatment options are often ineffective or incompletely understood. Recent studies have revealed the existence of a brain-wide paravascular pathway for cerebrospinal (CSF) and interstitial fluid (ISF) exchange. The current review critically examines the contribution of this ‘glymphatic’ system to the main types of brain edema. We propose that in cytotoxic ed...

  11. Drowning stars: reassessing the role of astrocytes in brain edema.

    Science.gov (United States)

    Thrane, Alexander S; Rangroo Thrane, Vinita; Nedergaard, Maiken

    2014-11-01

    Edema formation frequently complicates brain infarction, tumors, and trauma. Despite the significant mortality of this condition, current treatment options are often ineffective or incompletely understood. Recent studies have revealed the existence of a brain-wide paravascular pathway for cerebrospinal (CSF) and interstitial fluid (ISF) exchange. The current review critically examines the contribution of this 'glymphatic' system to the main types of brain edema. We propose that in cytotoxic edema, energy depletion enhances glymphatic CSF influx, whilst suppressing ISF efflux. We also argue that paravascular inflammation or 'paravasculitis' plays a critical role in vasogenic edema. Finally, recent advances in diagnostic imaging of glymphatic function may hold the key to defining the edema profile of individual patients, and thus enable more targeted therapy.

  12. Critical Care Management of Cerebral Edema in Brain Tumors.

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    Esquenazi, Yoshua; Lo, Victor P; Lee, Kiwon

    2017-01-01

    Cerebral edema associated with brain tumors is extremely common and can occur in both primary and metastatic tumors. The edema surrounding brain tumors results from leakage of plasma across the vessel wall into the parenchyma secondary to disruption of the blood-brain barrier. The clinical signs of brain tumor edema depend on the location of the tumor as well as the extent of the edema, which often exceeds the mass effect induced by the tumor itself. Uncontrolled cerebral edema may result in increased intracranial pressure and acute herniation syndromes that can result in permanent neurological dysfunction and potentially fatal herniation. Treatment strategies for elevated intracranial pressure consist of general measures, medical interventions, and surgery. Alhough the definitive treatment for the edema may ultimately be surgical resection of the tumor, the impact of the critical care management cannot be underestimated and thus patients must be vigilantly monitored in the intensive care unit. In this review, we discuss the pathology, pathophysiology, and clinical features of patients presenting with cerebral edema. Imaging findings and treatment modalities used in the intensive care unit are also discussed.

  13. Edema

    Science.gov (United States)

    Edema means swelling caused by fluid in your body's tissues. It usually occurs in the feet, ankles ... it can involve your entire body. Causes of edema include Eating too much salt Sunburn Heart failure ...

  14. Edema

    Science.gov (United States)

    ... problem worse. Edema can also be a side effect of taking certain medicines.Some health problems, such as congestive heart failure, liver disease and kidney disease, can cause edema. You cannot ...

  15. Effects of magnesium sulfate on traumatic brain edema in rats

    Institute of Scientific and Technical Information of China (English)

    冯东福; 朱志安; 卢亦成

    2004-01-01

    Objective: To investigate the effects of magnesium sulfate on traumatic brain edema and explore its possible mechanism.Methods: Forty-eight Sprague-Dawley ( SD ) rats were randomly divided into three groups: Control, Trauma and Treatment groups. In Treatment group, magnesium sulfate was intraperitoneally administered immediately after the induction of brain trauma. At 24 h after trauma, total tissue water content and Na + , K + , Ca2 + , Mg2+ contents were measured. Permeability of blood-brain barrier (BBB)was assessed quantitatively by Evans Blue (EB) dye technique. The pathological changes were also studied.Results: Water, Na + , Ca2 + and EB contents in Treatment group were significantly lower than those in Trauma group ( P < 0. 05 ). Results of light microscopy and electron microscopy confirmed that magnesium sulfate can attenuate traumatic brain injury and relieve BBB injury.Conclusions: Treatment with MgSO4 in the early stage can attenuate traumatic brain edema and prevent BBB injury.

  16. Edema

    Science.gov (United States)

    ... one position for too long Eating too much salty food Premenstrual signs and symptoms Pregnancy Edema can ... Do you restrict your intake of salt and salty foods? Do you drink alcohol? Do you seem ...

  17. Significance of Primary Tumor Location and Histology for Brain Metastasis Development and Peritumoral Brain Edema in Lung Cancer

    DEFF Research Database (Denmark)

    Fabian, Katalin; Gyulai, Marton; Furak, Jozsef;

    2016-01-01

    Background: Brain metastasis of lung cancer adversely affects overall survival (OS) and quality of life, while peritumoral brain edema is responsible for life-threatening complications. Methods: We retrospectively analyzed the clinicopathological and cerebral radiological data of 575 consecutive...... lung cancer patients with brain metastases. Results: In adenocarcinoma and squamous cell carcinoma, peritumoral brain edema was more pronounced than in small-cell lung cancer (p ... of peritumoral brain edema (p

  18. THE RELATIONSHIP BETWEEN PERITUMORAL BRAIN EDEMA AND VASCULAR ENDOTHELIAL GROWTH FACTOR EXPRESSION IN PATIENTS WITH MENINGIOMA

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective To determine whether VEGF plays a role in the development of peritumoral brain edema. Methods 50 meningioma patients and their VEGF expression were studied. We took a mono- clonal antibody from mouse to VEGF to stain the tumor cells, the vascular endothelial cells and the interstitial cells. The severity of brain edema was evaluated according to CT or MR scans by the following equation: edema index = Vtumor+edema/Vtumor. The relationship between VEGF expression and edema index was analyzed statisti- cally. Results VEGF was expressed in meningioma tumor cells, which is usually concentrated at the pe- ripheral sites of the tumor. There was a positive linear correlation between the expression and the brain edema index. Conclusion VEGF may play a role in the development of peritumoral brain edema in meningioma patient.

  19. [Study of cytokines content and gangliosides metabolism at experimental brain edema].

    Science.gov (United States)

    Zakarian, A V; Kazarian, G S; Zakarian, G V; Melkonian, M M; Ovsesian, L M

    2011-01-01

    The content of cytokines, and gangliosides metabolism, and the quantity of lipid peroxidation products were studied at experimental brain edema. Data obtained show increase the level of proinflammatory cytokins and decrease the level of antiinflammatory cytokines during development of brain edema. Along with this we reveal the accumulation of lipid peroxidation products (diene conjugates, hydroperoxides, and malonic dialdehyde). Each fraction of gangliosides decreased, but the product of their hydrolytic dissociation sphingosine increased at experimental brain edema.

  20. Brain expression of the water channels Aquaporin-1 and -4 in mice with acute liver injury, hyperammonemia and brain edema

    DEFF Research Database (Denmark)

    Eefsen, Martin; Jelnes, Peter; Schmidt, Lars E;

    2010-01-01

    Cerebral edema is a feared complication to acute liver failure (ALF), but the pathogenesis is still poorly understood. The water channels Aquaporin-1 (Aqp1) and -4 (Aqp4) has been associated with brain edema formation in several neuropathological conditions, indicating a possible role of Aqp1 and....../or Aqp4 in ALF mediated brain edema. We induced acute liver injury and hyperammonemia in mice, to evaluate brain edema formation and the parallel expression of Aqp1 and Aqp4 in ALF. Liver injury and hyperammonemia were induced by +D-galactosamine (GLN) plus lipopolysaccharide (LPS) intraperitoneally......(6266) (p edema in mice with ALF....

  1. Acetazolamide Mitigates Astrocyte Cellular Edema Following Mild Traumatic Brain Injury

    Science.gov (United States)

    Sturdivant, Nasya M.; Smith, Sean G.; Ali, Syed F.; Wolchok, Jeffrey C.; Balachandran, Kartik

    2016-09-01

    Non-penetrating or mild traumatic brain injury (mTBI) is commonly experienced in accidents, the battlefield and in full-contact sports. Astrocyte cellular edema is one of the major factors that leads to high morbidity post-mTBI. Various studies have reported an upregulation of aquaporin-4 (AQP4), a water channel protein, following brain injury. AZA is an antiepileptic drug that has been shown to inhibit AQP4 expression and in this study we investigate the drug as a therapeutic to mitigate the extent of mTBI induced cellular edema. We hypothesized that mTBI-mediated astrocyte dysfunction, initiated by increased intracellular volume, could be reduced when treated with AZA. We tested our hypothesis in a three-dimensional in vitro astrocyte model of mTBI. Samples were subject to no stretch (control) or one high-speed stretch (mTBI) injury. AQP4 expression was significantly increased 24 hours after mTBI. mTBI resulted in a significant increase in the cell swelling within 30 min of mTBI, which was significantly reduced in the presence of AZA. Cell death and expression of S100B was significantly reduced when AZA was added shortly before mTBI stretch. Overall, our data point to occurrence of astrocyte swelling immediately following mTBI, and AZA as a promising treatment to mitigate downstream cellular mortality.

  2. Peritumoral brain edema in intracranial meningiomas Edema peritumoral em meningiomas intracranianos

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    Nelson de Azambuja Pereira-Filho

    2010-06-01

    Full Text Available Occurrence of peritumoral brain edema (PBE in meningiomas has been associated with several factors in recent years, although its pathophysiological mechanism has not yet been fully elucidated. The aim of this study was to analyze the correlation between the presence / degree of PBE and factors such as gender, age, size and histological subtype of tumor. We analyzed the MRI images of 74 patients operated on Hospital Beneficência Portuguesa de Porto Alegre for the presence / degree of PBE and data was statistically correlated with the parameters of the patient. PBE was present in 70.1% of patients. Tumors with higher volume had more PBE. Tumors of the olfactory groove showed more PBE than sphenoid wing and parassagittal tumors. Transitional subtype showed more PBE than fibroblastic and meningothelial subtypes.A presença de edema cerebral peritumoral (ECP em meningiomas tem sido associada a diversos fatores nos últimos anos, embora o seu mecanismo fisiopatológico ainda não tenha sido inteiramente elucidado. O objetivo desse estudo foi analisar a correlação entre a presença/grau de ECP e fatores como sexo, idade, volume e subtipo histológico do tumor. Foram analisadas imagens de RM de 74 pacientes operados no Hospital Beneficência Portuguesa de Porto Alegre quanto à presença/grau de ECP e os dados correlacionados estatisticamente com os parâmetros do paciente. ECP estava presente em 70,1% dos pacientes. Tumores com maior volume apresentaram mais ECP. Tumores da goteira olfatória apresentaram mais ECP que os da asa do esfenóide e que os parassagitais. Meningiomas transicionais apresentaram mais ECP que os fibroblásticos e que os meningoteliais.

  3. Cerebral Edema in Traumatic Brain Injury: Pathophysiology and Prospective Therapeutic Targets.

    Science.gov (United States)

    Winkler, Ethan A; Minter, Daniel; Yue, John K; Manley, Geoffrey T

    2016-10-01

    Traumatic brain injury is a heterogeneous disorder resulting from an external force applied to the head. The development of cerebral edema plays a central role in the evolution of injury following brain trauma and is closely associated with neurologic outcomes. Recent advances in the understanding of the molecular and cellular pathways contributing to the posttraumatic development of cerebral edema have led to the identification of multiple prospective therapeutic targets. The authors summarize the pathogenic mechanisms underlying cerebral edema and highlight the molecular pathways that may be therapeutically targeted to mitigate cerebral edema and associated sequelae following traumatic brain injury.

  4. Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    YANG Xiao-feng; LIU Wei-guo; SHEN Hong; GONG Jiang-biao; YU Jun; HU Wei-wei; L(U) Shi-ting; ZHENG Xiu-jue; FU Wei-ming

    2005-01-01

    Objective: To study the correlation between brain edema, elevated intracranial pressure (ICP) and cell apoptosis in traumatic brain injury (TBI). Methods: In this study, totally 42 rabbits in 7 groups were studied. Six of the animals were identified as a control group, and the remaining 36 animals were equally divided into 6 TBI groups. TBI models were produced by the modified method of Feeney. After the impact, ICP of each subject was recorded continuously by an ICP monitor until the animal was sacrificed at scheduled time. The apoptotic brain cells were detected by an terminal deoxynucleotide-transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) assay. Cerebral water content (CWC) was measured with a drying method and calculated according to the Elliott formula. Then, an analysis was conducted to determine the correlation between the count of apoptotic cells and the clinical pathological changes of the brain. Results: Apoptotic cell count began to increase 2 h after the impact, and reached its maximum about 3 days after the impact. The peak value of CWC and ICP appeared 1 day and 3 days after the impact, respectively. Apoptotic cell count had a positive correlation with CWC and ICP. Conclusions: In TBI, occurrence of brain edema and ICP increase might lead to apoptosis of brain cells. Any therapy which can relieve brain edema and/or decrease ICP would be able to reduce neuron apoptosis, thereby to attenuate the secondary brain damage.

  5. Rapamycin alleviates brain edema after focal cerebral ischemia reperfusion in rats.

    Science.gov (United States)

    Guo, Wei; Feng, Guoying; Miao, Yanying; Liu, Guixiang; Xu, Chunsheng

    2014-06-01

    Brain edema is a major consequence of cerebral ischemia reperfusion. However, few effective therapeutic options are available for retarding the brain edema progression after cerebral ischemia. Recently, rapamycin has been shown to produce neuroprotective effects in rats after cerebral ischemia reperfusion. Whether rapamycin could alleviate this brain edema injury is still unclear. In this study, the rat stroke model was induced by a 1-h left transient middle cerebral artery occlusion using an intraluminal filament, followed by 48 h of reperfusion. The effects of rapamycin (250 μg/kg body weight, intraperitoneal; i.p.) on brain edema progression were evaluated. The results showed that rapamycin treatment significantly reduced the infarct volume, the water content of the brain tissue and the Evans blue extravasation through the blood-brain barrier (BBB). Rapamycin treatment could improve histological appearance of the brain tissue, increased the capillary lumen space and maintain the integrity of BBB. Rapamycin also inhibited matrix metalloproteinase 9 (MMP9) and aquaporin 4 (AQP4) expression. These data imply that rapamycin could improve brain edema progression after reperfusion injury through maintaining BBB integrity and inhibiting MMP9 and AQP4 expression. The data of this study provide a new possible approach for improving brain edema after cerebral ischemia reperfusion by administration of rapamycin.

  6. Fluid Intake Related to Brain Edema in Acute Middle Cerebral Artery Infarction.

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    Dharmasaroja, Pornpatr A

    2016-02-01

    Evidence of the appropriate amount of fluid intake during the first few days after acute stroke was scarce. Concerns were raised in patients with acute malignant middle cerebral infarction, who tended to have malignant brain edema later. The purpose of the study was to evaluate the effect of fluid intake on the occurrence of malignant brain edema in patients with acute middle cerebral artery infarction. Patients with acute middle cerebral artery infarction who had National Institute of Health Stroke Scale (NIHSS) score of at least 15 were included. Baseline characteristics and amount of fluid intake during the first few days were compared in patients with and without malignant brain edema. One hundred ninety-three patients were studied. Mean NIHSS score was 20. Malignant brain edema occurred in 69 patients (36%). Higher amount of fluid intake (>1650 ml or >28 ml/kg/day or >93% of daily maintenance fluid) showed a significant association with malignant brain edema (OR = 13.86, 95% CI 5.11-37.60, p value edema, 39 patients (39/65, 60%) died and only 11% (7/65 patients) had favorable outcome. High amount of fluid intake in the first few days of acute middle cerebral infarction was related to the occurrence of malignant brain edema.

  7. Hypoxia-inducible factor-1α contributes to brain edema after stroke by regulating aquaporins and glycerol distribution in brain.

    Science.gov (United States)

    Higashida, Tetsuhiro; Peng, Changya; Li, Jie; Dornbos, David; Teng, Kailing; Li, Xiaohua; Kinni, Harish; Guthikonda, Murali; Ding, Yuchuan

    2011-02-01

    Brain edema following stroke is a critical clinical problem due to its association with increased morbidity and mortality. Despite its significance, present treatment for brain edema simply provides symptomatic relief due to the fact that molecular mechanisms underlying brain edema remain poorly understood. The present study investigated the role of hypoxia-inducible factor-1α (HIF-1α) and aquaporins (AQP-4 and -9) in regulating cerebral glycerol accumulation and inducing brain edema in a rodent model of stroke. Two-hours of middle cerebral artery occlusion (MCAO) followed by reperfusion was performed in male Sprague-Dawley rats (250-280 g). Anti-AQP-4 antibody, anti-AQP-9 antibody, or 2-Methoxyestradiol (2ME2, an inhibitor of HIF-1α) was given at the time of MCAO. The rats were sacrificed at 1 and 24 hours after reperfusion and their brains were examined. Extracellular and intracellular glycerol concentration of brain tissue was calculated with an enzymatic glycerol assay. The protein expressions of HIF-1α, AQP-4 and AQP-9 were determined by Western blotting. Brain edema was measured by brain water content. Compared to control, edema (p < 0.01), increased glycerol (p < 0.05), and enhanced expressions of HIF-1α, AQP-4, and AQP-9 (p < 0.05) were observed after stroke. With inhibition of AQP-4, AQP-9 or HIF-1α, edema and extracellular glycerol were significantly (p < 0.01) decreased while intracellular glycerol was increased (p < 0.01) 1 hour after stroke. Inhibition of HIF-1α with 2ME2 suppressed (p < 0.01) the expression of AQP-4 and AQP-9. These findings suggest that HIF-1α serves as an upstream regulator of cerebral glycerol concentrations and brain edema via a molecular pathway involving AQP-4 and AQP-9. Pharmacological blockade of this pathway in stroke patients may provide novel therapeutic strategies.

  8. Differential aquaporin 4 expression during edema build-up and resolution phases of brain inflammation

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    Brochet Bruno

    2011-10-01

    Full Text Available Abstract Background Vasogenic edema dynamically accumulates in many brain disorders associated with brain inflammation, with the critical step of edema exacerbation feared in patient care. Water entrance through blood-brain barrier (BBB opening is thought to have a role in edema formation. Nevertheless, the mechanisms of edema resolution remain poorly understood. Because the water channel aquaporin 4 (AQP4 provides an important route for vasogenic edema resolution, we studied the time course of AQP4 expression to better understand its potential effect in countering the exacerbation of vasogenic edema. Methods Focal inflammation was induced in the rat brain by a lysolecithin injection and was evaluated at 1, 3, 7, 14 and 20 days using a combination of in vivo MRI with apparent diffusion coefficient (ADC measurements used as a marker of water content, and molecular and histological approaches for the quantification of AQP4 expression. Markers of active inflammation (macrophages, BBB permeability, and interleukin-1β and markers of scarring (gliosis were also quantified. Results This animal model of brain inflammation demonstrated two phases of edema development: an initial edema build-up phase during active inflammation that peaked after 3 days (ADC increase was followed by an edema resolution phase that lasted from 7 to 20 days post injection (ADC decrease and was accompanied by glial scar formation. A moderate upregulation in AQP4 was observed during the build-up phase, but a much stronger transcriptional and translational level of AQP4 expression was observed during the secondary edema resolution phase. Conclusions We conclude that a time lag in AQP4 expression occurs such that the more significant upregulation was achieved only after a delay period. This change in AQP4 expression appears to act as an important determinant in the exacerbation of edema, considering that AQP4 expression is insufficient to counter the water influx during the build

  9. CT diagnosis of non-traumatic subarachnoid haemorrhage in patients with brain edema

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    Avrahami, E.; Katz, R.; Rabin, A.; Friedman, V. [Department of Diagnostic Radiology, E. Wolfson Medical Center 58100 Holon (Israel)

    1998-10-01

    The aim of the study is to prove, retrospectively, that it is unlikely that the computerized tomography (CT) diagnosis of subarachnoid haemorrhage (SH) accompanies the CT diagnosis of generalized brain edema. A total of 100 comatose patients underwent CT of the brain. Of this number, 42 underwent an enhanced CT scan. In 26 patients, lumbar puncture was also performed. A control group of ten patients diagnosed with headache and having a normal CT scan underwent NECT and ECT. Measurements of the white and gray matter density in Hounsfield units (HU) were performed in all 110 cases, including the controls. The brain tissue density and the difference between the densities of the white and gray matter were lower in the cases with brain edema than in the controls. The data values were statistically significant. Small cerebral ventricles, sulci and cisterns and small differences between white and gray matter measurements were observed in the CT scans of the brain edema cases. All 100 patients had CT diagnosis of brain edema and SH. There was no bloody or xanthochromic CSF in any of the 26 lumbar punctures performed. In the enhanced CT scans, there was poor or no filling of the lateral sinuses. The compression of the lateral sinuses by the edematous brain tissue most probably results in their stenosis or obstruction due to disturbed brain venous drainage which can mimic CT findings of SH. (Copyright (c) 1998 Elsevier Science B.V., Amsterdam. All rights reserved.)

  10. Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.

    Directory of Open Access Journals (Sweden)

    Ralph Timaru-Kast

    Full Text Available After traumatic brain injury (TBI elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months and old (21 months male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2% compared to young (0%. This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1β expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral

  11. A new approach to ischemic brain edema and infarct

    Institute of Scientific and Technical Information of China (English)

    Zhai Yu; Jin Jia Xing; Liu De Ha

    2000-01-01

    Objective: To study the feasibility and efficiency of treatment in the patients with acute moderate and severe ischemic stroke with Neurotropin for its principle of inhibiting cerebral edema and repairing injured neurons. Methods: A randomized controlled trial with Neurotropin was performed in 50 patients admitted within 48h after an acute internal carotid artery infarction, Neurological deficits score ( Europe Stroke Scale-ESS ) <80 marks and the area of infarct and edema>2.25cm2. There were 31 patients in the Neurotropin group and 19 patients in the control group. Basic treatment was Troxerutin 250 mg intravenous drip per day for 21 days in two groups. Additionally, the patients in the Neurotropin group were intravenous injected 106 ampoule Neurotropin (3.6 unit per ampoule), divided into 11 days. We evaluated Neurological deficits score (ESS), ability of daily living (ADL)- Barthel Index, the size and average CT density of infarct and edema area on CT scan during different treatment stage and analyzed.them with statistics. Results: The percentage of improved patients (complete and partial recovery) reaches 64.5% in the Neurotropin group and 31.6% in the control group. The size of the infarct and edema area on CT scan is significantly reduced only in the Neurotropin group after treatment. The average range reduced is 28% on day 11 and 41.5% on day 21, and the average CT density in the Neurotropin group is more advanced than in the control group after onset. Conclusion: Neurotropin can be used as an effective therapy in acute ischemic stroke and ischemic cerebral edema.

  12. Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood-Brain Barrier Disruption after Experimental Stroke in Mice.

    Directory of Open Access Journals (Sweden)

    Emil Zeynalov

    Full Text Available Stroke is a major cause of morbidity and mortality. Stroke is complicated by brain edema and blood-brain barrier (BBB disruption, and is often accompanied by increased release of arginine-vasopressin (AVP. AVP acts through V1a and V2 receptors to trigger hyponatremia, vasospasm, and platelet aggregation which can exacerbate brain edema. The AVP receptor blockers conivaptan (V1a and V2 and tolvaptan (V2 are used to correct hyponatremia, but their effect on post-ischemic brain edema and BBB disruption remains to be elucidated. Therefore, we conducted this study to investigate if these drugs can prevent brain edema and BBB disruption in mice after stroke.Experimental mice underwent the filament model of middle cerebral artery occlusion (MCAO with reperfusion. Mice were treated with conivaptan, tolvaptan, or vehicle. Treatments were initiated immediately at reperfusion and administered IV (conivaptan or orally (tolvaptan for 48 hours. Physiological variables, neurological deficit scores (NDS, plasma and urine sodium and osmolality were recorded. Brain water content (BWC and Evans Blue (EB extravasation index were evaluated at the end point.Both conivaptan and tolvaptan produced aquaresis as indicated by changes in plasma and urine sodium levels. However plasma and urine osmolality was changed only by conivaptan. Unlike tolvaptan, conivaptan improved NDS and reduced BWC in the ipsilateral hemisphere: from 81.66 ± 0.43% (vehicle to 78.28 ± 0.48% (conivaptan, 0.2 mg, p < 0.05 vs vehicle. Conivaptan also attenuated the EB extravasation from 1.22 ± 0.08 (vehicle to 1.01 ± 0.02 (conivaptan, 0.2 mg, p < 0.05.Continuous IV infusion with conivaptan for 48 hours after experimental stroke reduces brain edema, and BBB disruption. Conivaptan but not tolvaptan may potentially be used in patients to prevent brain edema after stroke.

  13. Comparative observation with MRI and pathology of brain edema at the early stage of severe burn

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To investigate the correlation between MRI features and pathology in brain edema at the early stage of severe burn (50% TBSA Ⅲ degree) in dogs.Methods: Fifty-two dogs were randomized into control, simple burn (SB), burn plus sodium lactate (BSL), and burn plus glucose solution groups (BGS). The manifestation of the brain of control group was compared with that of burn groups at 6, 12, 18 and 24 hours postburn with MRI and pathological examination (gross appearance, electron microscopy and light microscopy).Results: The earliest findings of brain edema were seen at 12 hours after burn in BGS group, in which brain swelling was the main feature of MRI. The decrease of SIR on T1WI was not observed until it was exceeded 10%.Signal of T2WI increased by 8.29% at 24 hours after burn.It was difficult to distinguish the gray matter from the white matter at the boundary line, which became blurred later. Histological changes of brain edema were observed as early as 6 hours after burn, being accompanied by swelling of endothelial cells and peri-vescular astrocytes, and vacuolation took place in neurons at 12 hours after burn, with different degrees of necrosis of capillary endothelimn,neurons, and axons. These changes became more marked with elapse of time. The BGS group showed the most obvious changes mentioned above at 24 hours after burn.Conclusions: The model of the brain edema after severe burn has the feature of both vasogenic edema and cytotoxic edema on the MRI and pathology. Positive MRI findings lagged behind that of the pathomorphological changes.ed

  14. Blockage of transient receptor potential vanilloid 4 inhibits brain edema in middle cerebral artery occlusion mice.

    Science.gov (United States)

    Jie, Pinghui; Tian, Yujing; Hong, Zhiwen; Li, Lin; Zhou, Libin; Chen, Lei; Chen, Ling

    2015-01-01

    Brain edema is an important pathological process during stroke. Activation of transient receptor potential vanilloid 4 (TRPV4) causes an up-regulation of matrix metalloproteinases (MMPs) in lung tissue. MMP can digest the endothelial basal lamina to destroy blood brain barrier, leading to vasogenic brain edema. Herein, we tested whether TRPV4-blockage could inhibit brain edema through inhibiting MMPs in middle cerebral artery occlusion (MCAO) mice. We found that the brain water content and Evans blue extravasation at 48 h post-MCAO were reduced by a TRPV4 antagonist HC-067047. The increased MMP-2/9 protein expression in hippocampi of MCAO mice was attenuated by HC-067046, but only the increased MMP-9 activity was blocked by HC-067047. The loss of zonula occludens-1 (ZO-1) and occludin protein in MCAO mice was also attenuated by HC-067047. Moreover, MMP-2/9 protein expression increased in mice treated with a TRPV4 agonist GSK1016790A, but only MMP-9 activity was increased by GSK1016790A. Finally, ZO-1 and occludin protein expression was decreased by GSK1016790A, which was reversed by an MMP-9 inhibitor. We conclude that blockage of TRPV4 may inhibit brain edema in cerebral ischemia through inhibiting MMP-9 activation and the loss of tight junction protein.

  15. Synthesis of /sup 11/C-methylated inulin as a radiopharmaceutical for imaging brain edema and pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Hara, Toshihiko; Iio, Masaaki; Inagaki, Keizo

    1988-07-01

    /sup 11/C-methylated inulin, supposedly useful for imaging of brain edema and pulmonary edema, was prepared using cyclotron produced /sup 11/CO/sub 2/. The synthesis consists of the production of /sup 11/C-methyl iodide and its coupling with inulin alkoxide sodium in dimethylsulfoxide as solvent. /sup 11/C labeled inulin was purified by alcohol precipitation. The radiochemical yield of pure /sup 11/C-inulin was 34% of /sup 11/CO/sub 2/ 30 min after the end of bombardment. The blood clearance and body distribution of /sup 11/C was observed in rabbits after i.v. injection of /sup 11/C-inulin. The blood clearance curve was composed of a sum of three exponential functions. The gamma camera image showed that the /sup 11/C activity in blood moved quickly to kidneys and urine and a small dose of radioactivity remained persistently in edematous tissues, i.e. the edematous lung tissues produced by oleic acid treatment.

  16. Dimethyl fumarate attenuates cerebral edema formation by protecting the blood-brain barrier integrity.

    Science.gov (United States)

    Kunze, Reiner; Urrutia, Andrés; Hoffmann, Angelika; Liu, Hui; Helluy, Xavier; Pham, Mirko; Reischl, Stefan; Korff, Thomas; Marti, Hugo H

    2015-04-01

    Brain edema is a hallmark of various neuropathologies, but the underlying mechanisms are poorly understood. We aim to characterize how tissue hypoxia, together with oxidative stress and inflammation, leads to capillary dysfunction and breakdown of the blood-brain barrier (BBB). In a mouse stroke model we show that systemic treatment with dimethyl fumarate (DMF), an antioxidant drug clinically used for psoriasis and multiple sclerosis, significantly prevented edema formation in vivo. Indeed, DMF stabilized the BBB by preventing disruption of interendothelial tight junctions and gap formation, and decreased matrix metalloproteinase activity in brain tissue. In vitro, DMF directly sustained endothelial tight junctions, inhibited inflammatory cytokine expression, and attenuated leukocyte transmigration. We also demonstrate that these effects are mediated via activation of the redox sensitive transcription factor NF-E2 related factor 2 (Nrf2). DMF activated the Nrf2 pathway as shown by up-regulation of several Nrf2 target genes in the brain in vivo, as well as in cerebral endothelial cells and astrocytes in vitro, where DMF also increased protein abundance of nuclear Nrf2. Finally, Nrf2 knockdown in endothelial cells aggravated subcellular delocalization of tight junction proteins during ischemic conditions, and attenuated the protective effect exerted by DMF. Overall, our data suggest that DMF protects from cerebral edema formation during ischemic stroke by targeting interendothelial junctions in an Nrf2-dependent manner, and provide the basis for a completely new approach to treat brain edema.

  17. Enhanced Expression of Aquaporin-9 in Rat Brain Edema Induced by Bacterial Lipopolysaccharides

    Institute of Scientific and Technical Information of China (English)

    Huaili WANG; Runming JIN; Peichao TIAN; Zhihong ZHUO

    2009-01-01

    To investigate the role of AQP9 in brain edema,the expression of AQP9 in an infectious rat brain edema model induced by the injection of lipopolysaccharide (LPS) was examined.Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that the expressions of AQP9 mRNA and protein at all observed intervals were significantly increased in LPS-treated animals in comparison with the control animals.Time-course analysis showed that the first signs of blood-brain barrier disruption and the increase of brain water content in LPS-treated animals were evident 6 h after LPS injection,with maximum value appearing at 12 h,which coincided with the expression profiles of AQP9 mRNA and protein in LPS-treated animals.The further correlation analysis revealed strong positive correlations among the brain water content,the disruption of the blood-brain barrier and the enhanced expressions of AQP9 mRNA and protein in LPS-treated animals.These results suggested that the regulation of AQP9 expression may play important roles in water movement and in brain metabolic homeostasis associated with the pathophysiology of brain edema induced by LPS injection.

  18. Telmisartan reduced cerebral edema by inhibiting NLRP3 inflammasome in mice with cold brain injury.

    Science.gov (United States)

    Wei, Xin; Hu, Chen-Chen; Zhang, Ya-Li; Yao, Shang-Long; Mao, Wei-Ke

    2016-08-01

    The aim of this study was to investigate the possible beneficial role of telmisartan in cerebral edema after traumatic brain injury (TBI) and the potential mechanisms related to the nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) pyrin domain-containing 3 (NLRP3) inflammasome activation. TBI model was established by cold-induced brain injury. Male C57BL/6 mice were randomly assigned into 3, 6, 12, 24, 48 and 72 h survival groups to investigate cerebral edema development with time and received 0, 5, 10, 20 and 40 mg/kg telmisartan by oral gavage, 1 h prior to TBI to determine the efficient anti-edemic dose. The therapeutic window was identified by post-treating 30 min, 1 h, 2 h and 4 h after TBI. Blood-brain barrier (BBB) integrity, the neurological function and histological injury were assessed, at the same time, the mRNA and protein expression levels of NLRP3 inflammasome, IL-1β and IL-18 concentrations in peri-contused brain tissue were measured 24 h post TBI. The results showed that the traumatic cerebral edema occurred from 6 h, reached the peak at 24 h and recovered to the baseline 72 h after TBI. A single oral dose of 5, 10 and 20 mg/kg telmisartan could reduce cerebral edema. Post-treatment up to 2 h effectively limited the edema development. Furthermore, prophylactic administration of telmisartan markedly inhibited BBB impairment, NLRP3, apoptotic speck-containing protein (ASC) and Caspase-1 activation, as well as IL-1β and IL-18 maturation, subsequently improved the neurological outcomes. In conclusion, telmisartan can reduce traumatic cerebral edema by inhibiting the NLRP3 inflammasome-regulated IL-1β and IL-18 accumulation.

  19. A STUDY ON PERITUMORAL BRAIN EDEMA AROUND MENINGIOMAS BY MRI AND CONTRAST CT

    NARCIS (Netherlands)

    GO, KG; KAMMAN, RL; WILMINK, JT; MOOYAART, EL

    1994-01-01

    In the present study upon 9 meningiomas, the volume of peritumoral brain edema was calculated by integration of the cross-sectional edematous areas on serial MRI slices. It was zero in 3 cases and ranged from 11 to 176.4 ml in the other cases. There was disruption of the cortex in all cases, ranging

  20. Increased brain edema following 5-aminolevulinic acid mediated photodynamic in normal and tumor bearing rats

    Science.gov (United States)

    Hirschberg, Henry; Angell-Petersen, Even; Spetalen, Signe; Mathews, Marlon; Madsen, Steen J.

    2007-02-01

    Introduction: Failure of treatment for high grade gliomas is usually due to local recurrence at the site of surgical resection indicating that a more aggressive form of local therapy, such as PDT, could be of benefit. PDT causes damage to both tumor cells as well as cerebral blood vessels leading to degradation of the blood brain barrier with subsequent increase of brain edema. The increase in brain edema following ALA-PDT was evaluated in terms of animal survival, histopatological changes in normal brain and tumor tissue and MRI scanning. The effect of steroid treatment, to reduce post-treatment PDT induced edema, was also examined. Methods:Tumors were established in the brains of inbred BD-IX and Fisher rats. At various times following tumor induction the animals were injected with ALA ip. and four hours later light treatment at escalating fluences and fluence rates were given. Nontumor bearing control animals were also exposed to ALA-PDT in a similar manner to evaluate damage to normal brain and degree of blood brain barrier (BBB) disruption. Results: Despite a very low level of PpIX production in normal brain, with a 200:1 tumor to normal tissue selectivity ratio measured at a distance of 2 mm from the tumor border, many animals succumbed shortly after treatment. A total radiant energy of 54 J to non-tumor bearing animals resulted in 50% mortality within 5 days of treatment. Treatment of tumor bearing animals with moderate fluence levels produced similar brain edema compared to higher fluence levels. ALA PDT in nontumor bearing animals produced edema that was light dose dependent. PDT appeared to open the BBB for a period of 24-48 hrs after which it was restored. The addition of post operative steroid treatment reduced the incident of post treatment morbidity and mortality. Conclusions: T2 and contrast enhanced T1 MRI scanning proved to be a highly effective and non-evasive modality in following the development of the edema reaction and the degree and time

  1. Central role of maladapted astrocytic plasticity in ischemic brain edema formation

    Directory of Open Access Journals (Sweden)

    Yu-Feng eWang

    2016-05-01

    Full Text Available Brain edema formation and the ensuing brain damages are the major cause of high mortality and long term disability following the occurrence of ischemic stroke. In this process, oxygen and glucose deprivation and the ensuing reperfusion injury play primary roles. In response to the ischemic insult, the neurovascular unit experiences both intracellular and extracellular edemas; the two processes are interactive closely under the driving of maladapted astrocytic plasticity. The astrocytic plasticity includes both morphologic and functional plasticity. The former involves a reactive gliosis and the ensuing glial retraction. It relates to the capacity of astrocytes to buffer changes in extracellular chemical levels, particularly K+ and glutamate, as well as the integrity of the blood-brain barrier. The latter involves the expression and activity of a series of ion and water transport proteins. These molecules are grouped together around glial fibrillary acidic protein and water channel protein aquaporin 4 to form functional networks, regulate hydromineral balance across cell membranes and maintain the integrity of the blood-brain barrier. Intense ischemic challenges can disrupt these capacities of astrocytes and result in their maladaptation. The maladapted astrocytic plasticity in ischemic stroke cannot only disrupt the hydromineral homeostasis across astrocyte membrane and the blood-brain barrier, but also lead to disorders of the whole neurovascular unit. This review focuses on how the maladapted astrocytic plasticity in ischemic stroke plays the central role in the brain edema formation.

  2. Quantitative Apparent Diffusion Coefficients in the Characterization of Brain Tumors and Associated Peritumoral Edema

    Energy Technology Data Exchange (ETDEWEB)

    Server, A.; Schellhorn, T.; Nakstad, P.H. (Dept. of Neuroradiology, Div. of Radiology, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway)); Kulle, B. (Epi-Gen Faculty Div. Akershus Univ. Hospital and Dept. of Biostatistics, Univ. of Oslo, Oslo (Norway)); Maehlen, J.; Kumar, T. (Dept. of Pathology, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway)); Josefsen, R. (Dept. of Neurosurgery, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway)); Langberg, C.W. (Cancer Centre, Ullevaal Univ. Hospital, Univ. of Oslo, Oslo (Norway))

    2009-07-15

    Background: Conventional magnetic resonance (MR) imaging has a number of limitations in the diagnosis of the most common intracranial brain tumors, including tumor specification and the detection of tumoral infiltration in regions of peritumoral edema. Purpose: To prospectively assess if diffusion-weighted MR imaging (DWI) could be used to differentiate between different types of brain tumors and to distinguish between peritumoral infiltration in high-grade gliomas, lymphomas, and pure vasogenic edema in metastases and meningiomas. Material and Methods: MR imaging and DWI was performed on 93 patients with newly diagnosed brain tumors: 59 patients had histologically verified high-grade gliomas (37 glioblastomas multiforme, 22 anaplastic astrocytomas), 23 patients had metastatic brain tumors, five patients had primary cerebral lymphomas, and six patients had meningiomas. Apparent diffusion coefficient (ADC) values of tumor (enhancing regions or the solid portion of tumor) and peritumoral edema, and ADC ratios (ADC of tumor or peritumoral edema to ADC of contralateral white matter, ADC of tumor to ADC of peritumoral edema) were compared with the histologic diagnosis. ADC values and ratios of high-grade gliomas, primary cerebral lymphomas, metastases, and meningiomas were compared by using ANOVA and multiple comparisons. Optimal thresholds of ADC values and ADC ratios for distinguishing high-grade gliomas from metastases were determined by receiver operating characteristic (ROC) curve analysis. Results: Statistically significant differences were found for minimum and mean of ADC tumor and ADC tumor ratio values between metastases and high-grade gliomas when including only one factor at a time. Including a combination of in total four parameters (mean ADC tumor, and minimum, maximum and mean ADC tumor ratio) resulted in sensitivity, specificity, positive (PPV), and negative predictive values (NPV) of 72.9, 82.6, 91.5, and 54.3% respectively. In the ROC curve analysis

  3. Reduction of cerebral edema after traumatic brain injury using an osmotic transport device.

    Science.gov (United States)

    McBride, Devin W; Szu, Jenny I; Hale, Chris; Hsu, Mike S; Rodgers, Victor G J; Binder, Devin K

    2014-12-01

    Traumatic brain injury (TBI) is significant, from a public health standpoint, because it is a major cause of the morbidity and mortality of young people. Cerebral edema after a TBI, if untreated, can lead to devastating damage of the remaining tissue. The current therapies of severe TBI (sTBI), as outlined by the Brain Trauma Foundation, are often ineffective, thus a new method for the treatment of sTBI is necessary. Herein, the reduction of cerebral edema, after TBI, using an osmotic transport device (OTD) was evaluated. Controlled cortical impact (CCI) was performed on adult female CD-1 mice, and cerebral edema was allowed to form for 3 h, followed by 2 h of treatment. The treatment groups were craniectomy only, craniectomy with a hydrogel, OTD without bovine serum albumin (BSA), and OTD. After CCI, brain water content was significantly higher for animals treated with a craniectomy only, craniectomy with a hydrogel, and OTD without BSA, compared to that of control animals. However, when TBI animals were treated with an OTD, brain water content was not significantly higher than that of controls. Further, brain water content of TBI animals treated with an OTD was significantly reduced, compared to that of untreated TBI animals, TBI animals treated with a craniectomy and a hydrogel, and TBI animals treated with an OTD without BSA. Here, we demonstrate the successful reduction of cerebral edema, as determined by brain water content, after TBI using an OTD. These results demonstrate proof of principle for direct water extraction from edematous brain tissue by direct osmotherapy using an OTD.

  4. A fatal adverse effect of cefazolin administration: severe brain edema in a patient with multiple meningiomas

    Directory of Open Access Journals (Sweden)

    Tribuddharat S

    2016-02-01

    Full Text Available Sirirat Tribuddharat,1 Thepakorn Sathitkarnmanee,1 Amnat Kitkhuandee,2 Sunchai Theerapongpakdee,1 Kriangsak Ngamsaengsirisup,1 Sarinya Chanthawong,11Department of Anesthesiology, 2Department of Surgery, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand Abstract: Cefazolin is commonly administered before surgery as a prophylactic antibiotic. Hypersensitivity to cefazolin is not uncommon, and the symptoms mostly include urticaria, skin reaction, diarrhea, vomiting, and transient neutropenia, which are rarely life threatening. We present a rare case of fatal cefazolin hypersensitivity in a female who was diagnosed with multiple meningiomas and scheduled for craniotomy and tumor removal. Immediately after cefazolin IV administration, the patient developed acute hypertensive crisis, which resolved within 10 minutes after the treatment. This was followed by unexplained metabolic acidosis. The patient then developed severe brain edema 100 minutes later. The patient had facial edema when her face was exposed for the next 30 minutes. A computed tomography scan revealed global brain edema with herniation. She was admitted to the intensive care unit for symptomatic treatment and died 10 days after surgery from multiorgan failure. The serum IgE level was very high (734 IU/mL. Single-dose administration of cefazolin for surgical prophylaxis may lead to rare, fatal adverse reaction. The warning signs are sudden, unexplained metabolic acidosis, hypertensive crisis, tachycardia, and facial angioedema predominating with or without cutaneous symptoms like urticaria. Keywords: cefazolin, adverse effect, drug hypersensitivity, brain edema, hypertension

  5. Imaging experimental cerebral malaria in vivo: significant role of ischemic brain edema.

    Science.gov (United States)

    Penet, Marie-France; Viola, Angèle; Confort-Gouny, Sylviane; Le Fur, Yann; Duhamel, Guillaume; Kober, Frank; Ibarrola, Danielle; Izquierdo, Marguerite; Coltel, Nicolas; Gharib, Bouchra; Grau, Georges E; Cozzone, Patrick J

    2005-08-10

    The first in vivo magnetic resonance study of experimental cerebral malaria is presented. Cerebral involvement is a lethal complication of malaria. To explore the brain of susceptible mice infected with Plasmodium berghei ANKA, multimodal magnetic resonance techniques were applied (imaging, diffusion, perfusion, angiography, spectroscopy). They reveal vascular damage including blood-brain barrier disruption and hemorrhages attributable to inflammatory processes. We provide the first in vivo demonstration for blood-brain barrier breakdown in cerebral malaria. Major edema formation as well as reduced brain perfusion was detected and is accompanied by an ischemic metabolic profile with reduction of high-energy phosphates and elevated brain lactate. In addition, angiography supplies compelling evidence for major hemodynamics dysfunction. Actually, edema further worsens ischemia by compressing cerebral arteries, which subsequently leads to a collapse of the blood flow that ultimately represents the cause of death. These findings demonstrate the coexistence of inflammatory and ischemic lesions and prove the preponderant role of edema in the fatal outcome of experimental cerebral malaria. They improve our understanding of the pathogenesis of cerebral malaria and may provide the necessary noninvasive surrogate markers for quantitative monitoring of treatment.

  6. Vascular endothelial growth factor A protein level and gene expression in intracranial meningiomas with brain edema

    DEFF Research Database (Denmark)

    Nassehi, Damoun; Dyrbye, Henrik; Andresen, Morten;

    2011-01-01

    Meningiomas are the second most common primary intracranial tumors in adults. Although meningiomas are mostly benign, more than 50% of patients with meningioma develop peritumoral brain edema (PTBE), which may be fatal because of increased intracranial pressure. Vascular endothelial growth factor....... Forty-three patients had primary, solitary, supratentorial meningiomas with PTBE. In these, correlations in PTBE, edema index, VEGF-A protein, VEGF gene expression, capillary length, and tumor water content were investigated. DNA-branched hybridization was used for measuring VEGF gene expression...... in tissue homogenates prepared from frozen tissue samples. The method for VEGF-A analysis resembled an ELISA assay, but was based on chemiluminescence. The edema index was positively correlated to VEGF-A protein (p = 0.014) and VEGF gene expression (p

  7. Alleviation of ischemia-induced brain edema by activation of the central histaminergic system in rats.

    Science.gov (United States)

    Irisawa, Yumi; Adachi, Naoto; Liu, Keyue; Arai, Tatsuru; Nagaro, Takumi

    2008-09-01

    We have reported that facilitation of central histaminergic activity prevents the development of ischemia-induced brain injury. Since cerebral edema is a major cause of brain damage, we studied effects on brain edema of postischemic administration of L-histidine, a precursor of histamine, and thioperamide, a histamine H(3)-receptor antagonist, both of which enhance central histaminergic activity. Focal cerebral ischemia for 2 h was provoked by transient occlusion of the right middle cerebral artery in rats, and the water content and infarct size were determined 24 h after reperfusion. Changes in the extracellular concentration of histamine were examined in the striatum by a microdialysis procedure, and effects of these compounds were evaluated. Repeated administration of L-histidine (1000 mg/kg x 2, i.p.), immediately and 6 h after reperfusion, reduced the increase in the water contents in ischemic regions. Simultaneous administration of thioperamide (5 mg/kg, s.c.) with L-histidine (1000 mg/kg, i.p.) completely prevented edema formation and alleviated brain infarction, although a single dose of L-histidine, immediately after reperfusion, showed no benefits. The striatal histamine level was gradually increased after reperfusion as well as during ischemia. Simultaneous administration of thioperamide with L-histidine markedly increased the brain histamine concentration, and the value increased up to 230% of that in the saline group 5 - 6 h after reperfusion. L-Histidine alone did not affect the increase in the histamine output after ischemia. These findings suggest that further activation of the central histaminergic system after initiation of cerebral ischemia prevents development of ischemia-induced brain edema.

  8. Dexamethasone exacerbates cerebral edema and brain injury following lithium-pilocarpine induced status epilepticus.

    Science.gov (United States)

    Duffy, B A; Chun, K P; Ma, D; Lythgoe, M F; Scott, R C

    2014-03-01

    Anti-inflammatory therapies are the current most plausible drug candidates for anti-epileptogenesis and neuroprotection following prolonged seizures. Given that vasogenic edema is widely considered to be detrimental for outcome following status epilepticus, the anti-inflammatory agent dexamethasone is sometimes used in clinic for alleviating cerebral edema. In this study we perform longitudinal magnetic resonance imaging in order to assess the contribution of dexamethasone on cerebral edema and subsequent neuroprotection following status epilepticus. Lithium-pilocarpine was used to induce status epilepticus in rats. Following status epilepticus, rats were either post-treated with saline or with dexamethasone sodium phosphate (10mg/kg or 2mg/kg). Brain edema was assessed by means of magnetic resonance imaging (T2 relaxometry) and hippocampal volumetry was used as a marker of neuronal injury. T2 relaxometry was performed prior to, 48 h and 96 h following status epilepticus. Volume measurements were performed between 18 and 21 days after status epilepticus. Unexpectedly, cerebral edema was worse in rats that were treated with dexamethasone compared to controls. Furthermore, dexamethasone treated rats had lower hippocampal volumes compared to controls 3 weeks after the initial insult. The T2 measurements at 2 days and 4 days in the hippocampus correlated with hippocampal volumes at 3 weeks. Finally, the mortality rate in the first week following status epilepticus increased from 14% in untreated rats to 33% and 46% in rats treated with 2mg/kg and 10mg/kg dexamethasone respectively. These findings suggest that dexamethasone can exacerbate the acute cerebral edema and brain injury associated with status epilepticus.

  9. Hyperammonemia,brain edema and blood-brain barrier alterations in prehepatic portal hypertensive rats and paravrtamol intoxication

    Institute of Scientific and Technical Information of China (English)

    Camila Scorticati; Juan P. Prestifilippo; Francisco X. Eizayaga; José L. Castro; Salvador Romay; Maria A. Fernández; Abraham Lemberg; Juan C. Perazzo

    2004-01-01

    AIM: To study the blood-brain barrier integrity, brain edema,animal behavior and ammonia plasma levels in prehepatic portal hypertensive rats with and without acute liver intoxication.METHODS: Adults male Wistar rats were divided into four groups. Group Ⅰ: sham operation; Ⅱ: Prehepatic portal hypertension, produced by partial portal vein ligation; Ⅲ:Acetaminophen intoxication and Ⅳ: Prehepatic portal hypertension plus acetaminophen. Acetaminophen was administered to produce acute hepatic injury. Portal pressure, liver serum enzymes and ammonia plasma levels were determined. Brain cortex water content was registered and trypan blue was utilized to study blood brain barrier integrity. Reflexes and behavioral tests were recorded.RESULTS: Portal hypertension was significantly elevated in groups Ⅱ and Ⅳ. Liver enzymes and ammonia plasma levels were increased in groups Ⅱ, Ⅳ and Ⅳ. Prehepatic portal hypertension (group Ⅱ), acetaminophen intoxication (group Ⅲ) and both (group Ⅳ) had changes in the blood brain-barrier integrity (trypan blue) and hyperammonemia. Cortical edema was present in rats with acute hepatic injury in groups Ⅲ and Ⅳ. Behavioral test (rota rod) was altered in group Ⅳ.CONCLUSION: These results suggest the possibility of another pathway for cortical edema production because blood brain barrier was altered (vasogenic) and hyperammonemia was registered (cytotoxic). Group Ⅳ, with behavioral altered test, can be considered as a model for study at an early stage of portal-systemic encephalopathy.

  10. Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    Objective: To investigate the relationship between the changes of N-methyl-D-aspartate (NMDA) receptor activity and brain edema after injury in rats.   Methods: The brain injury models were made by using a free-falling body. The treatment model was induced by means of injecting AP5 into lateral ventricle before brain injury; water contents in brain cortex were measured with dry-wet method; and NMDA receptor activity was detected with a radio ligand binding assay.   Results: The water contents began to increase at 30 minutes and reached the peak at 6 hours after brain injury. The maximal binding (Bmax) of NMDA receptor increased significantly at 15 minutes and reached the peak at 30 minutes, then decreased gradually and had the lowest value 6 hours after brain injury. Followed the treatment with AP5, NMDA receptor activity in the injured brain showed a normal value; and the water contents were lower than that of AP5-free injury group 24 hours after brain injury.   Conclusions: It suggests that excessive activation of NMDA receptor may be one of the most important factors to induce the secondary cerebral impairments, and AP5 may protect the brain from edema after brain injury.

  11. Racking the brain: Detection of cerebral edema on postmortem computed tomography compared with forensic autopsy

    Energy Technology Data Exchange (ETDEWEB)

    Berger, Nicole [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Institute of Diagnostic and Interventional Radiology, University Hospital of Zurich, Raemistrasse 100, 8091 Zurich (Switzerland); Ampanozi, Garyfalia; Schweitzer, Wolf; Ross, Steffen G.; Gascho, Dominic [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Ruder, Thomas D. [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Institute of Diagnostic, Interventional and Pediatric Radiology, University Hospital of Bern, Freiburgstrasse, 3010 Bern (Switzerland); Thali, Michael J. [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Flach, Patricia M., E-mail: patricia.flach@irm.uzh.ch [Institute of Forensic Medicine, Virtopsy, University of Zurich, Winterthurerstrasse 190/52, 8057 Zurich (Switzerland); Institute of Diagnostic and Interventional Radiology, University Hospital of Zurich, Raemistrasse 100, 8091 Zurich (Switzerland)

    2015-04-15

    Graphical abstract: -- Highlights: •Postmortem swelling of the brain is a typical finding on PMCT and occurs concomitant with potential antemortem or agonal brain edema. •Cerebral edema despite normal postmortem swelling is indicated by narrowed temporal horns and symmetrical herniation of the cerebral tonsils on PMCT. •Cases with intoxication or asphyxia demonstrated higher deviations of the attenuation between white and gray matter (>20 Hounsfield Units) and a ratio >1.58 between the gray and white matter. •The Hounsfield measurements of the white and gray matter help to determine the cause of death in cases of intoxication or asphyxia. -- Abstract: Purpose: The purpose of this study was to compare postmortem computed tomography with forensic autopsy regarding their diagnostic reliability of differentiating between pre-existing cerebral edema and physiological postmortem brain swelling. Materials and methods: The study collective included a total of 109 cases (n = 109/200, 83 male, 26 female, mean age: 53.2 years) and were retrospectively evaluated for the following parameters (as related to the distinct age groups and causes of death): tonsillar herniation, the width of the outer and inner cerebrospinal fluid spaces and the radiodensity measurements (in Hounsfield Units) of the gray and white matter. The results were compared with the findings of subsequent autopsies as the gold standard for diagnosing cerebral edema. p-Values <0.05 were considered statistically significant. Results: Cerebellar edema (despite normal postmortem swelling) can be reliably assessed using postmortem computed tomography and is indicated by narrowed temporal horns and symmetrical herniation of the cerebellar tonsils (p < 0.001). There was a significant difference (p < 0.001) between intoxication (or asphyxia) and all other causes of death; the former causes demonstrated higher deviations of the attenuation between white and gray matter (>20 Hounsfield Units), and the gray to

  12. Ischemic Postconditioning Alleviates Brain Edema After Focal Cerebral Ischemia Reperfusion in Rats Through Down-Regulation of Aquaporin-4.

    Science.gov (United States)

    Han, Dong; Sun, Miao; He, Ping-Ping; Wen, Lu-Lu; Zhang, Hong; Feng, Juan

    2015-07-01

    Cerebral edema is a serious complication associated with cerebral ischemia/reperfusion (I/R). Aquaporin-4 (AQP4) plays a role in generating postischemic edema after reperfusion. Recently, ischemic postconditioning (Postcond) has been shown to produce neuroprotective effects and reduce brain edema in rats after cerebral I/R. It is unclear if ischemic Postcond alleviates brain edema injury through regulation of AQP4. In this study, middle cerebral artery occlusion (MCAO) was induced in rats by filament insertion for 2 h following 24-h reperfusion: ischemic Postcond treatment was performed before reperfusion in the experimental group. We used the wet-dry weight ratio and transmission electron microscopy to evaluate brain edema after 24 h of reperfusion. We used immunohistochemistry and Western blot analyses to evaluate the distribution and expression of AQP4. Ischemic Postcond significantly reduced the water content of the brain tissue and swelling of the astrocytic foot processes. AQP4 expression increased in the I/R and Postcond groups compared to the sham group, but it decreased in the Postcond group compared to the I/R group. The results of our study suggest that ischemic Postcond effectively reduces brain edema after reperfusion by inhibiting AQP4 expression. The data in this study support the use of ischemic Postcond for alleviating brain edema after cerebral I/R.

  13. Brain edema after intracerebral hemorrhage in rats: The role of inflammation

    Directory of Open Access Journals (Sweden)

    Zhang Xiangjian

    2006-01-01

    Full Text Available Background: Intracerebral hemorrhage (ICH results in secondary brain edema and injury that may lead to death and disability. ICH also causes inflammation. It is unclear whether inflammation contributes to brain edema and neuron injury or functions in repairing the brain tissue. Aims: To understand the effect of inflammation in ICH, we have carried out an investigation on the various aspects and the dynamic changes of inflammation. Settings and Design: An ICH model was generated by injecting 50 ml autologous tail artery blood stereotactically into the right caudate nucleus of 30 rats, which were randomly divided into five ICH groups. Similarly, five Sham control groups were generated by inserting the needle to the right caudate nucleus of rats. Materials and Methods: Rat behavior was evaluated over the time course (6 h, 24 h, 48 h, 72 h and 7 d in each group. The rats were then killed by administering an overdose of pentobarbital. Following the euthanasia, the brain water content, neuronal loss, glia proliferation, inflammatory infiltration and brain morphology of the rats were measured. Additionally, the expression of TNF-a,IL-6, ICAM-1, VEGF, NF-kB, C3 and CR2 was analyzed by immunohistochemistry. Statistical Analysis: The data were analyzed by student′s t test. Results: Rat brain water content increased progressively over the time course and reached its peak at 48h followed ICH. The maximum of inflammatory infiltrate (especially neutrophils and immunopositive cells of TNF-a, IL-6 and NF-kB, were at 48h. The expression of C3 and CR2 reached their peaks at 48-72h, while the expression ICAM-1 and VEGF were at maximum at 72h followed ICH. Conclusions: The results suggested that the inflammatory cytokines, complement system and VEGF may have a function in the development of the brain edema and neuron injury followed ICH.

  14. The apparent diffusion coefficient does not reflect cytotoxic edema on the uninjured side after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Hong Lu; Xiaoyan Lei

    2014-01-01

    After traumatic brain injury, vasogenic and cytotoxic edema appear sequentially on the in-volved side. Neuroimaging investigations of edema on the injured side have employed apparent diffusion coefficient measurements in diffusion tensor imaging. We investigated the changes occurring on the injured and uninjured sides using diffusion tensor imaging/apparent diffusion coefficient and histological samples in rats. We found that, on the injured side, that vasogen-ic edema appeared at 1 hour and intracellular edema appeared at 3 hours. Mixed edema was observed at 6 hours, worsening until 12-24 hours post-injury. Simultaneously, microglial cells proliferated at the trauma site. Apparent diffusion coefficient values increased at 1 hour, decreased at 6 hours, and increased at 12 hours. The uninjured side showed no significant pathological change at 1 hour after injury. Cytotoxic edema appeared at 3 hours, and vasogen-ic edema was visible at 6 hours. Cytotoxic edema persisted, but vasogenic edema tended to decrease after 12-24 hours. Despite this complex edema pattern on the uninjured side with associated pathologic changes, no significant change in apparent diffusion coefficient values was detected over the first 24 hours. Apparent diffusion coefficient values accurately detected the changes on the injured side, but did not detect the changes on the uninjured side, giving a false-negative result.

  15. Multi-fractal texture features for brain tumor and edema segmentation

    Science.gov (United States)

    Reza, S.; Iftekharuddin, K. M.

    2014-03-01

    In this work, we propose a fully automatic brain tumor and edema segmentation technique in brain magnetic resonance (MR) images. Different brain tissues are characterized using the novel texture features such as piece-wise triangular prism surface area (PTPSA), multi-fractional Brownian motion (mBm) and Gabor-like textons, along with regular intensity and intensity difference features. Classical Random Forest (RF) classifier is used to formulate the segmentation task as classification of these features in multi-modal MRIs. The segmentation performance is compared with other state-of-art works using a publicly available dataset known as Brain Tumor Segmentation (BRATS) 2012 [1]. Quantitative evaluation is done using the online evaluation tool from Kitware/MIDAS website [2]. The results show that our segmentation performance is more consistent and, on the average, outperforms other state-of-the art works in both training and challenge cases in the BRATS competition.

  16. Clinical and neuroradiological studies of eclampsia. Cerebral vasospasm and relation to the brain edema

    Energy Technology Data Exchange (ETDEWEB)

    Ito, Yasuhiro; Niwa, Hisayoshi; Ando, Tetsuo; Yasuda, Takeshi; Yanagi, Tsutomu [Nagoya Daini Red Cross Hospital, Aichi (Japan)

    1995-04-01

    Clinical and neuroradiological studies involving cerebral angiography were conducted in four patients with eclampsia. In three cases (case 1, 2 and 4), neurological focal signs, abnormal low density areas on cranial CT and T{sub 2} high intensity areas on cranial MRI disappeared within a month. But in one case (case 3), cerebral infarction occurred and right hemiparesis and aphasia persisted. Cerebral angiography in the acute phase demonstrated vasospasm in all cases and arterial occlusion in the middle cerebral artery due to vasospasm in case 3. Angiography demonstrated several types of spasms, including diffuse, peripheral and multi local. Furthermore, in some cases, diffuse vasospasms were recognized at the siphon and extracranial portions of the internal carotid artery. In one case (Case 4), segmental vasospasms were detected in the bilateral vertebral arteries. Three to four weeks later, follow-up cerebral angiography was performed in three cases. Cerebral vasospasms had partially or completely recovered. Subarachnoid hemorrhage (SAH) was excluded by lumbar puncture and neuroradiological findings in all cases. We concluded that eclampsia itself causes cerebral vasospasm and that the mechanism of vasospasm is different from that of SAH, since cerebral vasospasm occurred in the extracranial cerebral arteries. We suspected that cerebral vasospasm in eclampsia causes cerebral ischemia, which leads to cytotoxic edema and dysfunction of the blood-brain barrier (BBB) and cerebral autoregulation. With this background, brain edema, especially vasogenic edema, may easily occur and clinical symptoms of eclampsia may appear when the blood pressure rapidly increases. (author).

  17. The effects of Tanshinone IIA on blood-brain barrier and brain edema after transient middle cerebral artery occlusion in rats.

    Science.gov (United States)

    Tang, Chao; Xue, Hongli; Bai, Changlin; Fu, Rong; Wu, Anhua

    2010-12-01

    Disruption of blood-brain barrier (BBB) and edema formation play a key role in the development of neurological dysfunction after cerebral ischemia. In this study, the effects of Tanshinone IIA (Tan IIA), one of the active ingredients of Salvia miltiorrhiza root, on the BBB and brain edema after transient middle cerebral artery occlusion in rats were examined. Our study demonstrated that Tan IIA reduced brain infarct area, water content in the ischemic hemisphere. Furthermore, Tan IIA significantly decreased BBB permeability to Evans blue, suppressed the expression of intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase-9 (MMP-9), inhibited the degradation of tight junction proteins zonula occludens-1 (ZO-1) and Occludin. These results demonstrated that Tan IIA was effective for attenuating the extent of brain edema formation in response to ischemia injury in rats, partly by Tan IIA's protective effect on the BBB. Our results may have implications in the treatment of brain edema in cerebral ischemia.

  18. Rifaximin, but not growth factor 1, reduces brain edema in cirrhotic rats

    Institute of Scientific and Technical Information of China (English)

    Gemma (ò)dena; Mireia Miquel; Anna Serafín; Amparo Galan; Rosa Morillas; Ramon Planas; Ramon Bartolí

    2012-01-01

    AIM:To compare rifaximin and insulin-like growth factor (IGF)-1 treatment of hyperammonemia and brain edema in cirrhotic rats with portal occlusion.METHODS:Rats with CCl4-induced cirrhosis with ascites plus portal vein occlusion and controls were randomized into six groups:Cirrhosis; Cirrhosis + IGF-1;Cirrhosis + rifaximin; Controls; Controls + IGF-1; and Controls + rifaximin.An oral glutamine-challenge test was performed,and plasma and cerebral ammonia,glucose,bilirubin,transaminases,endotoxemia,brain water content and ileocecal cultures were measured and liver histology was assessed.RESULTS:Rifaximin treatment significantly reduced bacterial overgrowth and endotoxemia compared with cirrhosis groups,and improved some liver function parameters (bilirubin,alanine aminotransferase and aspartate aminotransferase).These effects were associated with a significant reduction in cerebral water content.Blood and cerebral ammonia levels,and area-underthe-curve values for oral glutamine-challenge tests were similar in rifaximin-treated cirrhotic rats and control group animals.By contrast,IGF-1 administration failed to improve most alterations observed in cirrhosis.CONCLUSION:By reducing gut bacterial overgrowth,only rifaximin was capable of normalizing plasma and brain ammonia and thereby abolishing low-grade brain edema,alterations associated with hepatic encephalopathy.

  19. Predictors of malignant brain edema in middle cerebral artery infarction observed on CT angiography.

    Science.gov (United States)

    Kim, Hoon; Jin, Seon Tak; Kim, Young Woo; Kim, Seong Rim; Park, Ik Seong; Jo, Kwang Wook

    2015-03-01

    Patients with middle cerebral artery (MCA) infarction accompanied by MCA occlusion with or without internal carotid artery (ICA) occlusion have a poor prognosis, as a result of brain cell damage caused by both the infarction and by space-occupying and life-threatening edema formation. Multiple treatments can reduce the likelihood of edema formation, but tend to show limited efficacy. Decompressive hemicraniectomy with duroplasty has been promising for improving functional outcomes and reducing mortality, particularly improved functional outcomes can be achieved with early decompressive surgery. Therefore, identifying patients at risk for developing fatal edema is important and should be performed as early as possible. Sixty-four patients diagnosed with major MCA infarction with MCA occlusion within 8 hours of symptom onset were retrospectively reviewed. Early clinical, laboratory, and computed tomography angiography (CTA) parameters were analyzed for malignant brain edema (MBE). Twenty of the 64 patients (31%) had MBE, and the clinical outcome was poor (3month modified Rankin Scale >2) in 95% of them. The National Institutes of Health Stroke Scale (NIHSS) score, Alberta Stroke Program Early Computed Tomography Score, Clot Burden Score, and Collateral Score (CS) showed statically significant differences in both groups. Multivariable analyses adjusted for age and sex identified the independent predictors of MBE: NIHSS score >18 (odds ratio [OR]: 4.4, 95% confidence interval [CI]: 1.2-16.0, p=0.023) and CS on CTA <2 (OR: 7.28, 95% CI: 1.7-30.3,p=0.006). Our results provide useful information for selecting patients in need of aggressive treatment such as decompressive surgery.

  20. Perforin expression by CD8 T cells is sufficient to cause fatal brain edema during experimental cerebral malaria.

    Science.gov (United States)

    Huggins, Matthew; Johnson, Holly L; Jin, Fang; N'Songo, Aurelie; Hanson, Lisa M; LaFrance, Stephanie J; Butler, Noah S; Harty, John T; Johnson, Aaron J

    2017-03-06

    Human cerebral malaria (HCM) is a serious complication of Plasmodium falciparum infection. The most severe outcomes for patients include coma, permanent neurological deficits, and death. Recently, a large-scale magnetic resonance imaging (MRI) study in humans identified brain swelling as the most prominent predictor of fatal HCM. Therefore, in this study we sought to define the mechanism controlling brain edema through the use of the murine experimental cerebral malaria (ECM) model. Specifically, we investigated the ability of CD8 T cells to initiate brain edema during ECM. We determined that areas of blood-brain barrier (BBB) permeability colocalized with a reduction of the cerebral endothelial cell tight junction proteins claudin-5 and occludin. Furthermore, through small animal MRI we analyzed edema and vascular leakage. Using gadolinium enhanced T1-weighted MRI we determined that vascular permeability is not homogeneous, but rather confined to specific regions of the brain. Our findings show that BBB permeability was localized within the brainstem, olfactory bulb, and lateral ventricle. Concurrently with the initiation of vascular permeability, T2-weighted MRI revealed edema and brain swelling. Importantly, ablation of the cytolytic effector molecule perforin fully protected against vascular permeability and edema. Furthermore, perforin production specifically by CD8 T cells was required to cause fatal edema during ECM. We propose that CD8 T cells initiate BBB breakdown through perforin mediated disruption of tight junctions. In turn, leakage from the vasculature into the parenchyma causes brain swelling and edema. This results in a breakdown of homeostatic maintenance that likely contributes to ECM pathology.

  1. Occludin and connexin 43 expression contribute to the pathogenesis of traumatic brain edema*

    Institute of Scientific and Technical Information of China (English)

    Wanyin Ren; Guojie Jing; Qin Shen; Xiaoteng Yao; Yingchao Jing; Feng Lin; Weidong Pan

    2013-01-01

    The experimental model of traumatic brain injury was established in Sprague-Dawley rats according to Feeney’s free fal ing method. The brains were harvested at 2, 6 and 24 hours, and at 3 and 5 days after injury. Changes in brain water content were determined using the wet and dry weights. Our results showed that water content of tissue significantly increased after traumatic brain injury, and reached minimum at 24 hours. Hematoxylin-eosin staining revealed pathological impairment of brain tissue at each time point after injury, particularly at 3 days, with nerve celledema, degenera-tion, and necrosis observed, and the apoptotic rate significantly increased. Immunohistochemistry and western blot analysis revealed that the expression of occludin at the injured site gradual y de-creased as injury time advanced and reached a minimum at 3 days after injury; the expression of connexin 43 gradual y increased as injury time advanced and reached a peak at 24 hours after in-jury. The experimental findings indicate that changes in occludin and connexin 43 expression were consistent with the development of brain edema, and may reflect the pathogenesis of brain injury.

  2. Minocycline-induced hypersensitivity syndrome presenting with meningitis and brain edema: a case report

    Directory of Open Access Journals (Sweden)

    Lefebvre Nicolas

    2007-05-01

    Full Text Available Background Hypersentivity Syndrome (HS may be a life-threatening condition. It frequently presents with fever, rash, eosinophilia and systemic manifestations. Mortality can be as high as 10% and is primarily due to hepatic failure. We describe what we believe to be the first case of minocycline-induced HS with accompanying lymphocytic meningitis and cerebral edema reported in the literature. Case presentation A 31-year-old HIV-positive female of African origin presented with acute fever, lymphocytic meningitis, brain edema, rash, eosinophilia, and cytolytic hepatitis. She had been started on minocycline for inflammatory acne 21 days prior to the onset of symptoms. HS was diagnosed clinically and after exclusion of infectious causes. Minocycline was withdrawn and steroids were administered from the second day after presentation because of the severity of the symptoms. All signs resolved by the seventh day and steroids were tailed off over a period of 8 months. Conclusion Clinicians should maintain a high index of suspicion for serious adverse reactions to minocycline including lymphocytic meningitis and cerebral edema among HIV-positive patients, especially if they are of African origin. Safer alternatives should be considered for treatment of acne vulgaris. Early recognition of the symptoms and prompt withdrawal of the drug are important to improve the outcome.

  3. The protective effect of HET0016 on brain edema and blood-brain barrier dysfunction after cerebral ischemia/reperfusion.

    Science.gov (United States)

    Liu, Yu; Wang, Di; Wang, Huan; Qu, Youyang; Xiao, Xingjun; Zhu, Yulan

    2014-01-28

    N-hydroxy-N-(4-butyl-2-methylphenyl) formamidine (HET0016) is a specific 20-hydroxyeicosatetraenoic acid (20-HETE) inhibitor which was first synthesized in 2001. It has been demonstrated that HET0016 reduces cerebral infarction volume in rat middle cerebral artery occlusion (MCAO) models. However, little is known about the role of HET0016 in the blood-brain barrier (BBB) dysfunction after cerebral ischemia/reperfusion (I/R) injury. The present study was designed to examine the effect of HET0016 in a MCAO and reperfusion rat model to determine whether it protects against brain edema and BBB disruption. Rats were subjected to 90 min MCAO, followed by 4, 24, 48, and 72 h reperfusion. Brain edema was measured according to the wet and dry weight method. BBB permeability based on the extravasation of Evans blue and sodium fluorescein was detected. BBB ultrastructure alterations were presented through transmission electron microscope. Superoxide production in ischemic tissue was also measured by dihydroethidium fluorescent probe. Western blot was used to analyze the expression of Claudin-5, ZO-1, MMP-9, and JNK pathway. At 24h after reperfusion, HET0016 reduced brain edema and BBB leakage. Ultrastructural damage of BBB and the increase of superoxide production were attenuated by HET0016 treatment. Western blot showed that HET0016 suppressed the activation of MMP-9 and JNK pathway but restored the expression of Claudin-5 and ZO-1. In conclusion, these results suggest that HET0016 protects BBB dysfunction after I/R by regulating the expression of MMP-9 and tight junction proteins. Furthermore, inhibition of oxidative stress and JNK pathway may be involved in this protecting effect.

  4. Synthesis and evaluation of the anti-inflammatory effects of niflumic acid lipophilic prodrugs in brain edema.

    Science.gov (United States)

    el Kihel, L; Bourass, J; Richomme, P; Petit, J Y; Letourneux, Y

    1996-11-01

    Five new lipophilic prodrugs of the non-steroidal anti-inflammatory drug, niflumic acid (Nifluril, CAS 4394-00-7), were synthetized and evaluated on the experimental brain edema (injection of phospholipase A2). The effect of these drugs in comparison with dexamethasone which elicits a marked effect on clinical and experimental brain edema was evaluated. Niflumic acid was vectorised by cholesterol, hexadecanol and by three 1,3-diacylglycerols. The anti-inflammatory activity of these compounds on experimental brain edema was evaluated by determination of the prostaglandin E2 (PGE2) brain tissue concentration. Niflumic acid reduced the prostaglandin E2 production more significantly than dexamethasone. Niflumic acid prodrug forms (1,3-dihexadecanoyl-2-[2-[3-(trifluoromethyl)anilino]nicotinoyl] glycerol and 1,3-dihexadecanoyl-2-[2-[3-(trifluoromethyl)anilino]nicotinoyloxybuta noyl] glycerol also showed a marked anti-inflammatory activity at low concentrations.

  5. Amelioration of cold injury-induced cortical brain edema formation by selective endothelin ETB receptor antagonists in mice.

    Directory of Open Access Journals (Sweden)

    Shotaro Michinaga

    Full Text Available Brain edema is a potentially fatal pathological condition that often occurs in stroke and head trauma. Following brain insults, endothelins (ETs are increased and promote several pathophysiological responses. This study examined the effects of ETB antagonists on brain edema formation and disruption of the blood-brain barrier in a mouse cold injury model (Five- to six-week-old male ddY mice. Cold injury increased the water content of the injured cerebrum, and promoted extravasation of both Evans blue and endogenous albumin. In the injury area, expression of prepro-ET-1 mRNA and ET-1 peptide increased. Intracerebroventricular (ICV administration of BQ788 (ETB antagonist, IRL-2500 (ETB antagonist, or FR139317 (ETA antagonist prior to cold injury significantly attenuated the increase in brain water content. Bolus administration of BQ788, IRL-2500, or FR139317 also inhibited the cold injury-induced extravasation of Evans blue and albumin. Repeated administration of BQ788 and IRL-2500 beginning at 24 h after cold injury attenuated both the increase in brain water content and extravasation of markers. In contrast, FR139317 had no effect on edema formation when administrated after cold injury. Cold injury stimulated induction of glial fibrillary acidic protein-positive reactive astrocytes in the injured cerebrum. Induction of reactive astrocytes after cold injury was attenuated by ICV administration of BQ788 or IRL-2500. These results suggest that ETB receptor antagonists may be an effective approach to ameliorate brain edema formation following brain insults.

  6. Pentoxifylline attenuates TNF-α protein levels and brain edema following temporary focal cerebral ischemia in rats.

    Science.gov (United States)

    Vakili, Abedin; Mojarrad, Somye; Akhavan, Maziar Mohammad; Rashidy-Pour, Ali

    2011-03-04

    Cerebral edema is the most common cause of neurological deterioration and mortality during acute ischemic stroke. Despite the clinical importance of cerebral ischemia, the underlying mechanisms remain poorly understood. Recent studies suggest a role for TNF-α in the brain edema formation. To further investigate whether TNF-α would play a role in brain edema formation, we examined the effects of pentoxifylline (PTX, an inhibitor of TNF-α synthesis) on the brain edema and TNF-α levels in a model of transient focal cerebral ischemia. The right middle cerebral artery (MCA) of rats was occluded for 60 min using the intraluminal filament method. The animals received PTX (60 mg/kg) immediately, 1, 3, or 6h post-ischemic induction. Twenty-four hours after induction of ischemic injury, permeability of the blood-brain barrier (BBB) and brain edema were determined by in situ brain perfusion of Evans Blue (EB) and wet-to-dry weight ratio, respectively. TNF-α protein levels in ischemic cortex were also measured at 1, 4, and 24h after the beginning of an ischemic stroke by using an enzyme-linked immunosorbent assay method. The administration of PTX up to 6h after occlusion of the MCA significantly reduced the brain edema. Moreover, PTX significantly reduced the concentration of TNF-α in ischemic brain cortex up to 4h post-transient focal stroke (Pedema in a model of transient focal cerebral ischemia. The beneficial effects of PTX may be mediated, at least in part, through a decline in TNF-α production and BBB breakdown.

  7. Near-infrared spectroscopy technique to evaluate the effects of drugs in treating traumatic brain edema

    Energy Technology Data Exchange (ETDEWEB)

    Xie, J; Qian, Z; Li, W; Hu, G [Department of Biomedical Engineering, Nanjing University of Aeronautics and Astronautics, 29 Yudao Street, Nanjing 210016 (China); Yang, T, E-mail: zhiyu@nuaa.edu.cn [School of Clinical Medicine, Southeast University, 87 Dingjiaqiao Road, Nanjing 210009 (China)

    2011-01-01

    The aim of this study was to evaluate the effects of several drugs in treating traumatic brain edema (TBE) following traumatic brain injury (TBI) using near-infrared spectroscopy (NIRs) technology. Rats with TBE models were given hypertonic saline (HS), mannitol and mannitol+HS respectively for different groups. Light scattering properties of rat's local cortex was measured by NIRs within the wavelength range from 700 to 850 nm. TBE models were built in rats' left brains. The scattering properties of the right and left target corresponding to the position of normal and TBE tissue were measured and recorded in vivo and real-time by a bifurcated needle probe. The brain water contents (BWC) were measured by the wet and dry weight method after injury and treatment hours 1, 6, 24, 72 and 120. A marked linear relationship was observed between reduced scattering coefficient ({mu}{sub s}') and BWC. By recording {mu}{sub s}' of rats' brains, the entire progressions of effects of several drugs were observed. The result may suggest that the NIRs techniques have a potential for assessing effects in vivo and real-time on treatment of the brain injury.

  8. Computer aided detection of tumor and edema in brain FLAIR magnetic resonance image using ANN

    Science.gov (United States)

    Pradhan, Nandita; Sinha, A. K.

    2008-03-01

    This paper presents an efficient region based segmentation technique for detecting pathological tissues (Tumor & Edema) of brain using fluid attenuated inversion recovery (FLAIR) magnetic resonance (MR) images. This work segments FLAIR brain images for normal and pathological tissues based on statistical features and wavelet transform coefficients using k-means algorithm. The image is divided into small blocks of 4×4 pixels. The k-means algorithm is used to cluster the image based on the feature vectors of blocks forming different classes representing different regions in the whole image. With the knowledge of the feature vectors of different segmented regions, supervised technique is used to train Artificial Neural Network using fuzzy back propagation algorithm (FBPA). Segmentation for detecting healthy tissues and tumors has been reported by several researchers by using conventional MRI sequences like T1, T2 and PD weighted sequences. This work successfully presents segmentation of healthy and pathological tissues (both Tumors and Edema) using FLAIR images. At the end pseudo coloring of segmented and classified regions are done for better human visualization.

  9. Purinergic receptor stimulation reduces cytotoxic edema and brain infarcts in mouse induced by photothrombosis by energizing glial mitochondria.

    Directory of Open Access Journals (Sweden)

    Wei Zheng

    Full Text Available Treatments to improve the neurological outcome of edema and cerebral ischemic stroke are severely limited. Here, we present the first in vivo single cell images of cortical mouse astrocytes documenting the impact of single vessel photothrombosis on cytotoxic edema and cerebral infarcts. The volume of astrocytes expressing green fluorescent protein (GFP increased by over 600% within 3 hours of ischemia. The subsequent growth of cerebral infarcts was easily followed as the loss of GFP fluorescence as astrocytes lysed. Cytotoxic edema and the magnitude of ischemic lesions were significantly reduced by treatment with the purinergic ligand 2-methylthioladenosine 5' diphosphate (2-MeSADP, an agonist with high specificity for the purinergic receptor type 1 isoform (P2Y(1R. At 24 hours, cytotoxic edema in astrocytes was still apparent at the penumbra and preceded the cell lysis that defined the infarct. Delayed 2MeSADP treatment, 24 hours after the initial thrombosis, also significantly reduced cytotoxic edema and the continued growth of the brain infarction. Pharmacological and genetic evidence are presented indicating that 2MeSADP protection is mediated by enhanced astrocyte mitochondrial metabolism via increased inositol trisphosphate (IP(3-dependent Ca(2+ release. We suggest that mitochondria play a critical role in astrocyte energy metabolism in the penumbra of ischemic lesions, where low ATP levels are widely accepted to be responsible for cytotoxic edema. Enhancement of this energy source could have similar protective benefits for a wide range of brain injuries.

  10. Mast cell blocking reduces brain edema and hematoma volume and improves outcome after experimental intracerebral hemorrhage.

    Science.gov (United States)

    Strbian, Daniel; Tatlisumak, Turgut; Ramadan, Usama Abo; Lindsberg, Perttu J

    2007-04-01

    Intracerebral hemorrhage (ICH) is associated with high mortality and disability, and there is no widely approved clinical therapy. Poor outcome after ICH results mostly from a mass effect owing to enlargement of the hematoma and brain swelling, leading to displacement and disruption of brain structures. Cerebral mast cells (MC) are resident inflammatory cells that are located perivascularly and contain potent vasoactive, proteolytic, and fibrinolytic substances. We previously found pharmacological MC stabilization and genetic MC deficiency to be associated with up to 50% reduction of postischemic brain swelling in rats. Here, we studied the role of MC and MC stabilization in ICH using in vivo magnetic resonance imaging and ex vivo digital imaging for calculating brain edema and hematoma volume. In a rat ICH model of autologous blood injection into the basal ganglia, four groups of Wistar rats received either saline or sodium cromoglycate (MC stabilizer, two groups) or compound 48/80 (MC degranulator). Evaluated 24 h later, MC stabilization had resulted in highly significantly better neurologic scores (Pbrain swelling (Pbrain swelling (P<0.05), and smaller hematoma growth (P<0.05) than WT. The role of MC deserves a close evaluation as a potential target in the development of novel forms of ICH therapy.

  11. Liposome-encapsulated hemoglobin alleviates brain edema after permanent occlusion of the middle cerebral artery in rats.

    Science.gov (United States)

    Kawaguchi, Akira T; Kurita, Daisaku; Furuya, Hiroyuki; Yamano, Mariko; Ogata, Yoshitaka; Haida, Munetaka

    2009-02-01

    Liposome-encapsulated hemoglobin (LEH) was proven to be protective in cerebral ischemia/reperfusion injury. The present study evaluated LEH in a rat model of permanent middle cerebral artery (MCA) occlusion to clarify its effect during ischemia and reperfusion. Five minutes after thread occlusion of the MCA, rats were infused with 10 mL/kg of LEH (LEH, n = 13), and compared with normal controls (n = 11). Additional animals received the same MCA occlusion with no treatment (CT, n = 11), saline (saline, n = 10), empty liposome solution (EL, n = 13), or washed red blood cells (RBC, n = 7). Severity of brain edema was determined 24 h later by signal strength in T2-weighted magnetic resonance imaging of the cortex, striatum, hippocampus, and pyriform lobe. The results showed that brain edema/infarction observed in any vehicle-infused control was significantly more severe than in LEH-treated rats. There was a tendency toward aggravated edema in rats receiving ELs. LEH infusion at a dose of 10 mL/kg significantly reduced edema formation as compared to other treatments in a wide area of the brain 24 h after permanent occlusion of the MCA. Low oncotic pressure of EL and LEH solution (vehicle solution) appeared to cause nonsignificant aggravation of edema and reduced protective effects of LEH.

  12. Effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    陈志刚; 卢亦成; 朱诚; 张光霁; 丁学华; 江基尧

    2003-01-01

    Objective: To observe the effects of ganglioside GM1 on reduction of brain edema and amelioration of cerebral metabolism after traumatic brain injury (TBI).Methods: An acute experimental closed TBI model in rats was induced by a fluid-percussion brain injury model. At five and sixty minutes after TBI, the animals were intraperitoneally injected by ganglioside GM1 (30 mg/kg) or the same volume of saline. At the 6th hour after TBI, effects of ganglioside GM1 or saline on changes of mean arterial pressure (MAP), contents of water, lactic acid (LA) and lipid peroxidation (LPO) in the injured cerebral tissues were observed.Results: After TBI, MAP decreased and contents of water, LA and LPO increased in brain injury group; however, MAP was back to normal levels and contents of water, LA and LPO decreased in ganglioside GM1 treated group, compared with those in brain injury group (P0.05) was observed.Conclusions: Ganglioside GM1 does have obvious neuroprotective effect on early TBI.

  13. Bilateral sphenoid wing metastases of prostate cancer presenting with extensive brain edema.

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    Lindsberg, P J; Tatlisumak, T; Tienari, J; Brander, A

    1999-05-01

    A 76-year-old man insidiously developed diffuse neurological symptoms: cognitive decline, dysphagia, dysphasia and mental disturbance. Computed tomography of the cranium revealed widespread bilateral brain edema and symmetrical bilateral sphenoid wing hyperostosis. Adjacent to the hyperostosis that resembled skull base meningiomas, two separate parenchymatous temporal lobe lesions enhancing with contrast medium were observed. The patient had earlier been diagnosed to have prostatic carcinoma. Dexamethasone therapy resulted in discontinuation of the neurological symptoms. The diagnosis of metastasized adenocarcinoma of the prostate was confirmed histologically on autopsy after a sudden death from pneumonia. Intracranial metastases of prostate cancer may have a predilection site at the sphenoid wing, and can mimic a skull base meningioma. Intracranial spread of prostatic adenocarcinoma should be considered in elderly men as a treatable cause of gradual neurological deterioration, especially if cranial malignancy or hyperostosis is found.

  14. Effect of Xingnaojing injection on cerebral edema and blood-brain barrier in rats following traumatic brain injury

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    XU Miao; SU Wei; XU Qiu-ping; HUANG Wei-dong

    2010-01-01

    Objective:To explore the effects of Xingnaojing injection on cerebral edema and blood-brain barrier (BBB) in rats following traumatic brain injury (TBI).Methods: A total of 108 adult male Sprague-Dawley rats were used as subjects and randomly assigned to three groups:sham-operation,TBI and Xingnaojing injection was set up by the improved device of Feeney's weightcontent and BBB permeability expressed as Evans blue content were measured at 1, 3, 5 and 7 days after surgery.Results: In sham-operation group, brain water content and Evans blue content in brain tissue were 78.97%±1.22%and 5.13μg±0.71μg. Following TBI, water content in brain tissue was increased significantly at 1, 3, 5 and 7 days (83.49%±0.54%, 82.74%±0.72%, 80.22%±0.68%, 79.21%±0.60%), being significantly higher than that in sham operation group (P<0.05). Evans blue content was increased in TBI group (16.54 μg±0.60 μg, 14.92μg±0.71μg, 12.44 μg ±0.92μg, 10.14μg±0.52 μg) as compared with sham-operation group(P<0.05). After treatment with Xingnaojing injection, brain water content decreased as compared with TBI group (81.91%±1.04%, 80.38%±0.72%, 79.54%±0.58%,78.60%±0.77%, P<0.05). Xingnaojing injection also reduced the leakage of BBB as compared with TBI group (15.11 μg± 0.63 μg, 13.62 μg±0.85μg, 10.06 μg±0.67 μg, 9.54 μg±0.41 μg,P<0.05).Conclusion: Xingnaojing injection could alleviate cerebral edema following TBI via reducing permeability ofBBB.

  15. Protection of Vascular Endothelial Growth Factor to Brain Edema Following Intracerebral Hemorrhage and Its Involved Mechanisms: Effect of Aquaporin-4.

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    Heling Chu

    Full Text Available Vascular endothelial growth factor (VEGF has protective effects on many neurological diseases. However, whether VEGF acts on brain edema following intracerebral hemorrhage (ICH is largely unknown. Our previous study has shown aquaporin-4 (AQP4 plays an important role in brain edema elimination following ICH. Meanwhile, there is close relationship between VEGF and AQP4. In this study, we aimed to test effects of VEGF on brain edema following ICH and examine whether they were AQP4 dependent. Recombinant human VEGF165 (rhVEGF165 was injected intracerebroventricularly 1 d after ICH induced by microinjecting autologous whole blood into striatum. We detected perihemotomal AQP4 protein expression, then examined the effects of rhVEGF165 on perihemotomal brain edema at 1 d, 3 d, and 7 d after injection in wild type (AQP4(+/+ and AQP4 knock-out (AQP4(-/- mice. Furthermore, we assessed the possible signal transduction pathways activated by VEGF to regulate AQP4 expression via astrocyte cultures. We found perihemotomal AQP4 protein expression was highly increased by rhVEGF165. RhVEGF165 alleviated perihemotomal brain edema in AQP4(+/+ mice at each time point, but had no effect on AQP4(-/- mice. Perihemotomal EB extravasation was increased by rhVEGF165 in AQP4(-/- mice, but not AQP4(+/+ mice. RhVEGF165 reduced neurological deficits and increased Nissl's staining cells surrounding hemotoma in both types of mice and these effects were related to AQP4. RhVEGF165 up-regulated phospharylation of C-Jun amino-terminal kinase (p-JNK and extracellular signal-regulated kinase (p-ERK and AQP4 protein in cultured astrocytes. The latter was inhibited by JNK and ERK inhibitors. In conclusion, VEGF reduces neurological deficits, brain edema, and neuronal death surrounding hemotoma but has no influence on BBB permeability. These effects are closely related to AQP4 up-regulation, possibly through activating JNK and ERK pathways. The current study may present new insights to

  16. Lycium barbarum extracts protect the brain from blood-brain barrier disruption and cerebral edema in experimental stroke.

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    Di Yang

    Full Text Available BACKGROUND AND PURPOSE: Ischemic stroke is a destructive cerebrovascular disease and a leading cause of death. Yet, no ideal neuroprotective agents are available, leaving prevention an attractive alternative. The extracts from the fruits of Lycium barbarum (LBP, a Chinese anti-aging medicine and food supplement, showed neuroprotective function in the retina when given prophylactically. We aim to evaluate the protective effects of LBP pre-treatment in an experimental stroke model. METHODS: C57BL/6N male mice were first fed with either vehicle (PBS or LBP (1 or 10 mg/kg daily for 7 days. Mice were then subjected to 2-hour transient middle cerebral artery occlusion (MCAO by the intraluminal method followed by 22-hour reperfusion upon filament removal. Mice were evaluated for neurological deficits just before sacrifice. Brains were harvested for infarct size estimation, water content measurement, immunohistochemical analysis, and Western blot experiments. Evans blue (EB extravasation was determined to assess blood-brain barrier (BBB disruption after MCAO. RESULTS: LBP pre-treatment significantly improved neurological deficits as well as decreased infarct size, hemispheric swelling, and water content. Fewer apoptotic cells were identified in LBP-treated brains by TUNEL assay. Reduced EB extravasation, fewer IgG-leaky vessels, and up-regulation of occludin expression were also observed in LBP-treated brains. Moreover, immunoreactivity for aquaporin-4 and glial fibrillary acidic protein were significantly decreased in LBP-treated brains. CONCLUSIONS: Seven-day oral LBP pre-treatment effectively improved neurological deficits, decreased infarct size and cerebral edema as well as protected the brain from BBB disruption, aquaporin-4 up-regulation, and glial activation. The present study suggests that LBP may be used as a prophylactic neuroprotectant in patients at high risk for ischemic stroke.

  17. Estrogen provides neuroprotection against brain edema and blood brain barrier disruption through both estrogen receptors α and β following traumatic brain injury

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    Vida Naderi

    2015-02-01

    Full Text Available Objective(s:Estrogen (E2 has neuroprotective effects on blood-brain-barrier (BBB after traumatic brain injury (TBI. In order to investigate the roles of estrogen receptors (ERs in these effects, ER-α antagonist (MPP and, ER-β antagonist (PHTPP, or non-selective estrogen receptors antagonist (ICI 182780 were administered. Materials and Methods: Ovariectomized rats were divided into 10 groups, as follows: Sham, TBI, E2, oil, MPP+E2, PHTPP+E2, MPP+PHTPP+E2, ICI+E2, MPP, and DMSO. E2 (33.3 µg/Kg or oil were administered 30 min after TBI. 1 dose (150 µg/Kg of each of MPP, PHTPP, and (4 mg/kg ICI182780 was injected two times, 24 hr apart, before TBI and estrogen treatment. BBB disruption (Evans blue content and brain edema (brain water content evaluated 5 hr and 24 hr after the TBI were evaluated, respectively. Results: The results showed that E2 reduced brain edema after TBI compared to vehicle (P

  18. Neuroprotective effects of nimodipine and MK-801 on acute infectious brain edema induced by injection of pertussis bacilli to neocortex of rats

    Institute of Scientific and Technical Information of China (English)

    陈立华; 刘丽旭; 杨于嘉; 刘运生; 曹美鸿

    2003-01-01

    Objective: To explore the mechanism and type of acute infectious brain edema induced by injection of pertussis bacilli (PB) in rat neocortex, to study the neuroprotective effect of non-competitive antagonist of N-methl-D-aspartate ( NMDA ) receptor ( MK-801 ) and antagonist of Ca2+ channels ( nimodipine )on brain edema, and to investigate the relationship between percentage of water content and cytosolic free calcium concentration ([Ca2+]i) in synaptosomes or content of Evans Blue (EB).Methods: 95 SD rats were randomly divided into five groups, ie, normal control group, sham-operated control group, PB group, nimodipine treatment group and MK-801 pretreatment group. The acute infectious brain edema was induced by injection of PB into the rats. Quantitative measurements of water content and the concentration of EB were performed. [Ca2+]i was determined in calcium fluorescent indication Fura-2/AM loaded neuronal synaptosome with a spectrofluorophotometer. To observe the effect of MK-801 and nimodipine, we administered MK-801 48 hours and 24 hours before the injection of PB in MK-801 pretreatment group, and nimodipine after the injection of PB in nimodipine treatment group. The specific binding of NMDA receptor was measured with [3H]-MK-801 in the neuronal membrane of cerebral cortex. Results: The levels of water content and EB content of brain tissues, and [Ca2+]i in the neuronal synaptosomes increased more significantly in the PB-injected cerebral hemisphere in the PB group than those of normal control group and sham-operated control group (P0.05). Conclusions: The changes in the permeability of blood-brain barrier (BBB) and Ca2+-overload may participate in the pathogenesis of infectious brain edema. Treatment with nimodipine can dramatically reduce the damage of brain edema and demonstrate neuroprotective effect on brain edema by inhibiting the excess of Ca2+ influx and reducing the permeability of BBB. MK-801 pretreatment may inhibit the delayed Ca2+ influx into

  19. Lack of functional P2X7 receptor aggravates brain edema development after middle cerebral artery occlusion.

    Science.gov (United States)

    Kaiser, Melanie; Penk, Anja; Franke, Heike; Krügel, Ute; Nörenberg, Wolfgang; Huster, Daniel; Schaefer, Michael

    2016-09-01

    Effective therapeutic measures against the development of brain edema, a life-threatening complication of cerebral ischemia, are necessary to improve the functional outcome for the patient. Here, we identified a beneficial role of purinergic receptor P2X7 activation in acute ischemic stroke. Involvement of P2X7 in the development of neurological deficits, infarct size, brain edema, and glial responses after ischemic cerebral infarction has been analyzed. Neurologic evaluation, magnetic resonance imaging, and immunofluorescence assays were used to characterize the receptor's effect on the disease progress during 72 h after transient middle cerebral artery occlusion (tMCAO). Sham-operated animals were included in all experiments for control purposes. We found P2X7-deficient mice to develop a more prominent brain edema with a trend towards more severe neurological deficits 24 h after tMCAO. Infarct sizes, T2 times, and apparent diffusion coefficients did not differ significantly between wild-type and P2X7(-/-) animals. Our results show a characteristic spatial distribution of reactive glia cells with strongly attenuated microglia activation in P2X7(-/-) mice 72 h after tMCAO. Our data indicate that P2X7 exerts a role in limiting the early edema formation, possibly by modulating glial responses, and supports later microglia activation.

  20. THE EFFECT OF FLUOROCARBON ARTIFICIAL BLOOD (FC-34 IN ACUTE VASOGENIC BRAIN EDEMA

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    M NEEMATBAKHSH

    2000-03-01

    Full Text Available Background. Oxygen transport to tissue after an acute ischemia is strongly important. Fluorocarbon liquids are able to facilitated the oxygen transport. An animal experiment was designed to study the effect of FC-34 in acute brain ischemia. Methods. The left common carotid arteries were ligated in three groups of anesthetized animals for 30 minutes to obtain acute brain edema. The animals were subjected to received 15 ml/kg saline (group 1, 10% monitol (group 2 or FC-43 (group 3. All animals were recovered, and they monitored for two weeks. The electrolytes, BUN, and creatinine were measured before (all animals and after two weeks (survived animals. Pathological investigation was obtained by light and electron microscope via pathological process. Findings. The group 1 animals were died during first five days, but one and four animals were survived by two weeks in groups 2 & 3 respectively (P < 0.05. The pathological determinations indicate less cellular damages in group 3. No significant differences were detected in potassium, calcium, BUN, and creatinine before and after the experiment. Conclusion. The particle size and oxygen solubility in FC-43 is the major factors for better oxygen transport in ischem

  1. Brain edema formation correlates with perfusion deficit during the first six hours after experimental subarachnoid hemorrhage in rats

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    Westermaier Thomas

    2012-07-01

    Full Text Available Abstract Background Severe brain edema is observed in a number of patients suffering from subarachnoid hemorrhage (SAH. Little is known about its pathogenesis and time-course in the first hours after SAH. This study was performed to investigate the development of brain edema and its correlation with brain perfusion after experimental SAH. Methods Male Sprague–Dawley rats, randomly assigned to one of six groups (n = 8, were subjected to SAH using the endovascular filament model or underwent a sham operation. Animals were sacrificed 15, 30, 60, 180 or 360 minutes after SAH. Intracranial pressure (ICP, mean arterial blood pressure (MABP, cerebral perfusion pressure (CPP and bilateral local cerebral blood flow (LCBF were continuously measured. Brain water content (BWC was determined by the wet/dry-weight method. Results After SAH, CPP and LCBF rapidly decreased. The decline of LCBF markedly exceeded the decline of CPP and persisted until the end of the observation period. BWC continuously increased. A significant correlation was observed between the BWC and the extent of the perfusion deficit in animals sacrificed after 180 and 360 minutes. Conclusions The significant correlation with the perfusion deficit after SAH suggests that the development of brain edema is related to the extent of ischemia and acute vasoconstriction in the first hours after SAH.

  2. Electron microscopic features of brain edema in rodent cerebral malaria in relation to glial fibrillary acidic protein expression.

    Science.gov (United States)

    Ampawong, Sumate; Chaisri, Urai; Viriyavejakul, Parnpen; Nontprasert, Apichart; Grau, Georges E; Pongponratn, Emsri

    2014-01-01

    The mechanisms leading to cerebral malaria (CM) are not completely understood. Brain edema has been suggested as having an important role in experimental CM. In this study, CBA/CaH mice were infected with Plasmodium berghei ANKA blood-stage and when typical symptoms of CM developed on day 7, brain tissues were processed for electron-microscopic and immunohistochemical studies. The study demonstrated ultrastructural hallmarks of cerebral edema by perivascular edema and astroglial dilatation confirming existing evidence of vasogenic and cytogenic edema. This correlates closely with the clinical features of CM. An adaptive response of astrocytic activity, represented by increasing glial fibrillary acidic protein (GFAP) expression in the perivascular area and increasing numbers of large astrocyte clusters were predominately found in the CM mice. The presence of multivesicular and lamellar bodies indicates the severity of cerebral damage in experimental CM. Congestion of the microvessels with occluded white blood cells (WBCs), parasitized red blood cells (PRBCs) and platelets is also a crucial covariate role for CM pathogenesis.

  3. Quantitation of brain edema and localisation of aquaporin 4 expression in relation to susceptibility to experimental cerebral malaria.

    Science.gov (United States)

    Ampawong, Sumate; Combes, Valéry; Hunt, Nicholas H; Radford, Jane; Chan-Ling, Tailoi; Pongponratn, Emsri; Grau, Georges E R

    2011-08-15

    The pathogenic mechanisms underlying the occurrence of cerebral malaria (CM) are still incompletely understood but, clearly, cerebral complications may result from concomitant microvessel obstruction and inflammation. The extent to which brain edema contributes to pathology has not been investigated. Using the model of P. berghei ANKA infection, we compared brain microvessel morphology of CM-susceptible and CM-resistant mice. By quantitative planimetry, we provide evidence that CM is characterized by enlarged perivascular spaces (PVS). We show a dramatic aquaporin 4 (AQP4) upregulation, selectively at the level of astrocytic foot processes, in both CM and non-CM disease, but significantly more pronounced in mice with malarial-induced neurological syndrome. This suggests that a threshold of AQP4 expression is needed to lead to neurovascular pathology, a view that is supported by significantly higher levels in mice with clinically overt CM. Numbers of intravascular leukocytes significantly correlated with both PVS enlargement and AQP4 overexpression. Thus, brain edema could be a contributing factor in CM pathogenesis and AQP4, specifically in its astrocytic location, a key molecule in this mechanism. Since experimental CM is associated with substantial brain edema, it models paediatric CM better than the adult syndrome and it is tempting to evaluate AQP4 in the former context. If AQP4 changes are confirmed in human CM, it may represent a novel target for therapeutic intervention.

  4. Reduced brain edema and infarct volume in aquaporin-4 deficient mice after transient focal cerebral ischemia.

    Science.gov (United States)

    Yao, Xiaoming; Derugin, Nikita; Manley, Geoffrey T; Verkman, A S

    2015-01-01

    Aquaporin-4 (AQP4) is a water channel expressed in astrocyte end-feet lining the blood-brain barrier. AQP4 deletion in mice is associated with improved outcomes in global cerebral ischemia produced by transient carotid artery occlusion, and focal cerebral ischemia produced by permanent middle cerebral artery occlusion (MCAO). Here, we investigated the consequences of 1-h transient MCAO produced by intraluminal suture blockade followed by 23 h of reperfusion. In nine AQP4(+/+) and nine AQP4(-/-) mice, infarct volume was significantly reduced by an average of 39 ± 4% at 24h in AQP4(-/-) mice, cerebral hemispheric edema was reduced by 23 ± 3%, and Evans Blue extravasation was reduced by 31 ± 2% (mean ± SEM). Diffusion-weighted magnetic resonance imaging showed greatest reduction in apparent diffusion coefficient around the occlusion site after reperfusion, with remarkably lesser reduction in AQP4(-/-) mice. The reduced infarct volume in AQP4(-/-) mice following transient MCAO supports the potential utility of therapeutic AQP4 inhibition in stroke.

  5. Brain edema and intracranial hypertension in fulminant hepatic failure: Pathophysiology and management

    Institute of Scientific and Technical Information of China (English)

    Olivier Detry; Arnaud De Roover; Pierre Honoré; Michel Meurisse

    2006-01-01

    Intracranial hypertension is a major cause of morbidity and mortality of patients suffering from fulminant hepatic failure. The etiology of this intracranial hypertension is not fully determined, and is probably multifactorial, combining a cytotoxic brain edema due to the astrocytic accumulation of glutamine, and an increase in cerebral blood volume and cerebral blood flow, in part due to inflammation, to glutamine and to toxic products of the diseased liver. Validated methods to control intracranial hypertension in fulminant hepatic failure patients mainly include mannitol, hypertonic saline, indomethacin, thiopental, and hyperventilation.However all these measures are often not sufficient in absence of liver transplantation, the only curative treatment of intracranial hypertension in fulminant hepatic failure to date. Induced moderate hypothermia seems very promising in this setting, but has to be validated by a controlled, randomized study. Artificial liver support systems have been under investigation for many decades. The bioartificial liver, based on both detoxification and swine liver cells, has shown some efficacy on reduction of intracranial pressure but did not show survival benefit in a controlled, randomized study.The Molecular Adsorbents Recirculating System has shown some efficacy in decreasing intracranial pressure in an animal model of liver failure, but has still to be evaluated in a phase Ⅲ trial.

  6. Attenuation of Acute Phase Injury in Rat Intracranial Hemorrhage by Cerebrolysin that Inhibits Brain Edema and Inflammatory Response.

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    Yang, Yang; Zhang, Yan; Wang, Zhaotao; Wang, Shanshan; Gao, Mou; Xu, Ruxiang; Liang, Chunyang; Zhang, Hongtian

    2016-04-01

    The outcome of intracerebral hemorrhage (ICH) is mainly determined by the volume of the hemorrhage core and the secondary brain damage to penumbral tissues due to brain swelling, microcirculation disturbance and inflammation. The present study aims to investigate the protective effects of cerebrolysin on brain edema and inhibition of the inflammation response surrounding the hematoma core in the acute stage after ICH. The ICH model was induced by administration of type VII bacterial collagenase into the stratum of adult rats, which were then randomly divided into three groups: ICH + saline; ICH + Cerebrolysin (5 ml/kg) and sham. Cerebrolysin or saline was administered intraperitoneally 1 h post surgery. Neurological scores, extent of brain edema content and Evans blue dye extravasation were recorded. The levels of pro-inflammatory factors (IL-1β, TNF-α and IL-6) were assayed by Real-time PCR and Elisa kits. Aquaporin-4 (AQP4) and tight junction proteins (TJPs; claudin-5, occludin and zonula occluden-1) expression were measured at multiple time points. The morphological and intercellular changes were characterized by Electron microscopy. It is found that cerebrolysin (5 ml/kg) improved the neurological behavior and reduced the ipsilateral brain water content and Evans blue dye extravasation. After cerebrolysin treated, the levels of pro-inflammatory factors and AQP4 in the peri-hematomal areas were markedly reduced and were accompanied with higher expression of TJPs. Electron microscopy showed the astrocytic swelling and concentrated chromatin in the ICH group and confirmed the cell junction changes. Thus, early cerebrolysin treatment ameliorates secondary injury after ICH and promotes behavioral performance during the acute phase by reducing brain edema, inflammatory response, and blood-brain barrier permeability.

  7. Minocycline effects on cerebral edema: relations with inflammatory and oxidative stress markers following traumatic brain injury in mice.

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    Homsi, Shadi; Federico, Fabiola; Croci, Nicole; Palmier, Bruno; Plotkine, Michel; Marchand-Leroux, Catherine; Jafarian-Tehrani, Mehrnaz

    2009-09-29

    One of the severe complications following traumatic brain injury (TBI) is cerebral edema and its effective treatment is of great interest to prevent further brain damage. This study investigated the effects of minocycline, known for its anti-inflammatory properties, on cerebral edema and its respective inflammatory markers by comparing different dose regimens, on oxidative stress and on neurological dysfunction following TBI. The weight drop model was used to induce TBI in mice. The brain water content was measured to evaluate cerebral edema. Inflammatory markers were detected by ELISA (IL-1beta), zymography and Western blot (MMP-9). The oxidative stress marker (glutathione levels) and neurological function were measured by Griffith technique and string test, respectively. Minocycline was administered i.p. once (5 min), twice (5 min and 3 h) or triple (5 min, 3 h and 9 h) following TBI. The first dose of minocycline only varied (45 or 90 mg/kg), whereas the following doses were all at 45 mg/kg. The single and double administrations of minocycline reduced the increase of inflammatory markers at 6 h post-TBI. Minocycline also reduced cerebral edema at this time point, only after double administration and at the high dose regimen, although with no effect on the TBI-induced oxidized glutathione increase. The anti-edematous effect of minocycline persisted up to 24 h, upon a triple administration, and accompanied by a neurological recovery. In conclusion, we reported an anti-edematous effect of minocycline after TBI in mice according to a specific treatment regimen. These findings emphasize that the beneficial effects of minocycline depend on the treatment regimen following a brain injury.

  8. Inhibition of Myosin light-chain kinase attenuates cerebral edema after traumatic brain injury in postnatal mice.

    Science.gov (United States)

    Rossi, Janet L; Todd, Tracey; Bazan, Nicolas G; Belayev, Ludmila

    2013-10-01

    Traumatic brain injury (TBI) in children less than 8 years of age leads to decline in intelligence and executive functioning. Neurological outcomes after TBI correlate to development of cerebral edema, which affect survival rates after TBI. It has been shown that myosin light-chain kinase (MLCK) increases cerebral edema and that pretreatment with an MLCK inhibitor (ML-7) reduces cerebral edema. The aim of this study was to determine whether inhibition of MLCK after TBI in postnatal day 24 (PND-24) mice would prevent breakdown of the blood-brain barrier (BBB) and development of cerebral edema and improve neurological outcome. We used a closed head injury model of TBI. ML-7 or saline treatment was administered at 4 h and every 24 h until sacrifice or 5 days after TBI. Mice were sacrificed at 24 h, 48 h, and 72 h and 7 days after impact. Mice treated with ML-7 after TBI had decreased levels of MLCK-expressing cells (20.7±4.8 vs. 149.3±40.6), less albumin extravasation (28.3±11.2 vs. 116.2±60.7 mm(2)) into surrounding parenchymal tissue, less Evans Blue extravasation (339±314 vs. 4017±560 ng/g), and showed a significant difference in wet/dry weight ratio (1.9±0.07 vs. 2.2±0.05 g), compared to saline-treated groups. Treatment with ML-7 also resulted in preserved neurological function measured by the wire hang test (57 vs. 21 sec) and two-object novel recognition test (old vs. new, 10.5 touches). We concluded that inhibition of MLCK reduces cerebral edema and preserves neurological function in PND-24 mice.

  9. A correlative study between AQP4 expression and the manifestation of DWI after the acute ischemic brain edema in rats

    Institute of Scientific and Technical Information of China (English)

    鲁宏; 孙善全

    2003-01-01

    Objective To investigate the rule of the aquaporin-4 (AQP4) expression in acute ischemic brain edema, and to study the correlation between AQP4 expression and diffusion-weighted imaging (DWI).Methods Thirty-six Wistar rats were divided into 2 groups randomly, control group (n=12) and operation group (n=24) in which right middle cerebral artery of each animal had been occluded unilaterally (MCAO) at interval times of: 15 minutes, 30 minutes, 1 hours, 3 hours, 6 hours and 24 hours, respectively. The operation process of the control group was the same as the operation group except for the MCAO. All groups were examined using DWI. The apparent diffusion coefficient (ADC), relative density (rd) and relative area (rs) of the biggest hyperintensity signal layer on DWI were measured. After that the animals were sacrificed and perfused with the mixture solution consisting of TTC. The biggest layers of the ischemic cerebral tissues in each rat corresponding to the DWI were stained with TTC and examined with immunochemistry (△S) , in situ hybridization (α) and histology.Results There was no significant change in the control group. In the operation group, a hyperintensity signal was found in the DWI of the right MAC territory at 15 minutes after MCAO. The ADC value decreased quickly within one hour after MCAO, while the AQP4 expression, rd-DWI and rs-DWI increased rapidly during this stage. As time progressed, the ADC value decreased further to (2.1±0.6)×10-4 mm2/s at 3 hours, and then began to increase slowly till 24 hours. But the AQP4 expression (△S and α) and rd as well as the rs continuously increased slowly between 1 hour and 6 hours after MCAO, followed a peak after 6 hours. The AQP4 expression (α) showed a positive relationship with the rs-DWI, they all presented two peaks and a plateau. The corresponding sequential pathologic changes were a gradual increase of intracellular edema (within one hour), then an emergence of vasogenic edema (1-6 hours), and final

  10. Treatment with the NK1 antagonist emend reduces blood brain barrier dysfunction and edema formation in an experimental model of brain tumors.

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    Elizabeth Harford-Wright

    Full Text Available The neuropeptide substance P (SP has been implicated in the disruption of the blood-brain barrier (BBB and development of cerebral edema in acute brain injury. Cerebral edema accumulates rapidly around brain tumors and has been linked to several tumor-associated deficits. Currently, the standard treatment for peritumoral edema is the corticosteroid dexamethasone, prolonged use of which is associated with a number of deleterious side effects. As SP is reported to increase in many cancer types, this study examined whether SP plays a role in the genesis of brain peritumoral edema. A-375 human melanoma cells were injected into the right striatum of male Balb/c nude mice to induce brain tumor growth, with culture medium injected in animals serving as controls. At 2, 3 or 4 weeks following tumor cell inoculation, non-treated animals were perfusion fixed for immunohistochemical detection of Albumin, SP and NK1 receptor. A further subgroup of animals was treated with a daily injection of the NK1 antagonist Emend (3 mg/kg, dexamethasone (8 mg/kg or saline vehicle at 3 weeks post-inoculation. Animals were sacrificed a week later to determine BBB permeability using Evan's Blue and brain water content. Non-treated animals demonstrated a significant increase in albumin, SP and NK1 receptor immunoreactivity in the peritumoral area as well as increased perivascular staining in the surrounding brain tissue. Brain water content and BBB permeability was significantly increased in tumor-inoculated animals when compared to controls (p<0.05. Treatment with Emend and dexamethasone reduced BBB permeability and brain water content when compared to vehicle-treated tumor-inoculated mice. The increase in peritumoral staining for both SP and the NK1 receptor, coupled with the reduction in brain water content and BBB permeability seen following treatment with the NK1 antagonist Emend, suggests that SP plays a role in the genesis of peritumoral edema, and thus warrants

  11. Brain edema and tumor necrosis factor-like weak inducer of apoptosis in rats with cerebral ischemia

    Institute of Scientific and Technical Information of China (English)

    Renlan Zhou; Peng Xie

    2008-01-01

    BACKGROUND: Recent studies have demonstrated that tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in brain edema. However, it is unclear whether blood-brain barrier (BBB) disruption is associated with TWEAK during the process of brain edema OBJECTIVE: To investigate the effects of TWEAK on BBB permeability in brain edema.DESIGN, TIME AND SETTING: An immunohistochemical observation, randomized, controlled animal experiment was pertbrmed at the Laboratory of Neurosurgical Anatomy, Xiangya Medical College, Central South University & Central Laboratory, Third Xiangya Hospital, Central South University between January 2006 and December 2007.MATERIALS: A total of 48 adult Wistar rats were randomly divided into three groups: normal control (n =8), sham-operated (n = 8), and ischemia/reperfusion (n = 32). Rats from the ischemia/reperfusion group were randomly assigned to four subgroups according to different time points, i.e., 2 hours of ischemia followed by 6 hours (n = 8), 12 hours {n = 8), 1 day (n = 8), or 12 days (n = 8) of reperfusion.METHODS: Focal cerebral ischemia/reperfusion injury was induced by middle cerebral artery occlusion (MCAO) using the suture method in rats from the ischemia/reperfusion group. Thread was introduced at a depth of 17-19 mm. Rats in the sham-operated group were subjected to experimental procedures similar to the ischemia/reperfusion group; however, the introducing depth of thread was 10 mm. The normal control group was not given any intervention.MAIN OUTCOME MEASURES: TWEAK expression was examined by immunohistochemistry; brain water content on the ischemic side was calculated as the ratio of dry to wet tissue weight; BBB permeability was measured by Evans blue extravasation.RESULTS: A total of eight rats died prior to and after surgery and an additional eight rats were randomly entered into the study. Thus 48 rats were included in the final analysis. In the ischemia/reperfusion group,TWEAK-positive cells were

  12. Peritumoral edema of meningiomas and metastatic brain tumors: differences in diffusion characteristics evaluated with diffusion-tensor MR imaging

    Energy Technology Data Exchange (ETDEWEB)

    Toh, Cheng-Hong; Wong, Alex M.-C; Wong, Ho-Fai; Wan, Yung-Liang [Chang Gung Memorial Hospital, Department of Medical Imaging and Intervention, Tao-Yuan (China); Chang Gung University, School of Medicine and Medical Technology, Tao-Yuan (China); Wei, Kuo-Chen [Chang Gung Memorial Hospital, Department of Neurosurgery, Tao-Yuan (China); Chang Gung University, School of Medicine and Medical Technology, Tao-Yuan (China); Ng, Shu-Hang [Chang Gung Memorial Hospital, Department of Medical Imaging and Intervention, Tao-Yuan (China); Chang Gung University, School of Medicine and Medical Technology, Tao-Yuan (China); Chang Gung Memorial Hospital, Molecular Image Center, Tao-Yuan (China)

    2007-06-15

    We prospectively compared the fractional anisotropy (FA) and mean diffusivity (MD) of the peritumoral edema of meningiomas and metastatic brain tumors with diffusion-tensor magnetic resonance (MR) imaging. The study protocol was approved by the local ethics committee, and written informed consent was obtained. Preoperative diffusion-tensor MR imaging was performed in 15 patients with meningiomas and 11 patients with metastatic brain tumors. Regions of interest (ROI) were placed in the peritumoral edema and normal-appearing white matter (NAWM) of the contralateral hemisphere to measure the FA and MD. The FA and MD ratios were calculated for each ROI in relation to the NAWM of the contralateral hemisphere. Changes in peritumoral MD and FA, in terms of primary values and ratios, were compared using a two-sample t-test; P < 0.05 was taken as indicating statistical significance. The mean MD values (x 10{sup -3} mm{sup 2}/s) of the peritumoral edema for metastases and meningiomas, respectively, were 0.902 {+-} 0.057 and 0.820 {+-} 0.094, the mean MD ratios were 220.3 {+-} 22.6 and 193.1 {+-} 23.4, the mean FA values were 0.146 {+-} 0.026 and 0.199 {+-} 0.052, and the mean FA ratios were 32.3 {+-} 5.9 and 46.0 {+-} 12.1. All the values were significantly different between metastases and meningiomas (MD values P = 0.016, MD ratios P = 0.006, FA values P = 0.005, FA ratios P = 0.002). The peritumoral edema of metastatic brain tumors and meningiomas show different MD and FA on diffusion-tensor MR imaging. (orig.)

  13. MRI findings of acute cerebral swelling and brain edema in the acute stage. A report of two cases

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    Oki, Hideo; Ueda, Shin; Matsumoto, Keizo; Kashihara, Michiharu; Furuichi, Masashi.

    1988-08-01

    We report two cases, one of acute cerebral swelling and the other with a major stroke, whose MRI has shown very interesting findings. Case 1, a 32-year-old male, was admitted to our service because of a lowering of his consciousness immediately after a head injury. On admission, the patient was semicomatous (E/sub 1/M/sub 2/V/sub 1/, with anisocoria (R > L). His plain skull X-ray was normal. A CT scan, however, demonstrated right isodensity hemispheric swelling associated with a subarachnoid hemorrhage in the right Sylvian fissure. A right carotid angiogram showed no vascular disorders. MR imaging of the spin density demonstrated a hyperintensitive thickening of the gray matter in the whole right hemisphere. Case 2, a 58-year-old female, was admitted because of a sudden onset of loss of consciousness, with right hemiparesis and dysarthria. On admission, her consciousness was semicomatous (E/sub 1/M/sub 3/V/sub 1/), and it deteriorated to a deep coma 1 hour later. A CT scan demonstrated a diffuse left hemispheric low density, with a finding of hemorrhagic infarction in the basal ganglia. MR imaging of the spin density showed a hyperintensitive thickening of the gray matter resembling that of Case 1. The findings of the spin-echo images of our two cases showed a hyperintensitive thickening of the gray matter in both. The hyperintensity and thickening of the gray matter apparently indicated a sort of hyperemia and brain edema. These findings led us to suspect that the hyperemia associated with acute cerebral swelling and ischemic brain edema of our two cases originated in the gray matter, although it has been considered that the pathogenesis of acute cerebral swelling is not known and that brain edema, especially vasogenic edema, will mostly develop in the white matter rather than in the gray matter.

  14. Purinergic 2Y1 receptor stimulation decreases cerebral edema and reactive gliosis in a traumatic brain injury model.

    Science.gov (United States)

    Talley Watts, Lora; Sprague, Shane; Zheng, Wei; Garling, R Justin; Jimenez, David; Digicaylioglu, Murat; Lechleiter, James

    2013-01-01

    Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adults. Neuroprotective agents that may promote repair or counteract damage after injury do not currently exist. We recently reported that stimulation of the purinergic receptor subtype P2Y(1)R using 2-methylthioladenosine 5' diphosphate (2MeSADP) significantly reduced cytotoxic edema induced by photothrombosis. Here, we tested whether P2Y(1)R stimulation was neuroprotective after TBI. A controlled closed head injury model was established for mice using a pneumatic impact device. Brains were harvested at 1, 3, or 7 days post-injury and assayed for morphological changes by immunocytochemistry, Western blot analysis, and wet/dry weight. Cerebral edema and expression of both aquaporin type 4 and glial fibrillary acidic protein were increased at all time points examined. Immunocytochemical measurements in both cortical and hippocampal slices also revealed significant neuronal swelling and reactive gliosis. Treatment of mice with 2MeSADP (100 μM) or MRS2365 (100 μM) 30 min after trauma significantly reduced all post-injury symptoms of TBI including edema, neuronal swelling, reactive gliosis, and AQ4 expression. The neuroprotective effect was lost in IP(3)R2-/- mice treated with 2MeSADP. Immunocytochemical labeling of brain slices confirmed that P2Y(1)R expression was defined to cortical and hippocampal astrocytes, but not neurons. Taken together, the data show that stimulation of astrocytic P2Y(1)Rs significantly reduces brain injury after acute trauma and is mediated by the IP(3)-signaling pathway. We suggest that enhancing astrocyte mitochondrial metabolism offers a promising neuroprotective strategy for a broad range of brain injuries.

  15. Hyperbaric oxygen therapy ameliorates local brain metabolism, brain edema and inflammatory response in a blast-induced traumatic brain injury model in rabbits.

    Science.gov (United States)

    Zhang, Yongming; Yang, Yanyan; Tang, Hong; Sun, Wenjiang; Xiong, Xiaoxing; Smerin, Daniel; Liu, Jiachuan

    2014-05-01

    Many studies suggest that hyperbaric oxygen therapy (HBOT) can provide some clinically curative effects on blast-induced traumatic brain injury (bTBI). The specific mechanism by which this occurs still remains unknown, and no standardized time or course of hyperbaric oxygen treatment is currently used. In this study, bTBI was produced by paper detonators equivalent to 600 mg of TNT exploding at 6.5 cm vertical to the rabbit's head. HBO (100% O2 at 2.0 absolute atmospheres) was used once, 12 h after injury. Magnetic resonance spectroscopy was performed to investigate the impact of HBOT on the metabolism of local injured nerves in brain tissue. We also examined blood-brain barrier (BBB) integrity, brain water content, apoptotic factors, and some inflammatory mediators. Our results demonstrate that hyperbaric oxygen could confer neuroprotection and improve prognosis after explosive injury by promoting the metabolism of local neurons, inhibiting brain edema, protecting BBB integrity, decreasing cell apoptosis, and inhibiting the inflammatory response. Furthermore, timely intervention within 1 week after injury might be more conducive to improving the prognosis of patients with bTBI.

  16. Activation of P2X7 promotes cerebral edema and neurological injury after traumatic brain injury in mice.

    Science.gov (United States)

    Kimbler, Donald E; Shields, Jessica; Yanasak, Nathan; Vender, John R; Dhandapani, Krishnan M

    2012-01-01

    Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP) and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/- mice) of the purinergic P2x7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-1β (IL-1β) and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, brilliant blue G (BBG), a clinically non-toxic P2X7 inhibitor, inhibited IL-1β expression, limited edemic development, and improved neurobehavioral outcomes after TBI. The beneficial effects of BBG followed either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP), a reactive astrocyte marker, and attenuated the expression of aquaporin-4 (AQP4), an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation.

  17. Activation of P2X7 promotes cerebral edema and neurological injury after traumatic brain injury in mice.

    Directory of Open Access Journals (Sweden)

    Donald E Kimbler

    Full Text Available Traumatic brain injury (TBI is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/- mice of the purinergic P2x7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-1β (IL-1β and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, brilliant blue G (BBG, a clinically non-toxic P2X7 inhibitor, inhibited IL-1β expression, limited edemic development, and improved neurobehavioral outcomes after TBI. The beneficial effects of BBG followed either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP, a reactive astrocyte marker, and attenuated the expression of aquaporin-4 (AQP4, an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation.

  18. Interferon-Stimulated Gene 15 Upregulation Precedes the Development of Blood-Brain Barrier Disruption and Cerebral Edema after Traumatic Brain Injury in Young Mice.

    Science.gov (United States)

    Rossi, Janet L; Todd, Tracey; Daniels, Zachary; Bazan, Nicolas G; Belayev, Ludmila

    2015-07-15

    Recent studies show that myosin light chain kinase (MLCK) plays a pivotal role in development of cerebral edema, a known complication following traumatic brain injury (TBI) in children and a contributing factor to worsened neurologic recovery. Interferon-stimulated gene 15 (ISG15) is upregulated after cerebral ischemia and is neuroprotective. The significant role of ISG15 after TBI has not been studied. Postnatal Day (PND) 21 and PND24 mice were subjected to lateral closed-skull injury with impact depth of 2.0 or 2.25 mm. Behavior was examined at 7 d using two-object novel recognition and Wire Hang tests. Mice were sacrificed at 6 h, 12 h, 24 h, 48 h, 72 h, and 7 d. ISG15 and MLCK were analyzed by Western blot and immunohistochemistry, blood-brain barrier (BBB) disruption with Evans Blue (EB), and cerebral edema with wet/dry weights. EB extravasation and edema peaked at 72 h in both ages. PND21 mice had more severe neurological deficits, compared with PND24 mice. PND24 mice showed peak ISG15 expression at 6 h, and PND21 mice at 72 h. MLCK peaked in both age groups at 12 h and co-localized with ISG15 on immunohistochemistry and co-immunoprecipitation. These studies provide evidence, ISG15 is elevated following TBI in mice, preceding MLCK elevation, development of BBB disruption, and cerebral edema.

  19. Cannabinoid type 2 receptor stimulation attenuates brain edema by reducing cerebral leukocyte infiltration following subarachnoid hemorrhage in rats.

    Science.gov (United States)

    Fujii, Mutsumi; Sherchan, Prativa; Krafft, Paul R; Rolland, William B; Soejima, Yoshiteru; Zhang, John H

    2014-07-15

    Early brain injury (EBI), following subarachnoid hemorrhage (SAH), comprises blood-brain barrier (BBB) disruption and consequent edema formation. Peripheral leukocytes can infiltrate the injured brain, thereby aggravating BBB leakage and neuroinflammation. Thus, anti-inflammatory pharmacotherapies may ameliorate EBI and provide neuroprotection after SAH. Cannabinoid type 2 receptor (CB2R) agonism has been shown to reduce neuroinflammation; however, the precise protective mechanisms remain to be elucidated. This study aimed to evaluate whether the selective CB2R agonist, JWH133 can ameliorate EBI by reducing brain-infiltrated leukocytes after SAH. Adult male Sprague-Dawley rats were randomly assigned to the following groups: sham-operated, SAH with vehicle, SAH with JWH133 (1.0mg/kg), or SAH with a co-administration of JWH133 and selective CB2R antagonist SR144528 (3.0mg/kg). SAH was induced by endovascular perforation, and JWH133 was administered 1h after surgery. Neurological deficits, brain water content, Evans blue dye extravasation, and Western blot assays were evaluated at 24h after surgery. JWH133 improved neurological scores and reduced brain water content; however, SR144528 reversed these treatment effects. JWH133 reduced Evans blue dye extravasation after SAH. Furthermore, JWH133 treatment significantly increased TGF-β1 expression and prevented an SAH-induced increase in E-selectin and myeloperoxidase. Lastly, SAH resulted in a decreased expression of the tight junction protein zonula occludens-1 (ZO-1); however, JWH133 treatment increased the ZO-1 expression. We suggest that CB2R stimulation attenuates neurological outcome and brain edema, by suppressing leukocyte infiltration into the brain through TGF-β1 up-regulation and E-selectin reduction, resulting in protection of the BBB after SAH.

  20. The effect of butylphthalide on the brain edema, blood-brain barrier of rats after focal cerebral infarction and the expression of Rho A.

    Science.gov (United States)

    Hu, Jinyang; Wen, Qingping; Wu, Yue; Li, Baozhu; Gao, Peng

    2014-06-01

    The aim of this study was to explore the effect of butylphthalide on the brain edema, blood-brain barrier of rats of rats after focal cerebral infarction and the expression of Rho A. A total of 195 sprague-dawley male rats were randomly divided into control group, model group, and butylphthalide group (40 mg/kg, once a day, by gavage). The model was made by photochemical method. After surgery 3, 12, 24, 72, and 144 h, brain water content was done to see the effect of butylphthalide for the cerebral edema. Evans blue extravasation method was done to see the changes in blood-brain barrier immunohistochemistry, and Western blot was done to see the expression of Rho A around the infarction. Compared with the control group, the brain water content of model group and butylphthalide group rats was increased, the permeability of blood-brain barrier of model group and butylphthalide group rats was increased, and the Rho A protein of model group and butylphthalide group rats was increased. Compared with the model group, the brain water content of butylphthalide group rats was induced (73.67 ± 0.67 vs 74.14 ± 0.46; 74.89 ± 0.57 vs 75.61 ± 0.52; 77.49 ± 0.34 vs 79.33 ± 0.49; 76.31 ± 0.56 vs 78.01 ± 0.48; 72.36 ± 0.44 vs 73.12 ± 0.73; P edema, protect the blood-brain barrier, and decrease the expression of Rho A around the infarction.

  1. Dietary Virgin Olive Oil Reduces Blood Brain Barrier Permeability, Brain Edema, and Brain Injury in Rats Subjected to Ischemia-Reperfusion

    Directory of Open Access Journals (Sweden)

    Fatemeh Mohagheghi

    2010-01-01

    Full Text Available Recent studies suggest that dietary virgin olive oil (VOO reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in an in vivo study of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively. After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO. After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p < 0.05, and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p < 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls. Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.

  2. Correlation of vascular endothelial growth factor to permeability of blood-brain barrier and brain edema during high-altitude exposure

    Institute of Scientific and Technical Information of China (English)

    Qiquan Zhou; Chang'e Liu; Jing Wang; Yunli Wang; Bo Zhou

    2009-01-01

    BACKGROUND:Many studies have evaluated the role of vascular endothelial growth factor (VEGF) in traumatic brain edema and hemorrhagic brain edema.OBJECTIVE:To observe the effects of VEGF expression on permeability of the blood-brain barrier (BBB) during high-altitude and hypoxia exposure,and to investigate the correlation between VEGF expression and BBB permeability with regard to Evans blue staining and brain edema during high-altitude exposure.DESIGN,TIME AND SETTING:The randomized,controlled,animal study was performed at the Tanggula Etape,Central Laboratory of Chengdu Medical College,and Central Laboratory of General Hospital of Chengdu Military Area Command of Chinese PLA,China,from July 2003 to November 2004.MATERIALS:Quantitative RT-PCR kit (Sigma,USA),VEGF ELISA kit (Biosource,USA),and Evans blue (Jingchun,China) were acquired for this study.METHODS:A total of 180 Wistar rats were equally and randomly assigned to 15 groups:low-altitude (500 m),middle-altitude (2 880 m),high-altitude (4 200 m),super-high-altitude (5 000 m),1,3,5,7,9,11,13,15,17,19,and 21 days of super high-altitude exposure.Wistar rats were exposed to various altitude gradients to establish a hypoxia model.MAIN OUTCOME MEASURES:Brain water content was calculated according to the wet-to-dry weight ratio.BBB permeability to Evans blue was determined by colorimetric method.VEGF mRNA and protein levels in brain tissues were detected using RT-PCR and double-antibody sandwich ELISA.RESULTS:Brain water content,BBB permeability to Evans blue,and VEGF mRNA and protein levels in brain tissues increased with increasing altitude and prolonged exposure to altitude.The greatest increase was determined on day 9 upon ascending 5 000 m.Simultaneously,VEGF expression positively correlated to BBB permeability of Evans blue and brain water content (r=0.975,0.917,P<0.01).CONCLUSION:Increased VEGF protein and mRNA expression was responsible for increased BBB permeability,which may be an important mechanism

  3. Suppressive effect of dexamethasone on the neutrophil expression of CD18 in rats with radiation induced brain edema

    Institute of Scientific and Technical Information of China (English)

    Laixing Wang; Yibin Fang; Xiaoping Zhou; Xiaowu Hu; Jianmin Liu

    2006-01-01

    BACKGROUND: Stereo-tactic radiation therapy (SRT) is widely used to treat intracranial diseases, but some patients suffered from radiation induced brain edema after SRT. Once radiation induced brain edema occurs,the treatment is quite difficult, and it always leads to a poor outcome. Dexamethasone has certain therapeutic effect on traumatic brain edema, but the biological mechanism is still unclear.OBJECTIVE: To observe the effect of dexamethasone on the neutrophil expression of CD18.DESIGN: A randomized control observation.SETTING: Changhai Hospital of the Second Military Medical University of Chinese PLA.MATERIALS : The experiment was carried out in Changhai Hospital of the Second Military Medical University of Chinese PLA from January 1999 to December 1999. Twenty SD rats (male and female each in half) weighing (250±50) g were used.METHODS: Twenty SD rats were divided into four groups at random. ① Blank control group (n=5): The rats were not treated without dexamethasone or irradiation; ② Irradiation group (n=5): The rats were given irradiation but no dexamethasone treatment; ③ Irradiation+1 mg/kg dexamethasone group (n=5):The rats were treated with irradiation and dexamethasone of 1 mg/kg; ④ Irradiation+5 mg/kg dexamethasone group (n=5): The rats were treated with irradiation and dexamethasone of 5 mg/kg. The heads of the rats were irradiated with 10 MeV X-ray (30 Gy), and brain tissue was removed after 2weeks to observe the pathological changes. Blood samples were taken from the carotid artery, gradient centrifugation was used, and neutrophile layer was obtained, the level of neutrophile expression of CD18 mRNA and quantity of membrane proteins in blood were detected with Northern blot and flow cytometry respectively.MAIN OUTCOME MEASURES: ① Blood cell count; ② Pathological results; ③ level of neutrophile expression of CD18 mRNA and quantity of membrane proteins.RESULTS: All the 20 SD rats were involved in the analysis of results without

  4. Posterior reversible encephalopathy syndrome (PRES, an acute neurological syndrome due to reversible multifactorial brain edema: a case report

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    Camilla Cicognani

    2013-04-01

    Full Text Available Background: The essential features of Posterior Reversible Encephalopathy Syndrome (PRES are headache, mental changes, seizures, visual symptoms and often arterial hypertension. Brain RMN typically shows cortico-sottocortical parieto-occipital edema, with a bilateral and symmetric distribution. PRES develops in clinical conditions as hypertensive encephalopathy, preeclampsia/ eclampsia, autoimmune diseases, after transplantation, infections and as an adverse effect of immunosuppressive drugs or chemotherapy. It usually completely reverses with treatment, although permanent sequelae are possible in case of delayed or missed diagnosis. Case report: We describe the case of a transsexual (M!F and tetraplegic patient, admitted for neck and low back pain. She suddenly developed headache, confusion, seizures and severe hypertension with normal blood tests. RMN showed multiple cortico-sottocortical areas of vasogenic and citotoxic edema in temporo-occipital, parietal, frontal, and cerebellar regions. Soon after the beginning of the antihypertensive therapy, clinical recovery was observed, as well as the disappearance of edema at RMN. Discussion and conclusions: Although PRES is usually associated with definite pathological conditions, it is not always the case, as was for the patient here described, who had no predisposing factors in her past clinical history, and presented hypertension only in the acute phase of the syndrome. Since, moreover, PRES usually presents with acute non specific features and it can be misdiagnosed with other serious diseases, the clinician will be helped by the knowledge of this syndrome to promptly start diagnostic workup and treatments, and avoid permanent neurological deficits.

  5. Diagnostic utility of C-reactive Protein combined with brain natriuretic peptide in acute pulmonary edema: a cross sectional study

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    Murakami Junji

    2011-06-01

    Full Text Available Abstract Introduction Discriminating acute lung injury (ALI or acute respiratory distress syndrome (ARDS from cardiogenic pulmonary edema (CPE using the plasma level of brain natriuretic peptide (BNP alone remains controversial. The aim of this study was to determine the diagnostic utility of combination measurements of BNP and C-reactive protein (CRP in critically ill patients with pulmonary edema. Methods This was a cross-sectional study. BNP and CRP data from 147 patients who presented to the emergency department due to acute respiratory failure with bilateral pulmonary infiltrates were analyzed. Results There were 53 patients with ALI/ARDS, 71 with CPE, and 23 with mixed edema. Median BNP and CRP levels were 202 (interquartile range 95-439 pg/mL and 119 (62-165 mg/L in ALI/ARDS, and 691 (416-1,194 pg/mL (p Conclusions Measurement of CRP is useful as well as that of BNP for distinguishing ALI/ARDS from CPE. Furthermore, a combination of BNP and CRP can provide higher accuracy for the diagnosis.

  6. The brain in acute liver failure. A tortuous path from hyperammonemia to cerebral edema

    DEFF Research Database (Denmark)

    Bjerring, Peter Nissen; Eefsen, Martin; Hansen, Bent Adel

    2008-01-01

    Acute liver failure (ALF) is a condition with an unfavourable prognosis. Multiorgan failure and circulatory collapse are frequent causes of death, but cerebral edema and intracranial hypertension (ICH) are also common complications with a high risk of fatal outcome. The underlying pathogenesis has...

  7. [The effects of a benzopyrone derivative in experimental brain edema due to cold in the rabbit].

    Science.gov (United States)

    Góngora Castillo, C; Gómez de Segura, I A; López Bravo, A; de Miguel del Campo, E

    1993-01-01

    On this study, parenchymal changes during a cerebral edema caused by thermic injury (cool) on the rabbit, are analyzed. The work was based on the ultrastructural findings obtained by transmission electronic microscopy and on the effects produced by a benzopironic derived (F-117 Hydrosmina). The injury was produced with solid CO2, previous a craniectomy, on the dura mater of the left hemisphere. Forty rabbits were included into the study, the animals were distributed into five groups (n = 8): a control group and 4 treatment groups. One of the groups received treatment without previous cerebral injury. The group of rabbits with doses of 50 mg/Kg of weight showed focal and diffuse areas of edema alternating with less damaged areas, the edema was evident on the white substance. This group also showed a dissociation of the myelinic fibers and an intracytoplasmatic tumefaction into the glial cells. These findings contrast with the histopathological findings obtained from the rabbits (V), the extracellular edema was poor, the myelinic fiber disorganization was minimal with no vacuolar degeneration and no structural mitochondrial changes had been showed. The discontinuance of the hematoencephalic barrier caused by the cool could be a possible mechanism that causes the opening of the endothelial unions from the capillary vessels, changing their membranes and resulting in a free penetration of the molecule into the cerebral parenchyma.(ABSTRACT TRUNCATED AT 250 WORDS)

  8. The effect of pre-nutrition of hydroalcoholic extractof Origanum vulgare on brain edema and neurologic deficits in a rat stroke model

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    Meysam Foroozandeh

    2015-10-01

    Full Text Available Background and Aim: Stroke is one of the most important factors of mortality and disability in the world. Free radicals are produced following ischemic stroke and they play a central role in breaking the blood-brain barrier and  causing brain edema formation. The aim of the current study was to evaluate the effect of hydro- alcoholic extract of Origanum vulgare on brain edema and neurologic deficit in a rat stroke model. Materials and Methods: In thisexperimental study, 35 male Wistar rats were randomly divided into 5 equal groups.  The first  two groups (control and Sham received distilled water, while three treatment groups received oral Origanum vulgare extract for 30days (50,75and 100 mg/kgdaily, respectively.  Two hours after the last dose of Origanum vulgare extract,each main group underwent  a 60 min middle cerebral artery occlusion.  Then, the assessment of blood brain edema, and neurologic deficits analysis were done . Brain edema (brain water content was analyzed by One-Way ANOVA using LSD method and neurologic deficits analysis by means of Mann-Whitney U, and P<0.05 was taken as the significant level. Results: Origanum vulgare extract reduced brain edema in the experimental groups of 50 (82.49±0.47, 75 (80.89±0.63 and 100 mg/kg/day (80.80±0.66 compared to the control group (84.46±0.67. The neurologic deficit scores in the experimental groups of 75and 100mg/kg/day, compared with control group, but neurologic deficit scores did not affect the group receiving the dose 50 mg/kg. Conclusion:  The obtained data indicate that Origanum vulgar extract via reduction of brain edema and neurologic deficits scorescan have a protective effect on the stroke model.

  9. Pulmonary edema

    Science.gov (United States)

    Lung congestion; Lung water; Pulmonary congestion; Heart failure - pulmonary edema ... Pulmonary edema is often caused by congestive heart failure . When the heart is not able to pump efficiently, ...

  10. Study on the relationship of cytochrome C expression and cerebral edema in perihematomal brain tissue in patients with hypertensive cerebral hemorrhage

    Institute of Scientific and Technical Information of China (English)

    CAI Heng; LIU Guixiang; XU Chunsheng; LIU Qingxin; XU Xiaobo

    2007-01-01

    Objective To investigate the expression of cytochrome C in perihematomal brain tissue and its relationship with the histopathological change and formation of cerebral edema in patients with hypertensive cerebral hemorrhage. Methods Thirty four patients (23 male, 11 female) of hypertensive cerebral hemorrhage in hospital from Sep. 2001 to Sep. 2002 were selected with a mean age 55.6± 10.2 years (from 35 to 75 years). The mean volume of hemorrhagic blood was 50.4±11.6 ml (from 25 to 85 ml). The perihematomal brain tissue was obtained from the minimally invasive surgery. Histopathological change and expressions of cytochrome C in perihematomal brain tissue was detected by histopathological and immunohistochemical techniques. The volume of perihematomal cerebral edema was determined by computed tomographic scan before operation. The results of staining and the volume of perihematomal cerebral edema were analyzed with double blind fashion. Results Perihematomal cerebral edema were found 12-72h after cerebral hemorrhage. Myelin sheath degeneration, condensation of nucleus and typical apopototic body were observed in perihematomal brain tissue. Expression of cytochrome C in perihematomal brain tissue was observed at 4 h and reached peak around 48-72 h after cerebral hemorrhage. Cytochrome C expressed higher positively in 16 patients and lower positively in 13 patients. Cytochrome C expression was not detected only in 5 patints. There were significant differences in volume of perihematomal cerebral edema with different expression of cytochrome C in perihematomal brain tissue (P<0.01). Conclusions Cytochrome C expression was upregulated in perihematomal brain tissue in patients with hypertensive cerebral hemorrhage. Cytochrome C might involve in the histopathological change and the formation of perihematomal cerebral edema.

  11. Inhaled nitric oxide for the brain dead donor with neurogenic pulmonary edema during anesthesia for organ donation: a case report

    Science.gov (United States)

    Park, Eun Sun; Lee, A-Ran; Lee, Sang Hyun; Kim, An Suk; Park, Soon Eun; Cho, Young Woo

    2014-01-01

    Neurogenic pulmonary edema (NPE) in brain dead organ donors occurring after an acute central nervous system insult threatens organ preservation of potential organ donors and the outcome of organ donation. Hence the active and immediate management of NPE is critical. In this case, a 50-year-old male was admitted to the intensive care unit (ICU) for organ donation. He was hypoxic due to NPE induced by spontaneous intracerebral hemorrhage and intraventricular hemorrhage. Protective ventilatory management, intermittent recruitment maneuvers, and supportive treatment were maintained in the ICU and the operating room (OR). Despite this management, the hypoxemia worsened after the OR admission. So inhaled nitric oxide (NO) therapy was performed during the operation, and the hypoxic phenomena showed remarkable improvement. The organ retrieval was successfully completed. Therefore, NO inhalation can be helpful in the improvement of hypoxemia caused by NPE in brain dead organ donors during anesthesia for the organ donation. PMID:25237451

  12. Influence of isoflurane, fentanyl, thiopental, and alpha-chloralose on formation of brain edema resulting from a focal cryogenic lesion.

    Science.gov (United States)

    Murr, R; Berger, S; Schürer, L; Peter, K; Baethmann, A

    1995-06-01

    The objective of this study was to analyze the effects of various anesthetics on the formation of brain edema resulting from a focal cryogenic lesion. Thirty rabbits (six per group) were anesthetized with isoflurane (1 minimum alveolar anesthetic concentration [MAC] 2.1 vol%), fentanyl (bolus 5 micrograms/kg; infusion rate 1.0-0.5 micrograms.kg-1.min-1), thiopental (32.5 mg.kg-1.h-1), or alpha-chloralose (50 mg/kg). Control animals (sham operation, no lesion) received alpha-chloralose (50 mg/kg). Regional cerebral blood flow (rCBF) in perifocal brain tissue was measured by H2-clearance. Animals anesthetized with isoflurane required support of arterial pressure by angiotensin II (0.15 micrograms.kg-1.min-1). Six hours after trauma the animals were killed. Formation of brain edema was studied by specific gravity of cortical gray matter, white matter, hippocampus, caudate nucleus, putamen, and thalamus. Brain tissue samples were collected at multiple sites close to and distant from the lesion. Mean arterial pressure, arterial PCO2 and PO2, hematocrit, body temperature, and blood glucose were not different between groups during the posttraumatic course (except for an increased arterial pressure with alpha-chloralose compared to thiopental 4-6 h after trauma). The specific gravity of cortical gray matter was significantly reduced up to a distance of 6 mm from the center of the lesion in animals anesthetized with isoflurane, thiopental, or alpha-chloralose and up to 9 mm in animals given fentanyl.(ABSTRACT TRUNCATED AT 250 WORDS)

  13. Changes in cannabinoid receptors, aquaporin 4 and vimentin expression after traumatic brain injury in adolescent male mice. Association with edema and neurological deficit.

    Science.gov (United States)

    Lopez-Rodriguez, Ana Belen; Acaz-Fonseca, Estefania; Viveros, Maria-Paz; Garcia-Segura, Luis M

    2015-01-01

    Traumatic brain injury (TBI) incidence rises during adolescence because during this critical neurodevelopmental period some risky behaviors increase. The purpose of this study was to assess the contribution of cannabinoid receptors (CB1 and CB2), blood brain barrier proteins (AQP4) and astrogliosis markers (vimentin) to neurological deficit and brain edema formation in a TBI weight drop model in adolescent male mice. These molecules were selected since they are known to change shortly after lesion. Here we extended their study in three different timepoints after TBI, including short (24h), early mid-term (72h) and late mid-term (two weeks). Our results showed that TBI induced an increase in brain edema up to 72 h after lesion that was directly associated with neurological deficit. Neurological deficit appeared 24 h after TBI and was completely recovered two weeks after trauma. CB1 receptor expression decreased after TBI and was negatively correlated with edema formation and behavioral impairments. CB2 receptor increased after injury and was associated with high neurological deficit whereas no correlation with edema was found. AQP4 increased after TBI and was positively correlated with edema and neurological impairments as occurred with vimentin expression in the same manner. The results suggest that CB1 and CB2 differ in the mechanisms to resolve TBI and also that some of their neuroprotective effects related to the control of reactive astrogliosis may be due to the regulation of AQP4 expression on the end-feet of astrocytes.

  14. Changes in cannabinoid receptors, aquaporin 4 and vimentin expression after traumatic brain injury in adolescent male mice. Association with edema and neurological deficit.

    Directory of Open Access Journals (Sweden)

    Ana Belen Lopez-Rodriguez

    Full Text Available Traumatic brain injury (TBI incidence rises during adolescence because during this critical neurodevelopmental period some risky behaviors increase. The purpose of this study was to assess the contribution of cannabinoid receptors (CB1 and CB2, blood brain barrier proteins (AQP4 and astrogliosis markers (vimentin to neurological deficit and brain edema formation in a TBI weight drop model in adolescent male mice. These molecules were selected since they are known to change shortly after lesion. Here we extended their study in three different timepoints after TBI, including short (24h, early mid-term (72h and late mid-term (two weeks. Our results showed that TBI induced an increase in brain edema up to 72 h after lesion that was directly associated with neurological deficit. Neurological deficit appeared 24 h after TBI and was completely recovered two weeks after trauma. CB1 receptor expression decreased after TBI and was negatively correlated with edema formation and behavioral impairments. CB2 receptor increased after injury and was associated with high neurological deficit whereas no correlation with edema was found. AQP4 increased after TBI and was positively correlated with edema and neurological impairments as occurred with vimentin expression in the same manner. The results suggest that CB1 and CB2 differ in the mechanisms to resolve TBI and also that some of their neuroprotective effects related to the control of reactive astrogliosis may be due to the regulation of AQP4 expression on the end-feet of astrocytes.

  15. Intravenous HOE-642 reduces brain edema and Na uptake in the rat permanent middle cerebral artery occlusion model of stroke: evidence for participation of the blood-brain barrier Na/H exchanger.

    Science.gov (United States)

    O'Donnell, Martha E; Chen, Yi-Je; Lam, Tina I; Taylor, Kelleen C; Walton, Jeffrey H; Anderson, Steven E

    2013-02-01

    Cerebral edema forms in the early hours of ischemic stroke by processes involving increased transport of Na and Cl from blood into brain across an intact blood-brain barrier (BBB). Our previous studies provided evidence that the BBB Na-K-Cl cotransporter is stimulated by the ischemic factors hypoxia, aglycemia, and arginine vasopressin (AVP), and that inhibition of the cotransporter by intravenous bumetanide greatly reduces edema and infarct in rats subjected to permanent middle cerebral artery occlusion (pMCAO). More recently, we showed that BBB Na/H exchanger activity is also stimulated by hypoxia, aglycemia, and AVP. The present study was conducted to further investigate the possibility that a BBB Na/H exchanger also participates in edema formation during ischemic stroke. Sprague-Dawley rats were subjected to pMCAO and then brain edema and Na content assessed by magnetic resonance imaging diffusion-weighed imaging and magnetic resonance spectroscopy Na spectroscopy, respectively, for up to 210 minutes. We found that intravenous administration of the specific Na/H exchange inhibitor HOE-642 significantly decreased brain Na uptake and reduced cerebral edema, brain swelling, and infarct volume. These findings support the hypothesis that edema formation and brain Na uptake during the early hours of cerebral ischemia involve BBB Na/H exchanger activity as well as Na-K-Cl cotransporter activity.

  16. High mobility group box protein-1 promotes cerebral edema after traumatic brain injury via activation of toll-like receptor 4.

    Science.gov (United States)

    Laird, Melissa D; Shields, Jessica S; Sukumari-Ramesh, Sangeetha; Kimbler, Donald E; Fessler, R David; Shakir, Basheer; Youssef, Patrick; Yanasak, Nathan; Vender, John R; Dhandapani, Krishnan M

    2014-01-01

    Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Cerebral edema, a life-threatening medical complication, contributes to elevated intracranial pressure (ICP) and a poor clinical prognosis after TBI. Unfortunately, treatment options to reduce post-traumatic edema remain suboptimal, due in part, to a dearth of viable therapeutic targets. Herein, we tested the hypothesis that cerebral innate immune responses contribute to edema development after TBI. Our results demonstrate that high-mobility group box protein 1 (HMGB1) was released from necrotic neurons via a NR2B-mediated mechanism. HMGB1 was clinically associated with elevated ICP in patients and functionally promoted cerebral edema after TBI in mice. The detrimental effects of HMGB1 were mediated, at least in part, via activation of microglial toll-like receptor 4 (TLR4) and the subsequent expression of the astrocytic water channel, aquaporin-4 (AQP4). Genetic or pharmacological (VGX-1027) TLR4 inhibition attenuated the neuroinflammatory response and limited post-traumatic edema with a delayed, clinically implementable therapeutic window. Human and rodent tissue culture studies further defined the cellular mechanisms demonstrating neuronal HMGB1 initiates the microglial release of interleukin-6 (IL-6) in a TLR4 dependent mechanism. In turn, microglial IL-6 increased the astrocytic expression of AQP4. Taken together, these data implicate microglia as key mediators of post-traumatic brain edema and suggest HMGB1-TLR4 signaling promotes neurovascular dysfunction after TBI.

  17. Nimodipine pretreatment improves cerebral blood flow and reduces brain edema in conscious rats subjected to focal cerebral ischemia.

    Science.gov (United States)

    Jacewicz, M; Brint, S; Tanabe, J; Wang, X J; Pulsinelli, W A

    1990-11-01

    The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 micrograms/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a "vascular steal" and reduced the volume of the ischemic core (cortex with CBF of less than 25 ml/100 g/min) and accompanying edema by approximately 50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50-75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20-30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.

  18. Estradiol reduces activity of the blood-brain barrier Na-K-Cl cotransporter and decreases edema formation in permanent middle cerebral artery occlusion.

    Science.gov (United States)

    O'Donnell, Martha E; Lam, Tina I; Tran, Lien Q; Foroutan, Shahin; Anderson, Steven E

    2006-10-01

    Estrogen has been shown to protect against stroke-induced brain damage, yet the mechanism is unknown. During the early hours of stroke, cerebral edema forms as increased transport of Na and Cl from blood into brain occurs across an intact blood-brain barrier (BBB). We showed previously that a luminal BBB Na-K-Cl cotransporter is stimulated by hypoxia and arginine vasopressin (AVP), factors present during cerebral ischemia, and that inhibition of the cotransporter by intravenous bumetanide greatly reduces edema in rats subjected to permanent middle cerebral artery occlusion (MCAO). The present study was conducted to determine whether estrogen protects in stroke at least in part by reducing activity of the BBB cotransporter, thereby decreasing edema formation. Ovariectomized rats were subjected to 210 mins of permanent MCAO after 7-day or 30-min pretreatment with 17beta-estradiol and then brain swelling and 2,3,5-triphenyltetrazolium chloride staining were assessed as measures of brain edema and lesion volume, respectively. Diffusion-weighed imaging was used to monitor permanent MCAO-induced decreases in apparent diffusion coefficient (ADC) values, an index of changes in brain water distribution and mobility. Na-K-Cl cotransporter activity of cerebral microvascular endothelial cells (CMECs) was assessed as bumetanide-sensitive K influx and cotransporter abundance by Western blot analysis after estradiol treatment. Estradiol significantly decreased brain swelling and lesion volume and attenuated the decrease in ADC values during permanent MCAO. Estradiol also abolished CMEC cotransporter stimulation by chemical hypoxia or AVP and decreased cotransporter abundance. These findings support the hypothesis that estrogen attenuates stimulation of BBB Na-K-Cl cotransporter activity, reducing edema formation during stroke.

  19. ASPHYXIA, INTRACRANIAL HEMORRHAGES AND BRAIN EDEMA OF RISK CHILDREN IN THE ADVISORY INSTITUTE IN BITOLA FROM 1989-1994

    Directory of Open Access Journals (Sweden)

    M. ILIEVSKA,

    1997-09-01

    Full Text Available 3986 files have been examined in the Advisory Institute for a five year period in relation to the present risk factors in the pre, peri and postnatal period, the occurrence of asphyxia, I.H. (intracranial hemorrhages and brain edema and their outcome for the children. There were 958 or 32% risk children, out of them 206 or 22% were with asphyxia, 25 or 3% were with brain edema and 14 or 1,5% were with intracranial hemorrhages.The analysis for the risk factors shows that 119 of them were abortive , and from them 15% were born with asphyxia; 124 were SFD and 21% of them with asphyxia; 272 children weighed over 4500 gr., 7% of them with asphyxia and 0.4% with I.H., there were 68 twins, 12% of them with asphyxia. Out of the children with no risk registered, 6 were born with I.H., or 0,2%.Mothers under the age of 18 gave birth to 13% children with asphyxia; treated for sterility and anemia during pregnancy 15%; with increased blood pressure 14%; and 5% with maintained pregnancy.The highest delivery risk is present with children born with vacuum extraction (30% or every third child is with asphyxia and 3% with I.H. and with children delivered by caesarean section (14% with asphyxia.As for the position of the fetus-Citus pedalicus gave 55% children with asphyxia, and Situs pelvicus 12%.The worst damage is suffered by infants with premature amnion disruption (62% are with asphyxia; with the umbilical cord round the neck-56% with asphyxia and 6% with I.H.; and with muddled amniotic fluid and placenta pelvia-50%.The order of risk factors related to asphyxia, I.H. and brain edema is as follows: the first is premature amnion disruption, then follows the umbilical cord round the neck, the muddled amniotic fluid, and placenta previa and Citus pedalicus-which are obstetric problems. The next are the vacuum extraction and S.C. As for the gestatory period the order is as follows: first the abortive, then the twins and hypertrofic infants. The outcome of the

  20. β-Dystroglycan cleavage by matrix metalloproteinase-2/-9 disturbs aquaporin-4 polarization and influences brain edema in acute cerebral ischemia.

    Science.gov (United States)

    Yan, W; Zhao, X; Chen, H; Zhong, D; Jin, J; Qin, Q; Zhang, H; Ma, S; Li, G

    2016-06-21

    Dystroglycan (DG) is widely expressed in various tissues, and throughout the cerebral microvasculature. It consists of two subunits, α-DG and β-DG, and the cleavage of the latter by matrix metalloproteinase (MMP)-2 and -9 underlies a number of physiological and pathological processes. However, the involvement of MMP-2/-9-mediated β-DG cleavage in cerebral ischemia remains uncertain. In astrocytes, DG is crucial for maintaining the polarization of aquaporin-4 (AQP4), which plays a role in the regulation of cytotoxic and vasogenic edema. The present study aimed to explore the effects of MMP-2/-9-mediated β-DG cleavage on AQP4 polarization and brain edema in acute cerebral ischemia. A model of cerebral ischemia was established via permanent middle cerebral artery occlusion (pMCAO) in male C57BL/6 mice. Western blotting, real-time polymerase chain reaction (PCR), immunohistochemical staining, immunofluorescent staining, electron microscopy, and light microscopy were used. Captopril was applied as a selective MMP-2/-9 inhibitor. Recombinant mouse MMP (rmMMP)-2 and -9 were used in an in vitro cleavage experiment. The present study demonstrated evidence of β-DG cleavage by MMP-2/-9 in pMCAO mouse brains; this cleavage was implicated in AQP4 redistribution and brain edema in cerebral ischemia. In addition, captopril exacerbated cytotoxic edema and ameliorated vasogenic edema at 24h after pMCAO, and alleviated brain edema and neurological deficit at 48h and 72h. In conclusion, this study provides novel insight into the effects of MMP-2/-9-mediated β-DG cleavage in acute cerebral ischemia. Such findings might facilitate the development of a therapeutic strategy for the optimization of MMP-2/-9 targeted treatment in cerebral ischemia.

  1. Forebrain Ischemia-Reperfusion Simulating Cardiac Arrest in Mice Induces Edema and DNA Fragmentation in the Brain

    Directory of Open Access Journals (Sweden)

    Christina H. Liu

    2007-05-01

    Full Text Available Brain injury affects one-third of persons who survive after heart attack, even with restoration of spontaneous circulation by cardiopulmonary resuscitation. We studied brain injury resulting from transient bilateral carotid artery occlusion (BCAO and reperfusion by simulating heart attack and restoration of circulation, respectively, in live C57Black6 mice. This model is known to induce neuronal death in the hippocampus, striatum, and cortex. We report the appearance of edema after transient BCAO of 60 minutes and 1 day of reperfusion. Hyperintensity in diffusion-weighted magnetic resonance imaging (MRI was detectable in the striatum, thalamus, and cortex but not in the hippocampus. To determine whether damage to the hippocampus can be detected in live animals, we infused a T2 susceptibility magnetic resonance contrast agent (superparamagnetic iron oxide nanoparticles [SPIONs] that was linked to single-stranded deoxyribonucleic acid (DNA complementary in sequence to c-fos messenger ribonucleic acid (SPION-cfos; we acquired in vivo T2*-weighted MRI 3 days later. SPION retention was measured as T2* (milliseconds signal reduction or R2* value (s−1 elevation. We found that animals treated with 60-minute BCAO and 7-day reperfusion exhibited significantly less SPION retention in the hippocampus and cortex than sham-operated animals. These findings suggest that brain injury induced by cardiac arrest can be detected in live animals.

  2. Cannabinoid CB2 receptor stimulation attenuates brain edema and neurological deficits in a germinal matrix hemorrhage rat model.

    Science.gov (United States)

    Tao, Yihao; Tang, Jun; Chen, Qianwei; Guo, Jing; Li, Lin; Yang, Liming; Feng, Hua; Zhu, Gang; Chen, Zhi

    2015-03-30

    Germinal matrix hemorrhage (GMH) is one of the most common and devastating cerebrovascular events that affect premature infants, resulting in a significant socioeconomic burden. However, GMH has been largely unpreventable, and clinical treatments are mostly inadequate. In the present study, we tested the hypothesis that JWH133, a selective CB2 receptor agonist, could attenuate brain injury and neurological deficits in a clostridial collagenase VII induced GMH model in seven-day-old (P7) S-D rat pups. Up to 1h post-injury, the administration of JWH133 (1mg/kg, intraperitoneal injection) significantly attenuated brain edema at 24h post-GMH, which was reversed by a selective CB2R antagonist, SR144528 (3mg/kg, intraperitoneal injection). Long-term brain morphology and neurofunctional outcomes were also improved. In contrast, JWH133 did not have a noticeable effect on the hematoma volume during the acute phase. These data also showed that microglia activation and inflammatory cytokine (TNF-α) release were significantly inhibited by JWH133 after GMH. This current study suggests a potential clinical utility for CB2R agonists as a potential therapy to reduce neurological injury and improve patient outcomes after GMH.

  3. Minocycline Attenuates Neonatal Germinal-Matrix-Hemorrhage-Induced Neuroinflammation and Brain Edema by Activating Cannabinoid Receptor 2.

    Science.gov (United States)

    Tang, Jun; Chen, Qianwei; Guo, Jing; Yang, Liming; Tao, Yihao; Li, Lin; Miao, Hongping; Feng, Hua; Chen, Zhi; Zhu, Gang

    2016-04-01

    Germinal matrix hemorrhage (GMH) is the most common neurological disease of premature newborns leading to detrimental neurological sequelae. Minocycline has been reported to play a key role in neurological inflammatory diseases by controlling some mechanisms that involve cannabinoid receptor 2 (CB2R). The current study investigated whether minocycline reduces neuroinflammation and protects the brain from injury in a rat model of collagenase-induced GMH by regulating CB2R activity. To test this hypothesis, the effects of minocycline and a CB2R antagonist (AM630) were evaluated in male rat pups that were post-natal day 7 (P7) after GMH. We found that minocycline can lead to increased CB2R mRNA expression and protein expression in microglia. Minocycline significantly reduced GMH-induced brain edema, microglial activation, and lateral ventricular volume. Additionally, minocycline enhanced cortical thickness after injury. All of these neuroprotective effects of minocycline were prevented by AM630. A cannabinoid CB2 agonist (JWH133) was used to strengthen the hypothesis, which showed the identical neuroprotective effects of minocycline. Our study demonstrates, for the first time, that minocycline attenuates neuroinflammation and brain injury in a rat model of GMH, and activation of CBR2 was partially involved in these processes.

  4. 采用CT技术研究颅脑损伤患者的早期神经功能恢复:脑水肿和脑肿胀的比较%CT study of patients neurological function recovery in the acute stage of brain injury:compared brain swelling and brain edema

    Institute of Scientific and Technical Information of China (English)

    李龙; 池晓宇; 黄新才; 刘卫国; 蒋德清

    2002-01-01

    @@ ckground: Secondary clinical manifestations following brain injury may be due to either intracranial hemorrhage or brain edema and brain swelling.But brain swelling hasn't been understand adequately in clinical practice.Objective: 71 patients with brain edema or brain swelling following brain injury admitted to our hospital during Jan 1998 to Dec 1999 were selected for this study.Their CT findings were compared,and CT characters of traumatic brain swelling and neurological function recovery were analyzed emphatically.Unit: Department of Radiology,Guangdong Provincial Corps Hospital,Chinese People's Armed Police Forces.

  5. YiQiFuMai powder injection ameliorates blood-brain barrier dysfunction and brain edema after focal cerebral ischemia-reperfusion injury in mice.

    Science.gov (United States)

    Cao, Guosheng; Ye, Xinyi; Xu, Yingqiong; Yin, Mingzhu; Chen, Honglin; Kou, Junping; Yu, Boyang

    2016-01-01

    YiQiFuMai powder injection (YQFM) is a modern preparation derived from the traditional Chinese medicine Sheng-Mai-San. YQFM is widely used in clinical practice in the People's Republic of China, mainly for the treatment of microcirculatory disturbance-related diseases. However, little is known about its role in animals with ischemic stroke. The aim of this study was to examine the effect of YQFM on brain edema and blood-brain barrier (BBB) dysfunction induced by cerebral ischemia-reperfusion (I/R) injury. Male C57BL/6J mice underwent right middle cerebral artery occlusion for 1 hour with a subsequent 24-hour reperfusion to produce I/R injury. YQFM (three doses: 0.336, 0.671, and 1.342 g/kg) was then given intraperitoneally (IP). The results demonstrated that YQFM significantly decreased infarct size, improved neurological deficits, reduced brain water content, and increased cerebral blood flow after I/R injury. 18F-fluorodeoxyglucose micro-positron emission tomography imaging and hematoxylin and eosin staining results indicated that YQFM is able to ameliorate brain metabolism and histopathological damage after I/R. Moreover, YQFM administration reduced BBB leakage and upregulated the expression of zona occludens-1 (ZO-1) and occludin, which was confirmed by Evans Blue extravasation, Western blotting, and immunofluorescence assay. Our findings suggest that YQFM provides protection against focal cerebral I/R injury in mice, possibly by improving BBB dysfunction via upregulation of the expression of tight junction proteins.

  6. Effect of propofol post-treatment on blood-brain barrier integrity and cerebral edema after transient cerebral ischemia in rats.

    Science.gov (United States)

    Lee, Jae Hoon; Cui, Hui Song; Shin, Seo Kyung; Kim, Jeong Min; Kim, So Yeon; Lee, Jong Eun; Koo, Bon-Nyeo

    2013-11-01

    Although propofol has been reported to offer neuroprotection against cerebral ischemia injury, its impact on cerebral edema following ischemia is not clear. The objective of this investigation is to evaluate the effects of propofol post-treatment on blood-brain barrier (BBB) integrity and cerebral edema after transient cerebral ischemia and its mechanism of action, focusing on modulation of aquaporins (AQPs), matrix metalloproteinases (MMPs), and hypoxia inducible factor (HIF)-1α. Cerebral ischemia was induced in male Sprague-Dawley rats (n = 78) by occlusion of the right middle cerebral artery for 1 h. For post-treatment with propofol, 1 mg kg(-1) min(-1) of propofol was administered for 1 h from the start of reperfusion. Nineteen rats undergoing sham surgery were also included in the investigation. Edema and BBB integrity were assessed by quantification of cerebral water content and extravasation of Evans blue, respectively, following 24 h of reperfusion. In addition, the expression of AQP-1, AQP-4, MMP-2, and MMP-9 was determined 24 h after reperfusion and the expression of HIF-1α was determined 8 h after reperfusion. Propofol post-treatment significantly reduced cerebral edema (P cerebral edema after transient cerebral ischemia, in association with reduced expression of AQP-1, AQP-4, MMP-2, and MMP-9. The decreased expression of AQPs and MMPs after propofol post-treatment might result from suppression of HIF-1α expression.

  7. EFFECT OF GINKGO BILOBA EXTRACT ON BRAIN EDEMA AFTER SUBARACHNOID HEMORRHAGE IN RATS

    Institute of Scientific and Technical Information of China (English)

    孙保亮; 夏作理; 杨明峰; 邱平明

    2001-01-01

    @@ The aim of this study was to investigate the protectiveeffect of Ginkgo biloba extract (EGb) on brain edemaafter subarachnoid hemorrhage . Eighty male and femaleWistar rats, weighing 300~ 350g, were used in the ex-periment. Animals were divided into pure SAH group andEGb-treated group. Dynamic changes of regional cerebralblood flow (rCBF) were detected in eight rats from eachgroup. Brain water and electrolytes contents at differenttime points were detected in thirty-two rats from eachgroup (eight rats at each time point from each group) .EGb. provided by Pizhou Pharmaceutical Factory(Xuzhou, Jiangsu, China), was injected intraperi-toneally 30 minutes before operation and repeated withsingle dose of 15mg/kg .every 6 hours.

  8. A new strategy of CyberKnife treatment system based radiosurgery followed by early use of adjuvant bevacizumab treatment for brain metastasis with extensive cerebral edema.

    Science.gov (United States)

    Wang, Yang; Wang, Enmin; Pan, Li; Dai, Jiazhong; Zhang, Nan; Wang, Xin; Liu, Xiaoxia; Mei, Guanghai; Sheng, Xiaofang

    2014-09-01

    Bevacizumab blocks the effects of vascular endothelial growth factor in leakage-prone capillaries and has been suggested as a new treatment for cerebral radiation edema and necrosis. CyberKnife is a new, frameless stereotactic radiosurgery system. This work investigated the safety and efficacy of CyberKnife followed by early bevacizumab treatment for brain metastasis with extensive cerebral edema. The eligibility criteria of the patients selected for radiosurgery followed by early use of adjuvant bevacizumab treatment were: (1) brain tumors from metastasis with one solitary brain lesion and symptomatic extensive cerebral edema; (2) >18 years of age; (3) the patient refused surgery due to the physical conditions and the risk of surgery; (4) no contraindications for bevacizumab. (5) bevacizumab was applied for a minimum of 2 injections and a maximum of 6 injections with a 2-week interval between treatments, beginning within 2 weeks of the CyberKnife therapy; (6) Karnofsky performance status (KPS) ≥30. Tumor size and edema were monitored by magnetic resonance imaging (MRI). Dexamethasone dosage, KPS, adverse event occurrence and associated clinical outcomes were also recorded. Eight patients were accrued for this new treatment. Radiation dose ranged from 20 to 33 Gy in one to five sessions, prescribed to the 61-71 % isodose line. Bevacizumab therapy was administered 3-10 days after completion of CyberKnife treatment for a minimum of two cycles (5 mg/kg, at 2-week intervals). MRI revealed average reductions of 55.8 % (post-gadolinium) and 63.4 % (T2/FLAIR). Seven patients showed significant clinical neurological improvements. Dexamethasone was reduced in all patients, with five successfully discontinuing dexamethasone treatment 4 weeks after bevacizumab initiation. Hypertension, a bevacizumab-related adverse event, occurred in one patient. After 3-8 months, all patients studied were alive and primary brain metastases were under control, 2 developed new brain

  9. YiQiFuMai powder injection ameliorates blood–brain barrier dysfunction and brain edema after focal cerebral ischemia–reperfusion injury in mice

    Directory of Open Access Journals (Sweden)

    Cao GS

    2016-01-01

    Full Text Available Guosheng Cao, Xinyi Ye, Yingqiong Xu, Mingzhu Yin, Honglin Chen, Junping Kou, Boyang Yu Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Department of Complex Prescription of TCM, China Pharmaceutical University, Nanjing, People’s Republic of China Abstract: YiQiFuMai powder injection (YQFM is a modern preparation derived from the traditional Chinese medicine Sheng-Mai-San. YQFM is widely used in clinical practice in the People’s Republic of China, mainly for the treatment of microcirculatory disturbance-related diseases. However, little is known about its role in animals with ischemic stroke. The aim of this study was to examine the effect of YQFM on brain edema and blood–brain barrier (BBB dysfunction induced by cerebral ischemia–reperfusion (I/R injury. Male C57BL/6J mice underwent right middle cerebral artery occlusion for 1 hour with a subsequent 24-hour reperfusion to produce I/R injury. YQFM (three doses: 0.336, 0.671, and 1.342 g/kg was then given intraperitoneally (IP. The results demonstrated that YQFM significantly decreased infarct size, improved neurological deficits, reduced brain water content, and increased cerebral blood flow after I/R injury. 18F-fluorodeoxyglucose micro-positron emission tomography imaging and hematoxylin and eosin staining results indicated that YQFM is able to ameliorate brain metabolism and histopathological damage after I/R. Moreover, YQFM administration reduced BBB leakage and upregulated the expression of zona occludens-1 (ZO-1 and occludin, which was confirmed by Evans Blue extravasation, Western blotting, and immunofluorescence assay. Our findings suggest that YQFM provides protection against focal cerebral I/R injury in mice, possibly by improving BBB dysfunction via upregulation of the expression of tight junction proteins. Keywords: YiQiFuMai powder injection, YQFM, ischemic stroke, blood–brain barrier, microvascular permeability, tight junctions

  10. Cerebral edema associated with acute hepatic failure.

    Directory of Open Access Journals (Sweden)

    Fujiwara,Masachika

    1985-02-01

    Full Text Available The clinicopathological findings of cerebral edema were investigated in patients with acute hepatic failure autopsied at Okayama University Hospital between 1970 and 1980 retrospectively. Nine (64% of 14 hepatic failure cases were found to have cerebral edema during a post-mortem examination of the brain. Clinical features of the patients with cerebral edema were not significantly different from those of the patients without cerebral edema. However, general convulsions were observed more frequently in patients later found to have cerebral edema. Moreover, the length of time from deep coma to death was much shorter in the brain edema cases with cerebral herniation than without herniation.

  11. The effect of saponification on the mucopolysaccharides of the ground substance of the human brain: the relation to focal edema and multiple sclerosis.

    Science.gov (United States)

    Feigin, I

    1981-03-01

    The acid mucopolysaccharides of brain tissues are disclosed by their metachromatic staining with toluidine blue following saponification with potassium hydroxide, presumably as a result of the liberation of acid groups previously esterified. Earlier histochemical studies had disclosed the presence of neutral mucopolysaccharides by staining with the periodic acid-Schiff technique, and such staining is intensified by prior saponification. Many biochemical studies have reported the presence of both acid and neutral mucopolysaccharides in brain tissues. Within the white matter following brain edema, the quantity of stained mucopolysaccharides is decreased in the plaques of multiple sclerosis and pontine myelinolysis, and in the lesions of diffuse sclerosis. All of these are characterized by myelin loss with relative preservation of axons. The known physiological effects of the mucopolysaccharides on the water content of normal tissues, and on the properties and diffusability of the increments of fluid that constitute edema, lead to the suggestion that edema may play a major role in the pathogenesis of the demyelinating diseases, including multiple sclerosis.

  12. Therapeutic implications of melatonin in cerebral edema.

    Science.gov (United States)

    Rathnasamy, Gurugirijha; Ling, Eng-Ang; Kaur, Charanjit

    2014-12-01

    Cerebral edema/brain edema refers to the accumulation of fluid in the brain and is one of the fatal conditions that require immediate medical attention. Cerebral edema develops as a consequence of cerebral trauma, cerebral infarction, hemorrhages, abscess, tumor, hypoxia, and other toxic or metabolic factors. Based on the causative factors cerebral edema is differentiated into cytotoxic cerebral edema, vasogenic cerebral edema, osmotic and interstitial cerebral edema. Treatment of cerebral edema depends on timely diagnosis and medical assistance. Pragmatic treatment strategies such as antihypertensive medications, nonsteroidal anti-inflammatory drugs, barbiturates, steroids, glutamate and N-methyl-D-aspartate receptor antagonists and trometamol are used in clinical practice. Although the above mentioned treatment approaches are being used, owing to the complexity of the mechanisms involved in cerebral edema, a single therapeutic strategy which could ameliorate cerebral edema is yet to be identified. However, recent experimental studies have suggested that melatonin, a neurohormone produced by the pineal gland, could be an effective alternative for treating cerebral edema. In animal models of stroke, melatonin was not only shown to reduce cerebral edema but also preserved the blood brain barrier. Melatonin's beneficial effects were attributed to its properties, such as being a potent anti-oxidant, and its ability to cross the blood brain barrier within minutes after its administration. This review summarizes the beneficial effects of melatonin when used for treating cerebral edema.

  13. Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review

    Science.gov (United States)

    Lin, Xiaoping; Xu, Zhijun; Wang, Pengfei; Xu, Yan; Zhang, Gensheng

    2016-01-01

    Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients. PMID:27698733

  14. Role of PiCCO monitoring for the integrated management of neurogenic pulmonary edema following traumatic brain injury: A case report and literature review.

    Science.gov (United States)

    Lin, Xiaoping; Xu, Zhijun; Wang, Pengfei; Xu, Yan; Zhang, Gensheng

    2016-10-01

    Neurogenic pulmonary edema (NPE) is occasionally observed in patients with traumatic brain injury (TBI); however, this condition is often underappreciated. NPE is frequently misdiagnosed due to its atypical clinical performance, thus delaying appropriate treatment. A comprehensive management protocol of NPE in patients with TBI has yet to be established. The current study reported the case of a 67-year-old man with severe TBI who was transferred to our intensive care unit (ICU). On day 7 after hospitalization, the patient suddenly suffered tachypnea, tachycardia, systemic hypertension and hypoxemia during lumbar cistern drainage. Intravenous diuretics, tranquilizer and glucocorticoid were administered due to suspected left heart failure attack. Chest radiography examination supported the diagnosis of pulmonary edema; however, hypotension and hypovolemia were subsequently observed. Pulse index continuous cardiac output (PiCCO) hemodynamic monitoring and bedside echocardiography were performed, which excluded the diagnosis of cardiac pulmonary edema, and thus the diagnosis of NPE was confirmed. Goal-directed therapy by dynamic PiCCO monitoring was then implemented. In addition, levosimendan, an inotropic agent, was introduced to improve cardiac output. The patient had complete recovered from pulmonary edema and regained consciousness on day 11 of hospitalization. The current case demonstrated that PiCCO monitoring may serve a central role in the integrated management of NPE in patients with TBI. Levosimendan may be a potential medicine in treating cardiac dysfunction, along with its benefit from improving neurological function in NPE patients.

  15. Increased toll-like receptor 4 in cerebral endothelial cells contributes to the astrocyte swelling and brain edema in acute hepatic encephalopathy.

    Science.gov (United States)

    Jayakumar, Arumugam R; Tong, Xiao Y; Curtis, Kevin M; Ruiz-Cordero, Roberto; Abreu, Maria T; Norenberg, Michael D

    2014-03-01

    Astrocyte swelling and the subsequent increase in intracranial pressure and brain herniation are major clinical consequences in patients with acute hepatic encephalopathy. We recently reported that conditioned media from brain endothelial cells (ECs) exposed to ammonia, a mixture of cytokines (CKs) or lipopolysaccharide (LPS), when added to astrocytes caused cell swelling. In this study, we investigated the possibility that ammonia and inflammatory agents activate the toll-like receptor 4 (TLR4) in ECs, resulting in the release of factors that ultimately cause astrocyte swelling. We found a significant increase in TLR4 protein expression when ECs were exposed to ammonia, CKs or LPS alone, while exposure of ECs to a combination of these agents potentiate such effects. In addition, astrocytes exposed to conditioned media from TLR4-silenced ECs that were treated with ammonia, CKs or LPS, resulted in a significant reduction in astrocyte swelling. TLR4 protein up-regulation was also detected in rat brain ECs after treatment with the liver toxin thioacetamide, and that thioacetamide-treated TLR4 knock-out mice exhibited a reduction in brain edema. These studies strongly suggest that ECs significantly contribute to the astrocyte swelling/brain edema in acute hepatic encephalopathy, likely as a consequence of increased TLR4 protein expression by blood-borne noxious agents.

  16. Molecular pathophysiology of cerebral edema.

    Science.gov (United States)

    Stokum, Jesse A; Gerzanich, Volodymyr; Simard, J Marc

    2016-03-01

    Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the study of cerebral edema is the study of maladaptive ion transport. Following acute CNS injury, cells of the neurovascular unit, particularly brain endothelial cells and astrocytes, undergo a program of pre- and post-transcriptional changes in the activity of ion channels and transporters. These changes can result in maladaptive ion transport and the generation of abnormal osmotic forces that, ultimately, manifest as cerebral edema. This review discusses past models and current knowledge regarding the molecular and cellular pathophysiology of cerebral edema.

  17. Elevated pulmonary artery pressure and brain natriuretic peptide in high altitude pulmonary edema susceptible non-mountaineers

    Science.gov (United States)

    Gupta, Rajinder K.; Himashree, G.; Singh, Krishan; Soree, Poonam; Desiraju, Koundinya; Agrawal, Anurag; Ghosh, Dishari; Dass, Deepak; Reddy, Prassana K.; Panjwani, Usha; Singh, Shashi Bala

    2016-01-01

    Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo2 = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects. Baseline Ppa (19.31 ± 3.63 vs 15.68 ± 2.79 mm Hg, p < 0.05) and plasma BNP levels (52.39 ± 32.9 vs 15.05 ± 9.6 pg/ml, p < 0.05) were high and stroke volume was less (p < 0.05) in HAPE-S subjects compared to control. Acute hypoxia produced an exaggerated increase in heart rate (p < 0.05), mean arterial pressure (p < 0.05) and Ppa (28.2 ± 5.8 vs 19.33 ± 3.74 mm Hg, p < 0.05) and fall in peripheral oxygen saturation (p < 0.05) in HAPE-S compared to control. Receiver operating characteristic (ROC) curves showed that Ppa response to acute hypoxia was the best variable to identify HAPE susceptibility (AUC 0.92) but BNP levels provided comparable information (AUC 0.85). BNP levels are easy to determine and may represent an important marker for the determination of HAPE susceptibility. PMID:26892302

  18. Pulmonary Edema

    OpenAIRE

    Tanser, Paul H.

    1981-01-01

    The physician who deals with pulmonary edema from a pathophysiologic basis will seldom make a diagnostic or therapeutic error. Recent additions to preload and afterload therapy have greatly helped in the emergency and ambulatory treatment of pulmonary edema due to left heart failure. Careful follow-up and patient self-monitoring are the most effective means of reducing hospitalization of chronic heart failure patients.

  19. Quantitative evaluation of benign meningioma and hemangiopericytoma with peritumoral brain edema by 64-slice CT perfusion imaging

    Institute of Scientific and Technical Information of China (English)

    REN Guang; CHEN Shuang; WANG Yin; ZHU Rui-jiang; GENG Dao-ying; FENG Xiao-yuan

    2010-01-01

    Background Hemangiopericytomas (HPCs) have a relentless tendency for local recurrence and metastases,differentiating between benign meningiomas and HPCs before surgery is important for both treatment planning and the prognosis appraisal.The purpose of this study was to evaluate the correlations between CT perfusion parameters and microvessel density (MVD) in extra-axial tumors and the possible role of CT perfusion imaging in preoperatively differentiating benign meningiomas and HPCs.Methods Seventeen patients with benign meningiomas and peritumoral edema, 12 patients with HPCs and peritumoral edema underwent 64-slice CT perfusion imaging pre-operation.Perfusion was calculated using the Patlak method.The quantitative parameters, include cerebral blood volume (CBV), permeability surface (PS) of parenchyma, peritumoral edema among benign meningiomas and HPCs were compared respectively.CBV and PS in parenchyma, peritumoral edema of benign meningiomas and HPCs were also compared to that of the contrallateral normal white matter respectively.The correlations between CBV, PS of tumoral parenchyma and MVD were examined.Results The value of CBV and PS in parenchyma of HPCs were significantly higher than that of benign meningiomas (P<0.05), while the values of CBV and PS in peritumoral edema of benign meningiomas and HPCs were not significantly different (P >0.05).MVD in parenchyma of HPCs were significantly higher than that of benign meningiomas (P<0.05).There were positive correlations between CBV and MVD (r=0.648, P<0.05), PS and MVD (r=0.541, P<0.05) respectively.Furthermore, the value of CBV and PS in parenchyma of benign meningiomas and HPCs were significantly higher than that of contrallateral normal white matter (P<0.05), the value of CBV in peritumoral edema of benign meningiomas and HPCs were significantly lower than that of contrallateral normal white matter (P<0.05), while the value of PS in peritumoral edema of benign meningiomas and HPCs were not

  20. Effect of siRNA‑induced inhibition of IL‑6 expression in rat cerebral gliocytes on cerebral edema following traumatic brain injury.

    Science.gov (United States)

    Xu, Bin; Yu, Dong-Ming; Liu, Fu-Sheng

    2014-10-01

    The present study aimed to investigate the effect of RNA interference (RNAi) on the inhibition of interleukin (IL)‑6 expression in rat cerebral gliocytes in vitro and rat cerebral traumatic tissues in vivo, as well as the effect of RNAi on cerebral edema. pSUPER vectors containing IL‑6 small hairpin RNA (pSUPER‑IL‑6 1‑5) were designed, constructed and transfected into C6 rat glioma cells using cationic liposomes. ELISA was used to select the plasmid with the strongest interference effect. A freefall method was used to generate a rat brain injury model and rats were randomly divided into treatment, empty plasmid and control groups (n=14/group). IL‑6 levels, water content and sodium content were determined in the brain tissues at 24 and 72 h post‑injury. pSUPER‑IL‑6 was effectively transfected into C6 cells and was found to inhibit the expression of IL‑6 rather than IL‑8. The pSUPER‑IL‑6 1 vector was most effective in inducing RNAi. In vivo, IL‑6 levels were observed to be lowest in the interference group and there were statistically significant differences in water and sodium content among the experimental groups (Pcerebral gliocytes, and the reduction of the IL‑6 levels was found to reduce post‑traumatic cerebral edema.

  1. Progress in Drug Treatment of Cerebral Edema.

    Science.gov (United States)

    Deng, Y Y; Shen, F C; Xie, D; Han, Q P; Fang, M; Chen, C B; Zeng, H K

    2016-01-01

    Cerebral edema causes intracranial hypertension (ICH) which leads to severe outcome of patients in the clinical setting. Effective anti-edema therapy may significantly decrease the mortality in a variety of neurological conditions. At present drug treatment is a cornerstone in the management of cerebral edema. Osmotherapy has been the mainstay of pharmacologic therapy. Mannitol and hypertonic saline (HS) are the most commonly used osmotic agents. The relative safety and efficacy of HS and mannitol in the treatment of cerebral edema and reduction of enhanced ICP have been demonstrated in the past decades. Apart from its osmotic force, HS exerts anti-edema effects partly through inhibition of Na(+)-K(+)-2Cl(-) Cotransporter-1 (NKCC1) and aquaporin 4 (AQP4) expression in astrocytes. Melatonin may also reduce brain edema and exert neuroprotective effect on several central nervous system diseases through inhibition of inflammatory response. The inhibitors of Na/H exchanger, NKCC and AQP4 may attenuate brain edema formation through inhibition of excessive transportation of ion and water from blood into the cerebral tissue. In this review we survey some of the most recent findings in the drug treatment of brain edema focusing on the use of osmotherapy, melatonin and inhibitors of ion cotransporters and water channels. A better understanding of the molecular mechanism of these agents would help to improve in the clinical management of patients with brain edema.

  2. Edema pulmonar de gran altura HIGH ALTITUDE PULMONARY EDEMA

    Directory of Open Access Journals (Sweden)

    FELIPE UNDURRAGA M

    2003-04-01

    Full Text Available Las enfermedades de altura son de causa cerebral y pulmonar. Las primeras se refieren fundamentalmente al mal agudo de montaña y al edema cerebral de altura y las segundas al edema pulmonar agudo de montaña. Actuales evidencias señalan que el edema cerebral sería un fenómeno universal de los que ascienden a altura y que tres de cada cuatro individuos sanos que se expongan a altura desarrollarán un edema pulmonar agudo de montaña subclínico. La hipoxia de altura es la responsable de estos cuadros y los sujetos susceptibles serían aquellos que genéticamente tienen una respuesta ventilatoria reducida a la hipoxia y una exagerada respuesta vasopresora pulmonar al ejercicio.Se presenta un caso de edema pulmonar agudo de montaña en un deportista previamente sano que participó en una expedición al cerro El Plomo (5.280 msnm en la Cordillera de los Andes central. Posteriormente, se comenta la fisiopatología y tratamiento de esta condiciónHigh altitude diseases are originated from brain and lung. The first are Acute Mountain Sickness and Brain edema and the second is High Altitude Pulmonary Edema (HAPE. Current evidence shows that brain edema is an universal event of the people who are exposed to high altitude. By other hand 3 out of 4 healthy subjects exposed to high altitude will present a subclinical HAPE. Hypoxia of altitude is the responsable for this condition. The susceptible subjects would be those who genetically have a low ventilatory response to hypoxia and an exaggerated increase of vascular pulmonary pressure during exercise. A clinical case of acute pulmonary edema in a young sportman who participated in an expedition to Cerro El Plomo (5.280 m in Chilean Central Andes Mountains is presented. Pathophysiology and treatment of these conditions are discussed

  3. Unilateral pulmonary edema following acute subglottic edema.

    Science.gov (United States)

    Morisaki, H; Ochiai, R; Takeda, J; Nagano, M

    1990-01-01

    Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.

  4. Dynamics of cerebral edema and the apparent diffusion coefficient of water changes in patients with severe traumatic brain injury. A prospective MRI study

    Energy Technology Data Exchange (ETDEWEB)

    Pasco, Anne [Larrey Hospital, Angers University, Department of Radiology, Cedex (France); Inserm, Angers (France); Angers University, Angers (France); Minassian, Aram Ter [Larrey Hospital, Angers University, Department of Anaesthesiology, Cedex (France); Chapon, Catherine; Lemaire, Laurent; Benoit, Jean-Pierre; Jeune, Jean-Jacques Le [Inserm, Angers (France); Angers University, Angers (France); Franconi, Florence [Angers University, SCAS, Angers (France); Darabi, Dana; Caron, Christine [Larrey Hospital, Angers University, Department of Radiology, Cedex (France)

    2006-07-15

    The distinction between intracellular (ICE) and extracellular edema (ECE) has a crucial prognostic and therapeutic importance in patients with severe traumatic brain injury (STBI). Indeed, ICE usually leads to cellular death, and maintenance of a cerebral perfusion pressure (CPP) above 70 mmHg is still under debate since this practice may increase ECE. The purpose of this study was to describe the ECE and ICE kinetics associated with STBI using quantitative diffusion MRI. Twelve patients were prospectively studied. The initial ADC in ICE measured on day 1.3{+-}0.7 is significantly reduced compared to normal-appearing parenchyma (0.51{+-}0.12 * 10{sup -3} mm{sup 2}/s vs. 0.76{+-}0.03 * 10{sup -3} mm{sup 2}/s, n=12, P<0.0001) and reaches normality on MRI 3 performed on day 14.2{+-}3.3. In patients presenting an extension of ICE on MRI 2 performed on day 6.7{+-}1.4 (ADC{sub MRI2}=0.40{+-}0.11 * 10{sup -3} mm{sup 2}/s), ADC values in the extension area at the first MRI were slightly, but not significantly reduced compared to normal parenchyma (0.69{+-}0.05 * 10{sup -3} mm{sup 2}/s, P=0.29). Normalization occurred equally by day 14. ADC in ECE (1.34{+-}0.22 * 10{sup -3} mm{sup 2}/s) was elevated and stable with time under CPP therapy. Therefore, ECE is not worsened by CCP therapy, and ICE appears more relevant than ECE in STBI. (orig.)

  5. Progress on the New Mechanism of Venom Defibrase in Brain Edema after Stroke%蛇毒降纤酶治疗脑卒中后脑水肿的机制研究新进展

    Institute of Scientific and Technical Information of China (English)

    卜宪聪

    2012-01-01

    脑卒中在我国是一种严重的疾病.脑水肿在脑出血后的继发性脑损伤中起着重要的作用,是严重的并发症,其机制不清.蛇毒降纤酶可有效抑制血栓的形成且溶解血栓,目前已被广泛用于急性缺血性脑卒中的治疗.动物研究表明,蛇毒素能清除氧自由基、下调c-fos基因的表达,以及减少补体浸润等作用,能减轻脑缺血后脑水肿和脑损伤.现将蛇毒降纤酶对脑卒中后脑水肿的机制研究现状予以综述.%Stroke is a serious disease in China. Brain edema plays an important role in intracerebral hemorrhage secondary brain injury,which is a serious complication,whereas the mechanism is unclear. Snake venom defibrase can effectively inhibit thrombus formation and dissolution of blood clots, which has been widely used in the treatment of acute ischemic stroke. Animal studies have shown that snake toxins can remove oxygen free radicals,reduced the expression of c-fos gene,reduce the role of complement infiltration,ischemic brain edema and brain damage. The mechanisms of venom defibrase function on brain edema after stroke is to be reviewed here.

  6. Cerebral edema in drug addicts

    Directory of Open Access Journals (Sweden)

    Daruši Dragana J.

    2014-01-01

    Full Text Available Background/Aim. The effect of drugs leaves permanent consequences on the brain, organic in type, followed by numerous manifestations, and it significantly affects the development of mental dysfunctions. The clinicians are often given a task to estimate a patient’s personality during treatment or during experts estimate of a drug addict. The aim of this research was to determine the differences, if any, in characteristics of addicts experience and personality traits in drug addicts with or without cerebral edema. Methods. The research was conducted on a sample of 252 male drug addicts, the average age of 23.3 (SD = 4.3 years. Cerebral edema was confirmed on magnetic resonance (MR images of the brain performed during the treatment of the addicts. The participants were tested by the psychologists using Minnesota Multiphasic Personality Inventory (MMPI-201 test, and the data were processed using canonical discriminate analysis within the SPSS program. The dependent variable in the study was cerebral edema. A block of independent variables, designed for the requirements of this study, consisted of two subgroups. The first one consisted of 12 variables describing the relevant characteristics of drug abuse. The second subgroup consisted of 8 psychopathological tendencies in the personality defined by the mentioned test. Results. Cerebral edema was confirmed in 52 (20.63% of the drug addicts. The differences between the groups of drug addicts with and without cerebral edema were determined in the following: the time span of taking drugs (0.301, use of alcohol parallel with drugs (0.466, and treatment for addiction (0.603. In the drug addicts with a cerebral edema, MMPI-201 confirmed the increase in the scales for hypochondria, psychopathic deviations and psychastenia, and the decrease in the scales for schizophrenia and depression. Conclusion. Our study confirmed a possible connection between cerebral edema and personality traits in a number of the

  7. Mechanisms of Astrocyte-Mediated Cerebral Edema

    Science.gov (United States)

    Stokum, Jesse A.; Kurland, David B.; Gerzanich, Volodymyr; Simard, J. Marc

    2014-01-01

    Cerebral edema formation stems from disruption of blood brain barrier (BBB) integrity and occurs after injury to the CNS. Due to the restrictive skull, relatively small increases in brain volume can translate into impaired tissue perfusion and brain herniation. In excess, cerebral edema can be gravely harmful. Astrocytes are key participants in cerebral edema by virtue of their relationship with the cerebral vasculature, their unique compliment of solute and water transport proteins, and their general role in brain volume homeostasis. Following the discovery of aquaporins, passive conduits of water flow, aquaporin 4 (AQP4) was identified as the predominant astrocyte water channel. Normally, AQP4 is highly enriched at perivascular endfeet, the outermost layer of the BBB, whereas after injury, AQP4 expression disseminates to the entire astrocytic plasmalemma, a phenomenon termed dysregulation. Arguably, the most important role of AQP4 is to rapidly neutralize osmotic gradients generated by ionic transporters. In pathological conditions, AQP4 is believed to be intimately involved in the formation and clearance of cerebral edema. In this review, we discuss aquaporin function and localization in the BBB during health and injury, and we examine post-injury ionic events that modulate AQP4- dependent edema formation. PMID:24996934

  8. Isolated unilateral disk edema

    Directory of Open Access Journals (Sweden)

    Varner P

    2011-07-01

    Full Text Available Paul VarnerJohn J Pershing VAMC, Poplar Bluff, MO, USAAbstract: Isolated unilateral disk edema is a familiar clinical presentation with myriad associations. Related, non-consensus terminology is a barrier to understanding a common pathogenesis. Mechanisms for the development of disk edema are reviewed, and a new framework for clinical differentiation of medical associations is presented.Keywords: disk edema, axoplasmic flow, clinical multiplier, optic neuritis, ischemic optic neuropathy, papilledema

  9. Isolated unilateral disk edema

    OpenAIRE

    Varner P

    2011-01-01

    Paul VarnerJohn J Pershing VAMC, Poplar Bluff, MO, USAAbstract: Isolated unilateral disk edema is a familiar clinical presentation with myriad associations. Related, non-consensus terminology is a barrier to understanding a common pathogenesis. Mechanisms for the development of disk edema are reviewed, and a new framework for clinical differentiation of medical associations is presented.Keywords: disk edema, axoplasmic flow, clinical multiplier, optic neuritis, ischemic optic neuropathy, papi...

  10. Effect observation of piracetam combined mannitol in the treatment of brain edema after intracerebral hemorrhage%吡拉西坦联合甘露醇治疗脑出血后脑水肿的效果观察

    Institute of Scientific and Technical Information of China (English)

    张三军

    2015-01-01

    Objective:To observe the effect of piracetam combined mannitol in the treatment of brain edema after intracerebral hemorrhage.Methods:90 cases of patients with brain edema after cerebral hemorrhage were divided into two groups.The control group were given mannitol treatment.The observation group were given piracetam combined mannitol therapy.The curative effect of the two groups were observed.Results:After treatment,the total effective rate of the observation group 95.56% was significantly higher than that of the control group 51.11%(P<0.05).The brain edema volume of the observation group(7.42±2.15)cm3 was less than that of the control group(15.56 ± 4.28)cm3.The differences were statistically significant(P<0.05).Conclusion:Piracetam combined mannitol in the treatment of brain edema after intracerebral hemorrhage had remarkable effect.%目的:观察脑出血后脑水肿行甘露醇与吡拉西坦联合治疗的效果。方法:收治脑出血后脑水肿患者90例,分为两组。对照组行甘露醇治疗,观察组行甘露醇与吡拉西坦联合治疗,观察两组疗效。结果:治疗后,观察组总有效率95.56%显著高于对照组的51.11%(P<0.05)。观察组脑水肿的体积(7.42±2.15)cm3少于对照组的(15.56±4.28)cm3,差异具有统计学意义(P<0.05)。结论:脑出血后脑水肿行甘露醇与吡拉西坦联合治疗的效果显著。

  11. Relationship and action mechanism between oxygen free radicals and aquaporin 4 in brain edema%氧自由基与水通道蛋白4在脑水肿中作用机制及联系

    Institute of Scientific and Technical Information of China (English)

    陈珊; 徐国海

    2011-01-01

    Background Aquaporin-4(AQP4) may be one of the candidates for inducing brain edema,however,it has not been reported whether AQP4 and oxidative free radical is involved in the formation of brain edema.Objective To study the effect as well as the mechanism of oxidative free radical and AQP4 on cerebral edema.Content Aquaporin (AQP) is a membrane water channel protein family.And AQP4 is abundant within the nervous system and is closely related to the physiological and pathological process particularly in the metabolism of water.Perihematoma antioxidant imbalance and oxidative free radical reactions further increase the cerebral edema in acute cerebral hemorrhage.Trend It will provide basis for further exploring of the pathogenesis of cerebral edema by studying the relationship between oxidative free radical and AQP.%背景 水通道蛋白4(aquaporin-4,AQP4)可能是导致脑水肿形成的调节因素之一,但AQP4与氧自由基作用与脑水肿形成尚未见报道.目的 将AQP4与氧自由基在脑水肿的作用及其机制作简要的概述.内容 水通道蛋白(aquaporin,AQP)是膜水通道蛋白家族,其中AQP4在神经系统内含量最丰富,与神经系统生理和病理过程尤其水的代谢密切相关,同时急性脑出血时血肿周围脑组织氧化抗氧化平衡紊乱及自由基反应病理性加剧进一步加重脑水肿.趋向 通过研究氧自由基与APQ关系,进一步为脑水肿的发病机制奠定基础.

  12. Edema control by cediranib, a vascular endothelial growth factor receptor-targeted kinase inhibitor, prolongs survival despite persistent brain tumor growth in mice

    DEFF Research Database (Denmark)

    Kamoun, Walid S; Ley, Carsten D; Farrar, Christian T

    2009-01-01

    by an increase in plasma collagen IV. These rapid changes in tumor vascular morphology and function led to edema alleviation -- as measured by MRI and by dry/wet weight measurement of water content -- but did not affect tumor growth. By immunohistochemistry, we found a transient decrease in macrophage...

  13. Role of Aquaporin-4 in Cerebral Edema and Stroke

    OpenAIRE

    Zador, Zsolt; Stiver, Shirley; Wang, Vincent; MANLEY, GEOFFREY T.

    2009-01-01

    Cerebral edema plays a central role in the pathophysiology of many diseases of the central nervous system (CNS) including ischemia, trauma, tumors, inflammation, and metabolic disturbances. The formation of cerebral edema results in an increase in tissue water content and brain swelling which, if unchecked, can lead to elevated intracranial pressure (ICP), reduced cerebral blood flow, and ultimately cerebral herniation and death. Despite the clinical significance of cerebral edema, the mechan...

  14. Transient cooling during early reperfusion attenuates delayed edema and infarct progression in the Spontaneously Hypertensive Rat. Distribution and time course of regional brain temperature change in a model of postischemic hypothermic protection.

    Science.gov (United States)

    Kurasako, Toshiaki; Zhao, Liang; Pulsinelli, William A; Nowak, Thaddeus S

    2007-12-01

    The temperature threshold for protection by brief postischemic cooling was evaluated in a model of transient focal ischemia in the Spontaneously Hypertensive Rat, using an array of epidural probes to monitor regional brain temperatures. Rats were subjected to 90 mins tandem occlusion of the right middle cerebral artery (MCA) and common carotid artery. Systemic cooling to 32 degrees C was initiated 5 mins before recirculation, with simultaneous brain cooling to temperatures ranging from 28 degrees C to 32 degrees C within the MCA territory by means of a temperature-controlled saline drip. Rewarming was initiated at 2 h recirculation and was complete within 30 mins. Tissue damage and edema volume showed clear temperature-dependent reductions when evaluated at 3 days survival, with no protection evident in the group at 32 degrees C but progressive effects on both parameters after deeper cooling. A particularly striking effect was the essentially complete elimination of edema progression between 1 and 3 days. Temperature at distal sites within the MCA territory better predicted reductions in lesion volume, indicating that protection required effective cooling of the penumbral regions destined to be spared. These results show that even brief cooling can be highly protective when initiated at the time of recirculation after focal ischemia, but indicate a substantially lower temperature threshold for hypothermic protection than has been reported for other strains, occlusion methods, and cooling durations.

  15. The clinical study of external application of mirabilite to treat the postoperative brain edema in brain injury patients%芒硝外敷治疗颅脑外伤术后脑水肿的临床研究

    Institute of Scientific and Technical Information of China (English)

    张珏; 许乐宜; 龚立; 书国伟; 王静予; 蔡佩浩; 邱锋; 孔令军; 费智敏

    2015-01-01

    Objective To study the effects of external application of mirabilite in the treatment of brain injury patients with brain edema postoperative of decompressive craniectomy.Methods 60 brain injury patients from the department of neurosurgery in shuguang hospital,who were underwent decompressive craniectomy, were randomly divided into a control group and an observation group, with 30 patients in each.. The observation group was treated according to the results of intracranial pressure (ICP) monitoring. The control group was underwent additional external application of mirabilite. Comparisons were conducted on daily ICP, bispectral index(BIS) and Glasgow coma scale (GCS) in postoperative one week. The hospitalization days and expense were also be analysed. All patients were treated for 3 months and the Glasgow outcome scale (GOS) was recorded. Result The ICP of control group was lower than the observational group in postoperative day 2,3 and 5 (32±2.2 mmHgvs. 35± 2.2 mmHg,t=2.351; 31±2.0 mmHgvs. 33±2.1 mmHg,t=2.224; 26±2.3 mmHgvs. 28±1.9 mmHg, t=2.536), the BIS is higher in day 3 and 5(47±4.3 vs.43±4.2 t=2.379; 55±5.3 vs.52±3.9, t=2.559). There was significant difference in hospitalization days between the two groups (16.5 ± 1.2 dvs. 17.2 ± 1.1 d, t=2.355,P=0.022). There was significant difference between the two groups(P<0.05). There was also significant difference in hospitalization expense with 7.37 ± 0.68(million yuan) in the control group and 8.14 ±1.12 in the observational group(t=2.056,P=0.042).Conclusion The external application of mirabilite was effective in the treatment of brain injury patient with brain edema postoperative of decompressive craniectomy.%目的 评价芒硝外敷治疗颅脑外伤去骨瓣减压术后脑水肿的临床疗效.方法 将符合纳入标准的颅脑外伤去骨瓣减压术后患者60例,按随机数字表法分为2组各30例,2组均在颅内压监测基础上行阶梯化治疗,常规治疗组在伤口处以消毒

  16. [Cardiogenic and non cardiogenic pulmonary edema: pathomechanisms and causes].

    Science.gov (United States)

    Glaus, T; Schellenberg, S; Lang, J

    2010-07-01

    The development of pulmonary edema is divided in cardiogenic and non-cardiogenic. Cardiogenic edema pathogenically is caused by elevated hydrostatic pressure in the pulmonary capillaries due to left sided congestive heart failure. Non-cardiogenic pulmonary edema is categorized depending on the underlying pathogenesis in low-alveolar pressure, elevated permeability or neurogenic edema. Some important examples of causes are upper airway obstruction like in laryngeal paralysis or strangulation for low alveolar pressure, leptospirosis and ARDS for elevated permeability, and epilepsy, brain trauma and electrocution for neurogenic edema. The differentiation between cardiogenic versus non-cardiogenic genesis is not always straightforward, but most relevant, because treatment markedly differs between the two. Of further importance is the identification of the specific underlying cause in non-cardiogenic edema, not only for therapeutic but particularly for prognostic reasons. Depending on the cause the prognosis ranges from very poor to good chance of complete recovery.

  17. Effect of mild hypothermia on the brain edema of severe head injury%亚低温对重型颅脑损伤后脑水肿的影响

    Institute of Scientific and Technical Information of China (English)

    夏永勤; 徐如祥; 王向宇

    2000-01-01

    目的 研究亚低温对重型颅脑损伤(SHI)后脑水肿的影响及其临床意义。方法 36例SHI患者,随机分为常规治疗对照组和常规治疗+亚低温治疗组,各18例。亚低温方法:患者接受冰帽、冰毯和冰袋降温措施处理及冬眠Ⅰ辅助降温,保持肛温在33℃左右,并维持3~5 d。手术后病人均监测颅内压。每例病人伤后0、1、3、7、14、21 d各行一次头颅CT检查,分析比较两组颅内压、伤灶脑水肿体积变化和预后状况。结果 颅内压:对照组和治疗组伤后第3天分别是(2.87±0.26)kPa和(1.67±0.23)kPa (P<0.01);第7天分别为 (3.15±0.24)kPa和(1.78±0.24)kPa (P<0.01)。伤灶脑水肿体积:对照组在伤后第14天最大 [(140.90±22.95)cm3],治疗组在伤后第3天最大[(95.83±14.97)cm3],治疗组比对照组在伤后第14天减少42%(P<0.05)。伤后一周内转清醒率:对照组为22.2%(4/18例),治疗组为55.6%(10/18例)(P<0.05);残死率:对照组为61.1%(11/18例),治疗组为33.3%(6/18例)。结论 亚低温能减轻脑水肿、稳定颅内压和改善预后。%Objective To investigate the effect of mild hypothermia on brain edema after severe head injury (SHI) and its clinical significance. Methods Thirty-six patients with SHI were randomly divided into conventional therapy group (control group) and mild hypothermia therapeutic group (therapeutic group), with 18 patients in each group. The patients in the therapeutic group were treated with ice-cap, ice-blanket and ice-bag and lytic cocktail Ⅰas adjuvants, and a rectal temperature of 33 ℃ was maintained for 3~5 d. Intracranial pressure (ICP) of all the patients after operation were monitored postoperatively. The size of brain edema was measured with CT on day 0, 1, 3, 7, 14, 21 respectively after SHI. The size of brain edema at the trauma cite and ICP as well as the clinical outcome were compared and

  18. Pulmonary edema: radiographic differential diagnosis

    Energy Technology Data Exchange (ETDEWEB)

    Yoo, Dong Soo; Choi, Young Hi; Kim, Seung Cheol; An, Ji Hyun; Lee, Jee Young; Park, Hee Hong [Dankook Univ. College of Medicine, Chonan (Korea, Republic of)

    1997-04-01

    To evaluate the feasibility of using chest radiography to differentiate between three different etiologies of pulmonary edema. Plain chest radiographs of 77 patients, who were clinically confirmed as having pulmonary edema, were retrospectively reviewed. The patients were classified into three groups : group 1 (cardiogenic edema : n = 35), group 2 (renal pulmonary edema : n = 16) and group 3 (permeability edema : n = 26). We analyzed the radiologic findings of air bronchogram, heart size, peribronchial cuffing, septal line, pleural effusion, vascular pedicle width, pulmonary blood flow distribution and distribution of pulmonary edema. In a search for radiologic findings which would help in the differentiation of these three etiologies, each finding was assessed. Cardiogenic and renal pulmonary edema showed overlapping radiologic findings, except for pulmonary blood flow distribution. In cardiogenic pulmonary edema (n=35), cardiomegaly (n=29), peribronchial cuffing (n=29), inverted pulmonary blood flow distribution (n=21) and basal distribution of edema (n=20) were common. In renal pulmonary edema (n=16), cardiomegaly (n=15), balanced blood flow distribution (n=12), and central (n=9) or basal distribution of edema (n=7) were common. Permeability edema (n=26) showed different findings. Air bronchogram (n=25), normal blood flow distribution (n=14) and peripheral distribution of edema (n=21) were frequent findings, while cardiomegaly (n=7), peribronchial cuffing (n=7) and septal line (n=5) were observed in only a few cases. On plain chest radiograph, permeability edema can be differentiated from cardiogenic or renal pulmonary edema. The radiographic findings which most reliably differentiated these two etiologies were air bronchogram, distribution of pulmonary edema, peribronchial cuffing and heart size. Only blood flow distribution was useful for radiographic differentiation of cardiogenic and renal edema.

  19. Latest advances in edema

    Science.gov (United States)

    Villavicencio, J. L.; Hargens, A. R.; Pikoulicz, E.

    1996-01-01

    Basic concepts in the physiopathology of edema are reviewed. The mechanisms of fluid exchange across the capillary endothelium are explained. Interstitial flow and lymph formation are examined. Clinical disorders of tissue and lymphatic transport, microcirculatory derangements in venous disorders, protein disorders, and lymphatic system disorders are explored. Techniques for investigational imaging of the lymphatic system are explained.

  20. Reperfusion pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Klausner, J.M.; Paterson, I.S.; Mannick, J.A.; Valeri, C.R.; Shepro, D.; Hechtman, H.B. (Harvard Medical School, Boston, MA (USA))

    1989-02-17

    Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B{sub 4} and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. The authors conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.

  1. Reexpansion pulmonary edema

    OpenAIRE

    Genofre Eduardo Henrique; Vargas Francisco S.; Teixeira Lisete R.; Vaz Marcelo Alexandre Costa; Marchi Evaldo

    2003-01-01

    Reexpansion pulmonary edema (RPE) is a rare, but frequently lethal, clinical condition. The precise pathophysiologic abnormalities associated with this disorder are still unknown, though decreased pulmonary surfactant levels and a pro-inflammatory status are putative mechanisms. Early diagnosis is crucial, since prognosis depends on early recognition and prompt treatment. Considering the high mortality rates related to RPE, preventive measures are still the best available strategy for patient...

  2. Acute Idiopathic Scrotal Edema

    Directory of Open Access Journals (Sweden)

    Micheál Breen

    2013-01-01

    Full Text Available We report a case of acute idiopathic scrotal edema (AISE in a 4-year-old boy who presented with acute scrotal pain and erythema. The clinical features, ultrasound appearance, and natural history of this rare diagnosis are reviewed. In this report, we highlight the importance of good ultrasound technique in differentiating the etiology of the acute scrotum and demonstrate the color Doppler “Fountain Sign” that is highly suggestive of AISE.

  3. Vasogenic edema characterizes pediatric acute disseminated encephalomyelitis

    Energy Technology Data Exchange (ETDEWEB)

    Zuccoli, Giulio; Panigrahy, Ashok; Sreedher, Gayathri; Bailey, Ariel [Children' s Hospital of Pittsburgh of UPMC, Department of Radiology, Section of Neuroradiology, Pittsburgh, PA (United States); Laney, Ernest John [Children' s Hospital of Pittsburgh of UPMC, Department of Radiology, Section of Neuroradiology, Pittsburgh, PA (United States); Rush University Medical Center, Department of Diagnostic Radiology, Chicago, IL (United States); La Colla, Luca [University of Parma, Department of Anesthesiology, Parma (Italy); UPMC Shadyside Hospital, Department of Emergency Medicine, Pittsburgh, PA (United States); Alper, Gulay [Children' s Hospital of Pittsburgh of UPMC, Department of Pediatric Neurology, Neuroimmunology Clinic, Pittsburgh, PA (United States)

    2014-08-15

    MR imaging criteria for diagnosing acute disseminated encephalomyelitis (ADEM) have not been clearly established. Due to the wide spectrum of differential considerations, new imaging features allowing early and accurate diagnosis for ADEM are needed. We hypothesized that ADEM lesions would be characterized by vasogenic edema due to the potential reversibility of the disease. Sixteen patients who met the diagnostic criteria for ADEM proposed by the International Pediatric Multiple Sclerosis Study Group (IPMSSG) and had complete MR imaging studies performed at our institution during the acute phase of the disease were identified retrospectively and evaluated by experienced pediatric neuroradiologists. Vasogenic edema was demonstrated on diffusion-weighted imaging (DWI) and corresponding apparent diffusion coefficient (ADC) maps in 12 out of 16 patients; cytotoxic edema was identified in two patients while the other two patients displayed no changes on DWI/ADC. ADC values for lesions and normal-appearing brain tissue were 1.39 ± 0.45 x 10{sup -3} and 0.81 ± 0.09 x 10{sup -3} mm/s{sup 2}, respectively (p = 0.002). When considering a cutoff of 5 days between acute and subacute disease, no difference between ADC values in acute vs. subacute phase was depicted. However, we found a significant correlation and an inverse and significant relationship between time and ADC value. We propose that vasogenic edema is a reliable diagnostic sign of acute neuroinflammation in ADEM. (orig.)

  4. Edema pulmonar neurogênico: relato de dois casos Neurogenic pulmonary edema: report of two cases

    Directory of Open Access Journals (Sweden)

    Desanka Dragosavac

    1997-06-01

    Full Text Available O edema pulmonar neurogênico é rara e grave complicação de pacientes com traumatismo craniencefálico (TCE. Pode ocorrer também em outras patologias do sistema nervoso central, tais como acidentes vasculares cerebrais (AVC, tumores ou após crises epilépticas, entre outras. Foram avaliados 36 casos com TCE grave e quatro pacientes com AVC, internados na UTI geral, no período de janeiro a setembro 1995. Nesse intervalo de tempo foram diagnosticados dois casos de edema pulmonar neurogênico, um ocorrendo em paciente com TCE grave e outro em paciente com AVC hemorrágico. O diagnóstico foi estabelecido pelo rápido desenvolvimento de edema pulmonar, com hipoxemia grave, queda da complacência pulmonar e infiltrados difusos bilaterais sem história prévia de aspiração traqueal ou outro fator de risco para o desenvolvimento de síndrome de angústia respiratória aguda. No primeiro paciente com trauma craniencefálico, o edema neurogênico foi diagnosticado na internação, uma hora após o trauma, com concomitante reação inflamatória grave e boa evolução em três dias. O outro caso, com AVC hemorrágico, desenvolveu edema neurogênico no quarto dia após drenagem de hematoma intraparenquimatoso, evoluindo para o óbito.Neurogenic pulmonary edema is a rare and serious complication in patients with head injury. It also may develop after a variety of cerebral insults such as subarachnoid hemorrhage, brain tumors and after epileptic seizures. Thirty six patients with severe head injury and four patients with cerebrovascular insults treated in Intensive Care Unit of HC-UNICAMP from January to September 1995 were evaluated. In this period there were two patients with neurogenic pulmonary edema, one with head injury and other with intracerebral hemorrhage. Diagnosis was made by rapid onset of pulmonary edema, severe hypoxemia, decrease of pulmonary complacence and diffuse pulmonary infiltrations, without previous history of tracheal

  5. Aneurysmal wall enhancement and perianeurysmal edema after endovascular treatment of unruptured cerebral aneurysms

    Energy Technology Data Exchange (ETDEWEB)

    Su, I. Chang [Toronto Western Hospital, Division of Neuroradiology, Department of Medical Imaging, Toronto, ON (Canada); Taipei Cathay General Hospital, Division of Neurosurgery, Department of Surgery, Taipei (China); Willinsky, Robert A.; Agid, Ronit [Toronto Western Hospital, Division of Neuroradiology, Department of Medical Imaging, Toronto, ON (Canada); Fanning, Noel F. [Cork University Hospital, Department of Interventional Neuroradiology, Cork (Ireland)

    2014-06-15

    Perianeurysmal edema and aneurysm wall enhancement are previously described phenomenon after coil embolization attributed to inflammatory reaction. We aimed to demonstrate the prevalence and natural course of these phenomena in unruptured aneurysms after endovascular treatment and to identify factors that contributed to their development. We performed a retrospective analysis of consecutively treated unruptured aneurysms between January 2000 and December 2011. The presence and evolution of wall enhancement and perianeurysmal edema on MRI after endovascular treatment were analyzed. Variable factors were compared among aneurysms with and without edema. One hundred thirty-two unruptured aneurysms in 124 patients underwent endovascular treatment. Eighty-five (64.4 %) aneurysms had wall enhancement, and 9 (6.8 %) aneurysms had perianeurysmal brain edema. Wall enhancement tends to persist for years with two patterns identified. Larger aneurysms and brain-embedded aneurysms were significantly associated with wall enhancement. In all edema cases, the aneurysms were embedded within the brain and had wall enhancement. Progressive thickening of wall enhancement was significantly associated with edema. Edema can be symptomatic when in eloquent brain and stabilizes or resolves over the years. Our study demonstrates the prevalence and some appreciation of the natural history of aneurysmal wall enhancement and perianeurysmal brain edema following endovascular treatment of unruptured aneurysms. Aneurysmal wall enhancement is a common phenomenon while perianeurysmal edema is rare. These phenomena are likely related to the presence of inflammatory reaction near the aneurysmal wall. Both phenomena are usually asymptomatic and self-limited, and prophylactic treatment is not recommended. (orig.)

  6. Edema pulmonar de gran altura HIGH ALTITUDE PULMONARY EDEMA

    OpenAIRE

    FELIPE UNDURRAGA M.; ALVARO UNDURRAGA P

    2003-01-01

    Las enfermedades de altura son de causa cerebral y pulmonar. Las primeras se refieren fundamentalmente al mal agudo de montaña y al edema cerebral de altura y las segundas al edema pulmonar agudo de montaña. Actuales evidencias señalan que el edema cerebral sería un fenómeno universal de los que ascienden a altura y que tres de cada cuatro individuos sanos que se expongan a altura desarrollarán un edema pulmonar agudo de montaña subclínico. La hipoxia de altura es la responsable de estos cuad...

  7. Diabetic Macular Edema

    Science.gov (United States)

    Lobo, Conceição; Pires, Isabel; Cunha-Vaz, José

    The optical coherence tomography (OCT), a noninvasive and noncontact diagnostic method, was introduced in 1995 for imaging macular diseases. In diabetic macular edema (DME), OCT scans show hyporeflectivity, due to intraretinal and/or subretinal fluid accumulation, related to inner and/or outer blood-retinal barrier breakdown. OCT tomograms may also reveal the presence of hard exudates, as hyperreflective spots with a shadow, in the outer retinal layers, among others. In conclusion, OCT is a particularly valuable diagnostic tool in DME, helpful both in the diagnosis and follow-up procedure.

  8. Negative-Pressure Pulmonary Edema.

    Science.gov (United States)

    Bhattacharya, Mallar; Kallet, Richard H; Ware, Lorraine B; Matthay, Michael A

    2016-10-01

    Negative-pressure pulmonary edema (NPPE) or postobstructive pulmonary edema is a well-described cause of acute respiratory failure that occurs after intense inspiratory effort against an obstructed airway, usually from upper airway infection, tumor, or laryngospasm. Patients with NPPE generate very negative airway pressures, which augment transvascular fluid filtration and precipitate interstitial and alveolar edema. Pulmonary edema fluid collected from most patients with NPPE has a low protein concentration, suggesting hydrostatic forces as the primary mechanism for the pathogenesis of NPPE. Supportive care should be directed at relieving the upper airway obstruction by endotracheal intubation or cricothyroidotomy, institution of lung-protective positive-pressure ventilation, and diuresis unless the patient is in shock. Resolution of the pulmonary edema is usually rapid, in part because alveolar fluid clearance mechanisms are intact. In this review, we discuss the clinical presentation, pathophysiology, and management of negative-pressure or postobstructive pulmonary edema.

  9. [Pathopshysiological mechanisms in macular edema].

    Science.gov (United States)

    Turlea, Cristian; Zolog, Ileana; Blăjan, Codruta; Roşca, C; Turlea, Magdalena; Munteanu, Mihnea; Boruga, Ovidiu

    2014-01-01

    The treatment of diabetic macular edema has known a fast development in the last 5 years where the transition from laser monotherapy to intravitreal pharmacotherapy is becoming standard practice. Intravitreal injections therapy is in a continuous development with promising positive results. The use of intratvitreal devices in the treatment of macular edema of vascular cause has become a viable alternative also in treating diabetic macular edema. Several clinical studies have revealed the superiority of intravitreal treatment versus laser monotherapy. This article is evaluating and reviewing present and future treatments used to combat diabetic macular edema. [corrected].

  10. Bone marrow edema syndrome

    Energy Technology Data Exchange (ETDEWEB)

    Korompilias, Anastasios V.; Lykissas, Marios G.; Beris, Alexandros E. [University of Ioannina, Department of Orthopaedic Surgery, School of Medicine, Ioannina (Greece); Karantanas, Apostolos H. [University of Crete School of Medicine, Department of Radiology, Heraklion (Greece)

    2009-05-15

    Bone marrow edema syndrome (BMES) refers to transient clinical conditions with unknown pathogenic mechanism, such as transient osteoporosis of the hip (TOH), regional migratory osteoporosis (RMO), and reflex sympathetic dystrophy (RSD). BMES is primarily characterized by bone marrow edema (BME) pattern. The disease mainly affects the hip, the knee, and the ankle of middle-aged males. Many hypotheses have been proposed to explain the pathogenesis of the disease. Unfortunately, the etiology of BMES remains obscure. The hallmark that separates BMES from other conditions presented with BME pattern is its self-limited nature. Laboratory tests usually do not contribute to the diagnosis. Histological examination of the lesion is unnecessary. Plain radiographs may reveal regional osseous demineralization. Magnetic resonance imaging is mainly used for the early diagnosis and monitoring the progression of the disease. Early differentiation from other aggressive conditions with long-term sequelae is essential in order to avoid unnecessary treatment. Clinical entities, such as TOH, RMO, and RSD are spontaneously resolving, and surgical treatment is not needed. On the other hand, early differential diagnosis and surgical treatment in case of osteonecrosis is of crucial importance. (orig.)

  11. 吡拉西坦联合甘露醇治疗脑出血后脑水肿的效果观察%Observation of the effect of piracetam combined with mannitol in the treatment of patients with brain edema after cerebral hemorrhage

    Institute of Scientific and Technical Information of China (English)

    赵宝顺

    2015-01-01

    目的:观察吡拉西坦联合甘露醇治疗脑出血后脑水肿的效果。方法:收治脑出血后脑水肿患者84例,随机平分为两组,对照组予以甘露醇治疗,观察组联合吡拉西坦治疗,观察并比较两组临床疗效及脑水肿体积情况。结果:观察组治疗总有效率80.95%高于对照组的59.52%,且治疗后脑水肿体积低于对照组(P<0.05)。结论:吡拉西坦联合甘露醇治疗脑出血后脑水肿效果显著,可有效减小脑水肿体积,降低颅内压,从而促进患者的神经功能恢复。%Objective:To observe the effect of piracetam combined with mannitol in the treatment of patients with brain edema after cerebral hemorrhage.Methods:84 patients with brain edema after cerebral hemorrhage were selected.They were randomly divided into the two groups with 42 patients in each group.Patients of the control group received mannitol treatment,and the observation group combined with piracetam for treatment.The clinical curative effect and cerebral edema volume of the two groups were observed and compared.Results:The total effective rate of the observation group of 80.95% was higher than the control group of 59.52% ,and the cerebral edema volume after treatment was lower than the control group(P<0.05).Conclusion:Piracetam combined with mannitol in the treatment of patients with brain edema after cerebral hemorrhage has significant effect can effectively reduce the volume of brain edema,and reduce intracranial pressure,in order to promote the recovery of neurological function.

  12. The relationship between thrombin and apotosis of brain cells and brain edema around the hematoma after intracerebral hemorrhage in rats%大鼠脑出血后血肿周围凝血酶与脑细胞凋亡和脑水肿的关系

    Institute of Scientific and Technical Information of China (English)

    惠卫宁; 李向东; 惠国祯; 周和平; 于晶; 刘燕飞; 王津津

    2010-01-01

    目的 研究大鼠脑出血后血肿周围脑组织中凝血酶的变化及其与脑细胞凋亡和脑水肿的关系.方法 105只成年雄性SD大鼠随机均分为脑出血组、生理盐水组和正常对照组.每组再随机均分为7个时相,分别为6 h、12 h、24 h、48 h、3 d、5 d、7 d;用立体定向脑内注射法制备脑出血模型;用ELISA法检测脑组织中凝血酶-抗凝血酶复合物的含量;用流式细胞仪检测脑细胞的凋亡率;用干-湿重法检测脑组织的含水量;用透射电镜观察脑组织的形态学变化.结果 制备动物模型后,脑出血组各时相血肿周围脑组织中凝血酶含量、脑细胞凋亡率、脑组织含水量均明显高于生理盐水组和正常对照组;血肿周围脑组织中凝血酶-抗凝血酶复合物的含量与脑细胞凋亡率和脑组织含水量之间均呈正相关;电镜下,在脑出血组各时相脑组织切片中均可见大量的脑细胞凋亡和毛细血管周围大片组织间隙水肿,以及神经纤维脱髓鞘改变.结论 脑出血后,血肿周围脑组织中凝血酶含量明显升高,可导致脑细胞凋亡和脑水肿,凝血酶的含量与脑细胞凋亡率和脑组织含水量呈正相关;尽早清除血肿有望改善凝血酶引起的继发性脑损伤.%Objective To study the development of thrombin (TB) following experimental intracetebral hemorrage(ICH) in rats, and to analyze the relationship between TB and the apoptosis of brain cells as well as brain edema around the hematoma. Method 105 adult male SD rats were randomly divided into 3 groups:ICH group,physiological saline group and normal control group. Each of the three groups was randomly divided into 7 time phases:6 h, 12h,24h, 48 h,3 d, 5 d and7 d. A model of ICH was established by using stereotactical injection technique Thrombin-anti-Thrombin(TAT) complex in brain tissue around the hematoma was determined with ELISA assay, the brain cell apoptosis rate was analyzed by flow cytometry, the

  13. Relationship of matrix metallo proteinase-9 dynamic expression at different time points with brain edema after cerebral hemorrhage%脑出血后不同时间点基质金属蛋白酶-9的动态变化及其与脑水肿的关系

    Institute of Scientific and Technical Information of China (English)

    崔巍; 谈颂; 许晓辉; 宋波; 许予明

    2010-01-01

    目的 探讨血清基质金属蛋白酶-9(MMP-9)水平在脑出血后不同时间点的动态变化在脑水肿形成过程中的作用.方法 采用放射免疫法检测90例符合纳入标准的急性脑出血患者及80例正常对照者24 h、72 h、7 d 和14 d时血清MMP-9水平,分析其在脑水肿形成过程中的作用.结果 脑水肿在入院72 h时达高峰,之后缓慢下降.在发病24 h 内患者血清MMP-9含量已明显升高,发病后72 h达高峰,与脑水肿高峰一致;7 d下降明显,与对照组比较均明显升高(P<0.01),第14天接近正常水平.血清MMP-9水平在脑出血后24 h、72 h与水肿体积、水肿比值呈正相关(P<0.01).结论 脑出血后血清MMP-9随着时间动态变化,MMP-9与脑水肿体积相关,与相对水肿体积相关性更强.%Objective To study the effect of dynamic expression at different time points of metallo proteinase-9 on brain edema after cerebral hemorrhage. Methods Serum levels of MMP-9 in 90 patients with brain hemorrhage and 80 normal patients were detected by radioimmunoassay on 24 h、72 h、7 d and 14 d.The relationship between levels of MMP-9 and brain edema after cerebral hemorrhage.Results Brain edema went up to the peak at 72 h and slowly decline after it. At 24 h, the serum level of MMP-9 were significantly higher, and reached the peak at 72 h according to the peak of cerebral edema, and then decreased significantly after 7 d. Cerebral hemorrhage group compared with the control group were significantly higher(P<0.01). The level of MMP-9 close to normal levels on 14 d. MMP-9 was positive correlated with edema volume and edema ratioat 24 h and 72 h (P=0.01).Conclusions Serum MMP-9 dynamic changes over time after cerebral hemorrhage. The level of MMP-9 was correlated with the brain edema volume and had more stronger correlation with relative size of brain edema. MMP-9 was correlated with inflammation after cerebral hemorrhage.

  14. Variations of brain edema and neurological function of rat models of cerebral infarction after hyperbaric oxygen therapy%高压氧干预脑梗死模型大鼠脑水肿及神经功能变化

    Institute of Scientific and Technical Information of China (English)

    田烜

    2015-01-01

    背景:研究认为,高压氧有较好保护脑神经和脑细胞的作用,应用高压氧可使氧分压快速弥撒到相对缺氧的脑组织中,增加脑组织的血氧含量,促进脑水肿及脑神经功能的恢复。目的:观察大脑中动脉阻塞造模后高压氧干预对大鼠脑梗死组织水肿的影响,并探讨其对脑梗死大鼠神经功能保护的可能作用机制。方法:成年雌性SD大鼠65只,造模成功60只,随机区组法分为假手术组、脑梗死组、高压氧组,每组20只,按照线栓线法建立大鼠大脑中动脉阻塞脑梗死模型。造模后3 d,通过TUNEL法检测各实验组大鼠脑梗死区神经细胞的凋亡情况。伤后72 h通过RT-PCR、Western blot检测脑梗死区周围AQP4/9、基质金属蛋白酶9/2基因转录和蛋白的表达,通过苏木精-伊红染色观察脑梗死区病理组织形态学变化,通过免疫组织化学法检测胶质纤维酸性蛋白的表达量,高压氧干预后24 h,3 d及伤后1、2周行Longa行为学评分,检测神经功能的损伤情况。结果与结论:①高压氧组Longa行为学评分在治疗后1,2 d均较脑梗死组显著降低(P <0.05)。②造模后3 d高压氧组细胞凋亡指数均明显低于脑梗死组(P<0.05)。③造模后72 h,与脑梗死组相比高压氧组AQP4/9、基质金属蛋白酶9/2基因和蛋白表达均较显著降低(P<0.05)。结果提示高压氧治疗通过减少大鼠脑梗死区神经细胞的凋亡和降低脑组织水肿,对脑梗死起到保护作用。%BACKGROUND:Several studies have suggested that hyperbaric oxygen could better protect cranial nerve and brain cels. Hyperbaric oxygen therapy can make oxygen partial pressure rapidly diffusing toward relatively hypoxic brain tissue, so as to increase blood oxygen content in the brain tissue, reduce brain edema and promote the recovery of brain function. OBJECTIVE: To observe the effects of hyperbaric oxygen therapy on brain tissue

  15. Pulmonary edema following lumbar puncture

    Directory of Open Access Journals (Sweden)

    Gupta D

    1977-01-01

    Full Text Available In a boy of 17 years with disseminated tuberculosis, sudden onset of pulmonary edema following lumbar puncture is described. Possible pat ho-mechanisms have been discussed. The link bet-ween the lumbar puncture and the development of pulmonary edema is not casual.

  16. 吡拉西坦治疗创伤性脑水肿62例疗效观察%Observation on Curative Effect of Piracetam Injection in Patients with traumatic brain edema 62 cases

    Institute of Scientific and Technical Information of China (English)

    丁绪元; 刘大军; 钱中琪

    2013-01-01

    Objective :To investigate the effect of piracetam injection on reduction the traumatic brain edema. Methods:62 patients with traumatic encephaledemal were divided into the treatment group and the control group,31 cases were injected by the 20% piracetam injection,the other 31 cases were injected by the 20% mannitol..Observing the manifestation including headach,vomit,consciousness,papil edma and encephaledema of cranial CT,Determining the change of renal function and electrolyte in blood.Results: The total effective rate of two group was 93.33% and 90.00%,no significant diffevence(P>0.05).No adverse reactions was observed in the treatment group during and after treatment.One case appeared with Mannitol renal disease in the control group after medicine for five days.Conclusion:The effect of piracetam injection on reduction the traumatic brain edema is safe and rehable,it was worthy of clinical promotion.%目的:观察吡拉西坦注射液治疗创伤性脑水肿的临床效果。方法:将我院近一年收治的62例创伤性脑水肿患者62例随机分为对照组和治疗组,其中:治疗组31例,静滴20%吡拉西坦注射液治疗;对照组31例,静滴20%甘露醇治疗。通过患者的头痛、呕吐症状,意识状态的变化,视乳头水肿以及头颅C T水肿带的好转等,观察药物的疗效。通过测定两组治疗前后肾功能以及血电解质的变化,观察药物的副作用。结果:治疗组显效4例,有效24例,无效2例;对照组显效5例,有效22例,无效3例.两组的总有效率分别为93.33%和90.00%,无显著性差异(P>0.05)。在用药期间和用药后治疗组没有观察到与所用药品有关的副作用,对照组有一例用药5天后出现甘露醇肾病。结论:吡拉西坦注射液治疗创伤性脑水肿疗效肯定且安全,值得临床推广。

  17. Progesterone is neuroprotective by inhibiting cerebral edema after ischemia

    Institute of Scientific and Technical Information of China (English)

    Yuan-zheng Zhao; Min Zhang; Heng-fang Liu; Jian-ping Wang

    2015-01-01

    Ischemic edema can alter the structure and permeability of the blood-brain barrier. Recent stud-ies have reported that progesterone reduces cerebral edema after cerebral ischemia. However, the underlying mechanism of this effect has not yet been elucidated. In the present study, pro-gesterone effectively reduced Evans blue extravasation in the ischemic penumbra, but not in the ischemic core, 48 hours after cerebral ischemia in rats. Progesterone also inhibited the down-reg-ulation of gene and protein levels of occludin and zonula occludens-1 in the penumbra. These results indicate that progesterone may effectively inhibit the down-regulation of tight junctions, thereby maintaining the integrity of the blood-brain barrier and reducing cerebral edema.

  18. What Is Macular Edema?

    Medline Plus

    Full Text Available ... brain and interpreted as the images you see. It is the macula that is responsible for your ... fluids. The macula does not function properly when it is swollen. Vision loss may be mild to ...

  19. Edema and malignancy in meningiomas Edema e malignidade em meningiomas

    Directory of Open Access Journals (Sweden)

    Tobias Alécio Mattei

    2005-06-01

    Full Text Available PURPOSE: In recent years there have been many attempts to define a subset of aggressive malignant meningiomas based on histopathology and imaging technologies. The purpose of this study was to evaluate the level of peritumoral edema and its volume using the imaging technologies, computer tomography and magnetic resonance imaging, and correlate these results with the histological WHO classification. Reported causes of tumoral edema and its relationships to the histological characteristics were also reviewed. METHODS: The cases of 55 patients with meningiomas who underwent surgery at the Hospital das Clinicas (Fac Med Univ Sao Paulo between September 1993 and September 1997 were reviewed. The level of edema according to the classification of Ide et al. (1995 was compared to the histological WHO classification. RESULTS: Classification of the degree of edema was: level 0 edema - 28 cases ; level I edema - 19 cases; level II edema - 8 cases. Histological classification was: benign meningioma - 43 cases; atypical meningiomas - 11 cases; malignant meningioma - 1 case. There was a significant (P = .0089 correlation between the degree of tumoral edema and the histological characteristics. CONCLUSIONS: These results suggest that the degree of edema as revealed by computer tomography and magnetic resonance imaging can be an important clinical predictive factor for the histological grade of the meningioma.OBJETIVO: Nos últimos anos têm-se descrito alguns subtipos de meningiomas de comportamento peculiarmente agressivo. Muitas tentativas têm sido feitas no intuito de estabelecer critérios imagenológicos ou histopatológicos de malignidade. O objetivo desse estudo é avaliar, através de Tomografia Computadorizada e Ressonância Nuclear Magnética o grau de edema peritumoral e seu volume, correlacionando-os com a classificação histológica da OMS. As causas relatadas de edema peritumoral e sua possível correlação histológica foram também revistos

  20. Effect of pulmonary edema after seawater drowning on the permeability of blood-brain barrier after draumatic brain injury in rats%海水淹溺性肺水肿对颅脑创伤后血脑屏障的影响

    Institute of Scientific and Technical Information of China (English)

    房文峰; 于明琨

    2011-01-01

    Objective To investigate the effect of the pulmonary edema after seawater drowning (PE-SWD) on the permeability of blood-brain barrier (BBB) after brain injury in rats. Methods Thirty-two male SD rats were equally randomized into 4 groups of A (seawater drowning), B(fresh water drowning),C(brain injury control) and D(blank control). The brain injury model in groups of A,B and C was established by lateral fluid percussion method and the rats were drowned by injecting seawater(group A) or fresh water(group B) 4 ml/kg intratracheally after brain injury. Colloidal gold (CG) was used to evaluate the permeability of BBB at 6 h after brain injury. The CG particles permeating BBB were observed by electron microscope. Results The neuronal mitochondrial swelling, disintegration of myelin, glial cell swelling, neurons chromosome margination and even nuclear condensation were seen in group A. Space around the brain microvessels was expanded and pinocytosis activity increased as well. Compared to groups of B and C, more CG particles were seen permeating BBB in group A. Conclusion The traumatic brain edema can be exacerbated by seawater drowning-produced increase of BBB permeability in rats.%目的 研究海水淹溺性肺水肿对大鼠颅脑创伤后血脑屏障通透性的影响.方法 32只雄性SD大鼠随机均分为海水淹溺(A)组、颅脑创伤合并淡水淹溺(B)组、单纯创伤(C)组和正常对照(D)组.采用侧方液压打击颅脑伤合并海水淹溺大鼠模型,用胶体金示踪血脑屏障通透性的变化.伤后6h取大鼠伤区脑组织做电镜检查,了解胶体金颗粒透过血脑屏障入脑情况.结果 A组可见神经元细胞线粒体肿胀,髓鞘崩解,胶质细胞肿胀.神经元细胞染色体边集,甚至出现核固缩.脑微血管周围间隙扩大,胞饮活动增强.与B、C组相比,A组电镜可见有更多胶体金颗粒透过血脑屏障入脑.结论 海水淹溺性肺水肿可增加血脑屏障的通透性,加重创伤性脑水肿.

  1. 抗脑抗体对创伤性脑损伤后血脑屏障和脑水肿的影响%Effect of antibrain-antibody on blood-brain barrier and cerebral edema after traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    苏海; 张毅; 苏祖禄; 陈皓

    2015-01-01

    Objective To investigate the changes of antibrain-antibody (AB-Ab) in blood serum and the effect of AB-Ab on blood-brain barrier (BBB) and cerebral edema after the traumatic brain injury (TBI) in rabbits.Methods Forty-five New Zealand rabbits were randomly divided into control group (n =5),sham operation group (fenestration only without injury,n =15) and TBI group (severe lateral fluid percussion brain injury,n =15) according to the random number table.Sham and TBI animals were subdivided at postoperative 1,3,7 and 14 days.Level of AB-Ab,BBB permeability and brain water content were determined after operation.Results At each time point,serum AB-Ab level,BBB permeability and brain water content were higher in sham operation group and TBI group than in control group (P <0.05).At postoperative 3,7 and 14 days,serum AB-Ab level,BBB permeability and brain water content were higher in TBI group than in sham operation group (P < 0.05).Conclusion Serum level of AB-Ab is significantly increased after TBI along with synchronous changes in BBB permeability and brain water content,indicating that AB-Ab may be associated with the increase of BBB permeability and brain edema.%目的 探讨兔创伤性脑损伤(TBI)后血清抗脑抗体(AB-Ab)水平的变化及其对血脑屏障(BBB)和脑水肿的影响. 方法 将45只新西兰兔按随机数字表法分为对照组(5只)、假手术组(20只)和TBI组(20只),TBI组又分为1,3,7,14 d亚组.假手术组只开骨窗不打击;TBI组建立脑单侧重型液压冲击TBI模型.分别于术后1,3,7,14d检测各组血清AB-Ab浓度、BBB通透性和脑含水量. 结果 假手术组、TBI组血清AB-Ab含量、BBB通透性和脑含水量在各时相点均高于对照组(P<0.05),TBI组血清AB-Ab含量、BBB通透性和脑含水量在3,7,14 d均高于假手术组(P<0.05). 结论 TBI后血清中AB-Ab与BBB通透性升高和脑水肿程度呈同步性改变,提示AB-Ab可能是BBB通透性升高和脑水肿的原因之一.

  2. 重型颅脑创伤大鼠后期脑水肿研究及牛磺酸转运体的作用%Protection role of taurine transporter in rats brain edema followed severe traumatic head injury

    Institute of Scientific and Technical Information of China (English)

    蔡英; 黄慧玲; 范维佳; 武俏丽; 李晓茜; 苏彦华; 温晓昶

    2015-01-01

    Objective To investigate the effect of taurine transporter in the process of protection of brain edema in rats with severe traumatic head injury. Methods A total of 24 Male Sprague-Dawley rats were randomly divided into 4 groups. Except the control rats (Group Sham), all other three groups were subjected to lateral fluid percussion head injury. The TBI (Traumatic brain injury) models (Group TBI) and surgical control rats (Group Sham) were injected with saline through caudal vein after surgery, while the Taurine prevention and Taurine treatment models (Group Pre Tau and Group Tau) were injected with 120 g/L taurine solution before or after surgeries respectively. Water content in each brain, mRNA and protein expres⁃sion of aquaporin 4 and taurine transporter in the injured rat brain hemispheres were all evaluated over the time course of the study (7 d) in each group. Results Compared with rats in Group Sham, water content in each brain increase, mRNA tran⁃scription and protein expression of AQP4 were both up regulated but the mRNA transcription and protein expression of TauT were both down-regulated in rats in TBI group. Compared with rats in TBI group, brain water content, mRNA transcription and protein expression of AQP4 all decrease while mRNA transcription and protein expression of TauT all increase in rats in Pre tau and Tau groups. There is no statistical difference of TauT expression between rats in pre-tau group and Tau group. Conclusion Taurine exert its neuron protection role through draining water content from brain and down regulating expres⁃sion of AQP4 but rising expression of TauT after TBI.%目的:研究牛磺酸转运体(TauT)在牛磺酸调节重型颅脑创伤大鼠后期脑水肿中的作用。方法将40只大鼠按随机数字表法分为4组:假手术组(Sham组)、脑外伤组(TBI组)、牛磺酸预防组(Pre-Tau组)和牛磺酸治疗组(Tau组)。液压冲击法制作重型颅脑创伤大鼠模型。Pre-Tau组和Tau

  3. Primary report of noninvasive impedance monitoring of cerebral hematoma and edema in patients with intracerebral hemorrhage

    Institute of Scientific and Technical Information of China (English)

    Xia Yi Lu; Dong Wei-Wei; Yang Hao; Long Men; Yang Hua

    2000-01-01

    Background and Objective Brain edema is one of the most important clinical process in many diseases. Tissue impedance monitoring offers a non-invasive, bedside, rapid, and reliable technique for the monitoring of the brain edema. Methods We use a bioelectrical impedance(BEI) monitoring unit to record the brain impedance in the healthy volunteer and the patients with intracerebral hemorrhage. Percent of BEI variations were calculation. Results and Conclusions Brain BEI haven f any difference between both hemispheres in normal ones. In 48hrs, BEI value at hematoma-side was obviously decreased; after 48hrs, BEI value was obviously increased and continue to tenth day. Brain bioelectrical impedance monitoring, particularly noninvasively, is a first time in this field. The primary results show brain BEI could reflect the evolution of cerebral hematoma and edema.

  4. Study on the feasibility of near infrared spectroscopy in real-time monitoring traumatic brain edema in vivo%近红外光谱技术实时监测创伤性脑水肿的可行性研究

    Institute of Scientific and Technical Information of China (English)

    何亮; 杨天明; 钱志余

    2011-01-01

    目的:探讨近红外光谱技术(NIRS)用于创伤性脑水肿活体实时监测的可行性.方法:采用Feeneys自由落体撞击法建立急性局灶性脑挫裂伤模型,以NIRS实时监测静脉注入脱水剂后脑组织优化散射系数(μs)的变化情况.结果:脑组织受到创伤后水肿即开始发生,μs值呈抛物线形上升,但伤侧水肿的程度和速度明显大于健侧,1 h后两者之间差异具有统计学意义(P<0.05);注入脱水剂后μs值呈U形变化,先迅速降低,达到并维持一个平台期2.5~3.0 h,然后逐渐回升,于注射后4.5~5.5 h回复到注射前水平;相同渗透浓度的高渗盐水与甘露醇相比,起效更快,发挥最大效用所需要的时间更短,维持时间更长.结论:μs是监测创伤性脑水肿的良好指标,能够较好地反映脑组织水肿程度以及脱水剂的作用效果.NIRS可以用于创伤性脑水肿的实时监测.%Objective : To investigate the feasibility of real- time monitoring traumatic brain edema in vivo using near- infrared spectroscopy ( NIRS) technology. Methods: Acute regional brain trauma models were applied according to Feeney's apparatus. The changes of reduced scattering coefficient (μs') value in brain was real- time monitored by NIRS after injecting the dehydration drugs. Results : Brain edema was found after trauma. The curves of μs' value showed a parabola pattern both in the injured side and the healthy side, however, the value of μs' rose faster and greater in the former. The difference between the two sides was found statistically 1 h later( P < 0. 05 ) .The curves of μs' value had a U- shaped variation after injecting the dehydration to the rats: first, it declined rapidly; then achieved a plateau and maintained about 2. 5-3 h; finally, recovered to the level of before injection gradually 4. 5-5.5 h later. Compare to the mannitol with the same osmasis, hypertonic saline had an earlier, faster and prolonged effect. Conclusion : The

  5. Sympathetic crashing acute pulmonary edema.

    Science.gov (United States)

    Agrawal, Naman; Kumar, Akshay; Aggarwal, Praveen; Jamshed, Nayer

    2016-12-01

    Sympathetic crashing acute pulmonary edema (SCAPE) is the extreme end of the spectrum of acute pulmonary edema. It is important to understand this disease as it is relatively common in the emergency department (ED) and has better outcomes when managed appropriately. The patients have an abrupt redistribution of fluid in the lungs, and when treated promptly and effectively, these patients will rapidly recover. Noninvasive ventilation and intravenous nitrates are the mainstay of treatment which should be started within minutes of the patient's arrival to the ED. Use of morphine and intravenous loop diuretics, although popular, has poor scientific evidence.

  6. Reexpansion pulmonary edema following thoracentesis

    Directory of Open Access Journals (Sweden)

    Ansuman Mukhopadhyay

    2016-01-01

    Full Text Available Reexpansion pulmonary edema is an uncommon complication of the treatment of lung atelectasis, pleural effusion or pneumothorax and pathogenesis is unknown. An elderly male patient presented to us with right-sided pleural effusion. 2 h after thoracentesis, he felt chest discomfort and increased breathlessness. His chest examination showed right-sided crackles. Chest radiograph showed right-sided heterogeneous opacity in right lower zone consistent with unilateral pulmonary edema. He was managed conservatively along with bilevel positive airway pressure ventilator support. His condition improved gradually and was discharged successfully after 2 days.

  7. Edema pulmonar pós-pneumonectomia Postpneumonectomy pulmonary edema

    Directory of Open Access Journals (Sweden)

    Marcos Naoyuki Samano

    2005-02-01

    Full Text Available A pneumonectomia, embora seja tecnicamente simples, está associada a alta incidência de complicações (cerca de 60%. As complicações respiratórias correspondem a aproximadamente 15% deste total. A mortalidade global dessa cirurgia é de 8,6%, mas em presença de complicações respiratórias, a taxa de mortalidade chega a 30%. O edema pulmonar pós-pneumonectomia é uma complicação rara (3% a 5%, mas muito grave, sendo fatal na maioria dos casos. Foi descrito pela primeira vez há pouco mais de vinte anos mas, apesar da gravidade alarmante, pouco sabemos acerca de sua fisiopatologia, embora muitas hipóteses tenham sido levantadas. Uma vez instalado, nenhuma medida é comprovadamente eficaz no seu tratamento. Vários fatores de risco estão associados ao aparecimento do edema pulmonar pós-pneumonectomia, dentre os quais a sobrecarga hídrica, que foi o primeiro fator evitado. Entretanto, muitos trabalhos mostram não haver relação direta entre o volume recebido e o desenvolvimento do edema. A prevenção é a melhor forma de evitá-lo e deve ser realizada de maneira multifatorial, envolvendo toda a equipe médica, desde o momento da anestesia até os cuidados cirúrgicos e na terapia intensiva. No entanto, tão importante quanto a prevenção, é a suspeita clínica precoce, identificando os pacientes em risco para essa grave complicação.Although pneumonectomy is a technically simple procedure, it has been associated with a high (60% incidence of complications. Respiratory complications account for approximately 15% of such complications. Worldwide, the mortality rate among patients subjected to pneumonectomy is 8.6%. However, the rate among patients developing respiratory complications is 30%. Although postpneumonectomy pulmonary edema is rare (occurring in 3% to 5% of cases, it is a serious complication and is almost always fatal. It was first described twenty years ago and, despite these alarming statistics, little is known

  8. The impact of valproic acid on brain edema and neuroprotection after traumatic brain injury in rats%丙戊酸对大鼠创伤性颅脑损伤后脑水肿和神经功能的影响

    Institute of Scientific and Technical Information of China (English)

    陈祥荣; 李亚松; 骆良钦; 胡伟鹏; 庄丽明

    2016-01-01

    目的 观察丙戊酸对大鼠创伤性颅脑损伤后脑水肿的影响及磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)信号通路在其中的作用.方法 采用Feeney法建立大鼠创伤性脑损伤模型.72只健康雄性成年SD大鼠,采用随机数字表法分为4组(n=18):假手术组(Sham组)、创伤性颅脑损伤组(TBI组)、TBI+丙戊酸处理组(TBI+ VPA组)和TBI+ PI3K特异性抑制剂LY29400组(TBI+ LY组).分别于伤后1、3、7d进行神经行为学评分(mNSS);采用干湿重法测损伤区脑组织脑水含量;免疫荧光染色测定脑组织中组蛋白去乙酰化酶1(HDAC1)、基质金属蛋白酶-9(MMP-9)蛋白表达;Westerrn blot检查脑组织HDAC1、MMP-9和PI3K/Akt信号通路相关蛋白(PI3K、p-PI3K、Akt和p-Akt)表达水平的变化.结果 建模后第1、3、7天,与Sham组比较,TBI、TBI+ VPA、TBI+ LY组的mNSS评分显著升高,脑水含量显著增高;TBI、TBI+ VPA、TBI+ LY组脑组织HDAC1、MMP-9和PI3K/Akt通路相关蛋白表达均显著上调(P<0.01).模型建立后第3、7天,与TBI组比较,TBI+ VPA组和TBI+ LY组的mNSS评分显著低于TBI(TBI+ VPA组:10.83±0.48比12.04 ±0.51、P<0.05,8.55±0.29比10.73±0.42、P<0.05;TBI+ LY组:10.24±0.38比12.04±0.51,P<0.05,7.83±0.26比10.73±0.42,P<0.01);脑组织含水量显著降低[TBI+VPA组:(80.01±0.61)%比(82.87±0.69)%,P <0.05,(75.88±0.52)%比(78.33±0.41)%,P <0.05;TBI+ LY组:(79.59±0.57)%比(82.87±0.69)%,P<0.05,(74.94±0.43)%比(78.33±0.41)%,P<0.01].模型建立后第3天,与TBI组比较,TBI+ VPA组和TBI+ LY组脑组织HDAC1和MMP-9蛋白,PI3K/Akt通路中p-PI3K和p-Akt表达下调(P<0.05).结论 丙戊酸可减轻大鼠创伤性脑损伤后脑水肿,改善伤后神经功能,其机制可能与抑制脑组织PI3K/Akt信号通路活化,降低MMP-9的表达相关.%Objective To investigate the effect of valproic acid (VPA) treatment on brain edema and the role of the phosphatidylinositol 3-kinases/protein Kinase B (PI3K

  9. 大鼠液压脑损伤后皮层微血管改变与脑水肿的关系%Association of the changes of cortical capillaries with brain edema after lateral fluid percussion brain injury in adult rat

    Institute of Scientific and Technical Information of China (English)

    马迎辉; 刘绍明; 邢国祥

    2013-01-01

    目的 探讨大鼠液压脑损伤后皮层微血管损伤情况及其与伤后脑水肿的关系.方法 成年SD大鼠30只,随机分为正常组(n=6)、假手术组(n=6)、损伤组(n=18),其中损伤组分为伤后6h、24 h、72 h三亚组,每亚组6只.利用液压冲击法建立大鼠颅脑损伤模型,显微镜下观察直接损伤侧和非直接损伤侧皮层微血管损伤情况,CD34标记血管内皮细胞评价血管密度改变,干湿重法检测脑组织含水量的变化.结果 大鼠皮层微血管损伤后6h可见血管支行迂曲、扩张、充血,伤后24 h可见少量血栓形成,损伤后72 h可见有较多血栓形成.损伤组CD34阳性细胞数明显低于假手术组和对照组(P<0.05),而脑组织含水量明显高于假手术组和对照组(P<0.05),而后两组无统计学差异(P>0.05).损伤组直接损伤侧皮层微血管损伤较非直接损伤组严重,而且伤后24h较伤后6、72 h严重.结论 颅脑损伤后脑微血管损伤为全脑性血管损伤,这可能是伤后脑水肿形成的机制之一.%Objective To investigate the changes of the cortical capillaries and brain edema after lateral fluid percussion brain injury in adult rat and their relationship.Methods Thirty adult Sprague-Dawley rats were randomly divided into three groups,i.e.,normal group (n=6),sham-operated group (n=6) and injured group (n=18).The rat model was made by lateral fluid percussion brain injury with an impact of 2.3 kPa.The rats in injured group were killed 6,24 and 72 hours after injury with six rats in each time point.The pathological changes of cerebral tissues were detected by HE staining.The changes of cortical capillaries were evaluated by counting the number of CD34 marked vascular endothelial cells.The brain water content was calculated by wet and dry method.Results The HE staining showed that many cortical capillaries with no congestion and endothelial cells with normal shape could be seen in normal group and sham-operated group

  10. Decreased light attenuation in cerebral cortex during cerebral edema detected using optical coherence tomography

    OpenAIRE

    Rodriguez, Carissa L. R.; Szu, Jenny I.; Eberle, Melissa M.; Wang, Yan; Hsu, Mike S.; Binder, Devin K.; Park, B. Hyle

    2014-01-01

    Abstract. Cerebral edema develops in response to a variety of conditions, including traumatic brain injury and stroke, and contributes to the poor prognosis associated with these injuries. This study examines the use of optical coherence tomography (OCT) for detecting cerebral edema in vivo. Three-dimensional imaging of an in vivo water intoxication model in mice was performed using a spectral-domain OCT system centered at 1300 nm. The change in attenuation coefficient was calculated and cere...

  11. Cerebral Edema in Chronic Mountain Sickness: a New Finding

    Science.gov (United States)

    Bao, Haihua; Wang, Duoyao; Zhao, Xipeng; Wu, Youshen; Yin, Guixiu; Meng, Li; Wang, Fangfang; Ma, Lan; Hackett, Peter; Ge, Ri-Li

    2017-01-01

    We observed patients with chronic mountain sickness (CMS) in our clinic who developed progressive neurological deterioration (encephalopathy) and we wished to investigate this. We studied nine such CMS patients, and compared them to 21 CMS patients without encephalopathy, and to 15 healthy control subjects without CMS. All 45 subjects lived permanently at 3200–4000 m. Measurements at 2260 m included CMS symptom score, multi-slice CT, perfusion CT, pulse oximetry (SpO2%), and hemoglobin concentration (Hb). One patient had MRI imaging but not CT; 5 had CSF pressure measurements. CMS subjects had lower SpO2, higher Hb, higher brain blood density, lower mean cerebral blood flow (CBF), and significant cerebral circulatory delay compared to controls. The nine CMS subjects with neurological deterioration showed diffuse cerebral edema on imaging and more deranged cerebral hemodynamics. CSF pressure was elevated in those with edema. We conclude that cerebral edema, a previously unrecognized complication, may develop in CMS patients and cause encephalopathy. Contributing factors appear to be exaggerated polycythemia and hypoxemia, and lower and sluggish CBF compared to CMS patients without cerebral edema; but what triggers this complication is unknown. Recognition and treatment of this serious complication will help reduce morbidity and mortality from CMS. PMID:28233815

  12. Distal clavicle edema; Distales Klavikulaoedem

    Energy Technology Data Exchange (ETDEWEB)

    Vahlensieck, M.; Schmittke, I. [Radiologie Haydnhaus, Bonn (Germany); Schmidt, H.M. [Universitaet Bonn (Germany). Anatomisches Institut

    2006-07-15

    Distal clavicle marrow edema: frequency, MRI in the early stage and macroscopic correlation to the bone marrow distribution and to evaluate frequency and diagnostic criteria of a posttraumatic clavicula disorder with an edema pattern on MRI. An additional macroscopic study of the clavicle should elucidate anatomic pecularities which could explain the reaction of the distal clavicle. 285 MRI of traumatized patients were analyzed for edema pattern of the distal clavicle. Pattern A edema within the clavicle and the acromion was distinguished from pattern B edema within the clavicle only. Dissection in 20 cadavers should reveal vascular pecularities and the bone marrow distribution within clavicle and acromion or vascular pecularities. In 38 patients (13,3%) we found edema within the distal clavicle. Pattern A was found in 28 (9,8%) and pattern B in 10 patients (3,5%). Pattern A was usually associated with swelling of the AC joint (27 out of 28). Other injuries were not evident. 18 cadavers showed hematopoetic marrow within the distal clavicle and fatty marrow within the acromion. The distale clavicle can frequently react with edema pattern after trauma without evidence for another injury. Distinguish in cases with and cases without synovitis of the AC joint could have impact on therapy. A peculier vascular supply of the distal clavicle could not be found. (orig.) [German] Bestimmung der Haeufigkeit und diagnostischer Kriterien einer posttraumatischen Klavikulaerkrankung, die mit einem MR-tomographischen Oedemmuster auffaellt. Makroskopische Besonderheiten der Markhoehle sollten gesucht werden, die die besondere Reaktionsform der distalen Klavikula mit erklaeren koennten. 285 Patienten mit traumaassoziierten, zeitversetzt nach dem Unfallereignis bestehenden Schulterbeschwerden, wurden auf MR-tomographische Oedemmuster in der distalen Klavikula untersucht. Das Oedemmuster wurde in ''Klavikula allein'' (Muster B) und ''mit Beteiligung des

  13. Glioma-related edema: new insight into molecular mechanisms and their clinical implications

    Institute of Scientific and Technical Information of China (English)

    Zhi-Xiong Lin

    2013-01-01

    Glioma-related edema (GRE) is a significant contributor to morbidity and mortality from glioma.GRE is a complicated process involving not only peritumoral edema but also the water content of the tumor body.In terms of etiology,this condition derives from both GRE in the untreated state and GRE secondary to clinical intervention,and different cell types contribute to distinct components of GRE.Peritumoral edema was previously believed to loosen glioma tissue,facilitating tumor-cell invasion;however,the nutrition hypothesis of the tumor microecosystem suggests that tumor cells invade for the sake of nutrition.Edema is the pathologic consequence of the reconstructed trophic linkage within the tumor microecosystem.Glioma cells induce peritumoral brain edema via an active process that supplies a suitable niche for peritumoral invasive cells,suggesting that glioma-related peritumoral brain edema is determined by the invasive property of tumor cells.There are differences between pivotal molecular events and reactive molecular events in the development of GRE.Molecular therapy should target the former,as targeting reactive molecular events will produce undesired or even adverse results.At present,brain glioma angiogenesis models have not been translated into a new understanding of the features of brain images.The effect of these models on peritumoral brain edema is unclear.Clinical approaches should be transformed on the basis of new knowledge of the molecular mechanism underlying GRE.Exploring clinical assessment methods,optimizing the existing control strategy of GRE,and simultaneously developing new treatments are essential.

  14. 高原地区脑水肿并发大面积脑梗1例治疗与护理%Treatment and nursing of 1 case with brain edema complicated with large area cerebral infarction in plateau area

    Institute of Scientific and Technical Information of China (English)

    田甜; 魏林节

    2014-01-01

    本文汇报了1例高原地区脑水肿并发大面积脑梗患者的治疗与护理方法,取得了较好的效果,指出及时、合理的治疗和精心护理及康复锻炼具有重要的意义。%In this paper,the author reported the treatment and nursing of 1 case with brain edema complicated with large area cerebral infarction in plateau area which had better effect,and pointed out that timely and reasonable treatment,careful nursing and rehabilitation exercise had the vital significance.

  15. Effect of Decompressive Craniectomy on Perihematomal Edema in Patients with Intracerebral Hemorrhage.

    Directory of Open Access Journals (Sweden)

    Christian Fung

    Full Text Available Perihematomal edema contributes to secondary brain injury in the course of intracerebral hemorrhage. The effect of decompressive surgery on perihematomal edema after intracerebral hemorrhage is unknown. This study analyzed the course of PHE in patients who were or were not treated with decompressive craniectomy.More than 100 computed tomography images from our published cohort of 25 patients were evaluated retrospectively at two university hospitals in Switzerland. Computed tomography scans covered the time from admission until day 100. Eleven patients were treated by decompressive craniectomy and 14 were treated conservatively. Absolute edema and hematoma volumes were assessed using 3-dimensional volumetric measurements. Relative edema volumes were calculated based on maximal hematoma volume.Absolute perihematomal edema increased from 42.9 ml to 125.6 ml (192.8% after 21 days in the decompressive craniectomy group, versus 50.4 ml to 67.2 ml (33.3% in the control group (Δ at day 21 = 58.4 ml, p = 0.031. Peak edema developed on days 25 and 35 in patients with decompressive craniectomy and controls respectively, and it took about 60 days for the edema to decline to baseline in both groups. Eight patients (73% in the decompressive craniectomy group and 6 patients (43% in the control group had a good outcome (modified Rankin Scale score 0 to 4 at 6 months (P = 0.23.Decompressive craniectomy is associated with a significant increase in perihematomal edema compared to patients who have been treated conservatively. Perihematomal edema itself lasts about 60 days if it is not treated, but decompressive craniectomy ameliorates the mass effect exerted by the intracerebral hemorrhage plus the perihematomal edema, as reflected by the reduced midline shift.

  16. Edema macular diabético Diabetic macular edema

    Directory of Open Access Journals (Sweden)

    J. Andonegui

    2008-01-01

    Full Text Available El edema macular diabético representa la primera causa de pérdida visual en los pacientes con diabetes mellitus. Su complejidad, unida a la aparición de nuevos métodos de diagnóstico así como de novedosas alternativas de tratamiento, hace que el enfoque de esta enfermedad suponga un importante reto para el oftalmólogo. A lo largo de este artículo se describen su patofisiología, manifestaciones clínicas, clasificación, diagnóstico y tratamiento, haciendo especial énfasis en los nuevos métodos diagnósticos y en las diferentes opciones terapéuticas.Diabetic macular edema is the principal cause of visual loss in patients with diabetes mellitus. Its complexity, together with the appearance of new methods of diagnosis and new alternatives for treatment, mean that the approach to this disease is an important challenge for ophthalmologists. This article describes its pathophysiology, clinical manifestations, classification, diagnosis and treatment, with special emphasis on the new diagnostic methods and on the different therapeutic options.

  17. [Therapeutic approach in persistent diabetic macular edema].

    Science.gov (United States)

    Brănişteanu, Daniel; Moraru, Andreea

    2014-01-01

    Terminology of persistent diabetic macular edema has been initially reserved to cases unresponsive to conventional laser photocoagulation according to ETDRS criteria. While knowledge about pathophysiology of macular edema evolved and new drugs became available, the terminology of persistent diabetic macular edema expanded to include resistance to most current therapies. The purpose of this paper is to review medical and surgical options in the treatment of such difficult cases according to literature data and personal experience.

  18. Acute cerebral and pulmonary edema induced by hemodialysis in a dog model

    Institute of Scientific and Technical Information of China (English)

    SHI Zhen-wei; WANG Zhi-gang

    2008-01-01

    Background The dialysis disequilibrium syndrome is characterized by neurologic deterioration and cerebral edema which occurs after hemodialysis. The purpose of this study was to investigate the pathogenesis of acute cerebral and pulmonary edema induced by hemodialysis.Methods We evaluated the effects of hemodialysis on the biochemical and hemodynamic parameters of the plasma and cerebrospinal fluid, including the intracranial pressure, dry/wet ratio, and pulmonary edema index, and we also examined the pathological changes of the brain and lung tissue in dogs suffering from uremia.Results Seventy-two hours after bilateral ureteral ligation, 10 uremic dogs were hemodialyzed for 2 hours, yielding a 73.6% and 60.1% decrease in the plasma urea and creatinine, respectively, a decrease in the plasma osmolality from (359±18) mOsm/kgH2O to (304±6) mOsm/kgH2O (P <0.01 ), a decrease in the dry/wet ratio of the lung and brain tissue,and an increase in the hemodynamic parameters (right atrial pressure, right ventricular pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure), intracranial pressure, total pulmonary resistance index, and pulmonary edema index. Moreover, the pathological examination revealed lung and brain edema in the dialyzed dogs. This group was compared to 3 control groups: 6 uremic dogs which were sham dialyzed without dialysate so that no fall in the plasma urea occurred, and 12 uremic and 12 nonuremic animals that were not dialyzed.However, the parameters mentioned above were not significantly changed among these 3 control groups.Conclusions The acute brain and lung edema in our model appeared to be primarily due to a large osmotic gradient between the plasma and the brain and lung. This is the "urea reverse effect" which promoted the osmotically-induced lung and brain swelling.

  19. The effect of ASK1 on vascular permeability and edema formation in cerebral ischemia.

    Science.gov (United States)

    Song, Juhyun; Cheon, So Yeong; Lee, Won Taek; Park, Kyung Ah; Lee, Jong Eun

    2015-01-21

    Apoptosis signal-regulating kinase-1 (ASK1) is the mitogen-activated protein kinase kinase kinase (MAPKKK) and participates in the various central nervous system (CNS) signaling pathways. In cerebral ischemia, vascular permeability in the brain is an important issue because regulation failure of it results in edema formation and blood-brain barrier (BBB) disruption. To determine the role of ASK1 on vascular permeability and edema formation following cerebral ischemia, we first investigated ASK1-related gene expression using microarray analyses of ischemic brain tissue. We then measured protein levels of ASK1 and vascular endothelial growth factor (VEGF) in brain endothelial cells after hypoxia injury. We also examined protein expression of ASK1 and VEGF, edema formation, and morphological alteration through cresyl violet staining in ischemic brain tissue using ASK1-small interference RNA (ASK1-siRNA). Finally, immunohistochemistry was performed to examine VEGF and aquaporin-1 (AQP-1) expression in ischemic brain injury. Based on our findings, we propose that ASK1 is a regulating factor of vascular permeability and edema formation in cerebral ischemia.

  20. Coexistent transient pulmonary edema and pericardial effusion

    Energy Technology Data Exchange (ETDEWEB)

    Newman, B.; Oh, K.S.; Park, S.C.

    1988-09-01

    Eight (23%) of 35 children with acute pericardial effusions due to infection or juvenile rheumatoid arthritis (JRA) had associated transient pulmonary edema demonstrated on plain chest radiographs. The presence or absence of radiographic pulmonary edema correlated well with clinical and hemodynamic parameters in patients with JRA but not in those with infectious pericarditis. There was no definite relationship between radiographic edema and amount of pericardial fluid as estimated echocardiographically or removed at pericardiocentesis. Rapidity of pericardial fluid accumulation could not be assessed in this study. Children of young age with underlying JRA were the most likely subjects to have radiographic pulmonary edema in conjunction with an acute pericardial effusion.

  1. Pulmonary edema in acute carbon monoxide poisoning

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Kun Sang; Chang, Kee Hyun; Lee, Myung Uk [Seoul National University College of Medicine, Seoul (Korea, Republic of)

    1974-10-15

    Acute carbon monoxide poisoning has frequently occurred in Korean, because of the coal briquette being widely used as fuel in Korean residences. Carbon monoxide poisoning has been extensively studied, but it has been sparsely reported that pulmonary edema may develop in acute CO poisoning. We have noticed nine cases of pulmonary edema in acute CO poisoning last year. Other possible causes of pulmonary edema could be exclude in all cases but one. The purpose of this paper is to describe nine cases of pulmonary edema complicated in acute CO poisoning and discuss the pathogenesis and the prognosis.

  2. Bone marrow edema in sports: General concepts

    Energy Technology Data Exchange (ETDEWEB)

    Vanhoenacker, F.M. [AZ Sint-Maarten Duffel-Mechelen, Department of Radiology, Rooienberg 25, B-2570 Duffel (Belgium) and University Hospital Antwerp, Department of Radiology, Wilrijkstraat 10, B-2650 Edegem (Belgium)]. E-mail: filip.vanhoenacker@telenet.be; Snoeckx, A. [AZ Sint-Maarten Duffel-Mechelen, Department of Radiology, Rooienberg 25, B-2570 Duffel (Belgium); University Hospital Antwerp, Department of Radiology, Wilrijkstraat 10, B-2650 Edegem (Belgium)

    2007-04-15

    This paper will discuss the value of medical imaging in the detection and follow-up of bone marrow edema (BME), resulting from acute and chronic trauma in sports. MR imaging is the only imaging technique that allows direct evaluation of bone marrow edema in sports medicine. The use of fat suppressed T2-weighted or STIR images is particularly appropriate to detect bone marrow edema. The extent of bone marrow edema reflects the biomechanics of trauma. Compressive forces between two bony structures will result in extensive areas of bone marrow edema, whereas distraction forces provoke more subtle areas of bone marrow edema at the insertion of supporting structures of joints. In most clinical situations, a combination of compression and distraction forces is present, causing a complex pattern of bone marrow edema. A meticulous pattern approach of the distribution of these bone marrow changes around a joint can reveal in most instances the underlying mechanism of trauma. This may be helpful to analyze which joint supporting structures may be at risk. In the acute setting, plain radiography and CT scan may have an additional role in the detection of small avulsion fractures occurring at the site of minor areas of bone marrow edema. The clinical significance and natural history of bone marrow edema is still a matter of debate.

  3. ECG Changes in 8-Year-Old Boy with Pulmonary Edema after Head Injury

    Directory of Open Access Journals (Sweden)

    Bojko Bjelakovic

    2006-01-01

    Full Text Available This is a case story of an 8-year-old boy with no prior history of cardiac disease who developed acute pulmonary edema with ECG changes similar to transmural myocardial infarction after basilar skull fracture. Biochemical evaluation showed elevated total creatine kinase activity –1,350 U/L with 12% MB isoenzyme fraction. The brain scan on admission showed cerebral edema with ethmoidal sinuses hemorrhage. Neurogenic pulmonary edema following CNS damage is an extremely rare entity in the pediatric population and there are few reports. There are many proposed mechanisms and explanations of its origin. Based on previous reports and experimental studies, the cause of “neurogenic” pulmonary edema may be of cardiac as well as of noncardiac origin.

  4. Clinical Application of Pulse-indicated Continuous Cardiac Output in Neurogenic Pulmonary Edema after Severe Brain Injury%PICCO在重型颅脑损伤并神经源性肺水肿患者抢救中的应用

    Institute of Scientific and Technical Information of China (English)

    李金庭; 陈甘海; 丁燕晶

    2013-01-01

      目的:观察探讨PICCO(脉搏轮廓温度稀释连续心排量)对重型颅脑损伤并神经源性肺水肿的疗效影响.方法:32例重型颅脑损伤并神经源性肺水肿患者随机分为对照组和治疗组各16例,对照组给予神经科常规治疗,治疗组在常规组治疗基础上应用PICCO监测血流动力学指标进行液体管理,比较两组治疗效果.结果:治疗组治疗1周后GCS评分高于对照组,撤机时间早于对照组,两组比较,差异有统计学意义(P<0.05).治疗组死亡率低于对照组,而恢复良好率显著高于对照组(P<0.05).结论:PICCO能提高重型颅脑损伤并神经源性肺水肿患者抢救成功率.%Objective:To evaluate the clinical significance of PICCO in patients with neurogenic pulmonary edema after severe brain injury. Method:32 cases with neurogenic pulmonary edema after severe brain injury were randomly divided into treatment group and control group. All the patients were treated by routine methods. In control group,fluid management was depended on center venous pressure(CVP),and PICCO was used in the treatment group. Result:The GCS score of treatment group was higher than that of the control group after 1 week,and weaning time was earlier than that of the control group(P<0.05). The death rate of the treatment group was lower than that of the control group,and good recovery rate was higher than that of the control group. Conclusion:PICCO in fluid management for severe brain injury can decrease the death rate and improve prognosis.

  5. Bilateral eyelid edema : Cutis laxa or blepharochalasis?

    NARCIS (Netherlands)

    Braakenburg, A; Nicolai, JPA

    2000-01-01

    A 59-year-old woman with massive bilateral edema of the upper and lower eyelids is presented. The edema occurred suddenly and without provocation. No cause could be identified despite a multitude of examinations. Initially the patient was diagnosed as having blepharochalasis, but later skin biopsy s

  6. 醒脑静对脑出血患者 S100B、神经肽 Y和脑水肿的影响%Impact of Xingnaojing on the S100B,neuropeptide Y and brain edema of patients with cerebral hemorrhage

    Institute of Scientific and Technical Information of China (English)

    刘颖

    2015-01-01

    Objective To investigate the impact of Xingnaojing on the S100B,neuropeptide Y and brain edema of patients with cerebral hemorrhage. Methods A total of 72 patients with cerebral hemorrhage were selected in the People's Hos-pital of Yichun in 2014,they were randomly divided into control group and observation group,36 cases in each group. Control group were given edaravone treatment,observation group were given Xingnaojing on the basis of control group. Before treatment and after treatment of 1,2 weeks S100B,neuropeptide Y levels,brain edema volume and incidence of adverse reactions be-tween the two groups were compared. Results There was interaction between time and method(P 0. 05),after treatment of 1 week,S100B levels,brain edema volume showed no significant differences between the two groups(P > 0. 05),after treatment of 1 week,neuropeptide Y levels of ob-servation group was lower than that of control group(P < 0. 05),after treatment of 2 week,S100B,neuropeptide Y levels of observation group were lower than those of control group,brain edema volume of observation group was less than that of control group(P < 0. 05);no one of the two groups occurred serious adverse reactions. Conclusion Xingnaojing can decrease S100B,neuropeptide Y levels of patients with cerebral hemorrhage,improve patients' brain edema.%目的:探讨醒脑静对脑出血患者 S100B、神经肽 Y 和脑水肿的影响。方法选取2014年宜春市人民医院收治的脑出血患者72例,随机分为对照组与观察组,各36例。对照组患者予以依达拉奉治疗,观察组患者在对照组基础上加用醒脑静治疗。观察两组患者治疗前及治疗1、2周 S100B、神经肽 Y 水平、脑水肿体积及不良反应发生情况。结果时间与方法有交互作用(P <0.05),组间比较,差异均有统计学意义( P <0.05),时间间比较,差异均有统计学意义(P <0.05),治疗前两组患者 S100B、神经肽 Y 水平、脑水肿体

  7. Immersion Pulmonary Edema in Female Triathletes

    Directory of Open Access Journals (Sweden)

    Eric A. Carter

    2011-01-01

    Full Text Available Pulmonary edema has been reported in SCUBA divers, apnea divers, and long-distance swimmers however, no instances of pulmonary edema in triathletes exist in the scientific literature. Pulmonary edema may cause seizures and loss of consciousness which in a water environment may become life threatening. This paper describes pulmonary edema in three female triathletes. Signs and symptoms including cough, fatigue, dyspnea, haemoptysis, and rales may occur within minutes of immersion. Contributing factors include hemodynamic changes due to water immersion, cold exposure, and exertion which elevate cardiac output, causing pulmonary capillary stress failure, resulting in extravasation of fluid into the airspace of the lung. Previous history is a major risk factor. Treatment involves immediate removal from immersion and in more serious cases, hospitalization, and oxygen administration. Immersion pulmonary edema is a critical environmental illness of which triathletes, race organizers, and medical staff, should be made aware.

  8. 伽玛刀同步贝伐珠单抗治疗伴广泛脑水肿的结直肠癌脑转移瘤:5例病例报道%Concurrent gamma knife radiosu rgery and bevacizumab treatment for brain metastasis from colorectal cancer with extensive cerebral edema:5 cases report

    Institute of Scientific and Technical Information of China (English)

    汤旭群; 江华; 魏立晨; 张南; 戴嘉中; 吴瀚峰; 潘力

    2016-01-01

    Objective To explore the efficacy and safety of concurrent gamma knife radiosurgery and bevacizumab treatment for brain metastasis from colorectal cancer with extensive cerebral edema. Methods Five patients with brain metastasis from colorectal cancer were included in this prospective investigation from March 2013 to October 2014. Bevacizumab therapy (5 mg/kg, at 2 to 3 week intervals) was administered the next day after completion of gamma knife radiosurgery for the median treatment cycle of 4. The patients were followed up for median period of 13 months, ranged from 7 to 18 months. Results Compared with the pretreatment, the lesions decreased by median of 42.85%, ranged from 29.51%to 100%on enhanced MRI T1WI sequence, and edema area decreased by median of 86.60%, ranged from 69.03%to 97.51%on T2WI sequence during short-term follow-up period after the treatment. Clinical symptoms were improved in all the 5 patients, and the KPS increased by a median of 30, ranged from 20 to 40 scores. At last follow-up, two patients died, one progressed and the other two kept tumor progression free. No symptomatic radiation or severe bevacizumab-related adverse events occurred. Conclusion Coadministration of gamma knife radiosurgery and bevacizumab as a promising salvage treatment is safe and effective for brain metastasis from colorectal cancer with extensive cerebral edema.%目的:探讨伽玛刀同步贝伐珠单抗治疗伴广泛脑水肿的结直肠癌脑转移瘤的有效性和安全性。方法2013年3月-2014年10月期间共5例结直肠癌脑转移瘤病人纳入该前瞻性研究。所有病人在伽玛刀治疗后第2天给予贝伐珠单抗静脉滴注(5 mg/kg,每2~3周重复1次),贝伐珠单抗中位治疗周期数为4。伽玛刀和贝伐珠单抗同步治疗后随访7~18个月(中位时间13个月)。结果近期随访显示:MRI T1WI 增强序列上病灶较治疗前缩小29.51%~100%(中位数42.85%),T2WI序列上病灶水肿区域缩小69.03%~97.51%(

  9. 促甲状腺激素释放激素类似物 YM14673对大鼠脑损伤性脑水肿的作用及机制%Effect and mechanism of YM14673,an analog of thyrotropin-releasing hormone,to cerebral edema induced by brain damage in rats

    Institute of Scientific and Technical Information of China (English)

    张绍东; 翟晶; 张辉; 张家瑾

    2004-01-01

    BACKGROUND:As an analog of thyrotropin-releasing hormone(TRH), YM14673 has protective effects on brain.Many researches aim to explore wether the protective effects on brain of YM14673 are realized by the inhibition of cerebral edema. OBJECTIVE:To observe the effects of analog of TRH-YM14673 on blood brain barrier after brain damage. DESIGN:Randomized case control study. SETTING and MATERIALS:Experimental site:Beijing Institute of Neurosurgery.Sixty Wistar rats were randomly divided into sham-operation group,saline group,administrative group I(0.1 mg/kg)and administrative group II(1 mg/kg)with each of 15 rats. INTERVENTIONS:Acute brain damage model of rats were made.Evans blue was injected into femoral vein to test the change of permeability of blood-brain barrier in advance.Rats of sham-operation group were opened bone window without any strike.Rats of other groups were taken strike.Saline or YM14673 solution was injected after strike. Rats were executed after 24 hours to assay the water content of brain and the Evans blue content in brain tissue and plasma.MAIN OUTCOME MEASURES:①Changes of water contents in both hemispheres in rats of each group; ②Changes of Evans blue content in both hemispheres and plasma of rats. RESULTS:After brain damage occurred,the water content in brain tissue of saline group was much higher than that of sham-operation group[Left hemisphere:saline group( 79.57± 0.47)%, sham- operation group(78.29 ± 0.63)%, t=3.98,P0.05).The Evans blue content of brain remarkably increased after acute brain damage. YM14673 did not influence the contents.There was no difference on Evans blue content in plasma between groups. CONCLUSION:YM14673 can relieve the cerebral edema induced by acute brain damage.However,there is no effect on increasing the permeability of blood-brain barrier.%背景: YM14673为促甲状腺激素释放激素( thyrotropin-releasing hormone,TRH)类似物 ,具有脑保护作用.目前的许多研究都在探讨其脑保护作用

  10. Update on treatments of diabetic macular edema

    Institute of Scientific and Technical Information of China (English)

    YANG Xiao-lu; LIU Kun; XU Xun

    2009-01-01

    Objective To review the update research progress about the treatment of diabetic macular edema and to give helpful guidelines in the treatment of diabetic macular edema based on available evidence to date.Data sources A literature search of all English articles was performed on the online electronic PubMed database dated 1984 to 2009. The keywords searched included: macular edema, therapy, laser coagulation, intravitreal triamcinolone acetonide, vascular endothelial growth factor inhibitor, protein kinase C inhibitor and Pars plana vitrectomy. After finding relevant articles within these search limits, a manual search was conducted through the references from these articles.Study selection Original articles and critical reviews were reviewed and selected to address the stated purpose.Results To date, demonstrated means to reduce the risk of vision loss from diabetic macular edema include focal/grid laser photocoagulation and improved metabolic control. Emerging pharmacologic therapies (intravitreal triamcinolone acetonide, vascular endothelial growth factor inhibitors and protein kinase C beta-isoform inhibitors) and Pars plana vitrectomy have shown early promise in the treatment of diabetic macular edema.Conclusions As there has been extensive development in multiple treatments of diabetic macular edema, choice of the most suitable treatment for specific patients becomes important. Combination therapy of laser, pharmacological and surgical treatment modalities may offer an alternative to treatment of diabetic macular edema.

  11. Pulmonary Edema: Classification, Mechanisms of Development, Diagnosis

    Directory of Open Access Journals (Sweden)

    V. V. Moroz

    2009-01-01

    Full Text Available Pulmonary edema remains a topical problem of modern reanimatology. In clinical practice, there is a need for continuous monitoring of the content of extravascular water in the lung and the pulmonary vascular permeability index for the timely detection and treatment of pulmonary edema. This literature review considers the minor mechanisms of pulmonary extravas-cular water exchange in health and in different types of pulmonary edema (acute lung injury, pneumonia, sepsis, postoperative period, burns, injuries etc., as well as the most accessible current (irradiation and dilution studies permitting an estimate of the level of pulmonary extravascular water and the pulmonary vascular permeability index in clinical practice. Key words: pulmonary edema, acute lung injury, pulmonary extravascular water, pulmonary vascular permeability index.

  12. Clinical Practice Guidelines for Acute Pulmonary Edema.

    Directory of Open Access Journals (Sweden)

    Pablo Rodríguez Díaz

    2009-03-01

    Full Text Available Clinical Practice Guidelines for Acute Pulmonary Edema. It has been defined as an abrupt and severe failure of the left ventricular function which causes pulmonary edema or cardiac origin interfering with the normal oxygen exchange at pulmonary level. This document includes a review and update of the main clinical aspects allowing the early diagnosis and immediate therapeutic treatment. It includes assessment guidelines focused on the most important aspects to be accomplished.

  13. Shifting bone marrow edema of the knee

    Energy Technology Data Exchange (ETDEWEB)

    Moosikasuwan, Josh B.; Schultz, Elizabeth [Department of Radiology, North Shore University Hospital, 300 Community Drive, NY 11030, Manhasset (United States); Miller, Theodore T. [Department of Radiology, North Shore University Hospital, 300 Community Drive, NY 11030, Manhasset (United States); Department of Radiology, North Shore University Hospital, 825 Northern Boulevard, NY 11021, Great Neck (United States); Math, Kevin [Department of Radiology, Beth Israel Medical Center, First Avenue at 16th Street, NY 10003, New York (United States)

    2004-07-01

    The purpose of our study is to describe shifting bone marrow edema in the knee as the MR imaging feature of intra-articular regional migratory osteoporosis of the knee. Five men, aged 45-73 years, were referred by orthopedic surgeons for MR imaging evaluation of knee pain, which had been present for 2 weeks to 6 months. One patient had a prior history of blunt trauma. None had risk factors for osteonecrosis. Four patients had two MR examinations and the patient with prior blunt trauma had four. Plain radiographs were obtained in all patients. In all cases, a large area of marrow edema initially involved a femoral condyle, with migration of the bone marrow edema to the other femoral condyle, tibia, and/or patella occurring over a 2- to 4-month period. Adjacent soft tissue edema was present in all five patients, while none had a joint effusion. Radiographs of two patients showed generalized osteopenia. In the absence of acute trauma or clinical suspicion of infection, a large area of bone marrow edema without a zone of demarcation may represent intra-articular regional migratory osteoporosis. Demonstration of shifting bone marrow edema on follow-up examinations suggests this diagnosis. (orig.)

  14. Olanzapine-induced tender pitting pre-tibial edema

    Directory of Open Access Journals (Sweden)

    Kaliaperumal Mathan

    2015-01-01

    Full Text Available Antipsychotic-induced edema is uncommonly encountered in clinical practice. We report a case of tender pitting pre-tibial edema with olanzapine in a woman with no medical comorbidities. The peculiar distribution of edema resulted in diagnostic confusion necessitating specific investigations. Eventually, the edema resolved following complete stoppage of the drug, but caused distress to the patient and the caregiver.

  15. Mitral Valve Regurgitation Causing Right Upper Lobe Pulmonary Edema

    OpenAIRE

    Young, Andrew L.; Langston, Charles S.; Schiffman, Robert L.; Shortsleeve, Michael J.

    2001-01-01

    When radiography is performed in patients with mitral regurgitation, cardiogenic pulmonary edema is a typical finding; however, asymmetric pulmonary edema has also been reported. We describe the case of a patient in whom mitral valve regurgitation caused isolated pulmonary edema in the right upper lung. We include a discussion of pulmonary edema in conjunction with mitral regurgitation.

  16. [Hyponatremic encephalopathy with non-cardiogenic pulmonary edema. Development following marathon run].

    Science.gov (United States)

    Wellershoff, G

    2013-04-01

    This article presents the case of a 52-year-old woman who developed exercise-associated hyponatremia (EAH) complicated by non-cardiogenic pulmonary edema after a marathon run. The condition of EAH is a potentially life-threatening complication of endurance exercise. The main cause seems to be inadequate intake of free water during or following exercise with enduring antidiuresis due to nonosmotic stimulation of ADH secretion. Known risk factors are female gender, slow running pace and lack of weight loss. Emergency therapy is fluid restriction and bolus infusion of 3% NaCl solution to rapidly reduce brain edema.

  17. Expression of AQP4 and susceptivity to high-altitude cerebral edema in bovine brain%黄牛脑水通道蛋白4的表达及其对高原脑水肿的易感性

    Institute of Scientific and Technical Information of China (English)

    宋国强; 王建林; 徐元青; 伍国芬; 邵宝平

    2011-01-01

    为了探讨黄牛对高原脑水肿的易感性,并为青藏高原养牛业提供参考,运用免疫组织化学SABC染色法并采用Image-Pro Plus 6.0软件,对成年黄牛大脑不同功能区水通道蛋白4(AQP4)的表达及分布特征进行了研究.结果显示,黄牛不同功能区脑组织中AQP4表达面积(S)和积分光密度(IOD)值的大小顺序为S扣带回>S中央前回>S丘脑>S尾状核,IOD扣带回>IOD中央前回>IOD丘脑>IOD尾状核,且扣带回和中央前回的S和IOD值均显著高于丘脑和尾状核(P<0.01).结果证实,成年黄牛脑不同功能区、同功能区不同层及同功能区同层不同类型细胞对水的通透性及代谢功能存在较大差异,对脑水肿的易感性是不同的.%To investigate the susceptivity of cattle to the high altitude cerebral edema as well as provide reference and theory evidence to the cattle-raising industry in Qinghai-Tibet Plateau, the expression and distributional characteristics of adult cattle cerebral aquaporin 4 (AQP4) in different functional area were studied by using immunohistochemical SABC and Image-Pro Plus 6.0 software. Statistical analysis showed that both the immunostaining area(S) and the integral optical density(IOD) value of the cingulated gyrus and precentral gyrus were significantly larger than thalamus and caudate nucleus(P<0. 01, Scingulated gyrus>Sprecentral gyrus > Sthalamus > Scaudate uncleus and IODcingulated gyrus > IODprecentral gyrus > IODthalamus > IODcaudate nucleus ). The results showed that there was comparatively large discrepancy of cell water permeability and metabolism function among different functional area in cattle brain, distinct peers of a functional area and distinguished type cells in the same functional area and peer which might have different susceptivity to cerebral edema.

  18. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HuaHu; Wei-PingZhang; LeiZhang; ZhongChen; Er-QingWei

    2004-01-01

    Aquaporin-4 (AQP4) is one of the aquaporins (AQPs), a water channel family. In the brain, AQP4 is expressed in astroeyte foot processes, and plays an important role in water homeostasis and in the formation of brain edema. In our study, AQP4 expression in human brain specimens from patients with traumatic brain injury or different brain tumors was detected

  19. Cerebral edema in children with diabetic ketoacidosis: vasogenic rather than cellular?

    Science.gov (United States)

    Tasker, Robert C; Acerini, Carlo L

    2014-06-01

    Cerebral edema (CE) is accumulation of water in the intracellular or extracellular spaces of the brain. Vasogenic edema occurs when there is breakdown of the tight endothelial junctions of the blood-brain barrier (BBB), leading to extravasation of intravascular protein and fluid into the interstitial space of the brain. In cellular edema the BBB remains intact and there is swelling of astrocytes with corresponding reduction in extracellular space. In this review we bring together clinical evidence from neuropathology and cerebral magnetic resonance (MR) studies in pediatric patients presenting in diabetic ketoacidosis (DKA), and use applied physiology to understand whether CE complicating DKA is vasogenic, rather than cellular in origin. Because the first-line of defense against CE is the interface between the intravascular compartment and the extracellular space in the brain much of the focus in this review is the BBB. The principal pathologic finding in fatal cases is perivascular with BBB disruption and albumin extravasation, suggesting increased vascular permeability. DKA induces an inflammatory response and the mechanism of BBB transcellular permeability may be an immunologic cascade that disrupts tight junctions. The principal MR finding in subclinical cases of CE is vasogenic rather than cellular edema. We propose that the following physiology be considered when treating cases: bolus dose of intravenous mannitol may result in fall in serum sodium concentration, and therefore clinical worsening. Failure to respond to mannitol should prompt the use of 3% hypertonic saline (HS). Bolus dose of intravenous 3% HS is expected to effect vasogenic edema provided that the reflection coefficient is close to 1. Failure to respond to 3% HS should prompt the use of mannitol.

  20. Neurogenic Pulmonary Edema (A Case Report

    Directory of Open Access Journals (Sweden)

    Funda Gümüş

    2012-08-01

    Full Text Available Neurogenic pulmonary edema is a life threatening complication of severe central nervous system injury. The most common cause of neurogenic pulmonary edema is subarachnoid hemorrhage followed by head trauma and epilepsy. The rare causes are cervical spine trauma, multiplesclerosis, cerebellar hemorrhage and intracranial tumors. Neurogenic pulmonary edema is characterized by an increase in extravascular lung water in patients who have sustained a sudden change in neurologic condition. The exact pathophysiology is unclear but it probably involves an adrenergic response to the central nervous system injury which leads to increased catecholamine, pulmonary hydrostatic pressure and increased lung capillary permeability. The presenting symptoms are nonspecific and often include dyspnea, tachypnea, tachycardia, hypoxemia, pinkfroty secretion, bilateral pulmonary infiltrates and crackles. These symptoms start within minutes or hours and resolves 48-72 hours that typically for neurogenic pulmonary edema. Basic principles of treatment, surgical decompression, reduce intracranial pressure, controlled ventilation with suplemental oxygen, positive end expiratory pressure and diuresis. We report a case with neurogenic pulmonary edema that occured after head trauma. (Journal of the Turkish Society Intensive Care 2012; 10: 59-62

  1. Leg edema from intrathecal opiate infusions.

    Science.gov (United States)

    Aldrete, J A; Couto da Silva JM

    2000-01-01

    Despite the increasing popularity of intrathecal infusions to treat patients with long-term non-cancer-related pain, this therapy is not without serious side-effects. Five out of 23 patients who had intrathecal infusions of opiates for longer than 24 months developed leg and feet edema. As predisposing factors, cardiovascular disease, deep venous thrombosis, peripheral vascular disease, and venous stasis of the lower extremities were considered. Every patient who developed pedal and leg edema after the implantation of an infusion pump was also found to have leg edema and venous stasis prior to the time when the pump was inserted. This complication was severe enough to limit their physical activity, and to produce lymphedema, ulcerations and hyperpigmentation of the skin. Reduction of the edema occurred when the dose of the opiate was decreased, and in two cases in which the infusion was discontinued, there was almost complete resolution of the syndrome. It appears that the pre-existence of pedal edema and of venous stasis is a relative contraindication to the long-term intrathecal infusion of opiates in patients with chronic non-cancer pain.

  2. Bilateral ankle edema with bilateral iritis.

    Science.gov (United States)

    Kumar, Sunil

    2007-07-01

    I report two patient presented to me with bilateral symmetrical ankle edema and bilateral acute iritis. A 42-year-old female of Indian origin and 30-year-old female from Somalia both presented with bilateral acute iritis. In the first patient, bilateral ankle edema preceded the onset of bilateral acute iritis. Bilateral ankle edema developed during the course of disease after onset of ocular symptoms in the second patient. Both patients did not suffer any significant ocular problem in the past, and on systemic examination, all clinical parameters were within normal limit. Lacrimal gland and conjunctival nodule biopsy established the final diagnosis of sarcoidosis in both cases, although the chest x-rays were normal.

  3. Combined therapy for diabetic macular edema

    Directory of Open Access Journals (Sweden)

    Saba Al Rashaed

    2013-01-01

    Full Text Available Diabetic macular edema (DME is the main cause of visual impairment in diabetic patients. Macular edema within 1 disk diameter of the fovea is present in 9% of the diabetic population. The management of DME is complex and often multiple treatment approaches are needed. This review demonstrates the benefits of intravitreal triamcinolone, bevacizumab and ranibizumab as adjunctive therapy to macular laser treatment in DME. The published results indicate that intravitreal injections of these agents may have a beneficial effect on macular thickness and visual acuity, independent of the type of macular edema that is present. Therefore, pharmacotherapy could complement focal/grid laser photocoagulation in the management of DME. For this review, we performed a literature search and summarized recent findings regarding combined therapy for DME.

  4. Massive ovarian edema, due to adjacent appendicitis.

    Science.gov (United States)

    Callen, Andrew L; Illangasekare, Tushani; Poder, Liina

    2016-09-01

    Massive ovarian edema is a benign clinical entity, the imaging findings of which can mimic an adnexal mass or ovarian torsion. In the setting of acute abdominal pain, identifying massive ovarian edema is a key in avoiding potential fertility-threatening surgery in young women. In addition, it is important to consider other contributing pathology when ovarian edema is secondary to another process. We present a case of a young woman presenting with subacute abdominal pain, whose initial workup revealed marked enlarged right ovary. Further imaging, diagnostic tests, and eventually diagnostic laparoscopy revealed that the ovarian enlargement was secondary to subacute appendicitis, rather than a primary adnexal process. We review the classic ultrasound and MRI imaging findings and pitfalls that relate to this diagnosis.

  5. Triazolam, obesity and non cardiac pulmonary edema

    Directory of Open Access Journals (Sweden)

    Fabio Di Stefano

    2012-12-01

    Full Text Available Introduction Triazolam belongs to the group of benzodiazepines and may have side effects on the respiratory system which include not only respiratory depression, but also transient benign non cardiac pulmonary edema.Case report A 52 year old obese woman developed pulmonary edema after she was taking triazolam for almost two weeks without any other medications. All possible cardiogenic and non cardiogenic causes were excluded. The condition was severe enough to require non invasive ventilation.Discussion This case differs from the other report of triazolam associated non cardiac pulmonary edema for its severity requiring non invasive ventilation. The pathogenetic mechanism is unknown. Despite the lack of objective evidence to explain pulmonary venous hypertensive changes in our case, we want to advice that triazolam should be used with caution in obese patients, as obesity might aggravate this described drug adverse reaction.

  6. Reexpansion pulmonary edema- A case report

    Directory of Open Access Journals (Sweden)

    Janmeja A

    2007-01-01

    Full Text Available A middle aged male presented to us with right side pneumothorax. Two hours after insertion of intercostals tube he felt discomfort and increased breathlessness. His chest examination showed crepitations. Chest radiograph showed partial expansion of right lung with opacity in right lower zone consistent with unilateral pulmonary edema. He was managed conservatively and improved with complete resolution on chest radiograph. Reexpansion pulmonary edema is an uncommon complication of the treatment of lung atelectasis, pleural effusion or pneumothorax and patho-genesis is unclear.

  7. Facial Edema Evaluation Using Digital Image Processing

    Directory of Open Access Journals (Sweden)

    A. E. Villafuerte-Nuñez

    2013-01-01

    Full Text Available The main objective of the facial edema evaluation is providing the needed information to determine the effectiveness of the anti-inflammatory drugs in development. This paper presents a system that measures the four main variables present in facial edemas: trismus, blush (coloration, temperature, and inflammation. Measurements are obtained by using image processing and the combination of different devices such as a projector, a PC, a digital camera, a thermographic camera, and a cephalostat. Data analysis and processing are performed using MATLAB. Facial inflammation is measured by comparing three-dimensional reconstructions of inflammatory variations using the fringe projection technique. Trismus is measured by converting pixels to centimeters in a digitally obtained image of an open mouth. Blushing changes are measured by obtaining and comparing the RGB histograms from facial edema images at different times. Finally, temperature changes are measured using a thermographic camera. Some tests using controlled measurements of every variable are presented in this paper. The results allow evaluating the measurement system before its use in a real test, using the pain model approved by the US Food and Drug Administration (FDA, which consists in extracting the third molar to generate the facial edema.

  8. Current status in diabetic macular edema treatments

    Institute of Scientific and Technical Information of China (English)

    Pedro; Romero-Aroca

    2013-01-01

    Diabetes is a serious chronic condition,which increase the risk of cardiovascular diseases,kidney failure and nerve damage leading to amputation.Furthermore the ocular complications include diabetic macular edema,is the leading cause of blindness among adults in the industrialized countries.Today,blindness from diabetic macular edema is largely preventable with timely detection and appropriate interventional therapy.The treatment should include an optimized control of glycemia,arterial tension,lipids and renal status.The photocoagulation laser is currently restricted to focal macular edema in some countries,but due the high cost of intravitreal drugs,the use of laser treatment for focal and diffuse diabetic macular edema(DME),can be valid as gold standard in many countries.The intravitreal anti vascular endothelial growth factor drugs(ranibizumab and bevacizumab),are indicated in the treatment of all types of DME,but the correct protocol for administration should be defined for the different Retina Scientific Societies.The corticosteroids for diffuse DME,has a place in pseudophakic patients,but its complications restricted the use of these drugs for some patients.Finally the intravitreal interface plays an important role and its exploration is mandatory in all DME patients.

  9. Acute pulmonary edema after near strangulation

    Energy Technology Data Exchange (ETDEWEB)

    Shumaker, D.; Kottamasu, S.; Preston, G.; Treloar, D.

    1988-11-01

    We report a case of acute, noncardiogenic pulmonary edema in an 11 year old boy who suffered strangulation during an altercation. The clinical presentation was characterized by moderate respiratory distress and hemoptysis. Both the radiographic and clinical findings resolved during the three day admission which followed. A review of the literature is presented, and possible pathogenesis is discussed.

  10. An uncommon cause of acute pulmonary edema.

    Science.gov (United States)

    Nepal, Santosh; Giri, Smith; Bhusal, Mohan; Siwakoti, Krishmita; Pathak, Ranjan

    2016-09-01

    Acute cardiogenic pulmonary edema secondary to catecholamine-induced cardiomyopathy is a very uncommon and fatal initial presentation of pheochromocytoma. However, with early clinical suspicion and aggressive management, the condition is reversible. This case report describes a patient who presented with hypertension, dyspnea, and cough with bloody streaks, and who recovered within 48 hours after appropriate treatment.

  11. Interstitial Pulmonary Edema Following Bromocarbamide Intoxication

    Science.gov (United States)

    Sugihara, H.; Hagedorn, M.; Bōttcher, D.; Neuhof, H.; Mittermayer, Ch.

    1974-01-01

    Bromocarbamides are sleep-inducing drugs which can lead, in man, to intoxication and death due to respiratory failure. To prove whether hemodynamic factors or the changed endothelial permeability induce pulmonary edema, animal experiments were performed. The fine structural changes in pulmonary edema in rabbits were observed at 60, 90 and 120 minutes after oral administration. The major findings were a) large blebs between capillary endothelium and alveolar epithelium and b) interstitial edema of the vessel wall. The bleb contents were much less electron dense than the blood contents in the capillary. Colloidal carbon did not enter the bleb or the edematous interstitial tissue. Exogenous peroxidase uptake in pinocytotie vesicles increased in pathologic cases. The hemodynamic measurements in animal receiving artificial respiration which maintained the blood pO2 at a steady state showed similar blebs in the pulmonary vessels, indicating that anoxia is not the major cause of the vascular lesion. Moreover, pulmonary arterial pressure and pulmonary vascular resistance could be held in the normal range in artificially respirated animals under bromocarbamide intoxication. Thus, hemodynamic factors are not likely to play a pathogenetic role in bringing about pulmonary edema. The chief, early factor is the increased endothelial permeability due to increased cytoplasmic transport. From this a practical suggestion for treating patients with bromocarbamide intoxication is derived: the usual fluid replacement in shock patients should be handled with great care to avoid fluid overload of the lung. ImagesFig 1Fig 2Fig 3Fig 4Fig 5Fig 6 PMID:4835993

  12. Evaluation of an Acute RNAi-Mediated Therapeutic for Visual Dysfunction Associated with Traumatic Brain Injury

    Science.gov (United States)

    2013-10-01

    brain injury (TBI) is the leading cause of death in children and young adults globally. Malignant cerebral edema plays a major role in the...pathophysiology which evolves after severe TBI. Added to this is the significant morbidity and mortality from cerebral edema associated with acute stroke...hypoxic ischemic coma, neurological cancers and brain infection. Therapeutic strategies to prevent cerebral edema are limited and if brain swelling

  13. Generalized edema associated with parvovirus B19 infection

    Directory of Open Access Journals (Sweden)

    Pieter J. Vlaar

    2014-12-01

    Full Text Available Generalized edema is a rare presentation of human parvovirus B19 infection. The etiology of this edema is unclear, particularly because signs of heart or renal failure are often not present. We report the case of a young adult presenting with generalized edema with serological and PCR evidence of parvovirus B19 infection, and discuss the potential mechanisms of edema based on the previous literature.

  14. An Adult Case of Diabetic Ketoacidosis Presenting with Cerebral Edema

    OpenAIRE

    Barış Akıncı; Abdurrahman Çömlekçi; Serkan Yener; Süleyman Men

    2009-01-01

    Cerebral edema is a life-threatening complication of diabetic ketoacidosis (DKA) which may predominantly develop in pediatric cases during the management of DKA.. Symptomatic cerebral edema in children is rarely detected at admission, before initiation of the treatment. Cerebral edema associated with DKA is extremely rare in adults. Here, we report an adult patient with DKA who presented with symptomatic cerebral edema. Turk Jem 2009; 13: 16-8

  15. Collaboration in the presence of cerebral edema: The complications of steroids

    Directory of Open Access Journals (Sweden)

    Camille Schwarzrock

    2016-01-01

    Conclusions: More high-quality, well-controlled studies are needed around dexamethasone dosing for the management of cerebral edema. Clinical practice guidelines need to encompass both the prescriber and nursing-based interventions. Collaboration between disciplines is a necessity when monitoring and managing steroid-induced toxicities in brain tumor patients. Future evidence-based guidelines need recommendations for appropriate interval screening tests and quantifiable tools needed to aid in monitoring steroid-induced complications.

  16. Hypothyroidism and non-cardiogenic pulmonary edema: are we missing something here?

    OpenAIRE

    Al-Sofiani, Mohammed; Nikolla, Dhimitri; Metta, V V S Ramesh

    2015-01-01

    Summary We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diag...

  17. Macular edema in uveitis with emphasis on ocular sarcoidosis

    NARCIS (Netherlands)

    Norel, J. van

    2015-01-01

    This thesis investigates the accumulation of fluid in the yellow spot (macular edema) in ocular inflammation (uveitis). Macular edema may result in definitive loss of vision.Two methods of imaging of macular edema are fluorescein angiography (FA) and optical coherence tomography (OCT). The first met

  18. Characterization and quantification of cerebral edema induced by synchrotron x-ray microbeam radiation therapy

    Energy Technology Data Exchange (ETDEWEB)

    Serduc, Raphael; Looij, Yohan van de; Francony, Gilles; Verdonck, Olivier; Sanden, Boudewijn van der; Farion, Regine; Segebarth, Christoph; Remy, Chantal; Lahrech, Hana [INSERM, U836, F-38043 Grenoble (France); Laissue, Jean [Institute of Pathology, University of Bern (Switzerland); Braeuer-Krisch, Elke; Siegbahn, Erik Albert; Bravin, Alberto; Prezado, Yolanda [European Synchrotron Radiation Facility, F-38043 Grenoble (France)], E-mail: serduc@esrf.fr

    2008-03-07

    Cerebral edema is one of the main acute complications arising after irradiation of brain tumors. Microbeam radiation therapy (MRT), an innovative experimental radiotherapy technique using spatially fractionated synchrotron x-rays, has been shown to spare radiosensitive tissues such as mammal brains. The aim of this study was to determine if cerebral edema occurs after MRT using diffusion-weighted MRI and microgravimetry. Prone Swiss nude mice's heads were positioned horizontally in the synchrotron x-ray beam and the upper part of the left hemisphere was irradiated in the antero-posterior direction by an array of 18 planar microbeams (25 mm wide, on-center spacing 211 mm, height 4 mm, entrance dose 312 Gy or 1000 Gy). An apparent diffusion coefficient (ADC) was measured at 7 T 1, 7, 14, 21 and 28 days after irradiation. Eventually, the cerebral water content (CWC) was determined by microgravimetry. The ADC and CWC in the irradiated (312 Gy or 1000 Gy) and in the contralateral non-irradiated hemispheres were not significantly different at all measurement times, with two exceptions: (1) a 9% ADC decrease (p < 0.05) was observed in the irradiated cortex 1 day after exposure to 312 Gy, (2) a 0.7% increase (p < 0.05) in the CWC was measured in the irradiated hemispheres 1 day after exposure to 1000 Gy. The results demonstrate the presence of a minor and transient cellular edema (ADC decrease) at 1 day after a 312 Gy exposure, without a significant CWC increase. One day after a 1000 Gy exposure, the CWC increased, while the ADC remained unchanged and may reflect the simultaneous presence of cellular and vasogenic edema. Both types of edema disappear within a week after microbeam exposure which may confirm the normal tissue sparing effect of MRT. For more information on this article, see medicalphysicsweb.org.

  19. The evolution of scuba divers pulmonary edema.

    Science.gov (United States)

    Edmonds, Carl

    2016-01-01

    The evolution of scuba divers pulmonary edema is described. When discovered in 1981, it was believed to be a cold-induced response in a submerged, otherwise healthy, scuba diver. The clinical features are described and discussed, as are the demographics. An alleged prevalence of 1.1% was complicated by problematic statistics and an apparent increase in reported cases. Recurrences both while diving and swimming or snorkeling were common. More recent case reports and surveys are described, identifying predisposing factors and associations, including cardiac pathology. Stress cardiomyopathies, reversible myocardial disorder or Takotsubo cardiomyopathy, may complicate the presentation, especially in older females. Relevant cardiac investigations and autopsy findings are reviewed. Disease severity and potential lethality of scuba divers pulmonary edema became more apparent early this century, and these influence our current recommendations to survivors. First aid and treatment are also discussed.

  20. Influenza leaves a TRAIL to pulmonary edema.

    Science.gov (United States)

    Brauer, Rena; Chen, Peter

    2016-04-01

    Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake. In this issue of the JCI, Peteranderl and colleagues define a paracrine communication between macrophages and type II alveolar epithelial cells during influenza infection where IFNα induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium. This reduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmonary edema. Inhibition of the TRAIL signaling pathway has been shown to improve lung injury after influenza infection, and future studies will be needed to determine if blocking this pathway is a viable option in the treatment of ARDS.

  1. Management of pseudophakic cystoid macular edema.

    Science.gov (United States)

    Guo, Suqin; Patel, Shriji; Baumrind, Ben; Johnson, Keegan; Levinsohn, Daniel; Marcus, Edward; Tannen, Brad; Roy, Monique; Bhagat, Neelakshi; Zarbin, Marco

    2015-01-01

    Pseudophakic cystoid macular edema (PCME) is a common complication following cataract surgery. Acute PCME may resolve spontaneously, but some patients will develop chronic macular edema that affects vision and is difficult to treat. This disease was described more than 50 years ago, and there are multiple options for clinical management. We discuss mechanisms, clinical efficacy, and adverse effects of these treatment modalities. Topical non-steroidal anti-inflammatory agents and corticosteroids are widely used and, when combined, may have a synergistic effect. Intravitreal corticosteroids and anti-vascular endothelial growth factor (anti-VEGF) agents have shown promise when topical medications either fail or have had limited effects. Randomized clinical studies evaluating anti-VEGF agents are needed to fully evaluate benefits and risks. When PCME is either refractory to medical therapy or is associated with significant vitreous involvement, pars plana vitrectomy has been shown to improve outcomes, though it is associated with additional risks.

  2. The non-opioid KOR agonist Salovinorin A reducing brain edema in rats with forebrain ischemia and reperfusion%非阿片类药物KOR激动剂Salvinorin A减轻前脑缺血再灌注大鼠脑水肿的作用

    Institute of Scientific and Technical Information of China (English)

    张燕; 王震虹; 何振洲; 忻纪华

    2015-01-01

    Objective To discuss the mechanism of Kappa opioid receptor (KOR) agonist Salvinorin A (SA) on decreas-ing brain edema after forebrain ischemia-reperfusion (I/R) injury in rats. Methods Male Sprague-Dawley rats were di-vided into 5 groups (n=10): sham operation group, I/R group, DMSO (vehicle) group, SA group and Norbinaltorphimine (nor-BIN, KOR antagonist) +SA group. Forebrain ischemia was performed by low artery pressure with bilateral carotid artery occlusion for 10 minutes. Intervenes (DMSO, SA, nor-BIN+SA) were performed after forebrain ischemia instantly. The animals were sacrificed 24 hours after reperfusion. The hippocampus was taken for pathology, and TdT-mediated dUTP nick end labeling (TUNEL) and immunohistochemical test were used for AQP4 detection. The wet-dry weight method was used to assess brain water content. Results Compared with sham operation group, hippocampus water con-tent increased in I/R group (P< 0.01). Hippocampus water content was significantly lower in SA group than that in I/R group (P<0.01). Hippocampus water content was significantly higher in nor-BIN+SA group than that in SA group (P<0.05). Compared with I/R and DMSO groups, hippocampus neurosis and apoptosis were alleviated significantly with treatment of SA 24 h after forebrain I/R (P<0.01), which effect was blunted by nor-BIN. Compared with sham opera-tion group, AQP4 expressed in hippocampus was promoted by I/R (P < 0.01). Compared with I/R group, AQP4 ex-pressed was depressed in SA group (P< 0.01). The expression of AQP4 increased significantly with treatment of nor-BIN+SA compared with SA (P< 0.05). Conclusion SA can reduce cerebral edema after forebrain ischemia and brain damage by inhibition of AQP4. Its mechanism may be correlated with KOR.%目的:探讨大鼠前脑缺血再灌注(I/R)损伤后,Kappa阿片受体(KOR)激动剂Salvinorin A(SA)减轻脑水肿的机制。方法成年健康雄性Sprague-Dawley(SD)大鼠随机分为5组(n=10):假手术组、I/R组、DMSO

  3. Cystoid Macular Edema in Bietti's Crystalline Retinopathy

    OpenAIRE

    Ali Osman Saatci; Hasan Can Doruk; Aylin Yaman

    2014-01-01

    A 27-year-old man with progressive bilateral visual decline was diagnosed to have Bietti's crystalline dystrophy (BCD). Fluorescein angiography revealed bilateral petaloid type late hyperfluorescence implicating concurrent cystoid macular edema (CME). Optical coherence tomography exhibited cystoid foveal lacunas OU. During the follow-up of six years, intraretinal crystals reduced in amount but CME persisted angiographically and tomographically. CME is among the rare macular features of BCD in...

  4. Cystoid Macular Edema in Bietti's Crystalline Retinopathy

    Directory of Open Access Journals (Sweden)

    Ali Osman Saatci

    2014-01-01

    Full Text Available A 27-year-old man with progressive bilateral visual decline was diagnosed to have Bietti's crystalline dystrophy (BCD. Fluorescein angiography revealed bilateral petaloid type late hyperfluorescence implicating concurrent cystoid macular edema (CME. Optical coherence tomography exhibited cystoid foveal lacunas OU. During the follow-up of six years, intraretinal crystals reduced in amount but CME persisted angiographically and tomographically. CME is among the rare macular features of BCD including subfoveal sensorial detachment, subretinal neovascular membrane, and macular hole.

  5. Acute pulmonary edema after intramyometrial prostodin

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    Neha Baduni

    2011-01-01

    Full Text Available A 25 year old, 68 kg, primigravida, was taken up for emergency caesarean section for meconium stained liquor and fetal distress. She was a known case of pre eclampsia and her blood pressure was controlled on tab methyl dopa. she was administered general anaesthesia. after delivery of baby she went into postpartum hemorrhage which was controlled with intramyometrial prostodin. but immediately after its administration she went into acute pulmonary edema.

  6. Diagnosis and management of cardiogenic pulmonary edema.

    Science.gov (United States)

    Alwi, Idrus

    2010-07-01

    Acute cardiogenic pulmonary edema (ACPE) is a common cardiogenic emergency with a quite high in-hospital mortality rate. ACPE is defined as pulmonary edema with increased secondary hydrostatic capillary pressure due to elevated pulmonary venous pressure. Increased hydrostatic pressure may result from various causes including excessive administration of intravascular volume, obstruction of pulmonary venous outflow or secondary left ventricular failure due to left ventricular systolic or diastolic dysfunction. ACPE must be distinguished from pulmonary edema associated with injury of alveolar capillary membrane caused by various etiologies, i.e. direct pulmonary injury such as pneumonia and indirect pulmonary injury such as sepsis. Numerous clinical manifestations may differentiate ACPE and Non-ACPE. ACPE usually presents with a history of acute cardiac catastrophe. Physical examination reveals a low-flow state, S3 gallop, jugular venous distention and fine crepitant rales with auscultation. The diagnosis of pulmonary edema is made based on symptoms and clinical signs are found through history taking, physical examination, ECG, chest X-ray, echocardiography and laboratory tests including blood gas analysis and specific biomarkers. Medical treatment of ACPE has 3 main objectives, i.e.: (1) reduced venous return (preload reduction); (2) reduced resistance of systemic vascular (afterload reduction); and (3) inotropic support in some cases. Treatment that can be administered includes: vasodilator when there is normal or high BP, diuretics when there is volume overload or fluid retention, and inotropic drugs when there is hypotension or signs of organ hypoperfusion. Intubation and mechanical ventilation may be necessary to achieve adequate oxygenation.

  7. 伽玛刀治疗癫痫致迟发性放射性脑水肿及脑坏死的临床研究%Gamma knife therapy in treating epilepsy patients with delayed radiation-induced edema and necrosis in the brain

    Institute of Scientific and Technical Information of China (English)

    陈登奎; 庄进学; 朱明霞; 薛峰; 程宏炜; 李海龙; 李伟; 袁树斌

    2010-01-01

    Objective To explore the clinical effect of gamma knife treatment in intractable epilepsy patients with delayed radiation-induced cerebral edema and/or necrosis.Methods The clinical feature,EEG,MRI and treatment modality data of 20 patients,admitted to our hospital from 1995 to 2008 and treated with gamma knife,were analyzed retrospectively.In all these patients,14 received conventional medical treatment and 6 adopted surgical removals of necrosis and epileptic focus resulting from the formation of necrotizing lesion,the apparent mass effect and aggravated seizures after conservative treatment.Results Except 1 patient died of cerebral hernia after giving up surgical treatment,all the other patients achieved good results in controlling the epilepsy and headache.Five in the medical group and 2 in the surgical group still needed anti-epileptic drugs.Two patients presented epilepsy of new type because of brain necrosis after radiation therapy and followed EEG demonstrated that radiation-induced delayed cerebral edema and/or necrosis could lead to new epileptogenie focus.Conclusions Radiation-induced cerebral edema and/or necrosis is a common complication in patients with epilepsy after gamma knife treatment which is unpredicted or repeated,thus early diagnosis and treatment are extremely important.Most patients can be cured with such drugs as corticosteroid combined with mannitol or Chinese herbal medicine.However,surgical treatment is needed in controlling the seizures and improving the symptoms once the cystic necrosis lesion,apparent mass effect and new epileptogenic focus appear.%目的 探讨药物难治性癫痫患者经伽玛刀治疗后迟发性放射性脑水肿、脑坏死的临床治疗.方法 总结解放军第452医院神经外科自1995年至2008年治疗的20例发生迟发性放射性脑水肿、脑坏死患者的临床特点,脑电图、MRI变化和治疗方法,其中14例患者接受药物保守治疗,6例有坏死灶形成、占位效应明显、癫

  8. Assessing local tissue edema in postmastectomy lymphedema.

    Science.gov (United States)

    Mayrovitz, H N

    2007-06-01

    Overall limb lymphedema can be assessed by several methods but none are suitable to determine local edema. Quantifying local edema could provide important information not previously available. Our goal was to determine the suitability of using the tissue dielectric constant (TDC) as and index of local tissue water to detect and quantify edema in postmastectomy patients with unilateral arm lymphedema. Segmental arm volume and TDC were measured in both arms of 18 women with unilateral lymphedema, and in 15 premenopausal and 15 postmenopausal controls. TDC was measured at a frequency of 300 MHz using open-ended coaxial probes with effective measuring depths of 0.5, 1.5, 2.5 and 5.0 mm. For patients and controls, absolute TDC depended on measurement depth but for any depth the TDC of lymphedematous segments was significantly greater than for non-affected contralateral arms (pTDC ratio between arms for patients was 1.64+/-0.30 vs.1.04+/-0.04 for both control groups (pTDC ratio was as low as 1.2 and no control subject's TDC ratio was as great as 1.2. Results suggest that this method is a good quantitative discriminator of the presence of lymphedema in patients with unilateral limb lymphedema.

  9. Radiological diagnosis of pulmonary edema in chronic renal failure

    Energy Technology Data Exchange (ETDEWEB)

    Tret' yakov, A.E. (Tsentral' naya Klinicheskaya Bol' nitsa, Moscow (USSR))

    Pulmonary edema has been revealed in 132 patients (51.6 %) during radiologic examination of 256 patients with chronic renal failure. The performance of anterio-posterior chest radiographs was in most cases necessary and quite sufficient for making diagnostic conclusions. Follow up study of patients with pulmonary edema and analysis of radiologic picture of the alterations permitted physicians to distinguish approximately 3 stages of the process development, which transit from one into another. Stage 1 involves early disorders and prodromes of pulmonary edema; Stage 2 interstitial lung edema; Stage 3 alveolar edema. The circulation enforcement of the upper lobar vessels has been the main feature of stage 1. Radiogramometry provided additional information for the pulmonary edema diagnosis. For instance, cardioradiometric data are useful for pulmonary edema diagnosis and evidence in favour of its close connection with heart disorders.

  10. Hypothyroidism and non-cardiogenic pulmonary edema: are we missing something here?

    Science.gov (United States)

    Nikolla, Dhimitri; Metta, V V S Ramesh

    2015-01-01

    Summary We report the case of a 42-year-old female with a history of hypothyroidism and asthma presenting with progressive dyspnea and orthopnea after 2 days of an upper respiratory tract infection (URTI). Based on the clinical and radiological findings, the patient was admitted as a case of cardiogenic pulmonary edema secondary to possible viral myocarditis. However, a normal brain natriuretic peptide (BNP) level with a normal ejection fraction (EF) on echocardiogram changed our working diagnosis from cardiogenic to non-cardiogenic pulmonary edema. Further questioning revealed a history of nocturnal snoring, frequent awakening, and daytime fatigue, suggesting a possible sleep apnea syndrome (SAS). In conclusion, we believe that SAS was the missing link between our patient's hypothyroidism and non-cardiogenic pulmonary edema. Learning points Always keep an open mind and look for a pathology that would explain the whole clinical scenario.The involvement of the respiratory system in hypothyroidism can range from SAS, pulmonary hypertension, hypoventilation, and severe respiratory failure.Hypothyroidism and SAS should be considered in the differential diagnosis of non-cardiogenic pulmonary edema.Patients should be instructed to take levothyroxine on an empty stomach 30–60 min before food to avoid erratic absorption of the hormone. PMID:25866647

  11. Impact of Clipping versus Coiling on Postoperative Hemodynamics and Pulmonary Edema after Subarachnoid Hemorrhage

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    Nobutaka Horie

    2014-01-01

    Full Text Available Volume management is critical for assessment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH. This multicenter prospective cohort study compared the impact of surgical clipping versus endovascular coiling on postoperative hemodynamics and pulmonary edema in patients with SAH. Hemodynamic parameters were measured for 14 days using a transpulmonary thermodilution system. The study included 202 patients, including 160 who underwent clipping and 42 who underwent coiling. There were no differences in global ejection fraction (GEF, cardiac index, systemic vascular resistance index, or global end-diastolic volume index between the clipping and coiling groups in the early period. However, extravascular lung water index (EVLWI and pulmonary vascular permeability index (PVPI were significantly higher in the clipping group in the vasospasm period. Postoperative C-reactive protein (CRP level was higher in the clipping group and was significantly correlated with postoperative brain natriuretic peptide level. Multivariate analysis found that PVPI and GEF were independently associated with high EVLWI in the early period, suggesting cardiogenic edema, and that CRP and PVPI, but not GEF, were independently associated with high EVLWI in the vasospasm period, suggesting noncardiogenic edema. In conclusion, clipping affects postoperative CRP level and may thereby increase noncardiogenic pulmonary edema in the vasospasm period. His trial is registered with University Hospital Medical Information Network UMIN000003794.

  12. Ataxia, acute mountain sickness, and high altitude cerebral edema

    Institute of Scientific and Technical Information of China (English)

    Wu Tianyi; Ma Siqing; Bian Huiping; Zhang Minming

    2013-01-01

    Previous investigations suggest that ataxia is common and often one of the most reliable warning signs of high altitude cerebral edema(HACE).The aim of this study was to investigate the diagnostic role of ataxia in acute mountain sickness (AMS) and HACE among mountain rescuers on the quake areas,and in approaching the relation between AMS and HACE.After the earthquake on April 14,2010,approximately 24080 lowland rescuers were rapidly transported from sea level or lowlands to the mountainous rescue sites at 3750 ~ 4568 m,and extremely hardly worked for an emergency treatment after arrival.Assessments of acute altitude illness on the quake areas were using the Lake Louise Scoring System.73 % of the rescuers were found to be developed AMS.The incidence of high altitude pulmonary edema(HAPE) and HACE was 0.73 % and 0.26 %,respectively,on the second to third day at altitude.Ataxia sign was measured by simple tests of coordination including a modified Romberg test.The clinical features of 62 patients with HACE were analyzed.It was found that the most frequent,serious neurological symptoms and signs were altered mental status(50/62,80.6 %)and truncal ataxia (47/62,75.8 %).Mental status change was rated slightly higher than ataxia,but ataxia occurred earlier than mental status change and other symptoms.The earliest sign of ataxia was a vague unsteadiness of gait,which may be present alone in association with or without AMS.Advanced ataxia was correlated with the AMS scores,but mild ataxia did not correlate with AMS scores at altitudes of 3750~4568 m.Of them,14 patients were further examined by computerized tomographic scanning of the brain and cerebral magnetic resonance imagines were examined in another 15 cases.These imaging studies indicated that the presence of the cerebral edema was in 97 % of cases who were clinically diagnosed as HACE (28/29).Ataxia seems to be a reliable sign of advanced AMS or HACE,so does altered mental status.

  13. Expression of aquaporin 4 in 1,2-dichloroethane-induced toxic brain edema in rats%水通道蛋白4在1,2-二氯乙烷中毒性脑水肿中表达研究

    Institute of Scientific and Technical Information of China (English)

    贾肖辉; 陆丰荣; 李国樑; 高洪彬; 王庆; 胡前胜; 黄振烈; 程浩; 徐丹丹; 范启明; 殷霄; 戎伟丰; 郑杰蔚; 黄曼琪; 曾丽海

    2016-01-01

    Objective To explore the effects of aquaporin 4 ( APQ4) in rat toxic brain edema induced by subacute 1,2-dichloroethane (1,2-DCE) exposure.Methods Thirty-two specific pathogen free healthy adult female SD rats were randomly divided into control (8 rats), low-dose (12 rats) and high-dose (12 rats) groups.The treatment groups were exposed to 1,2-DCE (low-dose:600 mg/m3;high-dose:1 800 mg/m3, nose-only) and the control group was exposed to fresh air by dynamic inhalation for 8 hours per day for consecutive 7 days.After exposure, histopathologic changes were examined in the cerebral cortex.Real-time polymerase chain reaction was used to detect the mRNA relative expression of matrix metalloproteinase 2 (MMP2), Na-K-Cl cotransporter-1 (NKCC1) and AQP4.The Western blotting was used to detect the expression of AQP4 protein in the cerebral cortex.Results The pathological results showed that the cerebral cortex tissues were loose around the peripheral vessels and the vessels tissue space appeared widen in low-dose exposure group.The pathological change was more serious in high-dose group than low-dose group, with obvious loosen vessels and vacuole.Compared with those of the control group and the low-dose group, the relative expression level of MMP2 mRNA in the high-dose group increased significantly[(1.07 ±0.41) vs (1.56 ±0.55), (1.21 ±0.59) vs (1.56 ±0.55), P0.05 ] .The relative expression level of AQP4 protein in the high-dose group was lower than that of the control group [(0.80 ±0.25) vs (1.19 ±0.42), P<0.05].Conclusion The brain edema induced by subacute inhalation of 1,2-DCE is of mixed types with vasogenic edema as its main symptom.Its pathogenesis is related to the changes of AQP4 expression.%目的:探讨水通道蛋白4(AQP4)在1,2-二氯乙烷(1,2-DCE)亚急性吸入所致中毒性脑水肿发生中的作用。方法无特定病原体级健康成年雌性SD大鼠,随机分为对照组(8只)、低剂量组(12

  14. 脑水肿分子机制的研究进展%Progression on Molecular Mechanisms of Cerebral Edema

    Institute of Scientific and Technical Information of China (English)

    武柠子; 马慧萍; 王宁; 贾正平

    2016-01-01

    Cerebral edema is a pathological sign of increased brain volume induced by accumulation of fluid in the brain,and it is the response of brain tissues to a variety of pathogenic factors. Intracranial injury,ischemia,hypoxia, inflammation,cerebral dysmetabolism,brain tumor and poisoning can all cause brain edema. Brain edema can induce el-evation of intracranial pressure,and functional and structural injuries can be found when level of intracranial pressure in-creases to a certain degree,and it also can lead to brain death. The previous study for the mechanism of cerebral edema includes blood-brain barrier theory,calcium ion theory,cerebral microcirculation disturbance theory and so on. The study of recent years has shown that incidence of cerebral edema closely relates to aquaporin-4(AQP4),matrix metalloprotein-ases(MMPs),tight junction(TJ)protein and inflammatory cytokines. This paper summarizes the molecular mechanisms of cerebral edema.%脑水肿是指脑内水分增加导致脑容积增大的一种病理现象,是脑组织对各种致病因素的反应。颅内损伤、缺血、缺氧、炎症、脑代谢障碍、肿瘤以及中毒都会引起脑水肿。脑水肿可导致颅内压的升高,当颅内压升高到一定程度时,脑组织就会发生功能和结构的损害,严重者导致脑死亡。先前对脑水肿发病机制的研究包括血脑屏障学说、钙离子学说、脑微循环障碍学说、脑细胞代谢障碍等。但是近年的研究表明脑水肿的发生与水通道蛋白4、基质金属蛋白酶、紧密连接蛋白、炎性细胞因子等密切相关。本文就脑水肿发生的分子机制进行综述。

  15. First 5-days follow-up and correlation study between urinary cysteinyl leukotrienes and edema values in primary spontaneous supratentorial intracerebral hemorrhage

    Directory of Open Access Journals (Sweden)

    Dolnenec-Baneva Natalija

    2014-07-01

    Full Text Available Background: After intracerebral hemorrhage cysteinyl leukotrienes (C4, D4, E4 are synthetisized in the contact brain parenchyma-extravasated blood and participate in producing of edema formation. The study aim is a 5-days follow up (admittance/3th day/5th day of urinary cysteinyl leukotrienes, hematoma and edema volume in patients with primary spontaneous supratentorial intracerebral hemorrhage and to determine the relationship: edema/haematoma and edema/leukotrienes. Methods: An enzyme immunoassay for leukotrienes measuring in the urine samples from 62 patients with hemorrhage during the first 5 days (admittance/3th day/5th day and 80 health controls is used. Hematoma and edema volume is visualised and measured by computed-tomography. Results: Admission values of leukotrienes were significantly higher in the hemorrhagic patients (min = 268.61; max = 5787.36; mean = 1842.20 ± 1413.19 pg/ml/mg creatinine versus control subjects (min = 297.8; max = 1684.2; mean = 918.6 ± 332 (p 0.05. The edema (mean: 12.86 ± 13.52; 22.38 ± 21.10; 28.45 ± 29.41 cm3 showed very high significance (p 0.05 of moderate strength is found between edema and hematoma; and significant positive correlation (r = 0.6; p 0.05 at admittance, r = - 0.05 (p > 0. 05 on the 3th day (nonexistence of linear correlation, the sign minus presents their tendency for the opposite movement in their values and r = 0.2 (p > 0.05 on the 5th day are found (positive linear nonsignificant correlation of slight strength. Conclusion: Significant urinary leukotrienes excretion (a brain capacity for significant leukotreienes synthesis and significant edema progression versus constant haematoma are found. The edema size followed the hematoma size of moderate extent. The edema showed an inverse dependence of the leukotrienes (a tendency for opposite movement of their values, the high leukotrienes values at admittance bring to greater edema volume on the third/the fifth day, respectively. Elevated

  16. Loss of vascular early response gene reduces edema formation after experimental stroke

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    Liu Fudong

    2012-06-01

    Full Text Available Abstract Vascular Early Response Gene (Verge is an immediate early gene (IEG that is up-regulated in endothelial cells in response to a number of stressors, including ischemic stroke. Endothelial cell lines that stably express Verge show enhanced permeability. Increased Verge expression has also been associated with blood brain barrier breakdown. In this study we investigated the role of Verge in ischemic injury induced by middle cerebral artery occlusion (MCAO in both Verge knockout (KO and wild type (WT mice. Verge KO mice had significantly less cerebral edema formation after MCAO compared to WT mice. However, stroke outcome (infarct size and neurological deficit scores evaluated at either 24 or 72 hours after stroke showed no differences between the two genotypes. Verge deletion leads to decreased edema formation after ischemia; however acute stroke outcomes were unchanged.

  17. Edema agudo hemorrágico da infância Acute hemorrhagic edema of infancy

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    Fabiana Britto Goulart

    2004-06-01

    Full Text Available Relatamos o caso de uma criança de oito meses de idade com infecção das vias aéreas superiores, seguida de irritabilidade e pelo aparecimento de lesões purpúricas na face, extremidades e pavilhões auriculares e edema de dorso dos pés e das mãos. Inicialmente recebeu dexametasona, ampicilina e cloranfenicol para tratamento de suposta meningococcemia. Entretanto, as lesões características e a boa evolução clínica do quadro levaram-nos ao diagnóstico de uma forma rara de vasculite cutânea: edema agudo hemorrágico da infância.We report the case of an eight-month child with upper airway infection followed by irritability and purpuric lesions in his face, ears and extremities and peripheral soft tissue edema. He was treated with dexamethasone, ampicillin and chloramphenicol for presumed meningococcemia, but the characteristics lesions and the benign course of the disease led us to the diagnosis of a rare form of cutaneous vasculitis called Acute Hemorrhagic Edema of Infancy (AHEI.

  18. Pulmonary Edema and Myocarditis Developing Due to Scorpion Stings

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    Sevdegul Karadas

    2015-11-01

    Full Text Available Although most of the scorpion stings are harmless, deadly species of scorpions may cause multiorgan failure, neurotoxicity, cardiotoxicity, and pulmonary edema. The cases should be observed in the emergency department against the possibility of development of systemic effects. Fatal complications, in particular such as pulmonary edema, and myocarditis should be considered. In this study, a case of myocarditis and pulmonary edema was detected on the patient who had applied to the emergency department due to a scorpion sting is presented.

  19. Acute edema blisters in a hereditary angioedema cutaneous attack.

    Science.gov (United States)

    Fernández Romero, D; Di Marco, P; Malbrán, A

    2008-01-01

    Hereditary angioedema is a rare autosomal dominant disease characterized by recurrent episodes of acute edema affecting the skin and the respiratory and digestive tracts. Acute edema blisters or hydro-static bullae develop after rapid accumulation of interstitial fluid usually associated to cardiac insufficiency. Lesions contain sterile fluid and break up easily resolving without scars. Blisters disappear when fluid accumulation resolves. We describe a patient developing recurrent acute edema blisters as a consequence of cutaneous hereditary angioedema attacks.

  20. Unicompartmental muscle edema: an early sign of deep venous thrombosis

    Energy Technology Data Exchange (ETDEWEB)

    Liu, Patrick T. [Mayo Clinic Scottsdale, Department of Diagnostic Radiology, 13400 E. Shea Boulevard, Scottsdale, AZ 85259 (United States); Ilaslan, Hakan [Mayo Clinic Rochester, Department of Diagnostic Radiology, Rochester, Minnesota (United States)

    2003-01-01

    The finding of muscle edema restricted to a single muscle compartment on MRI usually indicates a diagnosis of traumatic injury, myositis, denervation or neoplasm. This case demonstrates that deep venous thrombosis can also be the cause of isolated deep posterior compartment muscle edema in the calf and should be considered in the differential diagnosis even in the absence of diffuse soft tissue or subcutaneous edema. (orig.)

  1. Edema and vascular permeability in cerebral ischemia: comparison between ischemic neuronal damage and infarction.

    Science.gov (United States)

    Petito, C K; Pulsinelli, W A; Jacobson, G; Plum, F

    1982-07-01

    The respective influences of ischemic neuronal damage and infarction on the development of abnormal blood-brain barrier (BBB) permeability and cerebral edema were evaluated in a rat model of temporary four-vessel occlusion in which ischemic neuronal damage with only infrequent infarction is produced. Survival times ranged from 40 minutes to 5 days after ischemia. Evans blue and horseradish peroxidase (HRP) were given before sacrifice. The majority of brain showed moderate ischemic neuronal damage inthe striatum. In these areas there was neither leakage of Evans blue nor extravasation of HRP. Astrocytic processes were moderately swollen. Large, grossly-visible unilateral infarcts were present in only 5 animals, and all showed abnormal BBB permeability of HRP which occurred via enchanced pinocytosis, and occasionally via diffuse leakage through necrotic vessels. Astrocytic processes were markedly swollen and their plasma membranes were disrupted. Whole brain and regional water content in a parallel series of animals were measured from 15 minutes (min) to 48 hours (h) postischemia. They showed a transient, 1% increase in whole brain water content from 15 to 60 min postischemia, but no increase in regional water content at any postischemic interval. These studies suggest that ischemia produces BBB permeability to large molecules, and sustained cerebral edema only when the process damages blood vessels and astrocytes; neuronal necrosis alone is insufficient.

  2. 钾通道在新生大鼠星形胶质细胞缺氧缺血性水肿中的作用机制%Mechanism of potassium channel in hypoxca-ischemic brain edema: experiment with neonatal rat astrocyte

    Institute of Scientific and Technical Information of China (English)

    付雪梅; 向龙; 廖大清; 封志纯; 母得志

    2008-01-01

    目的 探讨钾通道在体外培养的新生大鼠星形胶质细胞缺氧缺血性水肿中的作用机制.方法 体外培养出生3 d新生大鼠的星形胶质细胞;采用RNA干扰技术制作水通道蛋白4(AQP4)敲低型(AQP4-/-)细胞模型;用放射性[3H]标记的甲基D-葡萄糖摄取,测定缺氧缺血性AQP4-/-和野生型(AQP4+/+)星形胶质细胞体积;利用全细胞膜片钳技术记录培养的星形胶质细胞电压依赖性钾通道(Kv)的电流特性,并记录缺氧缺血性星形胶质细胞Kv通道的电流变化.结果 AQP4+/+和AQP4-/-星形胶质细胞在缺氧缺血时均较其对照组细胞体积明显增加(AQP4+/+和AQP4+/+组细胞在缺氧缺血0.5、1、2、4 h组占所对应的对照组D-葡萄糖摄取值的百分数分别为104±7、109±6、126±12、152±9和97±7、105±9、109±7、132±6,均P<0.05),但相同缺氧缺血时间点AQP4-/-介导细胞水肿程度明显减轻(均P<0.05),而且细胞电流密度随着缺氧缺血时间延长,进行性下降(对照组和缺氧缺血0.5、1、2、4 h组细胞电流密度值分别为116±8,107±9,91±10,76±6,37±11,均P<0.05).结论 在细胞缺氧缺血时,细胞外向性钾通道下调,可能阻止细胞内堆积的钾离子流出细胞外,引起渗透性改变而导致水通过AQP4流入细胞内,从而出现细胞水肿.%Objective To investigate the mechanism of potassium channel in brain edema caused by hypoxia-ischemia (HI). Methods Astrecytes were obtained from 3-day-old SD rats, cultured, and randomly divided into 2 groups: normoxia group, cultured under normoxic condition, and hypoxic-ischemic group, cultured under hypoxic-ischemic condition. The cell volume was measured by radiologic method. Patch-clamp technique was used to observe the electric physiological properties of the voltage-gated potassium channels (Kv) in a whole cell configuration, and the change of voltage-gated potassium channel current (IKv) was recorded in cultured neonatal rat astrocyte during HI

  3. Edema pulmonar postobstructivo: reporte de 3 casos

    Directory of Open Access Journals (Sweden)

    Juan Ignacio Padilla

    2002-12-01

    Full Text Available El edema pulmonar postobstructivo (EPPO es una complicación postoperatoria cuyo manejo adecuado depende de un diagnóstico etiológico correcto. El EPPO se clasifica en dos tipos. El tipo I es secundario a la obstrucción aguda de la vía aérea superior. Por su parte, el tipo II ocurre luego de corregir quirúrgicamente una obstrucción crónica de la vía aérea. Fisiopatológicamente, el mecanismo que explica el cuadro es una disminución marcada de la presión intersticial en el nivel pericapilar pulmonar resultante de la inspiración forzada. Lo anterior produce fuga capilar y el consecuente edema de pulmón. El manejo de este cuadro requiere de soporte respiratorio que incluye ventilación mecánica e incluso presión positiva al final de la espiración (PEEP. El pronóstico es muy bueno si el diagnóstico es correcto y oportuno. Se reportan 3 casos que ilustran la entidad, su diagnóstico y manejo.

  4. Update on corticosteroids for diabetic macular edema

    Directory of Open Access Journals (Sweden)

    Schwartz SG

    2016-09-01

    Full Text Available Stephen G Schwartz,1 Ingrid U Scott,2,3 Michael W Stewart,4 Harry W Flynn Jr1 1Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, Miami, FL, 2Department of Ophthalmology, 3Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA, 4Department of Ophthalmology, Mayo Clinic Florida, Jacksonville, FL, USA Abstract: Diabetic macular edema (DME remains an important cause of visual loss. Although anti-vascular endothelial growth factor (VEGF agents are generally used as first-line treatments for patients with center-involving DME, there is an important role for corticosteroids as well. Corticosteroids may be especially useful in pseudophakic patients poorly responsive to anti-VEGF therapies, in patients wishing to reduce the number of required injections, and in pregnant patients. Intravitreal triamcinolone acetonide has been used for many years but is not approved for this indication. An extended-release bioerodable dexamethasone delivery system and an extended-release nonbioerodable fluocinolone acetonide insert have both achieved regulatory approval for the treatment of DME. All intravitreal corticosteroids are associated with risks of cataract progression, elevation of intraocular pressure, and endophthalmitis. There is no current consensus regarding the use of corticosteroids, but they are valuable for selected patients with center-involving DME. Keywords: diabetic macular edema, vascular endothelial growth factor, triamcinolone acetonide, dexamethasone, fluocinolone acetonide, randomized clinical trial

  5. New Compton densitometer for measuring pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Loo, B.W.; Goulding, F.S.; Simon, D.S.

    1985-10-01

    Pulmonary edema is the pathological increase of extravascular lung water found most often in patients with congestive heart failure and other critically ill patients who suffer from intravenous fluid overload. A non-invasive lung density monitor that is accurate, easily portable, safe and inexpensive is needed for clinical evaluation of pulmonary edema. Other researchers who have employed Compton scattering techniques generally used systems of extended size and detectors with poor energy resolution. This has resulted in significant systematic biases from multiply-scattered photons and larger errors in counting statistics at a given radiation dose to the patient. We are proposing a patented approach in which only backscattered photons are measured with a high-resolution HPGe detector in a compact system geometry. By proper design and a unique data extraction scheme, effects of the variable chest wall on lung density measurements are minimized. Preliminary test results indicate that with a radioactive source of under 30 GBq, it should be possible to make an accurate lung density measurement in one minute, with a risk of radiation exposure to the patient a thousand times smaller than that from a typical chest x-ray. The ability to make safe, frequent lung density measurements could be very helpful for monitoring the course of P.E. at the hospital bedside or outpatient clinics, and for evaluating the efficacy of therapy in clinical research. 6 refs., 5 figs.

  6. Unilateral pulmonary edema after laparoscopic nephrectomy

    Directory of Open Access Journals (Sweden)

    Shreepathi Krishna Achar

    2011-01-01

    Full Text Available Unilateral-dependent pulmonary edema though reported in laparoscopic donor nephrectomies, has not been reported after laparoscopic non-donor nephrectomies. A 75-kg, 61-year-old man, a diagnosed case of right renal cell carcinoma was scheduled for laparoscopic nephrectomy. After establishing general anesthesia, the patient was positioned in the left-sided modified kidney (flank position. During the 5.75-hour procedure, he was hemodynamically stable except for a transient drop in blood pressure immediately after positioning. Intra-abdominal pressure was maintained less than 15 mmHg throughout the procedure. Blood loss was approximately 50 mL and urine output was 100 mL in the first hour followed by a total of 20 mL in the next 4.75 hours. Total fluid received during the procedure included 1.5 L of Ringer′s lactate and 1.0 L of 6% hydroxyethyl starch. After an uneventful procedure he developed respiratory distress in the postoperative period with a radiological evidence of dependent lung edema. Clinical and radiological improvement followed noninvasive ventilation, intravenous diuretics and oxygen therapy.

  7. Noncardiac Pulmonary Edema induced by Sitagliptin Treatment

    Science.gov (United States)

    Belice, Tahir; Yuce, Suleyman; Kizilkaya, Bayram; Kurt, Aysel; Cure, Erkan

    2014-01-01

    A 74-year-old male patient with type 2 diabetes mellitus admitted to the emergency department with the complaints of progressive breathlessness, dry cough, and swollen lower extremities. Our patient had type 2 diabetes mellitus and hypertension for 3 years. His HbA1c was not within the target range so sitagliptin was added to on-going therapy. After 1 week of starting sitagliptin therapy, even though the patient had not heart failure he applied to the emergency department with a complaint of dyspnea. The cardiovascular safety and efficacy of many anti-hyperglycemic agents such as sitagliptin, saxagliptin are unclear. Our case has shown that dipeptidyl peptidase 4 inhibitors may cause pulmonary edema. Hence, it should be used with cautious, especially in patients with heart failure. PMID:25657966

  8. Serotonin syndrome presenting as pulmonary edema

    Directory of Open Access Journals (Sweden)

    Nilima Deepak Shah

    2016-01-01

    Full Text Available Serotonin syndrome (SS is a potentially life-threatening condition resulting from excessive central and peripheral serotonergic activity. Clinically, it is a triad of mental-status changes, neuromuscular abnormalities, and autonomic disturbances. It can be caused by intentional self-poisoning, overdose, or inadvertent drug interactions. We report the case of a 58-year-old male with type 2 diabetes mellitus and obsessive compulsive disorder who developed pulmonary edema as a possible complication of SS. SS was caused by a combination of three specific serotonin re-uptake inhibitors (fluoxetine, fluvoxamine, and sertraline, linezolid, and fentanyl. The hospital course was further complicated by difficult weaning from the ventilator. SS was identified and successfully treated with cyproheptadine and lorazepam. The case highlights the importance of effective consultation-liaison and prompt recognition of SS as the presentation may be complex in the presence of co-morbid medical illness.

  9. Serotonin syndrome presenting as pulmonary edema

    Science.gov (United States)

    Shah, Nilima Deepak; Jain, Ajay B.

    2016-01-01

    Serotonin syndrome (SS) is a potentially life-threatening condition resulting from excessive central and peripheral serotonergic activity. Clinically, it is a triad of mental-status changes, neuromuscular abnormalities, and autonomic disturbances. It can be caused by intentional self-poisoning, overdose, or inadvertent drug interactions. We report the case of a 58-year-old male with type 2 diabetes mellitus and obsessive compulsive disorder who developed pulmonary edema as a possible complication of SS. SS was caused by a combination of three specific serotonin re-uptake inhibitors (fluoxetine, fluvoxamine, and sertraline), linezolid, and fentanyl. The hospital course was further complicated by difficult weaning from the ventilator. SS was identified and successfully treated with cyproheptadine and lorazepam. The case highlights the importance of effective consultation-liaison and prompt recognition of SS as the presentation may be complex in the presence of co-morbid medical illness. PMID:26997733

  10. Pulmonary edema following transcatheter closure of atrial septal defect

    Directory of Open Access Journals (Sweden)

    Singhi Anil

    2010-01-01

    Full Text Available Pulmonary edema after device closure of atrial septal defect (ASD is a rare complication. We present illustrative images of a case of pulmonary edema after device closure of ASD in a 53 year old adult. Older patients undergoing ASD closure can benefit from their left atrial and left ventricular end diastolic pressures measurement before and after temporary balloon occlusion of ASD.

  11. Massive vulvar edema in 2 prepartum dairy cows.

    Science.gov (United States)

    Cheong, Soon Hon; Gilbert, Robert O

    2014-05-01

    Two late gestation Holstein cows about to begin the third lactation developed massive vulvar edema. These were the only affected animals in the herd of 500 milking cows. The vulvar edema spontaneously regressed postpartum for both cows. Massive vulvar swelling is seldom observed in dairy cows in advanced pregnancy and is not described in the literature.

  12. Methylprednisolone therapy in acute hemorrhagic edema of infancy

    DEFF Research Database (Denmark)

    Risikesan, Jeyanthini; Koppelhus, Uffe; Steiniche, Torben;

    2014-01-01

    We present a case of an 18-month-old boy who showed severe clinical signs indicative of acute hemorrhagic edema of infancy (AHEI) with painful purpuric skin affection primarily of the face and marked edema of the ears. The histological findings were diagnostic for leukocytoclastic vasculitis...

  13. Edema de pulmón precipitado por amlodipino

    Directory of Open Access Journals (Sweden)

    Teresa Chapela Castaño

    2013-09-01

    Full Text Available Múltiples fármacos pueden causar edema agudo de pulmón no cardiogénico. Establecer esta relación causal resulta muy difícil en muchos casos debido a la escasa incidencia documentada con algunos fármacos y a que la sintomatología no es específica. Si bien el edema periférico es un efecto secundario frecuente del amlodipino, solamente se han publicado en la literatura dos casos de edema pulmonar causado por amlodipino y ambos ocurrieron en el contexto de dosis supraterapéuticas. Se describe un caso de edema pulmonar posiblemente inducido por amlodipino administrado a dosis terapéutica y se discute el posible mecanismo fisiopatológico. Multiple drugs can cause acute pulmonary edema non-cardiogenic. Establishing this causal relationship is very difficult in many cases due to low reported incidence of some drugs and non specific symptoms. While peripheral edema is a common side effect of amlodipine, only have been published in the literature two cases of pulmonary edema caused by amlodipine and both occurred in the context of drug overdose. We describe a case of pulmonary edema probably induced by amlodipine at therapeutic doses and we discuss the possible pathophysiological mechanism.

  14. Pathophysiology and treatment of edema following femoropopliteal bypass surgery

    NARCIS (Netherlands)

    te Slaa, A.; Dolmans, D. E. J. G. J.; Ho, G. H.; Moll, F. L.; van der Laan, L.

    2012-01-01

    Substantial lower-limb edema affects the majority of patients who undergo peripheral bypass surgery. Edema has impairing effects on the microvascular and the macrovascular circulation, causes discomfort and might delay the rehabilitation process of the patient. However, the pathophysiology of this e

  15. Oxygen-deficient metabolism and corneal edema.

    Science.gov (United States)

    Leung, B K; Bonanno, J A; Radke, C J

    2011-11-01

    Wear of low-oxygen-transmissible soft contact lenses swells the cornea significantly, even during open eye. Although oxygen-deficient corneal edema is well-documented, a self-consistent quantitative prediction based on the underlying metabolic reactions is not available. We present a biochemical description of the human cornea that quantifies hypoxic swelling through the coupled transport of water, salt, and respiratory metabolites. Aerobic and anaerobic consumption of glucose, as well as acidosis and pH buffering, are incorporated in a seven-layer corneal model (anterior chamber, endothelium, stroma, epithelium, postlens tear film, contact lens, and prelens tear film). Corneal swelling is predicted from coupled transport of water, dissolved salts, and especially metabolites, along with membrane-transport resistances at the endothelium and epithelium. At the endothelium, the Na+/K+ - ATPase electrogenic channel actively transports bicarbonate ion from the stroma into the anterior chamber. As captured by the Kedem-Katchalsky membrane-transport formalism, the active bicarbonate-ion flux provides the driving force for corneal fluid pump-out needed to match the leak-in tendency of the stroma. Increased lactate-ion production during hypoxia osmotically lowers the pump-out rate requiring the stroma to swell to higher water content. Concentration profiles are predicted for glucose, water, oxygen, carbon dioxide, and hydronium, lactate, bicarbonate, sodium, and chloride ions, along with electrostatic potential and pressure profiles. Although the active bicarbonate-ion pump at the endothelium drives bicarbonate into the aqueous humor, we find a net flux of bicarbonate ion into the cornea that safeguards against acidosis. For the first time, we predict corneal swelling upon soft-contact-lens wear from fundamental biophysico-chemical principles. We also successfully predict that hypertonic tear alleviates contact-lens-induced edema.

  16. Smoke aldehyde component influences pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Hales, C.A.; Musto, S.W.; Janssens, S.; Jung, W.; Quinn, D.A.; Witten, M. (Department of Medicine (Pulmonary/Critical Care Unit), Massachusetts General Hospital, Boston (United States))

    1992-02-01

    The pulmonary edema of smoke inhalation is caused by the toxins of smoke and not the heat. We investigated the potential of smoke consisting of carbon in combination with either acrolein or formaldehyde (both common components of smoke) to cause pulmonary edema in anesthetized sheep. Seven animals received acrolein smoke, seven animals received a low-dose formaldehyde smoke, and five animals received a high-dose formaldehyde smoke. Pulmonary arterial pressure, pulmonary capillary wedge pressure, and cardiac output were not affected by smoke in any group. Peak airway pressure increased after acrolein (14 +/- 1 to 21 +/- 2 mmHg; P less than 0.05) and after low- and high-dose formaldehyde (14 +/- 1 to 21 +/- 1 and 20 +/- 1 mmHg, respectively; both P less than 0.05). The partial pressure of O2 in arterial blood fell sharply after acrolein (219 +/- 29 to 86 +/- 9 (SE) Torr; P less than 0.05) but not after formaldehyde. Only acrolein resulted in a rise in lung lymph flow (6.5 +/- 2.2 to 17.9 +/- 2.6 ml/h; P less than 0.05). Lung lymph-to-plasma protein ratio was unchanged for all three groups, but clearance of lymph protein was increased after acrolein. After acrolein, the blood-free extravascular lung water-to-lung dry weight ratio was elevated (P less than 0.05) compared with both low- and high-dose formaldehyde groups (4.8 +/- 0.4 to 3.3 +/- 0.2 and 3.6 +/- 0.2, respectively). Lymph clearance (ng/h) of thromboxane B2, leukotriene B4, and the sulfidopeptide leukotrienes was elevated after acrolein but not formaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

  17. Neurogenic Pulmonary Edema in Aneurysmal Subarachnoid Hemorrhage.

    Science.gov (United States)

    Saracen, A; Kotwica, Z; Woźniak-Kosek, A; Kasprzak, P

    2016-01-01

    Neurogenic pulmonary edema (NPE) is observed in cerebral injuries and has an impact on treatment results, being a predictor of fatal prognosis. In this study we retrospectively reviewed medical records of 250 consecutive patients with aneurysmal subarachnoid hemorrhage (SAH) for the frequency and treatment results of NPE. The following factors were taken under consideration: clinical status, aneurysm location, presence of NPE, intracranial pressure (ICP), and mortality. All patients had plain- and angio-computer tomography performed. NPE developed most frequently in case of the aneurysm located in the anterior communicating artery. The patients with grades I-III of SAH, according to the World Federation of Neurosurgeons staging, were immediately operated on, while those with poor grades IV and V had only an ICP sensor's implantation procedure performed. A hundred and eighty five patients (74.4 %) were admitted with grades I to III and 32 patients (12.8 %) were with grade IV and V each. NPE was not observed in SAH patients with grade I to III, but it developed in nine patients with grade IV and 11 patients with grade V. Of the 20 patients with NPE, 19 died. Of the 44 poor grade patients (grades IV-V) without NPE, 20 died. All poor grade patients had elevated ICP in a range of 24-56 mmHg. The patients with NPE had a greater ICP than those without NPE. Gender and age had no influence on the occurrence of NPE. We conclude that the development of neurogenic pulmonary edema in SAH patients with poor grades is a fatal prognostic as it about doubles the death rate to almost hundred percent.

  18. Visual Impairment Caused by Periorbital Edema in an Infant with Acute Hemorrhagic Edema of Infancy

    DEFF Research Database (Denmark)

    Freitas, Priscila; Bygum, Anette

    2013-01-01

    Acute hemorrhagic edema of infancy (AHEI) is a cutaneous vasculitis seen in children. Many consider it to be a clinical variant of Schönlein-Henoch purpura, but others regard it as a separate entity because of its benign nature, age of onset, lack of visceral involvement, and frequent absence......, or vaccination. Because of the unknown etiology and benign character, which leads to spontaneous complete recovery, there is no specific treatment necessary for AHEI, and according to the literature, systemic corticosteroids do not seem to alter the course of the disease. We report the case of an 11-month......-old boy who manifested massive periorbital edema along with all of the clinical characteristics of this entity and showed clear improvement of the symptoms after a 24-hour administration of systemic corticosteroid therapy. Given the positive effect of this therapy, we propose that systemic corticosteroids...

  19. LASER PHOTOCOAGULATION IN DIABETIC MACULAR EDEMA: EFFECTS ON VISUAL ACUITY AND MACULAR EDEMA

    Directory of Open Access Journals (Sweden)

    M.H. Dehghan

    1999-06-01

    Full Text Available Due to the importance of clinically significant macular edema in diabetic patients, this study is aimed to determine if laser photocoagulation is effective in the treatment of clinically significant diabetic macular edema. In addition, the effects of risk factors arc surveyed* This is an existing data study considering patients with clinically significant diabetic macular edema, treated with argon-green laser photocoagulation in Labbafinejad hospital, department of lasertherapy, from 1995 to 1997. in 60 (42.6% eyes the treatment method was focal, in 22 (15.6% eyes grid, and in 59 (41.84 modified grid laser photocoagulation was performed. The results are based upon deterioration of visual acuity, occurance of moderate visual loss and improvement or persistence of CSME. We studied 114 eyes from 87 patients. Two years after initial treatment, visual acuity improved in 19.1% of eyes, unchanged in 9.5% and worsened in 71.4% of eyes. After this period the rate of moderate visual loss was 28.6% and CSME was improved in 23.8% of eyes. According to our study, baseline visual acuity and retinopathy severity were two important intervening factors in response to lasertherapy. Comparing our results with natural course of diabetic macular edema, indicates that in assessing visual outcome laser photocoagulation is an effective modality in treatment of CSME, but it is not effective in maintaining or improving visual acuity, which is due to patients delay in visiting ophthalmologists and paying not enough attention to follow-up visits.

  20. Severe cerebral edema following nivolumab treatment for pediatric glioblastoma: case report.

    Science.gov (United States)

    Zhu, Xiao; McDowell, Michael M; Newman, William C; Mason, Gary E; Greene, Stephanie; Tamber, Mandeep S

    2017-02-01

    Nivolumab is an immune checkpoint inhibitor (ICI) currently undergoing Phase III clinical trials for the treatment of glioblastoma. The authors present the case of a 10-year-old girl with glioblastoma treated with nivolumab under compassionate-use guidelines. After the first dose of nivolumab the patient developed hemiparesis, cerebral edema, and significant midline shift due to severe tumor necrosis. She was managed using intravenous dexamethasone and discharged on a dexamethasone taper. The patient's condition rapidly deteriorated after the second dose of nivolumab, demonstrating hemiplegia, seizures, and eventually unresponsiveness with a fixed and dilated left pupil. Computed tomography of her brain revealed malignant cerebral edema requiring emergency decompressive hemicraniectomy. Repeat imaging demonstrated increased size of the lesion, reflecting immune-mediated inflammation and tumor necrosis. The patient remained densely hemiplegic, but became progressively more interactive and was ultimately extubated. She resumed nivolumab several weeks later, but again her condition deteriorated with headache, vomiting, swelling at the craniectomy site, and limited right-sided facial movement following the sixth dose. MRI demonstrated severe midline shift and uncal herniation despite her craniectomy. Her condition gradually declined, and she died several days later under "do not resuscitate/do not intubate" orders. To the authors' knowledge, this represents the first case of malignant cerebral edema requiring operative intervention following nivolumab treatment for glioblastoma in a pediatric patient.

  1. Pediatric cerebral stroke: susceptibility-weighted imaging may predict post-ischemic malignant edema.

    Science.gov (United States)

    Bosemani, Thangamadhan; Poretti, Andrea; Orman, Gunes; Meoded, Avner; Huisman, Thierry A G M

    2013-10-01

    Susceptibility-weighted imaging (SWI) is an advanced MRI technique providing information on the blood oxygenation level. Deoxyhemoglobin is increased in hypoperfused tissue characterized by SWI-hypointensity, while high oxyhemoglobin concentration within hyperperfused tissue results in a SWI iso- or hyperintensity compared to healthy brain tissue. We describe a child with a stroke, where SWI in addition to excluding hemorrhage and delineating the thrombus proved invaluable in determining regions of hyperperfusion or luxury perfusion, which contributed further to the prognosis including an increased risk of developing post-ischemic malignant edema.

  2. Dialysis Disequilibrium Syndrome-Induced Cerebral Edema in a Patient with Uremia Following Hemodialysis: A Case Report

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Jung Min; Kim, Heung Cheol [Dept. of Radiology, Chuncheon Sacred Heart Hospital, Hallym University College of Medicine, Chuncheon (Korea, Republic of)

    2012-03-15

    Dialysis disequilibrium syndrome is a metabolic complication that can be caused by rapid removal of plasma urea during hemodialysis. Dialysis disequilibrium syndrome can lead to osmotic demyelinating syndrome. This case report describes one case of encephalopathy accompanied by dialysis disequilibrium syndrome with imaging findings acquired immediately after hemodialysis in a 55-year-old woman with chronic renal failure. The patient was observed to present repetitive seizures and sudden deterioration of consciousness immediately after hemodialysis. Shortly after the onset of symptoms, the patient underwent a CT scan. The imaging findings of the CT scan reveal symmetrical diffuse white matter edema of bilateral cerebral hemispheres that extends to the pons along the internal capsule. A follow-up MRI taken two years later shows that reversible changes without damage have occurred in the lesions. The patient can thus be seen to present symptoms characteristically associated with dialysis disequilibrium syndrome, while brain imaging reveals dif-fuse reversible brain edema.

  3. Cortical thickness difference across the central sulcus visualized in the presence of vasogenic edema

    Energy Technology Data Exchange (ETDEWEB)

    Togao, Osamu [Department of Clinical Radiology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582 (Japan)], E-mail: togao@dr.hosp.kyushu-u.ac.jp; Yoshiura, Takashi; Mihara, Futoshi; Noguchi, Tomoyuki; Hiwatashi, Akio; Yamashita, Koji; Yoshitake, Tadamasa; Honda, Hiroshi [Department of Clinical Radiology, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582 (Japan)

    2008-05-15

    Purpose: To confirm the cortical thickness difference across the central sulcus (CS) visualized in the presence of vasogenic edema on MRI. Materials and methods: T2-weighted images of 70 cerebral hemispheres showing vasogenic edema infiltrating into subcortical white matter around the CS were studied retrospectively. Two neuroradiologists measured the cortical thickness of the anterior and posterior banks of the CS, precentral sulci (PrCS), and postcentral sulci (PoCS). Additionally, we compared the cortical thickness of the anterior and posterior banks of each sulcus visually using a grading scale. Results: On T2-weighted images, the cerebral cortex was highlighted by a high signal-intensity vasogenic edema in the adjacent white matter, and its thickness was readily measurable. The unique cortical thickness difference between the anterior and posterior banks of the CS were confirmed with measurements of 2.67 and 1.48 mm (p < 0.0001). The cortical measurements across other cerebral sulci were 2.04 and 1.95 mm (NS) for the PrCS, and 1.67 and 1.77 mm (NS) for the PoCS. The cortical thickness ratios were 1.86 for the CS, 1.05 for the PrCS, and 0.96 for the PoCS. On visual evaluation, the anterior bank of the CS was thicker than the posterior bank in 93% (65/70). For the PrCS and PoCS, the thickness of the anterior and posterior banks appeared to be equal in over 70% of the patients. Conclusion: A prominent cortical thickness difference across the CS in the presence of vasogenic edema was confirmed. This finding is considered to facilitate the identification of the CS in patients with brain tumors.

  4. Edema in renal diseases – current view on pathogenesis

    Directory of Open Access Journals (Sweden)

    Irina Bobkova

    2016-10-01

    Full Text Available Edema is a common complication of numerous renal disease. In the recent past several aspects of the pathophysiology of this condition have been elucidated. We herein present a case of nephrotic syndrome in a 30 year-old men. The discussion revolves around the following key questions on fluid accumulation in renal disease: 1. What is edema? What diseases can cause edema? 2. What are the mechanisms of edema in nephrotic syndrome?   2a. The “underfill” theory   2b. The “overfill” theory   2c. Tubulointerstitial inflammation   2d. Vascular permeability 3. What are the mechanisms of edema in nephritic syndrome? 4. How can the volume status be assessed in patients with nephrotic syndrome? 5. What are therapeutic strategies for edema management? 6. What are the factors affecting response to diuretics? 7. How can we overcome the diuretics resistance?   7a. Effective doses of loop diuretics   7b. Combined diuretic therapy   7c. Intravenous administration of diuretics   7d. Albumin infusions   7e. Alternative methods of edema management 8. Conclusion.

  5. Exercise-Induced Pulmonary Edema in a Triathlon

    Science.gov (United States)

    Yamanashi, Hirotomo; Koyamatsu, Jun; Nobuyoshi, Masaharu; Murase, Kunihiko; Maeda, Takahiro

    2015-01-01

    Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise. PMID:26229538

  6. Synthetic smoke with acrolein but not HCl produces pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Hales, C.A.; Barkin, P.W.; Jung, W.; Trautman, E.; Lamborghini, D.; Herrig, N.; Burke, J.

    1988-03-01

    The chemical toxins in smoke and not the heat are responsible for the pulmonary edema of smoke inhalation. We developed a synthetic smoke composed of carbon particles (mean diameter of 4.3 microns) to which toxins known to be in smoke, such as HCl or acrolein, could be added one at a time. We delivered synthetic smoke to dogs for 10 min and monitored extravascular lung water (EVLW) accumulation thereafter with a double-indicator thermodilution technique. Final EVLW correlated highly with gravimetric values (r = 0.93, P less than 0.01). HCl in concentrations of 0.1-6 N when added to heated carbon (120 degrees C) and cooled to 39 degrees C produced airway damage but no pulmonary edema. Acrolein, in contrast, produced airway damage but also pulmonary edema, whereas capillary wedge pressures remained stable. Low-dose acrolein smoke (less than 200 ppm) produced edema in two of five animals with a 2- to 4-h delay. Intermediate-dose acrolein smoke (200-300 ppm) always produced edema at an average of 147 +/- 57 min after smoke, whereas high-dose acrolein (greater than 300 ppm) produced edema at 65 +/- 16 min after smoke. Thus acrolein but not HCl, when presented as a synthetic smoke, produced a delayed-onset, noncardiogenic, and peribronchiolar edema in a roughly dose-dependent fashion.

  7. Exercise-Induced Pulmonary Edema in a Triathlon

    Directory of Open Access Journals (Sweden)

    Hirotomo Yamanashi

    2015-01-01

    Full Text Available Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE or swimming-induced pulmonary edema (SIPE. Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise.

  8. Exercise-Induced Pulmonary Edema in a Triathlon.

    Science.gov (United States)

    Yamanashi, Hirotomo; Koyamatsu, Jun; Nobuyoshi, Masaharu; Murase, Kunihiko; Maeda, Takahiro

    2015-01-01

    Introduction. Family physicians have more opportunities to attend athletic competitions as medical staff at first-aid centers because of the increasing popularity of endurance sports. Case. A 38-year-old man who participated in a triathlon race experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. His diagnosis was noncardiogenic pulmonary edema associated with exercise or swimming: exercise-induced pulmonary edema (EIPE) or swimming-induced pulmonary edema (SIPE). Treatment with furosemide and corticosteroid relieved his symptoms of pulmonary edema. Discussion. Noncardiogenic pulmonary edema associated with endurance sports is not common, but knowledge about EIPE/SIPE or neurogenic pulmonary edema associated with hyponatremia, which is called Ayus-Arieff syndrome, is crucial. Knowledge and caution for possible risk factors, such as exposure to cold water or overhydration, are essential for both medical staff and endurance athletes. Conclusion. To determine the presence of pulmonary edema associated with strenuous exercise, oxygen saturation should be used as a screening tool at a first-aid center. To avoid risks for EIPE/SIPE, knowledge about these diseases is essential for medical staff and for athletes who perform extreme exercise.

  9. A female survivor of childhood medulloblastoma presenting with growth-hormone-induced edema and inflammatory lesions: a case report

    Directory of Open Access Journals (Sweden)

    Biassoni Veronica

    2009-01-01

    Full Text Available Abstract Introduction The improved survival of children with brain tumors has increased concerns about treatment-related sequelae. Growth hormone deficiency is frequently observed after craniospinal irradiation for medulloblastoma. It has been widely reported that growth hormone replacement therapy does not increase the risk of second tumors, but there are reports in the literature of growth hormone, and its downstream mediator insulin-like Growth Factor 1, having an important proinflammatory action. There are few reports, however, on the "in-vivo" induction of edema and symptomatic inflammatory lesions during replacement therapy. Case presentation We report the case of a 7-year-old girl treated for metastatic medulloblastoma who developed growth hormone deficiency 2 years after oncological treatment. Three months after replacement therapy, magnetic resonance imaging showed exacerbation of her brain edema, which was already present after oncological treatment. We consequently suspended the growth hormone until a new magnetic resonance image obtained 3 months later documented a reduction of the inflammatory areas. We then re-introduced somatotropin at lower doses with no further increase in brain edema in subsequent radiological controls. Conclusion This case and its iconography suggest a strong association between growth hormone administration and the exacerbation of inflammatory reactions within the tumor bed. Replacement therapy should be carefully monitored in this particular subset of patients.

  10. Effect of Maixuekang enteric coated tablets on absorption of hematoma and treatment of acute cerebral hemorrhage patients with cerebral edema

    Institute of Scientific and Technical Information of China (English)

    Bing-Ding Lu; Chuan Wang

    2016-01-01

    Objective:To study the clinical efficacy of Maixuekang in treating acute cerebral hemorrhage hematomas and promoting brain hemorrhage.Methods: A total of 192 patients with acute intracerebral hemorrhage treated within 3 hours in our hospital during April 2013 to February 2015 were selected. After admission immediately apply brain CT, blood, coagulation function tests were carried out. They were randomly divided into 2 groups. Both groups had anti-infective, mannitol and other conventional treatment. Observation group were treated with enteric-coated tablets Maixuekang on this basis. Clinical efficacy, various stages of treatment of cerebral hematoma volume, brain edema volume, NIHSS score were compared.Results: Before treatment, difference in edema volume and HIHSS scores were not statistically significant (P>0.05). After14 d and 28 d treatment, edema volume of observation group were significantly smaller than those of control group (P<0.01); NIHSS score of observation group were significantly lower than those of control group (P<0.01); 28 d after treatment total effective rate of observation group was significantly higher than that of the control group (P<0.01).Conclusions:Maixuekang enteric-coated tablets as a thrombin inhibitor, can effectively reduce a series of pathological changes after acute cerebral hemorrhage caused by partial thrombin content, promote absorption of hematoma and neurological recovery. The side effects is small, safe and worthy of promotion.

  11. Effect of lavender oil (Lavandula angustifolia) on cerebral edema and its possible mechanisms in an experimental model of stroke.

    Science.gov (United States)

    Vakili, Abedin; Sharifat, Shaghayegh; Akhavan, Maziar Mohammad; Bandegi, Ahmad Reza

    2014-02-22

    Lavender belongs to the family Labiatae and has a variety of cosmetic uses as well as therapeutic purposes in herbal medicine. The present study was conducted to evaluate the protective effect of lavender oil against brain edema and its possible mechanisms in an experimental model of stroke. Under Laser-Doppler Flowmetry, focal cerebral ischemia was induced by the transient occlusion of the middle cerebral artery for 1h in rats. Lavender oil (100, 200, and 400 mg/kg ip (and/or vehicle was injected at the onset of ischemia. Infarct size, cerebral edema, functional outcome, and oxidative stress biomarkers were evaluated using standard methods. Western blotting was used to determine the protein expression of VEGF, Bax, and Bcl-2. Treatment with lavender oil at doses of 200 and 400 mg/kg significantly diminished infarct size, brain edema, and improved functional outcome after cerebral ischemia (P0.05). The results indicated that lavender oil has neuroprotective activity against cerebral ischemia and alleviated neurological function in rats, and the mechanism may be related to augmentation in endogenous antioxidant defense, inhibiting oxidative stress, and increasing VEGF expression in the rat brain. However, lavender oil could not suppress the apoptosis pathway.

  12. Volatile Anesthetics Influence Blood-Brain Barrier Integrity by Modulation of Tight Junction Protein Expression in Traumatic Brain Injury

    OpenAIRE

    Thal, Serge C.; Clara Luh; Eva-Verena Schaible; Ralph Timaru-Kast; Jana Hedrich; Luhmann, Heiko J.; Kristin Engelhard; Zehendner, Christoph M.

    2012-01-01

    Disruption of the blood-brain barrier (BBB) results in cerebral edema formation, which is a major cause for high mortalityrnafter traumatic brain injury (TBI). As anesthetic care is mandatory in patients suffering from severe TBI it may be importantrnto elucidate the effect of different anesthetics on cerebral edema formation. Tight junction proteins (TJ) such as zonularnoccludens-1 (ZO-1) and claudin-5 (cl5) play a central role for BBB stability. First, the influence of the volatile anesthet...

  13. [Physiopathology of macular edema in central vein occlusion].

    Science.gov (United States)

    Stanca, Horia T; Manea, Georgiana

    2012-01-01

    Retinal Vein Occlusions are vascular diseases affecting the Central Retinal Vein and its branches causing decreased retinal drainage resulting in significant clinical and functional pathological changes. RVO determines the increase of vascular permeability, with edema and hemorrhage and development of collateral vessels in a few weeks. Among the serious consequences of venous occlusion is the installation of macular edema to which depends long-term visual prognosis. Macular Edema is the accumulation of intraretinal serous fluid in the macular area caused by the breakdown of blood-retinal barrier.

  14. Melatonin lowers edema after spinal cord injur y

    Institute of Scientific and Technical Information of China (English)

    Cheng Li; Xiao Chen; Suchi Qiao; Xinwei Liu; Chang Liu; Degang Zhu; Jiacan Su; Zhiwei Wang

    2014-01-01

    Melatonin has been shown to diminish edema in rats. Melatonin can be used to treat spinal cord injury. This study presumed that melatonin could relieve spinal cord edema and examined how it might act. Our experiments found that melatonin (100 mg/kg, i.p.) could reduce the water content of the spinal cord, and suppress the expression of aquaporin-4 and glial ifbrillary acidic protein after spinal cord injury. This suggests that the mechanism by which melatonin alleviates the damage to the spinal cord by edema might be related to the expression of aquaporin-4 and glial ifbrillary acidic protein.

  15. Diabetic Macular Edema Pathophysiology: Vasogenic versus Inflammatory

    Science.gov (United States)

    Baget-Bernaldiz, Marc; Pareja-Rios, Alicia; Lopez-Galvez, Maribel; Navarro-Gil, Raul; Verges, Raquel

    2016-01-01

    Diabetic macular edema (DME) can cause blindness in diabetic patients suffering from diabetic retinopathy (DR). DM parameters controls (glycemia, arterial tension, and lipids) are the gold standard for preventing DR and DME. Although the vascular endothelial growth factor (VEGF) is known to play a role in the development of DME, the pathological processes leading to the onset of this disease are highly complex and the exact sequence in which they occur is still not completely understood. Angiogenesis and inflammation have been shown to be involved in the pathogenesis of this disease. However, it still remains to be clarified whether angiogenesis following VEGF overexpression is a cause or a consequence of inflammation. This paper provides a review of the data currently available, focusing on VEGF, angiogenesis, and inflammation. Our analysis suggests that angiogenesis and inflammation act interdependently during the development of DME. Knowledge of DME etiology seems to be important in treatments with anti-VEGF or anti-inflammatory drugs. Current diagnostic techniques do not permit us to differentiate between both etiologies. In the future, diagnosing the physiopathology of each patient with DME will help us to select the most effective drug.

  16. Diabetic Macular Edema Pathophysiology: Vasogenic versus Inflammatory

    Directory of Open Access Journals (Sweden)

    Pedro Romero-Aroca

    2016-01-01

    Full Text Available Diabetic macular edema (DME can cause blindness in diabetic patients suffering from diabetic retinopathy (DR. DM parameters controls (glycemia, arterial tension, and lipids are the gold standard for preventing DR and DME. Although the vascular endothelial growth factor (VEGF is known to play a role in the development of DME, the pathological processes leading to the onset of this disease are highly complex and the exact sequence in which they occur is still not completely understood. Angiogenesis and inflammation have been shown to be involved in the pathogenesis of this disease. However, it still remains to be clarified whether angiogenesis following VEGF overexpression is a cause or a consequence of inflammation. This paper provides a review of the data currently available, focusing on VEGF, angiogenesis, and inflammation. Our analysis suggests that angiogenesis and inflammation act interdependently during the development of DME. Knowledge of DME etiology seems to be important in treatments with anti-VEGF or anti-inflammatory drugs. Current diagnostic techniques do not permit us to differentiate between both etiologies. In the future, diagnosing the physiopathology of each patient with DME will help us to select the most effective drug.

  17. Glyphosate Poisoning with Acute Pulmonary Edema

    Science.gov (United States)

    Thakur, Darshana Sudip; Khot, Rajashree; Joshi, P. P.; Pandharipande, Madhuri; Nagpure, Keshav

    2014-01-01

    GlySH-surfactant herbicide (GlySH), one of the most commonly used herbicides worldwide, has been considered as minimally toxic to humans. However, clinical toxicologists occasionally encounter cases of severe systemic toxicity. The US Environmental Protection Agency (EPA) states that ‘GlySH’ is of relatively low oral and acute dermal toxicity. It does not have anticholinesterase effect and no organophosphate-like central nervous system (CNS) effects. The clinical features range from skin and throat irritation to hypotension and death. Severe GlySH-surfactant poisoning is manifested by gastroenteritis, respiratory disturbances, altered mental status, hypotension refractory to the treatment, renal failure, and shock.[1] GlySH intoxication has a case fatality rate 3.2–29.3%. Pulmonary toxicity and renal toxicity seem to be responsible for mortality. Metabolic acidosis, abnormal chest X-ray, arrhythmias, and elevated serum creatinine levels are useful prognostic factors for predicting GlySH mortality.[2] There is no antidote and the mainstay of treatment for systemic toxicity is decontamination and aggressive supportive therapy. We report a case of acute pulmonary edema, which is a rare but severe manifestation of oral GlySH poisoning, where patient survived with aggressive supportive therapy. PMID:25948977

  18. Twenty-Four-Hour Real-Time Continuous Monitoring of Cerebral Edema in Rabbits Based on a Noninvasive and Noncontact System of Magnetic Induction

    Directory of Open Access Journals (Sweden)

    Gen Li

    2017-03-01

    Full Text Available Cerebral edema is a common disease, secondary to craniocerebral injury, and real-time continuous monitoring of cerebral edema is crucial for treating patients after traumatic brain injury. This work established a noninvasive and noncontact system by monitoring the magnetic induction phase shift (MIPS which is associated with brain tissue conductivity. Sixteen rabbits (experimental group n = 10, control group, n = 6 were used to perform a 24 h MIPS and intracranial pressure (ICP simultaneously monitored experimental study. For the experimental group, after the establishment of epidural freeze-induced cerebral edema models, the MIPS presented a downward trend within 24 h, with a change magnitude of −13.1121 ± 2.3953°; the ICP presented an upward trend within 24 h, with a change magnitude of 12–41 mmHg. The ICP was negatively correlated with the MIPS. In the control group, the MIPS change amplitude was −0.87795 ± 1.5146 without obvious changes; the ICP fluctuated only slightly at the initial value of 12 mmHg. MIPS had a more sensitive performance than ICP in the early stage of cerebral edema. These results showed that this system is basically capable of monitoring gradual increases in the cerebral edema solution volume. To some extent, the MIPS has the potential to reflect the ICP changes.

  19. Aspectos atuais na fisiopatologia do edema macular diabético Recent aspects on physiopathology of diabetic macular edema

    Directory of Open Access Journals (Sweden)

    Mário Martins dos Santos Motta

    2008-02-01

    Full Text Available O edema macular é a principal causa de baixa visual em pacientes diabéticos. Seu mecanismo de formação é complexo e envolve alterações bioquímicas e estruturais. Os autores fazem uma revisão e atualização dos conceitos fisiopatológicos envolvidos na maculopatia diabética.Macular edema is the leading cause of poor vision in diabetic patients.The mechanism of edema formation is complex and involves biochemical and structural changes. The authors review and update the physiopathologic concepts related to diabetic maculopathy.

  20. Status epilepticus induces vasogenic edema via tumor necrosis factor-α/ endothelin-1-mediated two different pathways.

    Directory of Open Access Journals (Sweden)

    Ji-Eun Kim

    Full Text Available Status epilepticus (SE induces vasogenic edema in the piriform cortex with disruptions of the blood-brain barrier (BBB. However, the mechanisms of vasogenic edema formation following SE are still unknown. Here we investigated the endothelin B (ETB receptor-mediated pathway of SE-induced vasogenic edema. Following SE, the release of tumor necrosis factor-α (TNF-α stimulated endothelin-1 (ET-1 release and expression in neurons and endothelial cells. In addition, TNF-α-induced ET-1 increased BBB permeability via ETB receptor-mediated endothelial nitric oxide synthase (eNOS activation in endothelial cells. ETB receptor activation also increased intracellular reactive oxygen species by NADPH oxidase production in astrocytes. These findings suggest that SE results in BBB dysfunctions via endothelial-astroglial interactions through the TNF-α-ET-1-eNOS/NADPH oxidase pathway, and that these ETB receptor-mediated interactions may be an effective therapeutic strategy for vasogenic edema in various neurological diseases.

  1. Characterization and quantification of cerebral edema induced by synchrotron x-ray microbeam radiation therapy

    Science.gov (United States)

    Serduc, Raphaël; van de Looij, Yohan; Francony, Gilles; Verdonck, Olivier; van der Sanden, Boudewijn; Laissue, Jean; Farion, Régine; Bräuer-Krisch, Elke; Siegbahn, Erik Albert; Bravin, Alberto; Prezado, Yolanda; Segebarth, Christoph; Rémy, Chantal; Lahrech, Hana

    2008-03-01

    Cerebral edema is one of the main acute complications arising after irradiation of brain tumors. Microbeam radiation therapy (MRT), an innovative experimental radiotherapy technique using spatially fractionated synchrotron x-rays, has been shown to spare radiosensitive tissues such as mammal brains. The aim of this study was to determine if cerebral edema occurs after MRT using diffusion-weighted MRI and microgravimetry. Prone Swiss nude mice's heads were positioned horizontally in the synchrotron x-ray beam and the upper part of the left hemisphere was irradiated in the antero-posterior direction by an array of 18 planar microbeams (25 mm wide, on-center spacing 211 mm, height 4 mm, entrance dose 312 Gy or 1000 Gy). An apparent diffusion coefficient (ADC) was measured at 7 T 1, 7, 14, 21 and 28 days after irradiation. Eventually, the cerebral water content (CWC) was determined by microgravimetry. The ADC and CWC in the irradiated (312 Gy or 1000 Gy) and in the contralateral non-irradiated hemispheres were not significantly different at all measurement times, with two exceptions: (1) a 9% ADC decrease (p disappear within a week after microbeam exposure which may confirm the normal tissue sparing effect of MRT. For more information on this article, see medicalphysicsweb.org

  2. Pseudo subarachnoid Hemorrhage: A Finding of Diffuse Cerebral Edema Leading to Misdiagnosis

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    Eda Kılıç Çoban

    2015-12-01

    Full Text Available Increased attenuation of the basal cisterns and subarachnoid spaces on CT scans is a characteristic finding of acute subarachnoid hemorrhage. CT mimics of SAH have been called pseudo-SAH. Our case is presented to underline the differentiation of two diagnosis. A 63-year-old man was admitted to the emergency room with right-sided hemiparesis and aphasia. He had middle cerebral artery enfarct on his CT. A week after his hospitalisation his neurological examination was deteriorated. A plain CT-scan of brain was consistent with sub-arachnoid hemorrhage. His antiagregant therapy was ended and anti edema therapy started. Urgent neurosurgical consultation was sought & surgery was not planned. Brain death was the finding in his CT angiography. So the CT-scan findings turned out to be `pseudo sub-arachnoid haemorrhage’.Pseudo sub-arachnoid haemorrhage is a rare CT scan finding that has been reported in different cerebral disease with cerebral edema. MR imaging studies, CSF examination by lumbar puncture and the criterias proposed by Yazawa can be useful to make the diagnosis. The aim is the unnecessary termination of antiagregant and anticoagulant therapy.

  3. Effect of neutrophil depletion on gelatinase expression, edema formation and hemorrhagic transformation after focal ischemic stroke

    Directory of Open Access Journals (Sweden)

    Machado Livia S

    2005-08-01

    Full Text Available Abstract Background While gelatinase (MMP-2 and -9 activity is increased after focal ischemia/reperfusion injury in the brain, the relative contribution of neutrophils to the MMP activity and to the development of hemorrhagic transformation remains unknown. Results Anti-PMN treatment caused successful depletion of neutrophils in treated animals. There was no difference in either infarct volume or hemorrhage between control and PMN depleted animals. While there were significant increases in gelatinase (MMP-2 and MMP-9 expression and activity and edema formation associated with ischemia, neutrophil depletion failed to cause any change. Conclusion The main finding of this study is that, in the absence of circulating neutrophils, MMP-2 and MMP-9 expression and activity are still up-regulated following focal cerebral ischemia. Additionally, neutrophil depletion had no influence on indicators of ischemic brain damage including edema, hemorrhage, and infarct size. These findings indicate that, at least acutely, neutrophils are not a significant contributor of gelatinase activity associated with acute neurovascular damage after stroke.

  4. Patchy cerebral white matter edema in chronic renal failure

    Energy Technology Data Exchange (ETDEWEB)

    Anlar, B.; Erzen, C.; Saatci, U.

    1989-07-01

    Bilateral patchy cerebral white matter edema was observed in two children with chronic renal failure. Uremia in one case and hypertension or hyponatremia in the other appeared to be the cause of the neurological and radiological findings. (orig.).

  5. Postembolization perianeurysmal edema as a cause of uncinate seizures.

    Science.gov (United States)

    Cohen, José E; Itshayek, Eyal; Attia, Moshe; Moscovici, Samuel

    2012-03-01

    We report a patient with a giant unruptured supraclinoid aneurysm treated by endovascular embolization by means of bare coils and implantation of a flow diverterstent. Eight weeks after the embolization, she presented with uncinate seizures. Neuroradiological examination revealed de novo postembolization perianeurysmal edema, which has been described only rarely. A brief course of oral steroids successfully controlled the seizures. Perianeurysmal edema must be considered a potential complication after embolization of large aneurysms with coils and other means, and needs to be considered as a differential diagnosis in patients with unusual neurological symptoms at either the acute or delayed stages. To our knowledge, this is the first report of postembolization perianeurysmal edema occurring after successful occlusion by means of bare coils and a flow diverterstent. This report contributes to the growing evidence on adverse post-coiling inflammatory reactions, and specifically on perianeurysmal edema.

  6. Unilateral pulmonary edema during laparoscopic resection of adrenal tumor

    Science.gov (United States)

    Prakash, Smita; Nayar, Pavan; Virmani, Pooja; Bansal, Shipra; Pawar, Mridula

    2015-01-01

    Despite technological, therapeutic and diagnostic advancements, surgical intervention in pheochromocytoma may result in a life-threatening situation. We report a patient who developed unilateral pulmonary edema during laparoscopic resection of adrenal tumor. PMID:26330724

  7. Unilateral pulmonary edema during laparoscopic resection of adrenal tumor

    Directory of Open Access Journals (Sweden)

    Smita Prakash

    2015-01-01

    Full Text Available Despite technological, therapeutic and diagnostic advancements, surgical intervention in pheochromocytoma may result in a life-threatening situation. We report a patient who developed unilateral pulmonary edema during laparoscopic resection of adrenal tumor.

  8. Dexamethasone Intravitreal Implant for Diabetic Macular Edema During Pregnancy

    DEFF Research Database (Denmark)

    Concillado, Michael; Lund-Andersen, Henrik; Mathiesen, Elisabeth R;

    2016-01-01

    PURPOSE: To describe the management of diabetic macular edema during pregnancy with the use of a dexamethasone slow-release intravitreal implant. DESIGN: Retrospective, observational, consecutive case series. METHODS: The study included 5 pregnant women who presented with diabetic macular edema...... injection. RESULTS: Diabetic macular edema involving the foveal center was observed between gestational weeks 9 and 23 in 10 eyes of 5 patients. Dexamethasone intravitreal implant injection was given 10 times in 9 eyes with a mean preinjection center field retinal thickness of 535 μm (range, 239-727 μm...... center field thickness and in 6 of 8 eyes by an increase in BCVA of 5 or more approxETDRS letters. A mild transient rise in intraocular pressure occurred in 3 out of 8 eyes. CONCLUSION: Diabetic macular edema involving the foveal center that presented during pregnancy responded promptly to intravitreal...

  9. Successful treatment of pseudophakic cystoid macular edema with intravitreal bevacizumab.

    Science.gov (United States)

    Barone, Antonio; Prascina, Francesco; Russo, Vincenzo; Iaculli, Cristiana; Primavera, Vito; Querques, Giuseppe; Stella, Andrea; Delle Noci, Nicola

    2008-07-01

    A 67-year-old woman developed refractory pseudophakic cystoid macular edema (CME) after uneventful phacoemulsification. Three months after an intravitreal injection of bevacizumab (1.25 mg), the CME was completely resolved, with resultant improvement in visual acuity.

  10. The study of burn wound edema using dichromatic absorptiometry.

    Science.gov (United States)

    Demling, R H; Mazess, R B; Witt, R M; Wolberg, W H

    1978-02-01

    Burn wound edema is a source of major morbidity and mortality. To quantitatively study this edema, we have devised a noninvasive method called Dichromatic Absorptiometry (DA) which is precise (2-3%) and accurate (r equal to 0.99) in measuring changes in tissue fluid. A scanning technique using a dual photon source, 125I and 241Am, is used. The variable attenuation of the two photon energies allows for selective mass measurements of fluid, protein, lipid, and bone. In limbs with thermal injury the correlation of DA changes in fluid mass with circumference was (r equal to 0.97), but DA was more sensitive. In deep second- and third-degree burns, edema formation was maximum between 12 and 18 hours postburn with 80% of maximum already present at 4 hours. Resorption was complete by 1 week in second-degree burns, but significantly delayed in third-degree burns. Superimposed infection produced persistent edema.

  11. Acute macular edema following intracorporeal prostaglandin injection for erectile dysfunction

    Directory of Open Access Journals (Sweden)

    Asahi MG

    2015-07-01

    Full Text Available Masumi G Asahi, Calvin Chou, Ron P Gallemore Retina Macula Institute, Torrance, CA, USA Purpose: We aimed to describe the first case of macular edema following intracorporeal injection of alprostadil, a prostaglandin E1. Methods: This was a retrospective case report followed with optical coherence tomography, fundus photos, and fluorescein angiography images. Results: A patient developed bilateral cystoid macular edema following intracorporeal injection of alprostadil, a prostaglandin E1 for treatment of erectile dysfunction. The edema resolved following treatment with nonsteroidal anti-inflammatory drugs (NSAIDs and corticosteroids, with subsequent recovery in visual acuity. Discussion: Systemic prostaglandin administration can cause macular edema and vision loss, indicating that elevated systemic prostaglandin levels may affect visual function. This has potential implications for other systemic disorders and treatments that could affect macular function. Keywords: alprostadil, inflammation

  12. Effect of Foot Massage on Physiological Edema During Pregnancy

    OpenAIRE

    Fatemeh Rahimikian; Azadeh Shadmehr; Abbas Mehran; Mahdieh Kiani

    2015-01-01

    Introduction: One of the most common and annoying problems during pregnancy is physiological foot edema that may cause activity restrictions during pregnancy for pregnant women. Present study aimed to determine the effect of foot massage on physiological edema during pregnancy. Methods: This study was non-randomized clinical trial and performed in 2012. 120 pregnant women aged 20 to 35 years were non randomly assigned to treatment and control groups. Treatment group, received 20 minutes d...

  13. Neurogenic pulmonary edema due to delayed radiation necrosis

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    Mani R

    2005-01-01

    Full Text Available Neurogenic pulmonary edema is oftten missed in the ICU setting as it is mistaken for pneumonia or ARDS. The case presented here illustrates how a high index of suspicion in the appropriate setting can lead to the diagnosis. The patient in this report developed acute-on-chronic cerebral edema due to radiation necrosis following gamma-knife radiation therapy for cerebral arteriovenous malformation.

  14. Hypertrophic Cardiomyopathy Complicated by Pulmonary Edema in the Postpartum Period

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    Kate Hanneman

    2013-01-01

    Full Text Available We report the case of a 42-year-old patient with hypertrophic cardiomyopathy (HCM who presented to the emergency department with severe shortness of breath one week following uneventful cesarean delivery. Thoracic CT ruled out pulmonary embolus and confirmed pulmonary edema. Asymmetric interventricular septal thickening was clearly identified, demonstrating that the heart may be evaluated even on a non-ECG gated study. Acute pulmonary edema in the postpartum period is an unusual clinical presentation of HCM.

  15. Acute hemorrhagic edema of infancy-a rare entity

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    Saurabh R Jindal

    2013-01-01

    Full Text Available A patient presenting with fever and purpura often presents a diagnostic challenge for the dermatologist. Acute hemorrhagic edema of infancy (AHEI is a rare acute cutaneous leukocytoclastic vasculitic syndrome of infants leading to this presentation. We present an 18-month-old girl with AHEI who presented with fever, edema, and purpuric lesions involving the face, ears and extremities with uneventful complete recovery.

  16. Hemorrhagic Lacrimation and Epistaxis in Acute Hemorrhagic Edema of Infancy

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    Shireen Mreish

    2016-01-01

    Full Text Available Acute hemorrhagic edema of infancy is an uncommon benign cutaneous vasculitis. Despite its worrisome presentation, it carries good prognosis with rarely reported systemic involvement. Management of these cases has been an area of debate with majority of physicians adopting conservative modalities. We report a case that presented with classic triad of rash, low grade fever, and peripheral edema along with two rarely reported manifestations in literature: hemorrhagic lacrimation and epistaxis.

  17. Edema pulmonar agudo neurogênico: relato de caso

    OpenAIRE

    José Correia de Farias Brito; Maria Cerly Almeida Diniz; Roberto Ramalho Rosas; José Alberto Gonçalves Da Silva

    1995-01-01

    Os autores apresentam um caso de edema pulmonar agudo numa paciente de 28 anos de idade acometida de hemorragia subaracnóidea secundária à rotura de aneurisma intracraniano. A sintomatologia respiratória ocorreu durante o agravamento do quadro neurológico. Alguns aspectos etiológicos e fisiopatogênicos do edema pulmonar agudo neurogênico são analisados.

  18. Edema pulmonar agudo neurogênico: relato de caso

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    José Correia De Farias Brito

    1995-06-01

    Full Text Available Os autores apresentam um caso de edema pulmonar agudo numa paciente de 28 anos de idade acometida de hemorragia subaracnóidea secundária à rotura de aneurisma intracraniano. A sintomatologia respiratória ocorreu durante o agravamento do quadro neurológico. Alguns aspectos etiológicos e fisiopatogênicos do edema pulmonar agudo neurogênico são analisados.

  19. High altitude pulmonary edema among "Amarnath Yatris"

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    Parvaiz A Koul

    2013-01-01

    Full Text Available Background: Annual pilgrimage (Yatra to the cave shrine of Shri Amarnath Ji′ is a holy ritual among the Hindu devotees of Lord Shiva. Located in the Himalayan Mountain Range (altitude 13,000 ft in south Kashmir, the shrine is visited by thousands of devotees and altitude sickness is reportedly common. Materials and Methods: More than 600,000 pilgrims visited the cave shrine in 2011 and 2012 with 239 recorded deaths. Thirty one patients with suspected altitude sickness were referred from medical centers en-route the cave to Sher-i-Kashmir Institute of Medical Sciences, a tertiary-care center in capital Srinagar (5,000 ft. The clinical features and the response to treatment were recorded. Results: Thirty-one patients (all lowlanders, 19 male; age 18-60 years, median 41 had presented with acute onset breathlessness of 1-4 days (median 1.9 d starting within 12-24 h of a rapid ascent; accompanied by cough (68%, headache (8%, dizziness and nausea (65%. Sixteen patients had associated encephalopathy. Clinical features on admission included tachypnea ( n = 31, tachycardia ( n = 23, bilateral chest rales ( n = 29, cyanosis ( n = 22 and grade 2-4 encephalopathy. Hypoxemia was demonstrable in 24 cases and bilateral infiltrates on radiologic imaging in 29. Ten patients had evidence of high-altitude cerebral edema. All patients were managed with oxygen, steroids, nifedipine, sildenafil and other supportive measures including invasive ventilation ( n = 3. Three patients died due to multiorgan dysfunction. Conclusions: Altitude sickness is common among Amaranath Yatris from the plains and appropriate educational strategies should be invoked for prevention and prompt treatment.

  20. Diagnosis, prevention and management of postoperative pulmonary edema.

    Science.gov (United States)

    Bajwa, Sj Singh; Kulshrestha, A

    2012-07-01

    Postoperative pulmonary edema is a well-known postoperative complication caused as a result of numerous etiological factors which can be easily detected by a careful surveillance during postoperative period. However, there are no preoperative and intraoperative criteria which can successfully establish the possibilities for development of postoperative pulmonary edema. The aims were to review the possible etiologic and diagnostic challenges in timely detection of postoperative pulmonary edema and to discuss the various management strategies for prevention of this postoperative complication so as to decrease morbidity and mortality. The various search engines for preparation of this manuscript were used which included Entrez (including Pubmed and Pubmed Central), NIH.gov, Medknow.com, Medscape.com, WebMD.com, Scopus, Science Direct, MedHelp.org, yahoo.com and google.com. Manual search was carried out and various text books and journals of anesthesia and critical care medicine were also searched. From the information gathered, it was observed that postoperative cardiogenic pulmonary edema in patients with serious cardiovascular diseases is most common followed by noncardiogenic pulmonary edema which can be due to fluid overload in the postoperative period or it can be negative pressure pulmonary edema (NPPE). NPPE is an important clinical entity in immediate post-extubation period and occurs due to acute upper airway obstruction and creation of acute negative intrathoracic pressure. NPPE carries a good prognosis if promptly diagnosed and appropriately treated with or without mechanical ventilation.

  1. CT findings of pulmonary edema: comparison of various causes

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Hyae Young; Im, Jung Gi; Goo, Jin Mo [Seoul National University College of Medicine, Seoul (Korea, Republic of); Lee, Jae Kyo [Yeungnam University College of Medicine, Taegu (Korea, Republic of); Song, Jae Woo [Seoul City Boramae Hospital, Seoul (Korea, Republic of)

    1999-02-01

    To access the CT findings of pulmonary edema and to compare them, according to the cause. CT findings (thin section, 20 ; thick section, 16) of pulmonary edema in 36 patients [cardiac disease (group 1, n=20), renal disease (group 2, n=13), ARDS (group 3, n=3)] were analyzed and compared. There were 21 men and 15 women ranging in age from 27 to 77 years. Distribution (even, central, or peripheral) and patterns of pulmonary edema were compared between the three groups. The distribution of edema, appearing as consolidation or ground-glass opacity, was even in 75% (n=15) of group 1, even in 46% (n=6) and central in 38% (n=5) of group 2, and peripherally predominant in 100% (n=3) of group 3. Interlobular septal thickening was seen in 80% (n=16), 69% (n=9), and 0% of group 1, 2 and 3, respectively. Centrilobular ground-glass opacity was noted in six patients. In spite of various findings and considerable overlapping of the findings of pulmonary edema, the distribution and pattern of edema differed according to the cause, and this can be helpful for differential diagnosis.

  2. [Migraine with prolonged eyelid edema: a series of 10 cases].

    Science.gov (United States)

    Toribio-Díaz, M E; Cuadrado-Pérez, M L; Peláez, A; Aledo-Serrano, Angel; Pedraza, M Isabel; Porta-Etessam, Jesús; Guerrero-Peral, Angel L

    2014-05-01

    Introduccion. La migraña puede cursar con sintomas autonomicos craneales propios de las cefaleas trigeminoautonomicas, lo que plantea dificultades en el diagnostico. Objetivo. Describir una serie de diez pacientes con edema palpebral asociado a la migraña. Pacientes y metodos. Diez pacientes atendidos en la consulta de cefaleas de tres hospitales (nueve mujeres, un varon; edad: 26-53 años), con edema palpebral recurrente asociado a la migraña. Resultados. Segun los criterios diagnosticos de la Clasificacion Internacional de las Cefaleas (ICHD-III, version beta), ocho pacientes presentaban migraña sin aura, una tenia migraña con aura y otra, migraña cronica. El edema palpebral aparecia durante las crisis de migraña mas intensas, y tenia mayor duracion que la cefalea. Se descartaron causas farmacologicas o sistemicas del edema en todos los casos. Otros sintomas autonomicos asociados fueron la inyeccion conjuntival (n = 3), el lagrimeo (n = 2) y la rinorrea (n = 1). Tanto el dolor como el edema asociado respondieron a los tratamientos sintomaticos y preventivos de la migraña. Conclusiones. El edema palpebral es un posible acompañante de la migraña. Aparece en algunos pacientes con los episodios de mayor intensidad, y responde al tratamiento sintomatico y preventivo de la migraña.

  3. Blood pressure, edema and proteinuria in pregnancy. 7. Edema-plus-proteinuria relationships.

    Science.gov (United States)

    Sellmann, A H

    1976-01-01

    1. A total of 488 pregnancies had the combination of two-plus or more proteinuria and edema of the hands and face. Of these, 208 were white and 280 were black gravidas. In the white gravidas, 8 fetal and neonatal deaths occurred with a perinatal mortality of 38.5 per 1,000. There were 13 perinatal deaths in the black subgroup with a perinatal mortality rate of 46.4 per 1,000. The overall perinatal mortality rate was 43.0 per 1,000, which could be compared to the overall perinatal mortality rate of 32.8 per 1,000 for the segment of the study population without edema or proteinuria. This underscored the implication of increased hazard to fetal outcome of these clinical signs in combination. 2. The analysis of the matrix data showed scattered rates throughout gestation in white median-age nulliparas. Their black counterparts had comparable increased mortality rates. In the white multiparas of ages 20 to 34 years, the highest rates were found at relatively low blood pressure levels. The black median-age multiparas had rates associated with higher pressure readings, especially at or above 125/75. In teenage mulliparas with edema and proteinuria, perinatal mortality rates were similar for both subgroups and were found in somewhat lower blood pressures. 3. The incremental analysis was remarkable in that rates were scattered widely in the white subgroups, but tightly clustered in the black subgroups. The black median-age nulliparas had perinatal mortality concentrated about 115 to 134 mm. Hg systolic and 65 to 84 mm. Hg diastolic. The overall mortality rates of this subgroup were the highest of the subgroups studied. The black 20 to 34 year old multiparas had highest coassociated deaths in the 134-154 mm. Hg systolic levels throughout pregnancy. The clustering effect was most pronounced in black teenage nulliparas in both systolic and diastolic blood pressure groups at much lower levels. 4. The use of a critical cut-off blood pressure level of 125 mm. Hg systolic and 75 mm

  4. Lung ultrasound for monitoring cardiogenic pulmonary edema.

    Science.gov (United States)

    Cortellaro, Francesca; Ceriani, Elisa; Spinelli, Monica; Campanella, Carlo; Bossi, Ilaria; Coen, Daniele; Casazza, Giovanni; Cogliati, Chiara

    2016-07-29

    Several studies address the accuracy of lung ultrasound (LUS) in the diagnosis of cardiogenic pulmonary edema (CPE) evaluating the interstitial syndrome, which is characterized by multiple and diffuse vertical artifacts (B-lines), and correlates with extravascular lung water. We studied the potential role of LUS in monitoring CPE response to therapy, by evaluating the clearance of interstitial syndrome within the first 24 h after Emergency Department (ED) admission. LUS was performed at arrival (T0), after 3 (T3) and 24 (T24) hours. Eleven regions were evaluated in the antero-lateral chest; the B-lines burden was estimated in each region (0 = no B-lines, 1 = multiple B-lines, 2 = confluent B-lines/white lung) and a mean score (B-Score, range 0-2) was calculated. Patients received conventional CPE treatment. Blood chemistry, vital signs, blood gas analysis, diuresis at T0, T3, T24 were also recorded. A complete echocardiography was obtained during hospitalization. Forty-one patients were enrolled. Respiratory and hemodynamic parameters improved in all patients between T0 and T3 and between T3 and T24. Mean B-score significantly decreased at T3 (from 1.59 ± 0.40 to 0.73 ± 0.44, P < 0.001) and between T3 and T 24 (from 0.73 ± 0.44 to 0.38 ± 0.33, P < 0.001). B-score was higher in the lower pulmonary regions at any time. At final evaluation (T24) 75 % of apical and only 38 % of basal regions were cleared. LUS allows one to assess the clearance of interstitial syndrome and its distribution in the early hours of treatment of CPE, thus representing a possible tool to guide therapy titration.

  5. Intrapartum FHR monitoring and neonatal CT brain scan

    Energy Technology Data Exchange (ETDEWEB)

    Takahashi, Yoshiki; Ukita, Masahiko; Nakada, Eizo (Kurashiki Central Hospital, Okayama (Japan))

    1982-12-01

    The effect of fetal distress on the neonatal brain was investigated by neonatal CT brain scan, FHR monitoring and mode of delivery. This study involved 11 cases of full term vertex delivery in which FHR was recorded by fetal direct ECG during the second stage labor. All infants weighed 2,500 g or more. FHR monitoring was evaluated by Hon's classification. Neonatal brain edema was evaluated by cranial CT histgraphic analysis (Nakada's method). 1) Subdural hemorrhage was noted in 6 of 7 infants delivered by vacuum extraction or fundal pressure (Kristeller's method). 2) Intracranial hemorrhage was demonstrated in all of 3 infants with 5-min. Apgar score 7 or less. 3) Two cases with prolonged bradycardia and no variability had intraventricular or intracerebral hemorrhage which resulted in severe central nervous system damage. 4) The degree of neonatal brain edema correlated with 5-min. Apgar score. 5) One case with prolonged bradycardia and no variability resulted in severe neonatal brain edema. Four cases with variable deceleration and increased variability resulted in mild neonatal brain edema. Two cases with late deceleration and decreased variability resulted in no neonatal brain edema.

  6. A comparative study on the efficacy of 10% hypertonic saline and equal volume of 20% mannitol in the treatment of experimentally induced cerebral edema in adult rats

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    Fang Ming

    2010-12-01

    Full Text Available Abstract Background Hypertonic saline and mannitol are commonly used in the treatment of cerebral edema and elevated intracranial pressure (ICP at present. In this connection, 10% hypertonic saline (HS alleviates cerebral edema more effectively than the equal volume of 20% mannitol. However, the exact underlying mechanism for this remains obscure. This study aimed to explore the possible mechanism whereby 10% hypertonic saline can ameliorate cerebral edema more effectively than mannitol. Results Adult male Sprague-Dawley (SD rats were subjected to permanent right-sided middle cerebral artery occlusion (MCAO and treated with a continuous intravenous infusion of 10% HS, 20% mannitol or D-[1-3H(N]-mannitol. Brain water content (BWC as analyzed by wet-to-dry ratios in the ischemic hemisphere of SD rats decreased more significantly after 10% HS treatment compared with 20% mannitol. Concentration of serum Na+ and plasma crystal osmotic pressure of the 10% HS group at 2, 6, 12 and 18 h following permanent MCAO increased significantly when compared with 20% mannitol treated group. Moreover, there was negative correlation between the BWC of the ipsilateral ischemic hemisphere and concentration of serum Na+, plasma crystal osmotic pressure and difference value of concentration of serum Na+ and concentration of brain Na+ in ipsilateral ischemic hemisphere in the 10% HS group at the various time points after MCAO. A remarkable finding was the progressive accumulation of mannitol in the ischemic brain tissue. Conclusions We conclude that 10% HS is more effective in alleviating cerebral edema than the equal volume of 20% mannitol. This is because 10% HS contributes to establish a higher osmotic gradient across BBB and, furthermore, the progressive accumulation of mannitol in the ischemic brain tissue counteracts its therapeutic efficacy on cerebral edema.

  7. Connectivity of default-mode network is associated with cerebral edema in hepatic encephalopathy.

    Directory of Open Access Journals (Sweden)

    Wei-Che Lin

    Full Text Available Cerebral edema, a well-known feature of acute liver disease, can occur in cirrhotic patients regardless of hepatic encephalopathy (HE and adversely affect prognosis. This study characterized and correlated functional HE abnormalities in the brain to cerebral edema using resting-state functional magnetic resonance imaging (rs-fMRI and diffusion tensor imaging (DTI. Forty-one cirrhotic patients (16 without HE, 14 minimal HE, 11 overt HE and 32 healthy controls were assessed. The HE grade in cirrhotic patients was evaluated by the West Haven criteria and neuro-psychological examinations. Functional connectivity correlation coefficient (fc-CC of the default mode network (DMN was determined by rs-fMRI, while the corresponding mean diffusivity (MD was obtained from DTI. Correlations among inter-cortical fc-CC, DTI indices, Cognitive Ability Screening Instrument scores, and laboratory tests were also analyzed. Results showed that gradual reductions of HE-related consciousness levels, from "without HE" or "minimal HE" to "overt HE", correlated with decreased anterior-posterior fc-CC in DMN [F(4.415, p = 0.000]. The MD values from regions with anterior-posterior fc-CC differences in DMN revealed significant differences between the overt HE group and other groups. Increased MD in this network was inversely associated with decreased fc-CC in DMN and linearly correlated with poor cognitive performance. In conclusion, cerebral edema can be linked to altered cerebral temporal architecture that modifies both within- and between-network connectivity in HE. Reduced fc-CC in DMN is associated with behavior and consciousness deterioration. Through appropriate targets, rs-fMRI technology may provide relevant supplemental information for monitoring HE and serve as a new biomarker for clinical diagnosis.

  8. MRI of brain disease in veterinary patients part 1: Basic principles and congenital brain disorders.

    Science.gov (United States)

    Hecht, Silke; Adams, William H

    2010-01-01

    Magnetic resonance imaging (MRI) is increasingly being used in the diagnosis of central nervous system disorders in veterinary patients and is quickly becoming the imaging modality of choice in evaluation of brain and intracranial disease. This article provides an overview of the basic principles of MRI, a description of sequences and their applications in brain imaging, and an approach to interpretation of brain MRI. A detailed discussion of imaging findings in general intracranial disorders including hydrocephalus, vasogenic edema, brain herniation, and seizure-associated changes, and the MR diagnosis of congenital brain disorders is provided. MRI evaluation of acquired brain disorders is described in a second companion article.

  9. Endothelial transient receptor potential conical channel (TRPC)-3 activation induces vasogenic edema formation in the rat piriform cortex following status epilepticus.

    Science.gov (United States)

    Ryu, Hea Jin; Kim, Ji-Eun; Kim, Yeon-Joo; Kim, Ji-Yang; Kim, Won I L; Choi, So-Yeon; Kim, Min-Ju; Kang, Tae-Cheon

    2013-05-01

    Transient receptor potential canonical channel (TRPC) is a nonselective cation channel permeable to Ca(2+), which express in many cell types, including neurons. However the alterations in TRPC receptor expressions in response to status epilepticus (SE) have not been explored. Therefore, the present study was designated to elucidate the roles of TRPC3 in neuronal death and vasogenic edema within the rat piriform cortex (PC) following SE. In non-SE animals, TRPC3 immunoreactivity was abundantly detected in the PC. Following SE, TRPC3 immunoreactivity was increased in neurons. Furthermore, TRPC3 expression was detected in endothelial cells that did not contain it in non-SE animals. Loss of SMI-71 (a blood-brain barrier antigen) immunoreactivity was also observed in TRPC3 positive endothelial cells. In addition, FJB positive neurons and vasogenic edema were noticeably detected in the PC. To directly determine whether TRPC3 activation is correlated to SE-induced vasogenic edema formation and neuronal damages in the PC, the effect of Pyr-3 (a TRPC3 antagonist) on SE-induced insults were investigated. Pyr-3 infusion effectively attenuated vasogenic edema in the PC as compared to the vehicle. Therefore, our findings indicate that TRPC3 activation/overexpression induced by SE may involve BBB disruption and neuronal damages in the rat PC following SE. Therefore, the present study was TRPC3 may play an important role in SE-induced vasogenic edema formation through BBB disruptions in the rat PC.

  10. Bone marrow edema syndrome in postpartal women: treatment with iloprost.

    Science.gov (United States)

    Aigner, Nicholas; Meizer, Roland; Meraner, Dominik; Becker, Stephan; Meizer, Elizabeth; Landsiedl, Franz

    2009-04-01

    Bone marrow edema syndrome of the femoral head in pregnant women is a rare disease resulting in disabling coxalgia, beginning in the last 3 months of pregnancy and persisting for several months after parturition. The parenteral administration of the vasoactive drug iloprost constitutes a new approach to the treatment of painful bone marrow edema syndrome of the hip of pregnant women. Six postpartal women (8 hips) with bone marrow edema syndrome of the femoral head were treated with iloprost followed by 3 weeks of partial weight-bearing. Relief from pain, restoration of functional capacity, and normalization of the MRI signal pattern were rapidly achieved, thus avoiding the need for surgical intervention. As the substance is contraindicated in pregnancy, therapy may begin only some days after parturition, with a short discontinuation in breastfeeding.

  11. Cystoid Macular Edema Induced by Low Doses of Nicotinic Acid

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    Daniela Domanico

    2013-01-01

    Full Text Available Cystoid macular edema (CME is a condition that involves the macula, causing painless vision loss. In this paper, we report a case of niacin-induced bilateral cystoid macular edema (CME in a middle-age woman taking low dose of niacin (18 mg of nicotinic acid. Optical coherence tomography (OCT showed retinal thickening and cystoid spaces in both eyes, whereas fluorescein angiography (FA; HRA 2, Heidelberg Engineering revealed the absence of fluorescein leakage also in later phases. Four weeks after discontinuation of therapy there were a complete disappearance of macular edema at funduscopic examination and an improvement of visual acuity in both eyes. Furthermore OCT showed a normal retinal profile in both eyes. In our opinion considering the wide availability of niacin, medical monitoring and periodical examination should be considered during niacin administration. To our knowledge, this is the first report in the literature that described the very low-dose niacin-induced bilateral niacin maculopathy.

  12. Negative pressure pulmonary edema following choking on a cookie.

    Science.gov (United States)

    Toukan, Yazeed; Gur, Michal; Bentur, Lea

    2016-07-01

    A 12-year-old boy developed severe acute respiratory distress during a school break requiring resuscitative measures. The episode started shortly after a short choking episode with a cookie. History, physical examination, laboratory results, chest X-ray, and clinical course supported the diagnosis of negative pressure pulmonary edema (NPPE). NPPE occurring outside a hospital setting, especially following a short episode of choking on a cookie, is rarely reported in children. Understanding the pathophysiological mechanisms contributing to pulmonary edema can help in distinguishing NPPE from other causes of fulminant respiratory distress, and especially from other causes of noncardiogenic pulmonary edema. Pediatr Pulmonol. 2016;51:E25-E27. © 2016 Wiley Periodicals, Inc.

  13. Characterization of symptoms and edema distribution in premenstrual syndrome

    Science.gov (United States)

    Tacani, Pascale Mutti; Ribeiro, Danielle de Oliveira; Barros Guimarães, Barbara Evelyn; Machado, Aline Fernanda Perez; Tacani, Rogério Eduardo

    2015-01-01

    Background Premenstrual syndrome is a group of symptoms linked to the menstrual cycle, and edema is among these symptoms. Physiotherapy is often sought by many patients for the treatment of edema; however, for an adequate prescription of physiotherapeutic procedures, the distribution of edema throughout the body has yet to be characterized. Objective To determine the most frequent symptoms and body regions that present with edema in women during the premenstrual period. Subjects and methods Sixty women with a mean age of 24.6±4.7 years were evaluated during their premenstrual (between days 21 and 28) and menstrual period (between days 1 and 3), and the collected data included body mass, height, biotype (body-fat distribution), face, breast, limb-circumference measurements, and limb-volume estimate, and an adapted version of the Premenstrual Symptoms Screening Tool was used. Statistical analysis was performed using Student’s t-test and the test for equality of two proportions (P≤0.05). Results Premenstrual syndrome was identified in 91.7% of the women, and the most frequent symptoms were irritability (73.33%) and physical symptoms, including swelling (65%), and anxiety (58.3%). Edema was detected in the following areas: facial, epigastric, mammary, umbilical, and pubic, the mid-third of the arms, distal forearm, in both thighs and in the mid-third of the legs determined by circumference measurements, and in both upper and lower limbs, according to the estimated volume. Conclusion In this study population, the most frequent symptoms were irritability, physical symptoms, and anxiety, with distribution of edema in the face, breast, abdomen, pubic area, distal upper limb, and proximal lower limb. PMID:25792857

  14. Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors

    Institute of Scientific and Technical Information of China (English)

    HU Hua; YAO Hong-tian; ZHANG Wei-ping; ZHANG LEI; DING Wei; ZHANG Shi-hong; CHEN Zhong; WEI Er-qing

    2005-01-01

    Objective: To characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors. Methods: Nineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression. Results: AQP4 expression was increased from 15h to at least 8 d after injury. AQP4immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung.Conclusion: AQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

  15. MRI evidence: acute mountain sickness is not associated with cerebral edema formation during simulated high altitude.

    Science.gov (United States)

    Mairer, Klemens; Göbel, Markus; Defrancesco, Michaela; Wille, Maria; Messner, Hubert; Loizides, Alexander; Schocke, Michael; Burtscher, Martin

    2012-01-01

    Acute mountain sickness (AMS) is a common condition among non-acclimatized individuals ascending to high altitude. However, the underlying mechanisms causing the symptoms of AMS are still unknown. It has been suggested that AMS is a mild form of high-altitude cerebral edema both sharing a common pathophysiological mechanism. We hypothesized that brain swelling and consequently AMS development is more pronounced when subjects exercise in hypoxia compared to resting conditions. Twenty males were studied before and after an eight hour passive (PHE) and active (plus exercise) hypoxic exposure (AHE) (F(i)O(2) = 11.0%, P(i)O(2)∼80 mmHg). Cerebral edema formation was investigated with a 1.5 Tesla magnetic resonance scanner and analyzed by voxel based morphometry (VBM), AMS was assessed using the Lake Louise Score. During PHE and AHE AMS was diagnosed in 50% and 70% of participants, respectively (p>0.05). While PHE slightly increased gray and white matter volume and the apparent diffusion coefficient, these changes were clearly more pronounced during AHE but were unrelated to AMS. In conclusion, our findings indicate that rest and especially exercise in normobaric hypoxia are associated with accumulation of water in the extracellular space, however independent of AMS development. Thus, it is suggested that AMS and HACE do not share a common pathophysiological mechanism.

  16. Protective effect of ginkgolide B on high altitude cerebral edema of rats.

    Science.gov (United States)

    Botao, Yu; Ma, Jie; Xiao, Wenjing; Xiang, Qingyu; Fan, Kaihua; Hou, Jun; Wu, Juan; Jing, Weihua

    2013-03-01

    Ginkgolide B (GB) is one of the ginkgolides isolated from leaves of the Ginkgo biloba tree. The aim of this study was to investigate whether GB has a protective effect on high altitude cerebral edema (HACE) of rats. HACE was induced by hypobaric hypoxia exposure for 24 hours in an animal decompression chamber with the chamber pressure of 267 mmHg to simulate an altitude of 8000 m. Before the exposure, three doses (3, 6, and 12 mg·kg(-1)) of GB were given intraperitoneally (ip) daily for 3 days. Effects of GB on brain water content (BWC), activity of superoxide dismutase (SOD), concentration of glutathione (GSH) and malondialdehyde (MDA), expression of active caspase-3 and poly(ADP-ribose) polymerase (PARP) were measured. In GB pretreatment groups (6 and 12 mg·kg(-1), but not 3 mg·kg(-1)), BWC, the concentration of MDA, the expression of active caspase-3 and PARP were reduced significantly, while the activity of SOD and concentration of GSH were significantly increased. In conclusion, these results indicate that GB has a protective effect on cerebral edema caused by high altitude in rats. The protective effect of GB might be attributed to its antioxidant properties and suppression of the caspase-dependent apoptosis pathway.

  17. [Acute pulmonary edema secondary to acute upper airway obstruction].

    Science.gov (United States)

    Sánchez-Ortega, J L; Carpintero-Moreno, F; Olivares-López, A; Borrás-Rubio, E; Alvarez-López, M J; García-Izquierdo, A

    1992-01-01

    We report a 72 years old woman with mild arterial hypertension and no other pathological history who presented an acute pulmonary edema due to acute obstruction of the upper airway secondary to vocal chord paralysis developing during the immediate postoperative phase of thyroidectomy. The acute pulmonary edema resolved after application of tracheal reintubation, mechanical ventilation controlled with end expiratory positive pressure, diuretics, morphine, and liquid restriction. We discuss the possible etiopathogenic possibilities of this infrequent clinical picture and we suggest that all patients who suffered and acute obstruction of the upper airways require a careful clinical surveillance in order to prevent the development of the pulmonary syndrome.

  18. Neurogenic pulmonary edema: successful treatment with IV phentolamine.

    Science.gov (United States)

    Davison, Danielle L; Chawla, Lakhmir S; Selassie, Leelie; Tevar, Rahul; Junker, Christopher; Seneff, Michael G

    2012-03-01

    Neurogenic pulmonary edema (NPE) is a clinical syndrome characterized by the acute onset of pulmonary edema following a significant CNS insult. The cause is believed to be a surge of catecholamines that results in cardiopulmonary dysfunction. Although there are myriad case reports describing CNS events that are associated with this syndrome, few studies have identified specific treatment modalities. We present a case of NPE caused by an intracranial hemorrhage from a ruptured arteriovenous malformation. We uniquely document a rise and fall of serum catecholamine levels correlating with disease activity and a dramatic clinical response to IV phentolamine.

  19. Metal content ratio as a sensitive indicator of pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Maitani, T.; Suzuki, K.T.

    1981-11-01

    The sensitivity to detect edema fluid in the lungs of rats exposed to 4, 2, 0.8, and 0.4 ppm O3 was estimated using the metal content ratio (Ca/Mg) and wet/dry weight ratio methods. Metal content ratios were determined by inductively coupled plasma-atomic emission spectrometer (ICP-AES). The detection limits were 0.8 and 2.0 ppm for the former and latter methods, respectively. A transitory increase of edema fluid was observed at day 1 in 0.8 and 0.4 ppm experiments by the Ca/Mg ratio method.

  20. Edema de ubre en ganado bovino. II entrega

    OpenAIRE

    Saborío-Montero, Alejandro

    2014-01-01

    La inflamación excesiva de la glándula mamaria asociada al parto es un padecimiento frecuente en ganado bovino, éste desbalance se conoce con el nombre de “edema mamario” o “edema de ubre”. Particularmente las hembras primíparas experimentan este fenómeno de manera más severa. La inflamación de la ubre puede generar una serie de efectos detrimentales sobre el animal. El incremento en la propensión a mastitis, pezones dañados, ubres heridas y/o pendulosas han sido características asociadas al ...

  1. Perihematomal edema as predictor of outcome in spontaneous intracerebral hemorrhage

    Directory of Open Access Journals (Sweden)

    Mani Gupta

    2014-01-01

    Full Text Available Background: Spontaneous intracerebral hemorrhage (SICH is a form of cerebrovascular accident with a very high rate of morbidity and mortality. The determinants of prognosis include the demographic, clinical, laboratory, and radiologic factors. It is long known that the hematoma size has a negative impact on the outcome in SICH. The influence of perihematomal edema (PHE is not established to the extent same as that of hematoma volume. Hence, we planned this study to determine as to what role does PHE plays in the outcome in SICH. Aim of the Study: To evaluate the prognostic influence of absolute and relative edema (ratio of absolute edema to hematoma volume in the patients of SICH. Materials and Methods : This is a prospective case-controlled study. A total of 44 patients were enrolled after excluding the confounding factors. The patients were evaluated and their disability was assessed using modified Rankin scale (MRS. The imaging was done in the interval between 24 and 72 h and the hematoma volume, absolute edema volume, and the relative edema were calculated. The outcome was reassessed at 12 weeks and defined as favorable if MRS < 3. Results: A total of 69 patients were found to be having SICH on imaging; however, 25 patients were excluded as they had one of the criterion for exclusion. Hence, only 44 patients were included in the study. On univariate analysis, none of the demographic characteristics of the patients, vascular risk factors, presenting complaints, blood pressure, Glasgow coma scale, and MRS at admission, laboratory parameters were not significantly different in the two outcome groups. The hematoma volume was significantly higher in the poor outcome group (P < 0.0001 and the relative edema was associated with a favorable outcome at 12 weeks (P < 0.0001. On multivariate logistic regression, the hematoma volume and relative edema were found to have effect on the outcome similar to that seen on univariate analysis. Conclusion: In

  2. CSF transthyretin neuroprotection in a mouse model of brain ischemia

    DEFF Research Database (Denmark)

    Santos, Sofia Duque; Lambertsen, Kate Lykke; Clausen, Bettina Hjelm

    2010-01-01

    Brain injury caused by ischemia is a major cause of human mortality and physical/cognitive disability worldwide. Experimentally, brain ischemia can be induced surgically by permanent middle cerebral artery occlusion. Using this model, we studied the influence of transthyretin in ischemic stroke...... neuronal cell death, edema and inflammation, thereby influencing the survival of endangered neurons in cerebral ischemia....

  3. Accuracy of Non-Enhanced CT in Detecting Early Ischemic Edema Using Frequency Selective Non-Linear Blending.

    Directory of Open Access Journals (Sweden)

    Georg Bier

    Full Text Available Ischemic brain edema is subtle and hard to detect by computed tomography within the first hours of stroke onset. We hypothesize that non-enhanced CT (NECT post-processing with frequency-selective non-linear blending ("best contrast"/BC increases its accuracy in detecting edema and irreversible tissue damage (infarction.We retrospectively analyzed the NECT scans of 76 consecutive patients with ischemic stroke (exclusively middle cerebral artery territory-MCA before and after post-processing with BC both at baseline before reperfusion therapy and at follow-up (5.73±12.74 days after stroke onset using the Alberta Stroke Program Early CT Score (ASPECTS. We assessed the differences in ASPECTS between unprocessed and post-processed images and calculated sensitivity, specificity, and predictive values of baseline NECT using follow-up CT serving as reference standard for brain infarction.NECT detected brain tissue hypoattenuation in 35 of 76 patients (46.1%. This number increased to 71 patients (93.4% after post-processing with BC. Follow-up NECT confirmed brain infarctions in 65 patients (85.5%; p = 0.012. Post-processing increased the sensitivity of NECT for brain infarction from 35/65 (54% to 65/65 (100%, decreased its specificity from 11/11 (100% to 7/11 (64%, its positive predictive value (PPV from 35/35 (100% to 65/69 (94% and increased its accuracy 46/76 (61% to 72/76 (95%.This post-hoc analysis suggests that post-processing of NECT with BC may increase its sensitivity for ischemic brain damage significantly.

  4. Dichotomal role of TNF in experimental pulmonary edema reabsorption

    NARCIS (Netherlands)

    Braun, C; Hamacher, J; Morel, DR; Wendel, A; Lucas, R

    2005-01-01

    Distinct from its receptor binding sites, TNF carries a lectin-like domain, situated at the tip of the molecule, which specifically binds oligosaccharides, such as NN'-diacetylchitobiose. In view of the apparently conflicting data concerning TNF actions in pulmonary edema, we investigated the contri

  5. Acute effect of pure oxygen breathing on diabetic macular edema

    DEFF Research Database (Denmark)

    Vinten, Carl Martin; La Cour, Morten; Lund-Andersen, Henrik;

    2012-01-01

    Purpose. A small-scale pilot study of the pathophysiology of diabetic macular edema (DME) was made by assessing concomitant changes in macular volume (MV), mean arterial blood pressure (MABP), intraocular pressure (IOP), retinal artery diameter (RAD), and retinal vein diameter (RVD) in response...

  6. POST OBSTRUCTIVE PULMONARY EDEMA AFTER ATTEMPTED NYLON ROPE SUICIDAL HANGING

    Directory of Open Access Journals (Sweden)

    Rakesh

    2015-06-01

    Full Text Available Survival after nylon rope suicidal hanging is a rare occurance . We describe here a patient who attempted suicide by nylon rope hanging and developed post obstructive pulmonary edema was managed successfully . Patient recovered completely with ventilatory support in next 60 hours without any neurological deficit.This case highlights an unusual complication of hanging and its recovery.

  7. Postparacentesis vulvar edema in ovarian hyper stimulation syndrome

    Directory of Open Access Journals (Sweden)

    Sindhu Bhairavi

    2016-11-01

    Full Text Available Ovarian hyper stimulation syndrome (OHSS is a serious, potentially life threatening complication of ovulation induction. The clinical picture of severe OHSS includes ovarian enlargement, ascites, pleural effusion, increased coagulability, and electrolyte disorders. Very few cases of massive vulvar edema in OHSS have been reported in the literature. [Int J Reprod Contracept Obstet Gynecol 2016; 5(11.000: 4064-4066

  8. Prevention of edema disease in pigs by passive immunization

    DEFF Research Database (Denmark)

    Johansen, M.; Andresen, Lars Ole; Thomsen, L.K.

    2000-01-01

    The effect of treatment with verotoxin 2e (VT2e) specific antiserum was evaluated in 3 Danish pig herds with edema disease (ED). The antiserum was prepared by immunizing horses with a VT2e toroid. The study was performed as a randomized blind field trial with parallel treatment and control groups...

  9. New concepts about the pathophysiology of pulmonary edema.

    Science.gov (United States)

    Staub, N C

    1988-07-01

    Three new concepts concerning lung liquid and protein exchange are considered. The first is that the microvascular surface area is as important as the microvascular hydrostatic pressure in assessing filtration in the lung. One of the problems in differentiating hemodynamic from increased permeability edema is the inability to determine whether the microvascular surface area has changed. Several agents, as well as exercise, affect liquid filtration. A new, dynamic procedure that is more sensitive for the detection of increased permeability than static measurements of lung water content is described, along with its limitations. The second concept is that water and electrolytes are cleared from the alveoli by a separate mechanism from protein. Water clearance is fast and occurs mainly by an active process, which can be inhibited by amiloride or phloridzin and accelerated by beta-agonists. The mechanism appears to depend on metabolically regulated sodium transport across the alveolar epithelium. Protein clearance is very slow and is relatively independent of alveolar concentration. The protein clearance mechanism is unknown but may involve transcytosis. The third concept is that during edema formation there are two pathways for liquid clearance in addition to the lymphatic system: into the pleural space and along the bronchovascular connective tissue into the mediastinum. During recovery from edema, reabsorption into blood is important if the edema liquid has a low protein osmotic pressure. Clearance into the mediastinum may be the major pathway for liquid sequestered in the loose, binding connective tissue.

  10. Effects of the mitochondrial calcium uniporter on cerebral edema in a rat model of cerebral ischemia reperfusion injury

    Institute of Scientific and Technical Information of China (English)

    Linlin Li; Shilei Wang; Haihong Luan

    2011-01-01

    The present study investigated the effects of the mitochondrial calcium uniporter inhibitor ruthenium red and the agonist spermine on cerebral edema in rats with cerebral ischemia reperfusion injury.Left middle cerebral artery occlusion (MCAO) was induced in rats using the suture method.Following 24 hours of ischemic reperfusion, neurological function scores of rats with MCAO, and rats pretreated with ruthenium red and spermine were significantly lower, however, water content of brain tissue, aquaporin 4 expression and immunoglobulin G (IgG) exudation were significantly higher than those of sham-operated rats.Compared with MCAO rats and spermine-treated rats, neurological function scores were considerably higher, and brain tissue water content, aquaporin 4 expression and IgG exudation decreased in ruthenium red-treated rats.These findings suggest that preventive application of the mitochondrial calcium uniporter inhibitor ruthenium red can significantly decrease aquaporin 4 and IgG expression, influence the permeability of the blood brain barrier, and thereby decrease the extent of cerebral edema.

  11. Characterization of symptoms and edema distribution in premenstrual syndrome

    Directory of Open Access Journals (Sweden)

    Tacani PM

    2015-03-01

    Full Text Available Pascale Mutti Tacani,1 Danielle de Oliveira Ribeiro,1 Barbara Evelyn Barros Guimarães,1 Aline Fernanda Perez Machado,2 Rogério Eduardo Tacani1,2 1Physical Therapy Department, São Camilo University Center, 2Physical Therapy Department, São Paulo City University (UNICID, São Paulo, Brazil Background: Premenstrual syndrome is a group of symptoms linked to the menstrual cycle, and edema is among these symptoms. Physiotherapy is often sought by many patients for the treatment of edema; however, for an adequate prescription of physiotherapeutic procedures, the distribution of edema throughout the body has yet to be characterized. Objective: To determine the most frequent symptoms and body regions that present with edema in women during the premenstrual period.Subjects and methods: Sixty women with a mean age of 24.6±4.7 years were evaluated during their premenstrual (between days 21 and 28 and menstrual period (between days 1 and 3, and the collected data included body mass, height, biotype (body-fat distribution, face, breast, limb-circumference measurements, and limb-volume estimate, and an adapted version of the Premenstrual Symptoms Screening Tool was used. Statistical analysis was performed using Student’s t-test and the test for equality of two proportions (P≤0.05.Results: Premenstrual syndrome was identified in 91.7% of the women, and the most frequent symptoms were irritability (73.33% and physical symptoms, including swelling (65%, and anxiety (58.3%. Edema was detected in the following areas: facial, epigastric, mammary, umbilical, and pubic, the mid-third of the arms, distal forearm, in both thighs and in the mid-third of the legs determined by circumference measurements, and in both upper and lower limbs, according to the estimated volume.Conclusion: In this study population, the most frequent symptoms were irritability, physical symptoms, and anxiety, with distribution of edema in the face, breast, abdomen, pubic area, distal

  12. Effects of endostatin on C6 glioma-induced edema

    Institute of Scientific and Technical Information of China (English)

    YANG Li-juan; LIN Zhi-xiong; KANG De-zhi; WENG Shen-mei; LIN Jian-hua; HUANG Qiang; ZHANG Peng-fei

    2011-01-01

    Background Glioma-induced edema is considered as one of the most pathological characteristics of glioma and a significant source of morbidity and mortality.New strategies are needed for the treatment of peritumoral edema in glioma.Endostatin has been proven to be beneficial as an anti-angiogenic agent in experimental gliomas,but the effects are unclear.This study aimed to investigate the effects of endostatin on C6 glioma-induced edema.Methods Tumorigenic mice were established by subcutaneous injection of three glioma cell lines,C6-null cells and stable transfected-C6 cells overexpressing mock vector (C6-mock cells) and endostatin (C6-endo cells).Endostatin expression in xenograft C6 glioma was determined by immunostaining and Western blotting.Glioma-induced edema and tumor vessel permeability were assayed.The effect of endostatin on vascular enodothelial growth factor (VEGF) expression in vivo was analyzed by quantitative polymerase chain reaction (Q-PCR) and enzyme-linked immunosorbent assay (ELISA).The number of vesiculo-vascuolar organelles (VVOs) formed in tumor endothelia was calculated using electron microscopy.Data were analyzed by using one-way analysis of variance (ANOVA) followed by Dunnett's post hoc test for multiple comparisons to the control groups.Results Overexpression of endostatin (C6-endo cells) significantly suppressed tumor growth and reduced tumor edema and vessel permeability.ELISA analysis showed that the level of VEGF protein was markedly decreased in tumor from C6-endo cells compared with tumor from C6-null cells and C6-mock cells.Similar results were obtained by Q-PCR.Furthermore,the number of VVOs observed in tumor from C6-endo mice was significantly reduced compared with tumor from C6-null cells or C6-mock cells.Conclusions Our data provide primary evidence that endostatin reduces glioma-induced edema and vascular permeability.Using endostatin may be an effective strategy for treating glioma edema.

  13. Volatile anesthetics influence blood-brain barrier integrity by modulation of tight junction protein expression in traumatic brain injury.

    Directory of Open Access Journals (Sweden)

    Serge C Thal

    Full Text Available Disruption of the blood-brain barrier (BBB results in cerebral edema formation, which is a major cause for high mortality after traumatic brain injury (TBI. As anesthetic care is mandatory in patients suffering from severe TBI it may be important to elucidate the effect of different anesthetics on cerebral edema formation. Tight junction proteins (TJ such as zonula occludens-1 (ZO-1 and claudin-5 (cl5 play a central role for BBB stability. First, the influence of the volatile anesthetics sevoflurane and isoflurane on in-vitro BBB integrity was investigated by quantification of the electrical resistance (TEER in murine brain endothelial monolayers and neurovascular co-cultures of the BBB. Secondly brain edema and TJ expression of ZO-1 and cl5 were measured in-vivo after exposure towards volatile anesthetics in native mice and after controlled cortical impact (CCI. In in-vitro endothelial monocultures, both anesthetics significantly reduced TEER within 24 hours after exposure. In BBB co-cultures mimicking the neurovascular unit (NVU volatile anesthetics had no impact on TEER. In healthy mice, anesthesia did not influence brain water content and TJ expression, while 24 hours after CCI brain water content increased significantly stronger with isoflurane compared to sevoflurane. In line with the brain edema data, ZO-1 expression was significantly higher in sevoflurane compared to isoflurane exposed CCI animals. Immunohistochemical analyses revealed disruption of ZO-1 at the cerebrovascular level, while cl5 was less affected in the pericontusional area. The study demonstrates that anesthetics influence brain edema formation after experimental TBI. This effect may be attributed to modulation of BBB permeability by differential TJ protein expression. Therefore, selection of anesthetics may influence the barrier function and introduce a strong bias in experimental research on pathophysiology of BBB dysfunction. Future research is required to investigate

  14. Edema in the retropharyngeal space associated with head and neck tumors: CT imaging characteristics

    Energy Technology Data Exchange (ETDEWEB)

    Kurihara, Noriko; Nakamura, Mamoru; Tsuda, Masashi; Saito, Haruo [National Hospital Organization Sendai Medical Center, Department of Radiology, Sendai, Miyagi (Japan); Takahashi, Shoki; Higano, Shuichi [Tohoku University, Department of Diagnostic Radiology, Sendai, Miyagi (Japan)

    2005-08-01

    To determine computed tomographic (CT) imaging characteristics of retropharygeal edema, we reviewed CT images in 18 patients with head and neck tumors. Retropharyngeal edema spread craniocaudally between soft palate and upper half of thyroid cartilage in all patients. No edema fluid extended above soft palate and below thyroid cartilage. Horizontally, it spread symmetrically in ten and asymmetrically in eight patients. Predominance in asymmetrical retropharyngeal edema was found on the same side as that of unilateral predominance both in lymph nodes enlargement and jugular vein stenosis/occlusion. All patients had edema also in other cervical spaces. Edema of retropharyngeal and other spaces fluctuated synchronously. In 14 patients, as primary lesion and/or cervical lymph nodes regressed, retropharyngeal edema disappeared or decreased. Retropharyngeal edema had some imaging characteristics. With knowledge of that, we could avoid diagnostic confusion when evaluating head and neck CT images. (orig.)

  15. Multifocal electroretinogram in evaluating retinal function of diabetic macular edema after pars plana vitrectomy

    Institute of Scientific and Technical Information of China (English)

    马进; 吴德正; 高汝龙; 吕林; 张少冲; 文峰; 黄时洲

    2004-01-01

    @@ Beneficial effects of vitrectomy for diabetic macular edema (DME) have been demonstrated in a series of clinical trials. Vitreous surgery is useful in reducing the edema and improving visual acuity.

  16. Treatment of Traumatic Brain Injury by Localized Application of Sub-atmospheric Pressure to the Site of Cortical Impact

    Science.gov (United States)

    2013-07-01

    Resuscitation (MTR – the controlled application of vacuum) to the cerebral cortex following a controlled cortical impact (CCI) injury reduces brain... edema and the extent of injury, modulates metabolites in injured neuronal tissues, preserves neuronal tissue, and improves functional recovery. The...hyperintense region ipsilateral to the injured site. There was a large area of T2 hyperintensity ( edema ) sometimes associated with hypointensity

  17. Effects of angiopoietin-1 on hemorrhagic transformation and cerebral edema after tissue plasminogen activator treatment for ischemic stroke in rats.

    Science.gov (United States)

    Kawamura, Kunio; Takahashi, Tetsuya; Kanazawa, Masato; Igarashi, Hironaka; Nakada, Tsutomu; Nishizawa, Masatoyo; Shimohata, Takayoshi

    2014-01-01

    An angiogenesis factor, angiopoietin-1 (Ang1), is associated with the blood-brain barrier (BBB) disruption after focal cerebral ischemia. However, whether hemorrhagic transformation and cerebral edema after tissue plasminogen activator (tPA) treatment are related to the decrease in Ang1 expression in the BBB remains unknown. We hypothesized that administering Ang1 might attenuate hemorrhagic transformation and cerebral edema after tPA treatment by stabilizing blood vessels and inhibiting hyperpermeability. Sprague-Dawley rats subjected to thromboembolic focal cerebral ischemia were assigned to a permanent ischemia group (permanent middle cerebral artery occlusion; PMCAO) and groups treated with tPA at 1 h or 4 h after ischemia. Endogenous Ang1 expression was observed in pericytes, astrocytes, and neuronal cells. Western blot analyses revealed that Ang1 expression levels on the ischemic side of the cerebral cortex were decreased in the tPA-1h, tPA-4h, and PMCAO groups as compared to those in the control group (P = 0.014, 0.003, and 0.014, respectively). Ang1-positive vessel densities in the tPA-4h and PMCAO groups were less than that in the control group (p = 0.002 and cerebral homogenate (p = 0.007) and cerebral edema due to BBB damage (p = 0.038), as compared to administering COMP protein alone. In conclusion, Ang1 might be a promising target molecule for developing vasoprotective therapies for controlling hemorrhagic transformation and cerebral edema after tPA treatment.

  18. 脑创伤后脑水肿52例临床分析%Progress procedure of cerebral edema and clinical analysis of 52 cerebral trauma patients

    Institute of Scientific and Technical Information of China (English)

    李岩

    2012-01-01

    目的 了解脑创伤后不同时间窗内脑水肿和肿胀的发展过程及与预后的关系.方法 结合52例经CT和手术证实有脑水肿的脑外伤患者影像资料和术中所见,对其预后情况进行分析.结果 脑水肿较轻者,预后相对较好,11例恶性脑膨胀者,10例死亡,1例植物生存.结论 脑创伤后出现水肿-脑压高-脑缺血、缺氧-脑水肿的恶性循环而使脑水肿-脑肿胀-恶性脑膨胀,病情进行性恶化,应采取有效手段阻止颅内压进行性增高.%Objective To understand cerebral edema and development procedure of different time windows.Methods To analyze their prognosis through image document and operation findings of 52 cerebral trauma patients which were confirmed cerebral edema by CT and operation.Results he light cerebral oedema patients have a better prognosis,10 patients died and 1 patient became a plant man in 11 malignant brain dilatation patients.Conclusion The infernal circle of high brain pressure-cerebral ischemia,cerebral anoxia-cerebral edema result in cerebral edema-brain dilatation-malignant brain dilatation after cerebral trauma which leads to unremitting aggravated pathogenefic condition.So effective means should be used to interrupt the unremitting heightening ICP.

  19. Glyburide in Treating Malignant Cerebral Edema. Blocking Sulfonyl Urea One (SUR1) Receptors

    OpenAIRE

    Pallan, Tony V; Ahmed, Iftekhar

    2014-01-01

    Cerebral edema is a serious side effect of malignant stroke. On average 70,000 patients are diagnosed with malignant cerebral edema every year, of those patients, approximately 60-80% results in fatalities. The treatment of cerebral edema includes multimodality approaches.

  20. Imaging Findings Associated with Space-Occupying Edema in Patients with Large Middle Cerebral Artery Infarcts

    NARCIS (Netherlands)

    Horsch, A D; Dankbaar, J W; Stemerdink, T A; Bennink, E; van Seeters, T; Kappelle, L J; Hofmeijer, J; de Jong, H W; van der Graaf, Y; Velthuis, B K

    2016-01-01

    BACKGROUND AND PURPOSE: Prominent space-occupying cerebral edema is a devastating complication occurring in some but not all patients with large MCA infarcts. It is unclear why differences in the extent of edema exist. Better knowledge of factors related to prominent edema formation could aid treatm

  1. 9 CFR 309.8 - Cattle affected with anasarca and generalized edema.

    Science.gov (United States)

    2010-01-01

    ... generalized edema. 309.8 Section 309.8 Animals and Animal Products FOOD SAFETY AND INSPECTION SERVICE... anasarca and generalized edema. All cattle found on ante-mortem inspection to be affected with anasarca in advanced stages and characterized by an extensive and generalized edema shall be identified as...

  2. Grid pattern Argon Laser photocoagulation for diabetic diffuse macular edema

    Directory of Open Access Journals (Sweden)

    Karkhane R

    1998-05-01

    Full Text Available Purpose: to determine the effect of Grid pattern laser photocoagulation on diabetic diffuse macular edema with assessment of visual outcome. Patients & Methods: The author reviewed the medical records of 84 eyes of 62 patients with diabetic diffuse macular edema treated with Grid pattern green Argon laser photocoagulation in Farabi Eye Hospital between the years 1992-1995, the follow-up period was 16-48 months (average 24.55±6.42, median 28 mounths. Results: Visual acuity was improved in 11.9%; unchanged in 65.4% and worsened in 22.7% of eyes. Conclusion: In assessing long-term visual outcome, Grid laser photocoagulation is an effective modality in maintaining or improving visual acuity.

  3. Emma Kohman and the early history of nutritional edema.

    Science.gov (United States)

    Bing, F C

    1983-06-01

    Nutritional edema is a generalized edematous condition that afflicted whole populations of central European countries during World War 1--and other areas since that time--with a mortality rate of about 50%. An analogous condition in white rats was produced by Emma Kohman as a graduate student in Chicago (1916 to 1919). She fed the rats a diet similar to that consumed by human subjects but prevented or cured nutritional edema in the animals by feeding them good quality protein in suitable amounts. Her work, verified by others, was of immense practical significance and helped establish the value of animal experiments in the study of human diseases. Ms. Kohman gave up a scientific career to be a homemaker when she married in 1919.

  4. An index of pulmonary edema measured with emission computed tomography

    Energy Technology Data Exchange (ETDEWEB)

    Ahluwalia, B.D.; Brownell, G.L.; Hales, C.A.; Kazemi, H.

    1981-10-01

    Positron camera and short-lived biological isotopes are used to obtain transverse sections of lung volume, blood volume, and total lung water of dog lungs to assess the degree of pulmonary edema in normal and edematous dogs. At equilibration with specific isotope, 30 equally spaced angular profiles of the distribution are collected to obtain transverse section images. Emission computed number is obtained in the lung and heart areas for the images obtained with an intravascular marker (11CO) and intra- and extravascular marker (C15O2). The emission computed number ratio of lung to heart for C15O2 images is an index that is related to degree of edema. Emission computed number related to extravascular water can be obtained from normalized (C15O2--11CO) scintigrams. The technique is noninvasive.

  5. Cerebellar infarct with neurogenic pulmonary edema following viper bite

    Directory of Open Access Journals (Sweden)

    Salil Gupta

    2012-01-01

    Full Text Available Russell′s viper (Daboia russelli bites are well known to cause bleeding complications. However, thrombotic complications are rare. We present the case details of a female who was bitten by a Russell′s viper (Daboia russelli in her village. She then developed features of envenomation in the form of hemorrhagic episodes. She received 27 vials of polyvalent anti-snake venom to which the hemorrhagic complications responded. After about 48 h of the bite she developed features of cerebellar infarct along with pulmonary edema which was in all probability neurogenic in origin. She was managed with mechanical ventilation and extra ventricular drainage with good recovery. We discuss the likely pathogenesis of the infarct and pulmonary edema occurring in a patient with viper bite and other features of envenomation.

  6. Aripiprazole induced non-cardiogenic pulmonary edema: a case report.

    Science.gov (United States)

    Cetin, Mustafa; Celik, Mustafa; Cakıcı, Musa; Polat, Mustafa; Suner, Arif

    2014-01-01

    Aripiprazole is a second-generation antipsychotic drug with partial dopamine agonistic activity. Although the adverse cardiovascular effects of both typical and atypical antipsychotics are well known, similar data on aripiprazole, which was recently introduced, are scarce. Herein we report a 35-year-old female that presented to our emergency department with non-cardiogenic pulmonary edema. Chest X-ray and thoracic CT showed pulmonary edema and bilateral pleural effusion. Anamnesis showed that she had been taking sertraline 200 mg d-1 for obsessive-compulsive disorder for a long time and that aripiprazole10 mg d-1 was added for augmentation 2 months prior to presentation. We think that the CYP 2D6 inhibitor sertraline might have played a role in increasing the plasma concentration and toxicity of aripiprazole in the presented patient.

  7. Acute Pulmonary Edema in Patients with Cushing’s Syndrome

    OpenAIRE

    Mitra Niafar; Mehrnoush Toufan; Nooshin Milanchian; Farhad Niafar; Kavous Shahsavari Nia

    2015-01-01

    Introduction Dyspnea refers to difficulty in breathing, and short and shallow breaths. This sign is seen in numerous diseases due to pulmonary, cardiac, metabolic and neurological causes. Among cardiac causes, heart failure is considered the main cause of dyspnea. Cardiac failure is a clinical syndrome associated with a set of symptoms (dyspnea, and fatigue) and signs (edema and rales). Common causes of cardiac failure include: myocardial infarction, ischemic heart disease, hypertensi...

  8. Pulmonary tissue volume in dogs during pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Peterson, B.T.; Petrini, M.F.; Hyde, R.W.; Schreiner, B.F.

    1978-01-01

    Pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured in anesthetized dogs by analyzing end-expiratory concentrations of dimethyl ether (DME), acetylene (C/sub 2/H/sub 2/), and sulfur hexafluoride during a 30-s rebreathing maneuver. Vt was compared to the postmortem lung weight of control dogs and dogs with hemodynamic and nonhemodynamic (alloxan) pulmonary edema. Qc was compared to the cardiac output measured by dye dilution. A 100 ml increase in alveolar volume (Va) in the range of 1 to 2 liters resulted in a 9 +- 3 ml increase in Vt. Vt measured at a Va of 1.9 liters measures 114 +- 18% of the postmortem lung weight in 20 control dogs and in 6 dogs with moderate edema (lung weight <250% of predicted). Vt measured only 53 +- 14% of the lung weight in 11 dogs with more severe edema. DME and C/sub 2/H/sub 2/ gave the same mean values of Vt, but the reproducibility of a series of 3 to 7 measurements was greater with DME (coefficient of variation was 5% with DME and 8% C/sub 2/H/sub 2/). Qc measured 96 +- 15% of the cardiac output during the rebreathing maneuver, but the maneuver caused a 4 to 40% fall in the cardiac output. These data show that Vt determined by rebreathing DME is between 86% and 135% of the lung weight in dogs with pulmonary edema until the lung weight is greater than 250% of the predicted value.

  9. Positional shifting of HRCT findings in patients with pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Young Sun; Choi, Yo Won; Jeon, Seok Chol; Park, Choong Ki; Seo, Heung Suk; Lee, Seung Rho; Hahm, Chang Kok [Hanyang Univ. College of Medicine, Seoul (Korea, Republic of)

    2001-03-01

    To assess the value of positional shifting to a gravity-dependent area, as revealed by HRCT, in differentiating pulmonary edema (PE) from other conditions. Sixteen consecutive patients in whom plain radiographs suggested the presence of pulmonary edema but the clinical findings were indefinite underwent HRCT of the lung. For initial scanning they were in the supine position, and then in the prone position. Findings of ground-glass opacity, interlobular septal thickening and peribronchovascular interistitial thickening were analyzed in terms of the presence and degree of shifting to a gravity-dependent area, a grade of high, intermediate or low being assigned. PE was diagnosed in 8 of 16 cases, the remainder being designated as non-pulmonary edema (NPE). Ground-glass opacity was observed in all 16, while the degree of positional shifting was found to be high in ten (PE:NPE=6:4), intermediate in four (PE:NPE=2:2), and low in two (PE:NPE=0:2). There was no significant difference between the two groups ({rho} > 0.05). Interlobular septal thickening was observed in all but two NPE cases; the degree of shifting was high in six (PE:NPE=6:0), intermediate in one (PE), and low in seven (PE:NPE=1:6). Shifting was significantly more prominent in PE than in NPE case ({rho} <0.05). Peribronchovascular interstitial thickening was positive in all PE cases and one NPE case, with no positional shifting. Positional shifting of interlobular septal thickening to a gravity-dependent area, as demonstrated by HRCT, is the most specific indicator of pulmonary edema.

  10. Updates in the Management of Diabetic Macular Edema

    OpenAIRE

    Christopher Mathew; Anastasia Yunirakasiwi; Srinivasan Sanjay

    2015-01-01

    Diabetes mellitus is a chronic disease which has multiple effects on different end-organs, including the retina. In this paper, we discuss updates on diabetic macular edema (DME) and the management options. The underlying pathology of DME is the leakage of exudates from retinal microaneurysms, which trigger subsequent inflammatory reactions. Both clinical and imaging techniques are useful in diagnosing, classifying, and gauging the severity of DME. We performed a comprehensive literature sear...

  11. Radionuclide lymphoscintigraphy in the evaluation of peripheral edema

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Soon; Zeon, Seok Kil [School of Medicine, Keimyung Univ., Daegu (Korea, Republic of)

    2000-07-01

    It has been difficulty to visualize lymphatics in living patients. Conventional or direct lymphography has been the gold standard for delineation of the lymphatic system, but this procedure is invasive, difficulty to perform, and harmful to the lymphatic vascular endothelium. The aim of our study was to determine its severity, and to understand the drainage patterns on patients with peripheral edema by functional lymphatic studies. Tc-99m antimony sulfide colloid 25 MBq with 0.4 ml volume was injected intradermally in the first, second and third web space of the foot or hand in 40 patients with peripheral edema (5 in upper extremity and 35 in lower extremity). Initial flow after injection and whole body images at approximately 30 minutes. 1-4 hours were obtained. In 9/40 cases with peripheral edema normal lymphoscintigram were revealed, primary lymphedema was observed in 5/31 cases. The imaging patterns in primary lymphedema were absent (3 cases) or delayed (2 cases) transport, lymphatic duct dilatation (1), cutoff (1), decrease in size and number of lymph nodes (2). The Common caused of edema in secondry lymphedema (26/31) were carcinoma (13), inflammation (5), post-operation (5), and unknown origin (3). The common imaging findings in carcinoma showed non-visualization of lymph nodes (13), dermal backflow (8), collateral circulation (5), and in inflammation lymphatic obstruction (2), increase in size and number of lymph nodes (2), delayed transport (1), and in post-operation dermal backflow (3), delayed transport (2), decrease in number and size of lymph node (2) Clear images patterns were observed difference between primary lymphedema an secondary lymphedema. Radionuclide lymphoscintigraphy is essentially non-invasive, easy to perform repeatedly, and harmless to the lymphatic vascular endothelium for evaluation of a patient with lymphedema.

  12. Pulmonary tissue volume in dogs during pulmonary edema.

    Science.gov (United States)

    Peterson, B T; Petrini, M F; Hyde, R W; Schreiner, B F

    1978-05-01

    Pulmonary tissue volume (Vt) and pulmonary capillary blood flow (Qc) were measured in anesthetized dogs by analyzing end-expiratory concentrations of dimethyl ether (DME), acetylene (C2H2), and sulfur hexafluoride during a 30-s rebreathing maneuver. Vt was compared to the postmortem lung weight of control dogs and dogs with hemodynamic and nonhemodynamic (alloxan) pulmonary edema. Qc was compared to the cardiac output measured by dye dilution. A 100-ml increase in alveolar volume (VA) in the range of 1-2 liters resulted in a 9 +/- 3 ml increase in Vt. Vt measured at a VA of 1.9 liters measures 114 +/- 18% of the postmortem lung weight in 20 control dogs and in 6 dogs with moderate edema (lung weight smae mean values of Vt, but the reproducibility of a series of 3-7 measurements was greater with DME (coefficient of variation was 5% with DME and 8% C2H2). Qc measured 96 +/ 15% of the cardiac output during the rebreathing maneuver, but the maneuver caused a 4-40% fall in the cardiac output. These data show that Vt determined by rebreathing DME is between 86% and 135% of the lung weight in dogs with pulmonary edema until the lung weight is greater than 250% of the predicted value.

  13. A Case Report of Acute Hemorrhagic Edema of Infancy

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    M. Safari

    2005-10-01

    Full Text Available Introduction: Acute hemorrhagic edema of infancy is an acute and rare cutaneous disorder that affects children between 4 months to 2 years of age and characterized by cutaneous purpuric lesions with millimeters to centimeters diameter. Systemic involvement is rare. The disease is benign and spontaneously resolved in 1-3 weeks.Case Report: Here we described a 22-months old girl with acute hemorrhagic edema of infancy who hospitalized in department of pediatric with the presence of erythematous-purpuric lesions localized on the face, ears and lower limbs that developed suddenly two days before hospitalization. Laboratory examination revealed including normal cell blood counts, serum complements, serum electrolytes and creatinin. ANA was negative. Coagulation tests were normal. ESR was 45 mm/h. Urine analysis and stool examination revealed no abnormal findings. Disease resolved spontaneously without any problem.Conclusion: According to the contrast between the acuteness of the cutaneous sign, which are typical and unmistakable, and the general condition of the patient, which was good and the laboratory findings, our patient labeled as acute hemprrhagic edema of infancy.

  14. Management of upper airway edema caused by hereditary angioedema

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    Farkas Henriette

    2010-07-01

    Full Text Available Abstract Hereditary angioedema is a rare disorder with a genetic background involving mutations in the genes encoding C1-INH and of factor XII. Its etiology is unknown in a proportion of cases. Recurrent edema formation may involve the subcutis and the submucosa - the latter can produce obstruction in the upper airways and thereby lead to life-threatening asphyxia. This is the reason for the high, 30-to 50-per-cent mortality of undiagnosed or improperly managed cases. Airway obstruction can be prevented through early diagnosis, meaningful patient information, timely recognition of initial symptoms, state-of-the-art emergency therapy, and close monitoring of the patient. Prophylaxis can substantially mitigate the risk of upper airway edema and also improve the patients' quality of life. Notwithstanding the foregoing, any form of upper airway edema should be regarded as a potentially life-threatening condition. None of the currently available prophylactic modalities is capable of preventing UAE with absolute certainty.

  15. Postobstructive pulmonary edema after biopsy of a nasopharyngeal mass

    Science.gov (United States)

    Mehta, Keyur Kamlesh; Ahmad, Sabina Qureshi; Shah, Vikas; Lee, Haesoon

    2015-01-01

    We describe a case of 17 year-old male with a nasopharyngeal rhabdomyosarcoma who developed postobstructive pulmonary edema (POPE) after removing the endotracheal tube following biopsy. He developed muffled voice, rhinorrhea, dysphagia, odynophagia, and difficulty breathing through nose and weight loss of 20 pounds in the preceding 2 months. A nasopharyngoscopy revealed a fleshy nasopharyngeal mass compressing the soft and hard palate. Head and neck MRI revealed a large mass in the nasopharynx extending into the bilateral choana and oropharynx. Biopsy of the mass was taken under general anesthesia with endotracheal intubation. Immediately after extubation he developed oxygen desaturation, which did not improve with bag mask ventilation with 100% of oxygen, but improved after a dose of succinylcholine. He was re-intubated and pink, frothy fluid was suctioned from the endotracheal tube. Chest radiograph (CXR) was suggestive of an acute pulmonary edema. He improved with mechanical ventilation and intravenous furosemide. His pulmonary edema resolved over the next 24 h. POPE is a rare but serious complication associated with upper airway obstruction. The pathophysiology of POPE involves hemodynamic changes occurring in the lung and the heart during forceful inspiration against a closed airway due to an acute or chronic airway obstruction. This case illustrates the importance of considering the development of POPE with general anesthesia, laryngospasm and removal of endotracheal tube to make prompt diagnosis and to initiate appropriate management. PMID:26744691

  16. Postobstructive pulmonary edema after biopsy of a nasopharyngeal mass

    Directory of Open Access Journals (Sweden)

    Keyur Kamlesh Mehta

    2015-01-01

    Full Text Available We describe a case of 17 year-old male with a nasopharyngeal rhabdomyosarcoma who developed postobstructive pulmonary edema (POPE after removing the endotracheal tube following biopsy. He developed muffled voice, rhinorrhea, dysphagia, odynophagia, and difficulty breathing through nose and weight loss of 20 pounds in the preceding 2 months. A nasopharyngoscopy revealed a fleshy nasopharyngeal mass compressing the soft and hard palate. Head and neck MRI revealed a large mass in the nasopharynx extending into the bilateral choana and oropharynx. Biopsy of the mass was taken under general anesthesia with endotracheal intubation. Immediately after extubation he developed oxygen desaturation, which did not improve with bag mask ventilation with 100% of oxygen, but improved after a dose of succinylcholine. He was re-intubated and pink, frothy fluid was suctioned from the endotracheal tube. Chest radiograph (CXR was suggestive of an acute pulmonary edema. He improved with mechanical ventilation and intravenous furosemide. His pulmonary edema resolved over the next 24 h. POPE is a rare but serious complication associated with upper airway obstruction. The pathophysiology of POPE involves hemodynamic changes occurring in the lung and the heart during forceful inspiration against a closed airway due to an acute or chronic airway obstruction. This case illustrates the importance of considering the development of POPE with general anesthesia, laryngospasm and removal of endotracheal tube to make prompt diagnosis and to initiate appropriate management.

  17. [Acute heart failure: acute cardiogenic pulmonary edema and cardiogenic shock].

    Science.gov (United States)

    Sánchez Marteles, Marta; Urrutia, Agustín

    2014-03-01

    Acute cardiogenic pulmonary edema and cardiogenic shock are two of the main forms of presentation of acute heart failure. Both entities are serious, with high mortality, and require early diagnosis and prompt and aggressive management. Acute pulmonary edema is due to the passage of fluid through the alveolarcapillary membrane and is usually the result of an acute cardiac episode. Correct evaluation and clinical identification of the process is essential in the management of acute pulmonary edema. The initial aim of treatment is to ensure hemodynamic stability and to correct hypoxemia. Other measures that can be used are vasodilators such as nitroglycerin, loop diuretics and, in specific instances, opioids. Cardiogenic shock is characterized by sustained hypoperfusion, pulmonary wedge pressure > 18 mmHg and a cardiac index 30 mmHg) and absent or reduced diuresis (< 0.5 ml/kg/h). The most common cause is left ventricular failure due to acute myocardial infarction. Treatment consists of general measures to reverse acidosis and hypoxemia, as well as the use of vasopressors and inotropic drugs. Early coronary revascularization has been demonstrated to improve survival in shock associated with ischaemic heart disease.

  18. Update on high altitude cerebral edema including recent work on the eye.

    Science.gov (United States)

    Willmann, Gabriel; Gekeler, Florian; Schommer, Kai; Bärtsch, Peter

    2014-06-01

    This review summarizes recent research on high altitude cerebral edema (HACE) and on the eye with focus on the retina and optic nerve as visible brain tissue at high altitude. Hemosiderin deposits in the corpus callosum have been characterized as rather specific long-lasting footprints of HACE, indicating a leak of the blood-brain barrier (BBB) and resulting in microhemorrhages. These are compatible with the concept of increased capillary pressure due to venous outflow limitation as suggested by Wilson et al. There are no human data on the role of vascular permeability in HACE, while animal models of uncertain relevance for human HACE suggest that an impaired integrity of the BBB through VEGF and ROS is more important than hemodynamic changes. Examinations by ultrasound show an inconsistent increase of the optic nerve sheath diameter, whereas unequivocal optic disc swelling (ODS), increased retinal vessel diameter, as well as retinal vessel leakage occur at high altitude. However, whether these morphological changes correlate with symptoms of AMS as a possible precursor of HACE or high altitude headache supporting the concept of venous outflow limitation remains questionable and is discussed in detail in this article.

  19. 幼年鼠内毒素性脑水肿模型及脑组织钙离子和钙调素表达的研究%Intracellular free calcium and calmodulin expression in a brain edema model induced by endotoxin in infant rats

    Institute of Scientific and Technical Information of China (English)

    李梅; 蔡方成

    2003-01-01

    目的:建立简单、易复制的幼年鼠内毒素性脑水肿模型,并从Ca2+、钙调素(CaM)水平探讨脑水肿的发生发展.方法:45只幼鼠,随机分内毒素组(36只)和对照组(9只),分别于腹腔内注射内毒素(LPS)10mg/kg和等容量生理盐水,并用电镜观察其病理、用常规生化法测定脑含水量和伊文氏蓝(EB)含量、用荧光标记术和免疫印迹法分别测定脑组织细胞内[Ca2+]和CaM表达.结果:脑组织含水量和EB含量显著高于对照组;细胞内[Ca2+]明显增高,脑组织CaM表达增强;电镜显示血脑屏障(Blood-brain barrier,BBB)受损、神经元变性、胶质细胞肿胀、坏死等特征.结论:LPS导致了BBB通透性改变,并引起了混合性脑水肿.LPS引起了细胞内[Ca2+]增高,并激活了CaM,从而启动了Ca2+-CaM信号通路,这可能与其增加BBB通透性并导致脑水肿形成有密切关系.

  20. Edema cerebral crônico na neurocisticercose

    Directory of Open Access Journals (Sweden)

    AGAPEJEV SVETLANA

    1998-01-01

    Full Text Available Neste estudo retrospectivo, relatam-se as características clínicas do edema cerebral crônico (ECCr em 34 pacientes com neurocisticercose (NCC, que apresentavam edema cerebral difuso, à tomografia computadorizada (TC, como característica comum. Todos foram tratados com dextroclorofeniramina e, 32 deles, com albendazol. O ECCr predominou no sexo feminino (73,5% na faixa etária dos 11 - 40 anos (92,3%. A cefaléia ocorreu em 94,1% dos pacientes, náuseas/vômitos em 47,1%, crises epilépticas em 41,1% e distúrbios psíquicos em 38,2%. A hiperreflexia ocorreu em 82,3% e o papiledema em 58,8% e o exame neurológico normal em 11,8%. Na TC, o edema esteve associado a calcificações em 61,8% dos casos. As pressões liquóricas foram mais elevadas (p< 0,05 antes do tratamento. Atualmente, estão assintomáticos, ou com melhora clínica, 79,4% dos pacientes (57,1% deles sem medicação. Discute-se a possibilidade do ECCr, na NCC, ser uma manifestação antigênica, sem a presença concomitante de cistos parasitários, e poder representar mais uma condição clínica associada à hipertensão intracraniana benigna.

  1. Preventive treatment of alveolar pulmonary edema of cardiogenic origin

    Institute of Scientific and Technical Information of China (English)

    Gideon Charach; Michael Shochat; Alexander Rabinovich; Oded Ayzenberg; Jacob George; Lior Charach; Pavel Rabinovich

    2012-01-01

    Objective To evaluate the efficacy of preventive treatment (PT) on alveolar pulmonary edema (APE) of cardiogenic origin using a monitor based on principles of internal thoracic impedance (ITI) measurements. Methods We conducted blinded clinical trials on patients with ST-elevation myocardial infarction (STEMI) and monitored whether the condition would progress to APE. ITI was measured noninvasively by the Edema Guard Monitor (EGM, model RS-207) every 30 min. The measurement threshold for the diagnosis of APE was fixed at > 12% decrease in ITI from baseline as described in our methodology. The patients were divided into one group that received standard treatment after the appearance of clinical signs of APE without considering the prediction of APE by EGM devise (Group 1), and another group of asymptomatic patients in whom development of APE was predicted by using only EGM measurements (Group 2). The latter participants' PT consisted of furosemide, intravenous nitroglycerine and supplemental oxygen. Results One-hundred and fifty patients with acute STEMI were enrolled into this study. Group 1 included 100 patients (53% males, age 64.1 ± 12.6 years). Treatment was started after the clinical appearance of overt signs of APE. Group 2 included 50 patients (54% males, age 65.2 ± 11.9 years) who received PT based on EGM measurements. Group 2 had significantly fewer cases of APE (n = 4, 8%) than Group 1 (n = 100, 100%) (P > 0.001). While APE was lethal in six (6%) Group 1 patients, PT resulted in prompt resolution of APE in all four (8%) Group 2 patients. Conclusion ITI is a useful modality for early diagnosis and PT of pulmonary edema of cardiogenic origin.

  2. Pulmonary edema following transcatheter closure of atrial septal defect

    Directory of Open Access Journals (Sweden)

    Keerthi Chigurupati

    2015-01-01

    Full Text Available We describe an incident of development of acute pulmonary edema after the device closure of a secundum atrial septal defect in a 52-year-old lady, which was treated with inotropes, diuretics and artificial ventilation. Possibility of acute left ventricular dysfunction should be considered after the defect closure in the middle-aged patients as the left ventricular compliance may be reduced due to increased elastic stiffness and diastolic dysfunction. Baseline left atrial pressure may be > 10 mmHg in these patients. Associated risk factors for the left ventricular dysfunction are a large Qp:Qs ratio, systemic hypertension, severe pulmonary hypertension and paroxysmal atrial fibrillation.

  3. Practice management of french retinal specialists in diabetic macular edema

    OpenAIRE

    QU-KNAFO, Mo lise

    2015-01-01

    Purpose: To evaluate the practice management of french vitreoretinal (VR) specialists in the treatment of diabetic macular edema (DME)Methods: A 31-item survey investigating real life practice in diagnosis and treatment of DME was mailed to specialists identified from the Société Française d’Ophtalmologie and the Club Francophone des Spécialistes de la Rétine. Answers were analysed anonymously by an online survey software. Results: 95 specialists answered the survey. 25%, 36% and 32% of respo...

  4. Acute Pulmonary Edema Caused by a Giant Atrial Myxoma

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    Andrea Fisicaro

    2013-01-01

    Full Text Available Atrial myxoma is the most common primary cardiac tumor. Its clinical presentation spreads from asymptomatic incidental mass to serious life-threatening cardiovascular complications. We report the case of a 44-year-old man with evening fever and worsening dyspnea in the last weeks, admitted to our hospital for acute pulmonary edema. The cardiac auscultation was very suspicious for mitral valve stenosis, but the echocardiography revealed a huge atrial mass with a diastolic prolapse into mitral valve orifice causing an extremely high transmitral gradient pressure. Awareness of this uncommon acute presentation of atrial myxoma is necessary for timely diagnosis and prompt surgical intervention.

  5. Pulmonary edema following transcatheter closure of atrial septal defect

    Science.gov (United States)

    Chigurupati, Keerthi; Reshmi, Liza Jose; Gadhinglajkar, Shrinivas; Venkateshwaran, S.; Sreedhar, Rupa

    2015-01-01

    We describe an incident of development of acute pulmonary edema after the device closure of a secundum atrial septal defect in a 52-year-old lady, which was treated with inotropes, diuretics and artificial ventilation. Possibility of acute left ventricular dysfunction should be considered after the defect closure in the middle-aged patients as the left ventricular compliance may be reduced due to increased elastic stiffness and diastolic dysfunction. Baseline left atrial pressure may be > 10 mmHg in these patients. Associated risk factors for the left ventricular dysfunction are a large Qp:Qs ratio, systemic hypertension, severe pulmonary hypertension and paroxysmal atrial fibrillation. PMID:26139760

  6. Negative Pressure Pulmonary Edema Associated with Anterior Cervical Spine Surgery

    Science.gov (United States)

    Yoneda, Masana; Tanaka, Yasuhito

    2014-01-01

    We report a very rare case of negative pressure pulmonary edema (NPPE) that occurred immediately after anterior cervical discectomy and fusion (ACDF). The patient was a 25-year-old man who sustained a facet fracture-dislocation of C5 during a traffic accident. After ACDF, he developed NPPE and needed mechanical ventilation. Fortunately, he recovered fully within 24 hours. NPPE is a rare postoperative complication that may occur after cervical spine surgery. The aims of this report are to present information regarding the diagnosis and emergent treatment of NPPE, and to review the previous literature regarding this serious complication. PMID:25558327

  7. Is High Altitude Pulmonary Edema Relevant to Hawai‘i?

    Science.gov (United States)

    2014-01-01

    High altitude clinical syndromes have been described in the medical literature but may be under recognized in the state of Hawai‘i. As tourism increases, high altitude injuries may follow given the easy access to high altitude attractions. Visitors and clinicians should be aware of the dangers associated with the rapid ascent to high altitudes in the perceived comfort of a vehicle. This paper will review the basic pathophysiology, prevention, and treatment of the most serious of the high altitude clinical syndromes, high altitude pulmonary edema. PMID:25478294

  8. Acute pulmonary edema secondary to hyperbaric oxygen therapy

    Science.gov (United States)

    Obiagwu, Chukwudi; Paul, Vishesh; Chadha, Sameer; Hollander, Gerald; Shani, Jacob

    2015-01-01

    Hyperbaric oxygen therapy (HBOT) has been shown to be effective in the treatment of diabetic ulcers, air embolism, carbon monoxide poisoning and gas gangrene with minimal adverse effects. Very few cases of HBOT causing acute pulmonary edema (PE) has been described; with a study on dogs suggesting that a complication of this therapy could be PE. We describe the case of an 80-year-old man with a history of stable systolic heart failure and diabetes mellitus presenting with acute PE following treatment with HBOT for diabetic foot. PMID:25988073

  9. Development of tolerance to ozone in reference to pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Matzen, R.N.

    1957-01-01

    Four-hr exposure to O/sub 3/ concentration as low as 0.3 ppM (but not 0.1 ppM) prevented edema and death from subsequent LD/sub 50/ exposure (8 to 9 ppM). Protection increased with increasing dose up to toxic level. Tolerance was noted at 24 hr and was present for as long as 102 days. Some protection to doses as high as 2.5 LD/sub 50/ was observed. No tolerance was developed at low concentrations because that amount probably absorbed in upper respiratory tract of the mice.

  10. Acute Pulmonary Edema Associated With Propofol: An Unusual Complication

    Science.gov (United States)

    Waheed, Mian Adnan; Oud, Lavi

    2014-01-01

    Propofol is frequently used in the emergency department to provide procedural sedation for patients undergoing various procedures and is considered to be safe when administered by trained personnel. Pulmonary edema after administration of propofol has rarely been reported. We report a case of a 23-year-old healthy male who developed acute cough, hemoptysis and hypoxia following administration of propofol for splinting of a foot fracture. Chest radiography showed bilateral patchy infiltrates. The patient was treated successfully with supportive care. This report emphasizes the importance of this potentially fatal propofol-associated complication and discusses possible underlying mechanisms and related literature. PMID:25493132

  11. Negative Pressure Pulmonary Edema After Extubation in Appendectomy: Case Report

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    Tarik Purtuloglu

    2016-01-01

    Full Text Available Negative pressure pulmonary edema (NPPE is a rare complication that can occur after acute upper airway obstruction or secondary to relax chronic upper airway obstruction and a life-threatening fatal condition. The first cause in the etiology of NPPE is developed laryngospasm after intubation or extubation, while the other causes are epiglottitis, croup, hiccups, foreign body aspiration, pharyngeal hematoma and oropharyngeal tumors. Supportive therapy is usually the only treatment. The fundamental principle of treatment is early diagnosis and to provide adequate oxygenation. Application of positive airway pressure is often provided with CPAP in most of patients, but sometimes re-intubation and mechanical ventilation may be required.

  12. [Lupus erythematosus panniculitis presenting as palpebral edema and parotiditis].

    Science.gov (United States)

    Pérez-Pastor, G; Valcuende, F; Tomás, G; Moreno, M

    2007-10-01

    Lupus erythematosus panniculitis or lupus erythematosus profundus is characterized by inflammation of the deep dermis and subcutaneous tissue. It can occur in isolation or associated with chronic systemic or discoid lupus erythematosus. It usually consists of nodules and hardened subcutaneous plaques on the forehead, cheeks, proximal extremities, and buttocks. Periorbital and parotid involvement are rare and can lead to misdiagnosis. We present the case of a patient with lupus erythematosus panniculitis who presented with palpebral edema and involvement of the periocular fat and parotid gland.

  13. Echocardiographic changes during acute pulmonary edema subsequent to scorpion sting

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    K Delma

    2012-01-01

    Full Text Available Acute pulmonary edema (APE occurring after scorpion sting is the leading cause of death of the victims of scorpion envenomation. The APE origin is still questioned by physicians treating these patients. Based on echocardiographic study of 20 patients with severe envenomation treated in Ouargla Hospital resuscitation ward during the last four years, the APE etiology seems more likely cardiogenic, referring to cardiac symptoms confirmed by echocardiography although other mechanisms may also be involved. This hypothesis is further confirmed by the positive response of patients to the administration of dobutamine.

  14. Dexamethasone intravitreal implant in the treatment of diabetic macular edema

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    Dugel PU

    2015-07-01

    Full Text Available Pravin U Dugel,1,2 Francesco Bandello,3 Anat Loewenstein4 1Retinal Consultants of Arizona, Phoenix, AZ, 2Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA; 3Department of Ophthalmology, University Vita-Salute Scientific Institute San Raffaele, Milan, Italy; 4Department of Ophthalmology, Tel Aviv Medical Center and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel Abstract: Diabetic macular edema (DME resembles a chronic, low-grade inflammatory reaction, and is characterized by blood–retinal barrier (BRB breakdown and retinal capillary leakage. Corticosteroids are of therapeutic benefit because of their anti-inflammatory, antiangiogenic, and BRB-stabilizing properties. Delivery modes include periocular and intravitreal (via pars plana injection. To offset the short intravitreal half-life of corticosteroid solutions (~3 hours and the need for frequent intravitreal injections, sustained-release intravitreal corticosteroid implants have been developed. Dexamethasone intravitreal implant provides retinal drug delivery for ≤6 months and recently has been approved for use in the treatment of DME. Pooled findings (n=1,048 from two large-scale, randomized Phase III trials indicated that dexamethasone intravitreal implant (0.35 mg and 0.7 mg administered at ≥6-month intervals produced sustained improvements in best-corrected visual acuity (BCVA and macular edema. Significantly more patients showed a ≥15-letter gain in BCVA at 3 years with dexamethasone intravitreal implant 0.35 mg and 0.7 mg than with sham injection (18.4% and 22.2% vs 12.0%. Anatomical assessments showed rapid and sustained reductions in macular edema and slowing of retinopathy progression. Phase II study findings suggest that dexamethasone intravitreal implant is effective in focal, cystoid, and diffuse DME, in vitrectomized eyes, and in combination with laser therapy. Ocular complications of

  15. Edema pulmonar agudo posoperatorio de presión negativa

    OpenAIRE

    Faridt Hernán Criollo-Muñoz; Juan José Espinosa-Espinoza

    2014-01-01

    No es extraño que durante la práctica anestésica diaria se encuentrenpacientes sin padecimientos crónicos conocidos que expliquen eldesarrollo de edema pulmonar agudo durante el perioperatorio. Eledema pulmonar de presión negativa se ha reportado en la literatura,aun en pacientes sanos, como una entidad en el perioperatorio de buenpronóstico con tratamiento oportuno multidisciplinario. Se expone elcaso de un paciente de 29 años de edad, sin antecedentes patológicosconocidos, a quien se le rea...

  16. Relationship between AQP4 expression and DWI of the cerebral ischemic edema in rats

    Institute of Scientific and Technical Information of China (English)

    鲁宏; 孙善全

    2003-01-01

    Objective: To study the correlation between aquaporin-4(AQP4) expression and diffusion-weighted imaging (DWI) in the process of ischemic brain edema for the molecular biologic mechanism of DWI. Methods: A total of 34 Wistar rats were divided into 8 groups randomly: Non-operated group (n=4), sham-operated group (n=6), and operated group, receiving right middle cerebral artery occlusion (MCAO) for 15 and 30 min, and 1, 3, 6 and 24 h respectively (6 subgroups, n=4). All groups were imaged with DWI and T2WI. The apparent diffusion coefficient (ADC), relevant density (rd) and relevant area (rs) of hyperintensity of the lesions on DWI and T2WI were measured. Relevant ADC (rADC), relevant area of immunohistochemical staining for AQP4 (rS), optical density of AQP4 hybridization (α) were calculated. After that the animals were sacrificed and perfused at different time intervals, correlations between DWI, ADC, and AQP4 expression (rS, α) in ischemic tissue was made. Results: There was a significant correlation between rS and α (r=0.949). The abnormal high intensity was found in DWI of the ipsilateral MAC territory at 15 min after MCAO. The ADC value decreased quickly within 1 h after MCAO, the rd and rs of DWI increased rapidly and the expression of AQP4 increased quickly, too. However, there was no change on the T2WI. In the period of time (15 min-1 h), the AQP4 expression(α) had a strong relation to the rd and rs( r=0.914, 0.895). With the progress of the time, the ADC value of MCAO decreased further to (2.1±0.6)×10-4 mm2/s at 3 h, and then followed an increased slowly till 24 h, but the rd and the rs as well as the expression of AQP4 continuously increased during the stage. The T2WI detected the lesion at the average time (1.4 h) after MCAO, and the rs of T2WI was less than that of DWI at the same time in the same layer (P<0.05). Conclusion: The results imply that high expression of AQP4 may play a key role in ischemic brain edema. It is, certainly, one of the

  17. Evaluation of the Prevalence of Concomitant Idiopathic Cyclic Edema and Cellulite

    OpenAIRE

    José Maria Pereira de Godoy, Maria de Fátima Guerreiro de Godoy

    2011-01-01

    The aim of this study was to evaluate the prevalence of concomitant idiopathic cyclic edema with Grade II and III cellulite. All patients treated for Grade II and III cellulite were evaluated for idiopathic cyclic edema in a retrospective, quantitative and cross-sectional study. The study was carried out at the Godoy Clinic in the period from 2006 to 2010. All patients with body mass indexes > 25, Grade I cellulite and other causes of edema were excluded. The diagnosis of idiopathic cycli...

  18. Pulmonary Edema Assessed by Ultrasound: Impact in Cardiology and Intensive Care Practice.

    Science.gov (United States)

    Blanco, Pablo A; Cianciulli, Tomás F

    2016-05-01

    Pulmonary edema is a frequent condition found in adult patients hospitalized in cardiology wards and intensive care units. Ultrasonography is a diagnostic modality with a high sensitivity for the detection of extravascular lung water, visualized as B lines, and usually caused by cardiogenic or noncardiogenic pulmonary edema. This paper highlights a simple method for the assessment of patients with pulmonary edema, which allows for a differential diagnosis of its possible mechanism and contributes to therapeutic intervention guiding and monitoring.

  19. Modeling tumor-associated edema in gliomas during anti-angiogenic therapy and its impact on imageable tumor

    Directory of Open Access Journals (Sweden)

    Andrea eHawkins-Daarud

    2013-04-01

    Full Text Available Glioblastoma, the most aggressive form of primary brain tumor is predominantly assessed with gadolinium-enhanced T1-weighted (T1Gd and T2-weighted magnetic resonance imaging (MRI. Pixel intensity enhancement on the T1Gd image is understood to correspond to the gadolinium contrast agent leaking from the tumor-induced neovasculature, while hyperintensity on the T2/FLAIR images corresponds with edema and infiltrated tumor cells. None of these modalities directly show tumor cells; rather, they capture abnormalities in the microenvironment caused by the presence of tumor cells. Thus, assessing disease response after treatments impacting the microenvironment remains challenging through the obscuring lens of MR imaging. Anti-angiogenic therapies have been used in the treatment of gliomas with spurious results ranging from no apparent response to significant imaging improvement with the potential for extremely diffuse patterns of tumor recurrence on imaging and autopsy. Anti-angiogenic treatment normalizes the vasculature, effectively decreasing vessel permeability and thus reducing tumor-induced edema, drastically altering T2-weighted MRI. We extend a previously developed mathematical model of glioma growth to explicitly incorporate edema formation allowing us to directly characterize and potentially predict the effects of anti-angiogenics on imageable tumor growth. A comparison of simulated glioma growth and imaging enhancement with and without bevacizumab supports the current understanding that anti-angiogenic treatment can serve as a surrogate for steroids and the clinically-driven hypothesis that anti-angiogenic treatment may not have any significant effect on the growth dynamics of the overall tumor-cell populations. However, the simulations do illustrate a potentially large impact on the level of edematous extracellular fluid, and thus on what would be imageable on T2/FLAIR MR for tumors with lower proliferation rates.

  20. Our patients followed up with a diagnosis of neurogenic pulmonary edema

    Science.gov (United States)

    Sarı, Mehmet Yusuf; Yıldızdaş, Rıza Dinçer; Yükselmiş, Ufuk; Horoz, Özden Ögür

    2015-01-01

    Neurogenic pulmonary edema is a clinical situation which developes as a result of central nervous system injury. It is rare in the childhood. Neurogenic pulmonary edema is a clinical diagnosis. Although the pathogenesis is not elucidated well, there is increase in pulmonary interstitial and alveolar fluid. The main principle in treatment of neurogenic pulmonary edema is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome. In this article, clinical properties of our two patients diagnosed with neurogenic pulmonary edema developed as a result of central nervous system injury are presented. PMID:26884694

  1. Profiling of ARDS Pulmonary Edema Fluid Identifies a Metabolically Distinct Subset.

    Science.gov (United States)

    Rogers, Angela J; Contrepois, Kevin; Wu, Manhong; Zheng, Ming; Peltz, Gary; Ware, Lorraine B; Matthay, Michael A

    2017-03-03

    There is considerable biologic and physiologic heterogeneity among patients who meet standard clinical criteria for acute respiratory distress syndrome (ARDS). In this study, we tested the hypothesis that there exists a sub-group of ARDS patients who exhibit a metabolically distinct profile. We examined undiluted pulmonary edema fluid obtained at the time of endotracheal intubation from 16 clinically phenotyped ARDS patients and 13 control patients with hydrostatic pulmonary edema. Non-targeted metabolic profiling was carried out on the undiluted edema fluid. Univariate and multivariate statistical analyses including principal components analysis (PCA) and partial least squares discriminant analysis (PLSDA) were conducted to find discriminant metabolites. 760 unique metabolites were identified in the pulmonary edema fluid of these 29 patients. We found that a subset of ARDS patients (6/16, 38%) presented a distinct metabolic profile with the overrepresentation of 235 metabolites compared to edema fluid from the other 10 ARDS patients, whose edema fluid metabolic profile was indistinguishable from those of the 13 control patients with hydrostatic edema. This "high metabolite" endotype was characterized by higher concentrations of metabolites belonging to all of the main metabolic classes including lipids, amino acids, and carbohydrates. This distinct group with high metabolite levels in the edema fluid was also associated with a higher mortality rate. Thus, metabolic profiling of the edema fluid of ARDS patients supports the hypothesis that there is considerable biologic heterogeneity among ARDS patients who meet standard clinical and physiologic criteria for ARDS.

  2. Our patients followed up with a diagnosis of neurogenic pulmonary edema.

    Science.gov (United States)

    Sarı, Mehmet Yusuf; Yıldızdaş, Rıza Dinçer; Yükselmiş, Ufuk; Horoz, Özden Ögür

    2015-12-01

    Neurogenic pulmonary edema is a clinical situation which developes as a result of central nervous system injury. It is rare in the childhood. Neurogenic pulmonary edema is a clinical diagnosis. Although the pathogenesis is not elucidated well, there is increase in pulmonary interstitial and alveolar fluid. The main principle in treatment of neurogenic pulmonary edema is supportive treatment and decreasing intracranial pressure as in acute respiratory distress syndrome. In this article, clinical properties of our two patients diagnosed with neurogenic pulmonary edema developed as a result of central nervous system injury are presented.

  3. Diagnostic usefulness of periIesional edema around intracerebral hemorrhage in predicting underlying causes

    Energy Technology Data Exchange (ETDEWEB)

    Yim, Nam Yeol; Seo, Jeong Jin; Yoon, Woong; Shin, Sang Soo; Lim, Hyo Soon; Chung, Tae Woong; Jeong, Gwang Woo; Kang, Heoung Keun [Chonnam National Univ. Hospital, Gwangju (Korea, Republic of)

    2004-07-01

    We attempted to evaluate the diagnostic usefulness of the degree of perilesional edema around intracerebral hematoma in predicting the underlying cause. This study included 54 patients with intracerebral hematoma for whom the underlying cause was confirmed by biopsy, radiological or clinical methods. Cases of subarachnoid hemorrhage, hemorrhagic transformation of cerebral infarction and intraventricular hemorrhage were excluded. The lesion size was defined as the average value of the longest axis and the axis perpendicular to this. The size of the perilesional edema was defined as the longest width of the edema. In all cases, the sizes of the lesion and edema were measured on the T2 weighted image. We defined the edema ratio as the edema size divided by the lesion size. 23 cases were diagnosed as intracerebral hemorrhage due to neoplastic conditions, such as metastasis (n=17), glioblastoma (n=5), hemangioblastoma (n=1). 31 cases were caused by non-neoplastic conditions, such as spontaneous hypertensive hemorrhage (n=23), arteriovenous malformation (n=4), cavernous angioma (n=3), and moya-moya disease (n=1). In fourteen cases, which were confirmed as malignant intracerebral hemorrhage, the edema ratio was more than 100%. Of the other cases, only 8 were confirmed as malignant intracerebral hemorrhage. It was found that the larger the edema ratio, the more malignant the intracerebral hemorrhage, and this result was statistically significant (p<0.001). Measurement of perilesional edema and the intracerebral hematoma ratio may be useful in predicting the underlying causes.

  4. In vivo photoacoustic tomography of mouse cerebral edema induced by cold injury

    Science.gov (United States)

    Xu, Zhun; Zhu, Quing; Wang, Lihong V.

    2011-06-01

    For the first time, we have implemented photoacoustic tomography (PAT) to image the water content of an edema in vivo. We produced and imaged a cold-induced cerebral edema transcranially, then obtained blood vessel and water accumulation images at 610 and 975 nm, respectively. We tracked the changes at 12, 24, and 36 h after the cold injury. The blood volume decreased after the cold injury, and the maximum area of edema was observed 24 h after the cold injury. We validated PAT of the water content of the edema through magnetic Resonance Imaging and the water spectrum from the spectrophotometric measurement.

  5. Ibuprofen prevents synthetic smoke-induced pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Shinozawa, Y.; Hales, C.; Jung, W.; Burke, J.

    1986-12-01

    Multiple potentially injurious agents are present in smoke but the importance of each of these agents in producing lung injury as well as the mechanisms by which the lung injury is produced are unknown. In order to study smoke inhalation injury, we developed a synthetic smoke composed of a carrier of hot carbon particles of known size to which a single known common toxic agent in smoke, in this case HCI, could be added. We then exposed rats to the smoke, assayed their blood for the metabolites of thromboxane and prostacyclin, and intervened shortly after smoke with the cyclooxygenase inhibitors indomethacin or ibuprofen to see if the resulting lung injury could be prevented. Smoke exposure produced mild pulmonary edema after 6 h with a wet-to-dry weight ratio of 5.6 +/- 0.2 SEM (n = 11) compared with the non-smoke-exposed control animals with a wet-to-dry weight ratio of 4.3 +/- 0.2 (n = 12), p less than 0.001. Thromboxane B, and 6-keto-prostaglandin F1 alpha rose to 1660 +/- 250 pg/ml (p less than 0.01) and to 600 +/- 100 pg/ml (p greater than 0.1), respectively, in the smoke-injured animals compared with 770 +/- 150 pg/ml and 400 +/- 100 pg/ml in the non-smoke-exposed control animals. Indomethacin (n = 11) blocked the increase in both thromboxane and prostacyclin metabolites but failed to prevent lung edema.

  6. [Non-cardiogenic pulmonary edema, acute respiratory distress syndrome].

    Science.gov (United States)

    Skalická, Hana; Bělohlávek, Jan

    2015-01-01

    Non-cardiogenic pulmonary edema is a clinical syndrome manifested by rapidly progressive respiratory distress leading, without therapy, to severe respiratory insufficiency and subsequent multiorgan failure. The pathophysiological causes are: the change in the pressure gradients in the pulmonary capillaries, the impaired membrane permeability of the alveolocapillary in the lungs, and impaired lymphatic drainage. Unlike in cardiogenic pulmonary edema, cardiac disease is not a cause, and there is no increase in wedge pressure (< 18 mm Hg). The aetiological base is diverse and includes more clinical pathological factors. The diagnosis and evaluation are usually very difficult due to the rapidly deteriorating clinical condition of the patients. A decisive, quick and comprehensive approach, using all available invasive and non-invasive methods is necessary. The basic steps of treatment are: the use of different types of ventilatory support in order to achieve adequate oxygenation, dealing with possible hemodynamic instability, and, when needed, other specific procedures. It is always important to keep in mind that this is a very serious condition with a high mortality rate. And there is a need for fast and efficient access to the best specialized clinic.

  7. Brain Basics

    Medline Plus

    Full Text Available ... News About Us Home > Health & Education > Educational Resources Brain Basics Introduction The Growing Brain The Working Brain ... to mental disorders, such as depression. The Growing Brain Inside the Brain: Neurons & Neural Circuits Neurons are ...

  8. Brain Basics

    Science.gov (United States)

    ... News About Us Home > Health & Education > Educational Resources Brain Basics Introduction The Growing Brain The Working Brain ... to mental disorders, such as depression. The Growing Brain Inside the Brain: Neurons & Neural Circuits Neurons are ...

  9. Massive vulval edema with severe preeclampsia. Case report Edema vulvar masivo con preeclampsia grave. Presentación de un caso.

    Directory of Open Access Journals (Sweden)

    José Luis Gómez Miranda.

    2009-11-01

    Full Text Available Massive vulval edema with severe preeclampsia is presented as one of the consequences that may appear on patients with hypertension disorders during pregnancy, therefore the attention in the Obstetrics and Gynecology Service must be systematical and permanent. On women with hypertensive disorders during pregnancy, although edemas may not be constant, they may either appear at minor, barely perceptible extents, or even in the most severe ways, such as anasarca. A very peculiar manifestation of edema on preeclampsia is massive vulval edema, which appears as a highly rare complication, in whose basis there is a complex, systemic pathological process involved. We present a case of a pregnant woman who was admitted with high blood pressure values and excessive weight gain, plus very noticeable general edemas, and during her stay developed massive vulval edema. No data on this complication were found in the bibliography reviewed. Very few experienced professionals recall having dealt with similar cases in the last fifteen years, hence the decision to publish it.El edema vulvar masivo con preeclampsia grave se presenta como una de las consecuencias que pueden aparecer en pacientes con trastornos de hipertensión en el embarazo, por lo que la atención en el Servicio de Obstetricia debe ser sistemática y permanente. En las mujeres con trastornos hipertensivos del embarazo, los edemas, aunque no son constantes, se manifiestan desde las formas más leves, apenas perceptibles, hasta las más severas, como la anasarca. Una manifestación particular del edema en la preeclampsia, es el edema vulvar masivo, que se presenta como una complicación sumamente rara, en cuya base hay un proceso patológico sistémico y complejo. Se presenta el caso de una embarazada que ingresó con cifras elevadas de presión arterial y aumento de peso exagerado, con edemas generalizados muy acentuados, que durante su estancia desarrolló un edema vulvar masivo. En la bibliograf

  10. Clinical Studies of Cerebral Edema Recanalization After Thrombolysis in Acute Cerebral Infarction%急性脑梗死动脉溶栓血管再通后的脑水肿临床研究

    Institute of Scientific and Technical Information of China (English)

    王喜春; 马冲; 张健莉; 于杰

    2015-01-01

    目的:探讨急性缺血性脑卒中动脉溶栓血管再通后脑水肿的临床研究,旨在为此类疾病患者的下一步临床工作提供借鉴。方法选择通过动脉溶栓血管再通的患者40例。将患者分为1~3 h组(A组)、>3~6h组(B组)。头颅CT监测、随访脑水肿情况。记录溶栓前、术后1周及1年NIHSS评分、MRS评分及BI指数。结果动脉溶栓血管再通后脑水肿发生率为100%,随访发现脑水肿局部有明显软化灶。两组患者脑水肿及临床结局比较差异无统计学意义(P>0.05)。结论动脉溶栓血管再通后脑水肿的及其脑组织缺失发生率极高,脑水肿局部有明显软化灶,良好的脑内局部循环和全身状况是改善此类脑水肿的重要因素。%Objective To investigate the acute arterial ischemic stroke thrombolytic recanalization clinical studies of cerebral edema, designed to provide a reference for the next clinical disease in these patients.Methods arterial thrombolysis recanalization by 40 patients. Patients were divided into 1 ~ 3h group (A),> 3 ~ 6h group (group B). Cranial CT monitoring, follow-up of brain edema. Recorded before thrombolysis, after 1 week and 1 year NIHSS score, MRS score and BI index.Results arterial thrombolysis recanalization rate was 97.5% of cerebral edema, cerebral edema partial follow-up found a significant malacia. Two groups of patients and clinical outcomes of cerebral edema was no significant difference (P> 0.05).Conclusion The arterial thrombolysis recanalization of cerebral edema and high incidence of brain tissue loss, good local circulation in the brain and body condition is such an important factor in improving brain edema.

  11. Neural and Behavioral Sequelae of Blast-Related Traumatic Brain Injury

    Science.gov (United States)

    2012-11-01

    bipolar disorder, schizophrenia ) with the exception of post-traumatic stress disorder (PTSD), penetrating gunshot wound to the brain or contraindications...matter degeneration16, increased levels of mortality, brain edema17, and downregulation of genes associated with hippocampal neurogenesis.18

  12. Alteration of water-soluble S-100 protein content in microembolized rat brain.

    Directory of Open Access Journals (Sweden)

    Harada,Yasuhiro

    1982-12-01

    Full Text Available The amount of S-100 protein in rat brain embolized with carbon microspheres decreased in parallel with the development of cerebral edema as judged by water content, recovering to the normal range by 24h after embolization. These results suggest the participation of S-100 protein in the permeability characterisitics of nervous system capillaries known as the blood-brain barrier.

  13. Strategy for the Management of Diabetic Macular Edema: The European Vitreo-Retinal Society Macular Edema Study

    Directory of Open Access Journals (Sweden)

    Ron Adelman

    2015-01-01

    Full Text Available Objective. To compare the efficacy of different therapies in the treatment of diabetic macular edema (DME. Design. Nonrandomized, multicenter clinical study. Participants. 86 retina specialists from 29 countries provided clinical information on 2,603 patients with macular edema including 870 patients with DME. Methods. Reported data included the type and number of treatment(s performed, the pre- and posttreatment visual acuities, and other clinical findings. The results were analyzed by the French INSEE (National Institute of Statistics and Economic Studies. Main Outcome Measures. Mean change of visual acuity and mean number of treatments performed. Results. The change in visual acuity over time in response to each treatment was plotted in second order polynomial regression trend lines. Intravitreal triamcinolone monotherapy resulted in some improvement in vision. Treatment with threshold or subthreshold grid laser also resulted in minimal vision gain. Anti-VEGF therapy resulted in more significant visual improvement. Treatment with pars plana vitrectomy and internal limiting membrane (ILM peeling alone resulted in an improvement in vision greater than that observed with anti-VEGF injection alone. In our DME study, treatment with vitrectomy and ILM peeling alone resulted in the better visual improvement compared to other therapies.

  14. Neural histamine in the tuberomammillary nucleus regulates the onset of neurogenic pulmonary edema in rabbits

    Institute of Scientific and Technical Information of China (English)

    Rong Dong; Xiaohong Zhang; Lijuan Shi

    2009-01-01

    Objective:To explore the effect of neural histamine in the tuberomammillary nucleus(TM) on neurogenic pulmonary edema (NPE) onset in rabbits and the function of the rostral ventrolateral medulla(RVLM) in the neural histamine modulation of NPE.Methods:NPE was produced by the intracisternal injections of fibrinogen and thrombin.The contents of histamine in the TM and RVLM in rabbits were measured with high performance liquid chromatography(HPLC).Rabbits were placed on a stereotaxic frame and microinjection cannulae were inserted into the TM and RVLM using brain atlas coordinates.Animals were pretreated with R-α-methylhistamine(MeHA) in the TM and chlorphenamine Mmaleate/cimetidine in the RVLM prior to establishing the NPE model.Changes in the lung water ratio and mean arterial pressure(MAP) were recorded,and paraffin sections of lung tissue were observed by light microscope.Results:We found that the contents of histamine(HA) in the TM and RVLM increased significantly with the onset of NPE.Pretreatment with MeHA in the TM and chlorphenamine Mmaleate in the RVLM significantly decreased MAP,and the lung water ratio and histological characteristics of the NPE in the rabbit model.Pretreatment with cimetidine in the RVLM had no effect on NPE.Conculsion:The results suggest that neural histamine in the TM is involved in the onset of NPE,and this effect of neural histamine is mediated by H receptor in the RVLM.

  15. Dynorphin A(6-12) analogs suppress thermal edema.

    Science.gov (United States)

    Wei, E T; Thomas, H A; Gjerde, E A; Reed, R K; Burov, S V; Korolkov, V I; Glynskaya, O V; Dorosh, M Y; Vlasov, G P

    1998-01-01

    Dynorphin A (Dyn A) is a 17-residue opioid peptide derived from prodynorphin precursors found in mammalian tissues. Removal of Tyr1 from Dyn A produces a peptide that is more potent than Dyn A in attenuating the acute phase of the inflammatory response, as measured by inhibition of heat-induced edema in the anesthetized rat's paw (exposure to 58 degrees C water for 1 min). Dyn A(2-17), however, no longer interacts with opioid receptors. It was postulated that the non-opioid anti-inflammatory actions of Dyn A(2-17) may reside in Dyn A(6-12); that is, Arg-Arg-Ile-Arg-Pro-Lys-Leu. here we report on the activities of Dyn A(6-12) analogs modified by substitutions on the N terminus, by single N-methyl substitution and by single replacement of residues by alanine. The results indicated that the minimal sequence required for an anti-edema ED50 of <1.0 micromol/kg i.v. was anisoyl-Arg6-Arg7-Xaa8-Arg9-Pro10)-Xaa11-+ ++Xaa12-NH2. A prototype, p-anisoyl-[D-Leu12] Dyn A(6-12)-NH2, with an ED50 of 0.20 micromol/kg i.v. compared to an ED50 of 0.08 micromol/kg i.v. for Dyn A(2-17), was selected for further tests of biological activity. This analog, like Dyn A(2-17), lowered blood pressure in anesthetized rats. In a model of neurogenic inflammation, produced by antidromic stimulation of the vagus in the anesthetized rat, p-anisoyl-[D-Leu12] Dyn A(6-12)-NH2, 0.23 micromol/kg i.v., attenuated the negativity of tracheal tissue interstitial pressure (Pif), which normally develops after nerve stimulation. Modulation of interstitial pressure may be the mechanistic basis for the anti-edema properties of these Dyn A(6-12) analogs.

  16. Dexamethasone intravitreal implant in the treatment of diabetic macular edema.

    Science.gov (United States)

    Dugel, Pravin U; Bandello, Francesco; Loewenstein, Anat

    2015-01-01

    Diabetic macular edema (DME) resembles a chronic, low-grade inflammatory reaction, and is characterized by blood-retinal barrier (BRB) breakdown and retinal capillary leakage. Corticosteroids are of therapeutic benefit because of their anti-inflammatory, antiangiogenic, and BRB-stabilizing properties. Delivery modes include periocular and intravitreal (via pars plana) injection. To offset the short intravitreal half-life of corticosteroid solutions (~3 hours) and the need for frequent intravitreal injections, sustained-release intravitreal corticosteroid implants have been developed. Dexamethasone intravitreal implant provides retinal drug delivery for ≤6 months and recently has been approved for use in the treatment of DME. Pooled findings (n=1,048) from two large-scale, randomized Phase III trials indicated that dexamethasone intravitreal implant (0.35 mg and 0.7 mg) administered at ≥6-month intervals produced sustained improvements in best-corrected visual acuity (BCVA) and macular edema. Significantly more patients showed a ≥15-letter gain in BCVA at 3 years with dexamethasone intravitreal implant 0.35 mg and 0.7 mg than with sham injection (18.4% and 22.2% vs 12.0%). Anatomical assessments showed rapid and sustained reductions in macular edema and slowing of retinopathy progression. Phase II study findings suggest that dexamethasone intravitreal implant is effective in focal, cystoid, and diffuse DME, in vitrectomized eyes, and in combination with laser therapy. Ocular complications of dexamethasone intravitreal implant in Phase III trials included cataract-related events (66.0% in phakic patients), intraocular pressure elevation ≥25 mmHg (29.7%), conjunctival hemorrhage (23.5%), vitreous hemorrhage (10.0%), macular fibrosis (8.3%), conjunctival hyperemia (7.2%), eye pain (6.1%), vitreous detachment (5.8%), and dry eye (5.8%); injection-related complications (eg, retinal tear/detachment, vitreous loss, endophthalmitis) were infrequent (implant offers a

  17. Massive vulval edema with severe preeclampsia. Case report Edema vulvar masivo con preeclampsia grave. Presentación de un caso.

    OpenAIRE

    José Luis Gómez Miranda.; José Luis Durán Páez; Nelson Pérez Rumbaut

    2009-01-01

    Massive vulval edema with severe preeclampsia is presented as one of the consequences that may appear on patients with hypertension disorders during pregnancy, therefore the attention in the Obstetrics and Gynecology Service must be systematical and permanent. On women with hypertensive disorders during pregnancy, although edemas may not be constant, they may either appear at minor, barely perceptible extents, or even in the most severe ways, such as anasarca. A very peculiar manifestation of...

  18. Recirculation usually precedes malignant edema in middle cerebral artery infarcts

    DEFF Research Database (Denmark)

    Nielsen, T H; Ståhl, N; Schalén, W;

    2012-01-01

    In patients with large middle cerebral artery (MCA) infarcts, maximum brain swelling leading to cerebral herniation and death usually occurs 2-5 days after onset of stroke. The study aimed at exploring the pattern of compounds related to cerebral energy metabolism in infarcted brain tissue....

  19. Neuroleptic malignant syndrome presenting as pulmonary edema and severe bronchorrhea.

    Science.gov (United States)

    Patel, U; Agrawal, M; Krishnan, P; Niranjan, S

    2002-04-01

    Neuroleptic malignant syndrome is a rare (incidence, 0.02%-3.2%) but dangerous complication following the use of neuroleptic drugs. When not promptly recognized, this disease carries a high mortality (10%-20%) and morbidity rate. We report an unusual case of neuroleptic malignant syndrome that presented predominantly with autonomic instability in the form of recurrent episodes of respiratory distress. The respiratory distress was initially caused by pulmonary edema and later was caused by severe bronchorrhea. We propose that aspiration pneumonia resulting in respiratory failure, the leading cause of death in neuroleptic malignant syndrome, may be a result of a combination of altered mental status and bronchorrhea. This has therapeutic implications because early institution of bromocriptine/dantrolene can prevent aspiration pneumonia and, hence, mortality from respiratory failure.

  20. Evidence-Based Treatment of Diabetic Macular Edema.

    Science.gov (United States)

    Barham, Rasha; El Rami, Hala; Sun, Jennifer K; Silva, Paolo S

    2017-01-01

    Diabetes mellitus is a chronic disease that affects 415 million people worldwide. Despite treatment advances, diabetic eye disease remains a leading cause of vision loss worldwide. Diabetic macular edema (DME) is a common cause of vision loss in diabetic patients. The pathophysiology is complex and involves multiple pathways that ultimately lead to central retinal thickening and, if untreated, visual loss. First-line treatment of DME has evolved from focal/grid laser established by the Early Treatment of Diabetic Retinopathy Study (ETDRS) to intravitreous pharmacologic therapy. Landmark prospective clinical trials examining the effect of intravitreous injections of vascular endothelial growth factor (VEGF) inhibitors in the treatment of DME have demonstrated improved visual outcomes over focal grid laser. This review focuses on the scientific evidence treatment of DME, disease pathophysiology, clinical disease course, current treatment standards, and emerging novel therapeutic approaches.

  1. Pulmonary edema of environmental origin--newer concepts

    Energy Technology Data Exchange (ETDEWEB)

    Cordasco, E.M.; Demeter, S.R.; Kester, L.; Cordasco, M.A.; Lammert, G.; Beerel, F.

    1986-06-01

    Pulmonary edema of non-cardiac origin is usually an urgent clinical problem, which has recently increased in frequency throughout the world in the past few years. This is partly due to sociological factors and to pre-eminent advances in industrial technology. Recent severe massive toxic gas explosions have had national and worldwide implications. Therefore, urgent and appropriate therapy is of utmost importance in most of these patients. The use of high flow oxygen with Constant Positive Pressure Breathing are the main inhalational therapeutic approaches. Newer modalities of treatment include: (1) earlier Fiberoptic bronchoscopy in those individuals afflicted with aspiration problems and (2) certain specific chemical blocking agents for the management of phosgene intoxication and hydrogen sulfide toxicity. Preventive environmental measures are also important.

  2. A rare cause of pulmonary edema in the postoperative period

    Directory of Open Access Journals (Sweden)

    Kshitij Chatterjee

    2017-01-01

    Full Text Available With the increasing longevity of the population, the annual rates of hip arthroplasties performed have been steadily increasing over the past decade. Given the presence of medical comorbidities in the older patients, the peri-operative care of these individuals requires multi-specialty care, now more than ever. Hip arthroplasty is generally well tolerated, with early mortality after the procedure being <1%. Bone cement implantation syndrome (BCIS is an entity that is occasionally encountered during or after the surgery. It is characterized by hypoxemia, hypotension, cardiac arrhythmias, and cardiac arrest leading to death, in severe cases. We report a case of a middle-aged female who developed refractory hypotension and pulmonary edema while undergoing hemiarthroplasty for a pathological femoral neck fracture and experienced cardiac arrest in the immediate postoperative period. Critical care physicians must familiarize themselves with promptly diagnosing and managing BCIS.

  3. A Rare Cause of Pulmonary Edema in the Postoperative Period.

    Science.gov (United States)

    Chatterjee, Kshitij; Mittadodla, Penchala S; Colaco, Clinton; Jagana, Rajani

    2017-02-01

    With the increasing longevity of the population, the annual rates of hip arthroplasties performed have been steadily increasing over the past decade. Given the presence of medical comorbidities in the older patients, the peri-operative care of these individuals requires multi-specialty care, now more than ever. Hip arthroplasty is generally well tolerated, with early mortality after the procedure being <1%. Bone cement implantation syndrome (BCIS) is an entity that is occasionally encountered during or after the surgery. It is characterized by hypoxemia, hypotension, cardiac arrhythmias, and cardiac arrest leading to death, in severe cases. We report a case of a middle-aged female who developed refractory hypotension and pulmonary edema while undergoing hemiarthroplasty for a pathological femoral neck fracture and experienced cardiac arrest in the immediate postoperative period. Critical care physicians must familiarize themselves with promptly diagnosing and managing BCIS.

  4. Neurogenic pulmonary edema in head injuries: analysis of 5 cases

    Institute of Scientific and Technical Information of China (English)

    QIN Shi-qiang; SUN Wei; WANG Han-bin; ZHANG Qing-lin

    2005-01-01

    Objective: To review the pathophysiology and study the diagnosis and clinical management of neurogenic pulmonary edema (NPE). Methods: The data of 5 patients who developed NPE after head injury treated in our hospital form December 1995 to May 2003 were collected and analyzed.Results: The patients developed dyspnea and respiratory failure 2-8 hours after neurologic event. Four of the 5 patients presented with pink frothy sputum. Chest radiography showed bilateral diffuse infiltrations in all the 5 patients. After supportive measures such as oxygen support and pharmacologic therapy, 4 patients recovered in 72 hours and one patient died. Conclusions: The pathophysiologic mechanisms of NPE is unclear. In acute respiratory failure following head injury, NPE must be given much attention and timely and effective measures should be taken.

  5. Negative pressure pulmonary edema revisited: Pathophysiology and review of management

    Directory of Open Access Journals (Sweden)

    Balu Bhaskar

    2011-01-01

    Full Text Available Negative pressure pulmonary edema (NPPE is a dangerous and potentially fatal condition with a multifactorial pathogenesis. Frequently, NPPE is a manifestation of upper airway obstruction, the large negative intrathoracic pressure generated by forced inspiration against an obstructed airway is thought to be the principal mechanism involved. This negative pressure leads to an increase in pulmonary vascular volume and pulmonary capillary transmural pressure, creating a risk of disruption of the alveolar-capillary membrane. The early detection of the signs of this syndrome is vital to the treatment and to patient outcome. The purpose of this review is to highlight the available literature on NPPE, while probing the pathophysiological mechanisms relevant in both the development of this condition and that involved in its resolution.

  6. [Nursing assessment and management of patients with cardiogenic pulmonary edema].

    Science.gov (United States)

    Wang, Yu-Jyuan; Liao, Chieh-Yin; Kao, Chi-Wen

    2012-02-01

    Cardiogenic pulmonary edema (CPE) is a clinical health problem that induces impaired gas exchange, dyspnea and hypoxia. This serious condition results in acute respiratory failure and high mortality rate. This article suggests an effective approach to CPE patient clinical symptom assessment and management. In accordance with evidence-based methods, we searched Cochrane, CINAHL and ScienceDirect and identified four Oxford Ia or Ib reports that employed a randomized controlled trial, systematic review and meta-analysis. Results suggest that prompt application of a non-invasive positive ventilator, especially continuous positive or bi-level positive airway pressure, can help patients reduce intubation risks, ICU stay days, and mortality rates. The authors hope to see more clinical trials on this topic to support evidence-based clinical nursing care.

  7. Localized bi-nasal macular edema in optic chiasmal syndrome

    Directory of Open Access Journals (Sweden)

    Alejandro J Lavaque

    2013-01-01

    Full Text Available A 28-year-old healthy male complaining of vision loss in his right eye was discovered to have localized bi-nasal macular edema in the presence of a pituitary adenoma. The presence of a junctional scotoma composed by a central scotoma in the right eye associated with superior temporal quadrantanopia in the fellow eye was seen. The pattern detected in the visual field suggested the presence of an expansive mass at the level of the optic chiasm. Optical coherence tomography findings also revealed subtle macular thickness beyond normal in the superior and nasal quadrants of both maculae. This report illustrates the importance of suspecting a pituitary adenoma in the light of uncharacteristic retinal alterations.

  8. Topical ethosomal capsaicin attenuates edema and nociception in arthritic rats.

    Science.gov (United States)

    Kumar Sarwa, Khomendra; Rudrapal, Mithun; Mazumder, Bhaskar

    2015-12-01

    In this study, topical ethosomal formulation of capsaicin was prepared and evaluated for bio-efficacy in arthritic rats. Physical and biological characterizations of prepared capsaicin-loaded nano vesicular systems were also carried out. Ethosomal capsaicin showed significant reduction of rat paw edema along with promising antinociceptive action. The topical antiarthritic efficacy of prepared formulation of capsaicin was found more than that of Thermagel, a marketed gel of capsaicin. From toxicological study, no predictable signs of toxicity such as skin irritation (of experimental rats) were observed. Based on this finding, ethosomal capsaicin could be proposed as an effective as well as a safe topical delivery system for the long-term treatment of arthritis and associated inflammo-musculoskeletal disorders. Such exciting result would eventually enlighten the analgesic and anti-inflammatory potential of capsaicin for topical remedy.

  9. Cystoid macular edema in a patient with Danon disease

    Directory of Open Access Journals (Sweden)

    Heather G Mack

    2014-01-01

    Full Text Available To report a patient with Danon retinopathy with cystoid macular edema treated with topical dorzolamide 2% eye drops and oral acetazolamide. A 37-year-old Caucasian man with Danon disease treated with topical and oral carbonic anhydrase inhibitors participated in the study. Examinations performed before and during treatment included visual acuity (VA, spectral-domain optical coherence tomography, and electroretinography. Following total 48 weeks of treatment, VA decreased from 20/30 OD, 20/200 OS, to 20/40 OD, CF OS. The mean central retinal thickness was unchanged from baseline 263 μm OD , 226 μm OS, after treatment 283 μm OD and 202 μm OS. In our case, carbonic anydrase inhibitors were not effective. However, a general recommendation cannot be given based on a single case.

  10. Evaluation of the Prevalence of Concomitant Idiopathic Cyclic Edema and Cellulite

    Directory of Open Access Journals (Sweden)

    José Maria Pereira de Godoy, Maria de Fátima Guerreiro de Godoy

    2011-01-01

    Full Text Available The aim of this study was to evaluate the prevalence of concomitant idiopathic cyclic edema with Grade II and III cellulite. All patients treated for Grade II and III cellulite were evaluated for idiopathic cyclic edema in a retrospective, quantitative and cross-sectional study. The study was carried out at the Godoy Clinic in the period from 2006 to 2010. All patients with body mass indexes > 25, Grade I cellulite and other causes of edema were excluded. The diagnosis of idiopathic cyclic edema was based on a clinical history and fluid retention throughout the day, in particular difficulty in removing rings on waking in the morning which improves later in the day. All patients with cyclic edema were treated with 75 mg aminaphtone three times daily. Statistical analysis considered the frequency of edema.Of the 82 women evaluated with ages between 18 and 58 years old (mean of 34.9 years 41 (50.0% were diagnosed with idiopathic cyclic edema.Idiopathic cyclic edema is an aggravating factor for cellulite and is frequently associated with the more advanced stages of the disease. Its control is essential in the treatment of cellulite.

  11. Evaluation of the prevalence of concomitant idiopathic cyclic edema and cellulite.

    Science.gov (United States)

    de Godoy, José Maria Pereira; de Godoy, Maria de Fátima Guerreiro

    2011-01-01

    The aim of this study was to evaluate the prevalence of concomitant idiopathic cyclic edema with Grade II and III cellulite. All patients treated for Grade II and III cellulite were evaluated for idiopathic cyclic edema in a retrospective, quantitative and cross-sectional study. The study was carried out at the Godoy Clinic in the period from 2006 to 2010. All patients with body mass indexes > 25, Grade I cellulite and other causes of edema were excluded. The diagnosis of idiopathic cyclic edema was based on a clinical history and fluid retention throughout the day, in particular difficulty in removing rings on waking in the morning which improves later in the day. All patients with cyclic edema were treated with 75 mg aminaphtone three times daily. Statistical analysis considered the frequency of edema. Of the 82 women evaluated with ages between 18 and 58 years old (mean of 34.9 years) 41 (50.0%) were diagnosed with idiopathic cyclic edema. Idiopathic cyclic edema is an aggravating factor for cellulite and is frequently associated with the more advanced stages of the disease. Its control is essential in the treatment of cellulite.

  12. Persistent corneal edema secondary to presumed dead adult filarial worm in the anterior chamber

    Directory of Open Access Journals (Sweden)

    Basak Samar

    2007-01-01

    Full Text Available We present three cases of persistent corneal edema secondary to presumed dead adult filarial worms lying in the anterior chamber with their attachment to the endothelium. Two of them were initially diagnosed as descemet′s fold with corneal edema. Two patients underwent penetrating keratoplasty and in one case, surgical removal was partly possible with clearing of cornea.

  13. Increased pulmonary vascular permeability as a cause of re-expansion edema in rabbits

    Energy Technology Data Exchange (ETDEWEB)

    Pavlin, D.J.; Nessly, M.L.; Cheney, F.W.

    1981-01-01

    In order to study the mechanism(s) underlying re-expansion edema, we measured the concentration of labeled albumin (RISA) in the extravascular, extracellular water (EVECW) of the lung as a measure of pulmonary vascular permeability. Re-expansion edema was first induced by rapid re-expansion of rabbit lungs that had been collapsed for 1 wk by pneumothorax. The RISA in EVECW was expressed as a fraction of its plasma concentration: (RISA)L/(RISA)PL. The volume of EVECW (ml/gm dry lung) was measured using a /sup 24/Na indicator. Results in re-expansion edema were compared with normal control lungs and with oleic acid edema as a model of permeability edema. In re-expanded lungs, EVECW (3.41 +/- SD 1.24 ml/g) and (RISA)L/(RISA)PL 0.84 +/- SD 0.15) were significantly increased when compared with normal control lungs (2.25 +/- 0.41 ml/g and 0.51 +/- 0.20, respectively). Results in oleic acid edema (5.66 +/- 2.23 ml/g and 0.84 +/- 0.23) were similar to re-expansion edema. This suggested that re-expansion edema is due to increased pulmonary vascular permeability caused by mechanical stresses applied to the lung during re-expansion.

  14. Acute pulmonary edema after intravenous administration of nonionic contrast media: a case report

    Energy Technology Data Exchange (ETDEWEB)

    Cheon, Jung Eun; Im, Jung Gi; Chung, Jin Wook; Park, Jae Hyung; Han, Man Chung [Seoul National Univ. College of Medicine, Seoul (Korea, Republic of)

    1997-02-01

    We describe high-resolution CT findings of pulmonary edema following the administration of intravenous nonionic contrast media in a patient who had no previous history of cardiovascular disease; areas of ground glass opacity and interlobular septal thickenings which partly disappeared on scans obtained 90 minutes after the initial scans. The proposed mechanisms of pulmonary edema are briefly discussed.

  15. Takotsubo Cardiomyopathy in the Setting of Immersion Pulmonary Edema: Case Series

    Science.gov (United States)

    Sorrentino, Dante; Azuma, Steven

    2015-01-01

    Immersion Pulmonary Edema is a unique medical condition being increasingly described in the medical literature as sudden-onset pulmonary edema in the setting of scuba diving and or swimming. Case reports have associated immersion pulmonary edema with cardiac dysfunction, but there are no known case reports describing submersion pulmonary edema resulting in Takotsubo cardiomyopathy. We report on three patients with unique presentations of immersion pulmonary edema with associated Takotsubo cardiomyopathy. All three cases occurred in O‘ahu, Hawai‘i and were seen by the same cardiologist within a span of seven years. Each patient was scuba diving with sudden dyspnea with pulmonary edema on chest X-ray. Cardiac catheterization revealed no significant epicardial stenosis. Wall motion abnormalities resolved. EKG's showed typical evolution of symmetric T wave inversion. Immersion pulmonary edema and Takotsubo cardiomyopathy may occur together and may be more common than initially thought. Dyspnea has been long known to be stressful as in “waterboarding.” Stressful events are known to trigger Takotsubo cardiomyopathy. Takotsubo cardiomyopathy should be considered as a possible complication of immersion pulmonary edema and EKG's, troponins, echocardiogram and in the appropriate situation cardiac catheterization should be considered.

  16. Necrosis de médula espinal, edema cerebral y glioblastoma

    OpenAIRE

    Iglesias Rozas, José Rafael, 1942-

    1987-01-01

    Cinco imágenes de una necrosis de la médula espinal, un edema cerebral y un glioblastoma en una paciente de 76 años. Five pictures of a spinal cord necrosis, a cerebral edema and a glioblastoma in a 76-year-old female patient.

  17. Pharm GKB: Acute bovine pulmonary emphysema AND edema [PharmGKB

    Lifescience Database Archive (English)

    Full Text Available Overview Alternate Names: Synonym ABPE; Acute bovine pulmonary emphysema and edema;...63 External Vocabularies MeSH: Pneumonia, Atypical Interstitial, of Cattle (D011016) SnoMedCT: Acute bovine ...ia, Atypical Interstitial, of Cattle [Disease/Finding] (N0000010988) Common Searches Search Medline Plus Search CTD Pharm GKB: Acute bovine pulmonary emphysema AND edema ...

  18. Chronic edema of the lower extremities: international consensus recommendations for compression therapy clinical research trials.

    Science.gov (United States)

    Stout, N; Partsch, H; Szolnoky, G; Forner-Cordero, I; Mosti, G; Mortimer, P; Flour, M; Damstra, R; Piller, N; Geyer, M J; Benigni, J-P; Moffat, C; Cornu-Thenard, A; Schingale, F; Clark, M; Chauveau, M

    2012-08-01

    Chronic edema is a multifactorial condition affecting patients with various diseases. Although the pathophysiology of edema varies, compression therapy is a basic tenant of treatment, vital to reducing swelling. Clinical trials are disparate or lacking regarding specific protocols and application recommendations for compression materials and methodology to enable optimal efficacy. Compression therapy is a basic treatment modality for chronic leg edema; however, the evidence base for the optimal application, duration and intensity of compression therapy is lacking. The aim of this document was to present the proceedings of a day-long international expert consensus group meeting that examined the current state of the science for the use of compression therapy in chronic edema. An expert consensus group met in Brighton, UK, in March 2010 to examine the current state of the science for compression therapy in chronic edema of the lower extremities. Panel discussions and open space discussions examined the current literature, clinical practice patterns, common materials and emerging technologies for the management of chronic edema. This document outlines a proposed clinical research agenda focusing on compression therapy in chronic edema. Future trials comparing different compression devices, materials, pressures and parameters for application are needed to enhance the evidence base for optimal chronic oedema management. Important outcomes measures and methods of pressure and oedema quantification are outlined. Future trials are encouraged to optimize compression therapy in chronic edema of the lower extremities.

  19. Mechanisms of edema formation in myxedema--increased protein extravasation and relatively slow lymphatic drainage

    DEFF Research Database (Denmark)

    Parving, H H; Hansen, J M; Nielsen, S L;

    1979-01-01

    of generalized edema (P less than 0.05). All variables returned to normal during l-thyroxine treatment. The extravascular accumulation of albumin, and presumably of all other plasma proteins, is important in the generalized edema typically found in myxedema. Inadequate lymphatic drainage may also explain...

  20. Transthoracic lung ultrasound in normal dogs and dogs with cardiogenic pulmonary edema: a pilot study.

    Science.gov (United States)

    Rademacher, Nathalie; Pariaut, Romain; Pate, Julie; Saelinger, Carley; Kearney, Michael T; Gaschen, Lorrie

    2014-01-01

    Pulmonary edema is the most common complication of left-sided heart failure in dogs and early detection is important for effective clinical management. In people, pulmonary edema is commonly diagnosed based on transthoracic ultrasonography and detection of B line artifacts (vertical, narrow-based, well-defined hyperechoic rays arising from the pleural surface). The purpose of this study was to determine whether B line artifacts could also be useful diagnostic predictors for cardiogenic pulmonary edema in dogs. Thirty-one normal dogs and nine dogs with cardiogenic pulmonary edema were prospectively recruited. For each dog, presence or absence of cardiogenic pulmonary edema was based on physical examination, heartworm testing, thoracic radiographs, and echocardiography. A single observer performed transthoracic ultrasonography in all dogs and recorded video clips and still images for each of four quadrants in each hemithorax. Distribution, sonographic characteristics, and number of B lines per thoracic quadrant were determined and compared between groups. B lines were detected in 31% of normal dogs (mean 0.9 ± 0.3 SD per dog) and 100% of dogs with cardiogenic pulmonary edema (mean 6.2 ± 3.8 SD per dog). Artifacts were more numerous and widely distributed in dogs with congestive heart failure (P edema on radiographs. Findings from the current study supported the use of thoracic ultrasonography and detection of B lines as techniques for diagnosing cardiogenic pulmonary edema in dogs.

  1. Reducing Secondary Insults in Traumatic Brain Injury

    Science.gov (United States)

    2015-03-01

    distinguished by aligning data from the data logger accelerometer against the simultaneous data streams of ICP, mean anerial pressure, and cerebral ... edema of central nervous system tissue within the closed confines of the cranial vault. The ability to estab- lish and maintain an appropriate...source of cerebral ischemia following severe brain injury in the Trau- matic Coma Data Bank . Acta Neurochir Suppl (Wien) 1993; 59: 121-5. II. Jeremitsky

  2. Production of Hypoxia-induced Corneal Edema in Aged Eyes

    Institute of Scientific and Technical Information of China (English)

    Alan K. Cheung; Andrew W. Siu; Digby W. Cheung; Edwin C. Mo

    2004-01-01

    Purpose:Corneal thickness assessment is a common clinical procedure applied in corneal and contact lens care. This study aims to investigate the effect of age on hypoxiainduced corneal swelling.Methods:Eighteen male subjects were equally divided into the younger [(23.7±0.8) and older [(74.4±2.5) years old]groups.Each subject wore a thick soft contact lens (uniform thickness of 0.3 mm) on the left cornea. With the contact lens in place, the baseline central corneal thickness was measured using a specially designed photo-pachometer. The lens was then patched behind the closed eyelids, producing an extremely hypoxic stress to the cornea. The change in central corneal thickness was monitored every 20 minutes with momentary disruptions to the hypoxic stress over the next 2 hours. The increase in thickness was taken as an index of corneal edema. The rate of change in corneal thickness, as derived from a non-linear mathematical model, was compared between groups. Results:The corneal thickness of both age groups increased significantly with time (P<0.000 1 ). The mean corneal swelling constant for the older subjects was 16.5 × 10-3 (S.E.M. = 2.65 × 10-3) and the value for the younger subjects was 46.5 × 10-3 (S.E.M. = 3.25× 10-3). The difference was statistically significant (P < 0.000 1 ).Conclusion:Aging cornea has a slower hypoxia-induced edema response compared with the younger group. Whether it is caused by a decreased corneal lactate production or an increased resistance to physical expansion deserves further investigation. Eye Science2004;20:1-5.

  3. Brain herniation

    Science.gov (United States)

    ... herniation; Uncal herniation; Subfalcine herniation; Tonsillar herniation; Herniation - brain ... Brain herniation occurs when something inside the skull produces pressure that moves brain tissues. This is most ...

  4. Acute pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman undergoing transvaginal cervical cerclage

    Science.gov (United States)

    Lee, Jae-Young; Kwon, Hyun-Jung; Park, Sang-Wook; Lee, Yu-Mi

    2017-01-01

    Abstract Background: The physiological changes associated with pregnancy may predispose pregnant women to pulmonary edema. Other known causes of pulmonary edema during pregnancy include tocolytic drugs, preeclampsia, eclampsia, and peripartum cardiomyopathy. Methods: We describe a rare case of pulmonary edema caused by takotsubo cardiomyopathy in a pregnant woman at 14 weeks of gestation who was undergoing emergency transvaginal cervical cerclage. Results: Intraoperative chest radiography revealed severe pulmonary edema and echocardiography indicated moderate left ventricular dysfunction with akinesia of the mid to apical left ventricular wall segment, which is reflective of takotsubo cardiomyopathy. Conclusion: With early detection and appropriate management, the patient was stabilized in a relatively short period of time. Based on her clinical signs and symptoms, we suspect that the pulmonary edema was caused by takotsubo cardiomyopathy. PMID:28072695

  5. Fluid distribution in progressive pulmonary edema: a low-temperature scanning-electron-microscopy study

    Energy Technology Data Exchange (ETDEWEB)

    Hook, G.R.

    1981-06-01

    High pressure pulmonary edema is a common medical disorder caused by venous hypertension following left ventricular heart failure. Abnormal fluid accumulation in the alveolar air spaces results in a life-threatening loss of respiratory function. The primary component of the fluid is water and therefore the study of water distribution in the alveolus can provide insight into high pressure pulmonary edema pathology. The new method of freeze-fracture, low temperature SEM has been developed and applied to the study of pulmonary edema. This method combines freeze-fracture sample preservation with SEM observation and retains pulmonary fluids in the frozen hydrated state for direct three-dimensional SEM imaging of alveoli. Quantitative measurements of alveolar structures resulting from high-pressure pulmonary edema were made from SEM micrographs. From these measurements a model for alveolar fluid distribution resulting from progressive high pressure edema was made.

  6. Etiology and treatment of the inflammatory causes of cystoid macular edema

    Directory of Open Access Journals (Sweden)

    Hyung Cho

    2009-10-01

    Full Text Available Hyung Cho1, Assumpta Madu11Department of Ophthalmology, Albert Einstein College of Medicine, Montefiore Medical Center, Bronx, New York, USAAbstract: Cystoid macular edema in its various forms can be considered one of the leading causes of central vision loss in the developed world. It occurs in a wide variety of pathologic conditions and represents the final common pathway of several basic processes. Therapeutic approaches to cystoid macular edema depend on a clear understanding of its contributing pathophysiologic mechanisms. This review will discuss the mechanism of ocular inflammation in cystoid macular edema with a particular focus on the inflammatory causes: post-operative, uveitic, and after laser procedures. A variety of pharmacologic agents targeting inflammatory molecules have been shown to reduce macular edema and improve visual function. However, the long-term efficacy and safety of most new therapies have yet to be established in controlled clinical trials.Keywords: ocular inflammation, cystoid macular edema, uveitis

  7. One day wonder: Fast resolution of macular edema following intravitreal ranibizumab in retinal venous occlusions

    Directory of Open Access Journals (Sweden)

    Lalit Verma

    2013-01-01

    Full Text Available Macular edema is a significant cause of vision loss in patients with central retinal vein occlusions and branch retinal vein occlusions. Vascular endothelial growth factor (VEGF appears to be a key factor in the pathogenesis of this disease. Anti-VEGF therapy, such as intravitreal ranibizumab provides an effective treatment against vision-threatening macular edema. We report three patients of retinal vein occlusion with macular edema who demonstrated overnight resolution of macular edema following treatment with intravitreal ranibizumab (0.5 mg. 3D optical coherence tomography (Optovue was used as a tool for comparison of the macular thickness before and after treatment. The significant reductions in the central foveal thickness demonstrated in these patients one night after intravitreal injections could have significant influence on modifying current treatment protocols. Early treatment of macular edema related to retinal venous occlusive disease with anti-VEGF injections could result in faster visual rehabilitation in these patients.

  8. Evaluation of pharmacological efficacy of anti-edema agents in a rat cerebral infarction model by MRI image analysis

    Energy Technology Data Exchange (ETDEWEB)

    Izumi, Yoshio; Haida, Munetaka; Kurita, Daisaku; Shinohara, Yukito [Tokai Univ., Isehara, Kanagawa (Japan). School of Medicine; Sugiura, Takeo

    1997-04-01

    We investigated the efficacy of drugs used to treat brain edema in a rat acute cerebral infarction model by MRI image analysis. Twenty-six Sprague-Dawley rats were anesthetized with halothane, and the right middle cerebral artery was permanently occluded via a transvascular approach using a nylon 2-0 suture. At 24 hours after the occlusion, axial T{sub 2}-weighted MRI images were taken before and 2 hours after intraperitoneal administration of a test drug. After the administration of 1.7 g/kg glycerol (n=9), 3.3 g/kg mannitol (n=9) or 17 mg/kg furosemide (n=8), the high intensity area (HIA) in the whole brain amounted to 92% (p<0.01), 94% (p=0.07), or 95% (p=0.03), respectively as compared to the corresponding HIA before administration. The HIA in the cerebral cortex amounted to 87% (p<0.01), 89% (p=0.03), or 98% (p=0.47), and that in the striatum to 102%, 106%, or 87% (p<0.05), respectively. The signal intensity change (before{yields}after) was 54{yields}49 (p<0.01), 54{yields}50 (p<0.01), or 55{yields}54 in the left side normal cortex; 102{yields}97 (p<0.0l), 100{yields}98, or 98{yields}97 in the injured side cortex; and 100{yields}93 (p<0.0l), 94{yields}88 (p=0.03), or 94{yields}94 in the injured side striatum, respectively. Improvement of edema by the drugs was observed as a reduction in HIA and a decrease in signal intensity on MRI, and the changes were significant in the case of administration of each of glycerol, mannitol and furosemide. (author)

  9. Posterior Lumbar Subcutaneous Edema on Spine Magnetic Resonance Images: What Is the Cause?

    Energy Technology Data Exchange (ETDEWEB)

    Han, Ga Jin; Lee, In Sook; Han, In Ho; Lee, Jung Sub [Pusan National University Hospital, Pusan National University School of Medicine, Busan (Korea, Republic of); Moon, Tae Yong [Dept. of Radiology, Pusan National University Yangsan Hospital, Yangsan (Korea, Republic of); Song, Jong Woon [Dept. of Radiology, Inje University Haeundae Paik Hospital, Busan (Korea, Republic of)

    2013-04-15

    Posterior lumbar subcutaneous (PLS) edema on spine magnetic resonance (MR) images is a common incidental, though neglected finding. This study was undertaken to investigate the relations between PLS edema and pathologic conditions. Between January and December 2009, 138 patients with PLS edema, but without a spinal tumor or a history of recent surgery or trauma, and 80 infectious spondylitis patients without PLS edema were enrolled in this retrospective study. Available medical records and lumbar spine MR images were evaluated. The degree of edema was quantified using an arbitrary scoring system. Further, the correlations between the degree of edema and age, sex, body mass index (BMI), degeneration of posterior spinal structures (PSS) and infectious spondylitis were analyzed. Of the 93 cases with a calculable BMI, 61 (66%) had a BMI of > 23 kg/m2. Correlations between the degree of edema and sex, age and BMI grade were all statistically non-significant. Thirty-three cases (24%) had an underlying disease, such as heart problem, diabetes mellitus, liver cirrhosis, chronic renal failure, extra-spinal tumor or connective tissue disorder. The numbers of cases with infectious spondylitis and an idiopathic condition was 61 (44%) and 44 (32%), respectively. The grade of infectious spondylitis was not found to be significantly associated with the degree of edema (p = 0.084). In cases with an idiopathic condition, the correlation between the degree of edema and PSS degeneration was statistically significant (p = 0.042). Radiologists should not disregard PLS edema, because it is related to an underlying disease and thus may be of clinical significance.

  10. Involvement of COX2-thromboxane pathway in TCDD-induced precardiac edema in developing zebrafish.

    Science.gov (United States)

    Teraoka, Hiroki; Okuno, Yuki; Nijoukubo, Daisuke; Yamakoshi, Ayumi; Peterson, Richard E; Stegeman, John J; Kitazawa, Takio; Hiraga, Takeo; Kubota, Akira

    2014-09-01

    The cardiovascular system is one of the most characteristic and important targets for developmental toxicity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in fish larvae. However, knowledge of the mechanism of TCDD-induced edema after heterodimerization of aryl hydrocarbon receptor type 2 (AHR2) and AHR nuclear translocator type 1 (ARNT1) is still limited. In the present study, microscopic analysis with a high-speed camera revealed that TCDD increased the size of a small cavity between the heart and body wall in early eleutheroembryos, a toxic effect that we designate as precardiac edema. A concentration-response curve for precardiac edema at 2 days post fertilization (dpf) showed close similarity to that for conventional pericardial edema at 3 dpf. Precardiac edema caused by TCDD was reduced by morpholino knockdown of AHR2 and ARNT1, as well as by an antioxidant (ascorbic acid). A selective inhibitor of cyclooxygenase type 2 (COX2), NS398, also markedly inhibited TCDD-induced precardiac edema. A thromboxane receptor (TP) antagonist, ICI-192,605 almost abolished TCDD-induced precardiac edema and this effect was canceled by U46619, a TP agonist, which was not influential in the action of TCDD by itself. Knockdown of COX2b and thromboxane A synthase 1 (TBXS), but not COX2a, strongly reduced TCDD-induced precardiac edema. Knockdown of COX2b was without effect on mesencephalic circulation failure caused by TCDD. The edema by TCDD was also inhibited by knockdown of c-mpl, a thrombopoietin receptor necessary for thromobocyte production. Finally, induction of COX2b, but not COX2a, by TCDD was seen in eleutheroembryos at 3 dpf. These results suggest a role of the COX2b-thromboxane pathway in precardiac edema formation following TCDD exposure in developing zebrafish.

  11. Morphine blocks the Mesobuthus tamulus venom-induced augmentation of phenyldiguanide reflex and pulmonary edema in anesthetized rats

    Directory of Open Access Journals (Sweden)

    Aparna Akella

    2016-01-01

    Conclusion: The results reveal that morphine prevents the MBT venom-induced augmentation of PDG reflex response and pulmonary edema. Thus, morphine can be useful in scorpion envenomation syndrome associated with pulmonary edema.

  12. Prevention and management of brain edema in patients with acute liver failure

    DEFF Research Database (Denmark)

    Wendon, J.; Larsen, Finn Stolze

    2008-01-01

    ) and an increase in cerebral blood flow while the cerebrospinal fluid volume remains constant. 3. The development of intracranial hypertension in patients with acute liver failure may be controlled by manipulation of the position, body temperature, plasma tonicity, arterial carbon dioxide tension, and arterial...

  13. Role of dietary polyphenols in attenuating brain edema and cell swelling in cerebral ischemia

    Science.gov (United States)

    Polyphenols are natural substances with variable phenolic structures and are enriched in vegetables, fruits, grains, bark, roots, tea, and wine. There are over 8000 polyphenolic structures identified in plants, but edible plants contain only several hundred polyphenolic structures. Recent interest...

  14. Neuroprotective effects of vagus nerve stimulation on traumatic brain injury.

    Science.gov (United States)

    Zhou, Long; Lin, Jinhuang; Lin, Junming; Kui, Guoju; Zhang, Jianhua; Yu, Yigang

    2014-09-01

    Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue.

  15. Neuroprotective effects of vagus nerve stimulation on traumatic brain injury

    Science.gov (United States)

    Zhou, Long; Lin, Jinhuang; Lin, Junming; Kui, Guoju; Zhang, Jianhua; Yu, Yigang

    2014-01-01

    Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue. PMID:25368644

  16. Histopathological Findings in Brains of Patients Who Died in the Acute Stage of Poor-grade Subarachnoid Hemorrhage

    Science.gov (United States)

    SATOMI, Junichiro; HADEISHI, Hiromu; YOSHIDA, Yasuji; SUZUKI, Akifumi; NAGAHIRO, Shinji

    2016-01-01

    Patients with poor-grade aneurysmal subarachnoid hemorrhage (SAH) are likely to die due to irreversible acute-stage primary brain damage. However, the mechanism(s) and pathology responsible for their high mortality rate remain unclear. We report our findings on the brains of individuals who died in the acute stage of SAH. An autopsy was performed on the brains of 11 SAH patients (World Federation of Neurosurgical Societies grade 5) who died within 3 days of admission and who did not receive respiratory assistance. All brains were free of intracranial hematoma and hydrocephalus; all harbored ruptured aneurysms. In all brains, multiple infarcts with perifocal edema were scattered throughout the cortex and subcortical white matter of the whole brain. Infarcts with a patchy – were more often seen than infarcts with a wedge-shaped pattern. Microscopic examination revealed multiple areas with cytotoxic edema and neuronal death indicative of acute ischemic changes. Edema and congestion were more obvious in areas where the subarachnoid clot tightly adhered to the pia mater. Pathologically, the brains of deceased patients with acute poor-grade SAH were characterized by edema and multifocal infarcts spread throughout the whole brain; they were thought to be attributable to venous ischemia. Diffuse disturbance in venous drainage attributable to an abrupt increase in the intracranial pressure and focal disturbances due to tight adhesion of the subarachnoid clot to the pia mater, may contribute strongly to irreversible brain damage in the acute stage of SAH. PMID:27357086

  17. Tumor necrosis factor-α-mediated threonine 435 phosphorylation of p65 nuclear factor-κB subunit in endothelial cells induces vasogenic edema and neutrophil infiltration in the rat piriform cortex following status epilepticus

    Directory of Open Access Journals (Sweden)

    Kim Ji-Eun

    2012-01-01

    Full Text Available Abstract Background Status epilepticus (SE induces severe vasogenic edema in the piriform cortex (PC accompanied by neuronal and astroglial damages. To elucidate the mechanism of SE-induced vasogenic edema, we investigated the roles of tumor necrosis factor (TNF-α in blood-brain barrier (BBB disruption during vasogenic edema and its related events in rat epilepsy models provoked by pilocarpine-induced SE. Methods SE was induced by pilocarpine in rats that were intracerebroventricularly infused with saline-, and soluble TNF p55 receptor (sTNFp55R prior to SE induction. Thereafter, we performed Fluoro-Jade B staining and immunohistochemical studies for TNF-α and NF-κB subunits. Results Following SE, most activated microglia showed strong TNF-α immunoreactivity. In addition, TNF p75 receptor expression was detected in endothelial cells as well as astrocytes. In addition, only p65-Thr435 phosphorylation was increased in endothelial cells accompanied by SMI-71 expression (an endothelial barrier antigen. Neutralization of TNF-α by soluble TNF p55 receptor (sTNFp55R infusion attenuated SE-induced vasogenic edema and neuronal damages via inhibition of p65-Thr435 phosphorylation in endothelial cells. Furthermore, sTNFp55R infusion reduced SE-induced neutrophil infiltration in the PC. Conclusion These findings suggest that impairments of endothelial cell functions via TNF-α-mediated p65-Thr 485 NF-κB phosphorylation may be involved in SE-induced vasogenic edema. Subsequently, vasogenic edema results in extensive neutrophil infiltration and neuronal-astroglial loss.

  18. Aquaporin 9 in rat brain after severe traumatic brain injury

    Directory of Open Access Journals (Sweden)

    Hui Liu

    2012-03-01

    Full Text Available OBJECTIVE: To reveal the expression and possible roles of aquaporin 9 (AQP9 in rat brain, after severe traumatic brain injury (TBI. METHODS: Brain water content (BWC, tetrazolium chloride staining, Evans blue staining, immunohistochemistry (IHC, immunofluorescence (IF, western blot, and real-time polymerase chain reaction were used. RESULTS: The BWC reached the first and second (highest peaks at 6 and 72 hours, and the blood brain barrier (BBB was severely destroyed at six hours after the TBI. The worst brain ischemia occurred at 72 hours after TBI. Widespread AQP9-positive astrocytes and neurons in the hypothalamus were detected by means of IHC and IF after TBI. The abundance of AQP9 and its mRNA increased after TBI and reached two peaks at 6 and 72 hours, respectively, after TBI. CONCLUSIONS: Increased AQP9 might contribute to clearance of excess water and lactate in the early stage of TBI. Widespread AQP9-positive astrocytes might help lactate move into neurons and result in cellular brain edema in the later stage of TBI. AQP9-positive neurons suggest that AQP9 plays a role in energy balance after TBI.

  19. Transplantation of autologous bone marrow-derived mesenchymal stem cells for traumatic brain injury

    Institute of Scientific and Technical Information of China (English)

    Jindou Jiang; Xingyao Bu; Meng Liu; Peixun Cheng

    2012-01-01

    Results from the present study demonstrated that transplantation of autologous bone marrow-derived mesenchymal stem cells into the lesion site in rat brain significantly ameliorated brain tissue pathological changes and brain edema, attenuated glial cell proliferation, and increased brain-derived neurotrophic factor expression. In addition, the number of cells double-labeled for 5-bromodeoxyuridine/glial fibrillary acidic protein and cells expressing nestin increased. Finally, blood vessels were newly generated, and the rats exhibited improved motor and cognitive functions. These results suggested that transplantation of autologous bone marrow-derived mesenchymal stem cells promoted brain remodeling and improved neurological functions following traumatic brain injury.

  20. EFFICACY AND SAFETY OF GRID PHOTOCOAGULATION IN DIFFUSE DIABETIC MACULAR EDEMA IN RURAL SETUP

    Directory of Open Access Journals (Sweden)

    Narendra P

    2014-04-01

    Full Text Available Macular edema is a common cause of visual impairment in non-proliferative diabetic retinopathy. Laser photocoagulation is considered to be the standard treatment for diabetic macular edema. This study was taken up to find out the efficacy and safety of grid photocoagulation in diffuse diabetic macular edema in our rural setup. OBJECTIVES: To assess visual improvement and document adverse effects if any in diffuse diabetic macular edema after grid photocoagulation. MATERIALS AND METHODS: In this study, 30 eyes of 17 patients with diffuse diabetic macular edema were evaluated at retina clinic at Tamaka, Kolar. The visual acuities, fundoscopic findings and adverse effects at 3 months, 6 months and 1 year checkup following laser were used in present analysis. RESULTS: After one year of follow up, visual acuity in 8 eyes (26.6% improved by one or more line, 17 (56.6% did not change and 5 (16.6% lost by one or more lines. Macular edema was found to regress in 23 (76.6% lasered eyes, found same in 6 (20%, worsened in 1 (3.3%. In our study 83.33% had positive visual acuity and 96.66% had positive fundoscopic finding. CONCLUSION: Grid photocoagulation is of benefit in maintaining vision and resolution of diffuse diabetic macular edema

  1. The effect of TIP on pneumovirus-induced pulmonary edema in mice.

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    Elske van den Berg

    Full Text Available BACKGROUND: Pulmonary edema plays a pivotal role in the pathophysiology of respiratory syncytial virus (RSV-induced respiratory failure. In this study we determined whether treatment with TIP (AP301, a synthetic cyclic peptide that mimics the lectin-like domain of human TNF, decreases pulmonary edema in a mouse model of severe human RSV infection. TIP is currently undergoing clinical trials as a therapy for pulmonary permeability edema and has been shown to decrease pulmonary edema in different lung injury models. METHODS: C57BL/6 mice were infected with pneumonia virus of mice (PVM and received TIP or saline (control group by intratracheal instillation on day five (early administration or day seven (late administration after infection. In a separate set of experiments the effect of multiple dose administration of TIP versus saline was tested. Pulmonary edema was determined by the lung wet-to-dry (W/D weight ratio and was assessed at different time-points after the administration of TIP. Secondary outcomes included clinical scores and lung cellular response. RESULTS: TIP did not have an effect on pulmonary edema in different dose regimens at different time points during PVM infection. In addition, TIP administration did not affect clinical severity scores or lung cellular response. CONCLUSION: In this murine model of severe RSV infection TIP did not affect pulmonary edema nor course of disease.

  2. Blood pressure, edema and proteinuria in pregnancy. 3. Study design, population and data characteristics.

    Science.gov (United States)

    Vollman, R F

    1976-01-01

    1. The mean blood pressure runs a curvilinear pattern during the course of pregnancy, with the lowest reading between 20 and 27 weeks of gestation, a continuous rise from 28 to 36 weeks, followed by a plateau. 2. the mean blood pressure in pregnancies without edema and proteinuria are lowest throughout pregnancy. However, the mean blood pressures in pregnancies complicated by edema, proteinuria, or both, are less than 5 mm. Hg higher after 28 weeks of gestation. 3. The mean blood pressures are lower in black gravidas than in white gravidas throughout pregnancy, independent of the presence or absence of edema, proteinuria, or their combinations. 4. The mean blood pressure is related to age and parity. Median-age gravidas (20-34 years) of parity 1-5 have the lowest mean blood pressures overall at any time during gestation. The mean blood pressure of nulliparas, independent of age, is elevated over the mean blood pressure of comparable multiparas. Independent of parity, maternal age systematically affects the mean blood pressure. 5. The standard deviations for the mean diastolic and systolic blood pressures are approximately 9 and 11 mm. Hg, respectively, independent of the weeks of gestation. They are affected very little by the absence or presence of edema or proteinuria, or both. 6. Edema of hands and/or face occurs more often in black gravidas. 7. The overall perinatal mortality rates in pregnancies complicated by edema are not higher than in pregnancies without edema. Perinatal mortality rates in pregnancies with proteinuria, or edema and proteinuria, on the other hand, are approximately double the rates for pregnancies without edema and proteinuria.

  3. Bone marrow edema of the knee joint; Differenzialdiagnosen des Knochenmarkoedems am Kniegelenk

    Energy Technology Data Exchange (ETDEWEB)

    Breitenseher, M.J. [Waldviertelklinikum Horn (Austria). Institut fuer Radiologie; Universitaetsklinik fuer Radiodiagnostik Wien (Austria). Abteilung Osteologie; Kramer, J. [Institut fuer CT- und MRT-Diagnostik, Linz (Austria); Mayerhoefer, M.E. [Universitaetsklinik fuer Radiodiagnostik Wien (Austria). Abteilung Osteologie; Aigner, N. [Orthopaedisches Krankenhaus Speising, Erste Orthopaedische Abteilung, Wien (Austria); Hofmann, S. [LKH Stolzalpe (Austria). Orthopaedische Abteilung

    2006-01-01

    Bone marrow edema of the knee joint is a frequent clinical picture in MR diagnostics. It can be accompanied by symptoms and pain in the joint. Diseases that are associated with bone marrow edema can be classified into different groups. Group 1 includes vascular ischemic bone marrow edema with osteonecrosis (synonyms: SONK or Ahlbaeck's disease), osteochondrosis dissecans, and bone marrow edema syndrome. Group 2 comprises traumatic or mechanical bone marrow edema. Group 3 encompasses reactive bone marrow edemas such as those occurring in gonarthrosis, postoperative bone marrow edemas, and reactive edemas in tumors or tumorlike diseases. Evidence for bone marrow edema is effectively provided by MRI, but purely morphological MR information is often unspecific so that anamnestic and clinical details are necessary in most cases for definitive disease classification. (orig.) [German] Das Knochenmarkoedem des Kniegelenks ist ein haeufiges Erscheinungsbild in der MR-Diagnostik. Es kann mit Symptomen und Schmerzen des Gelenks einhergehen. Erkrankungen, die mit einem Knochenmarkoedem vergesellschaftet sind, koennen in verschiedene Gruppen eingeteilt werden. Zur 1. Gruppe gehoeren das vaskulaer-ischaemische Knochenmarkoedem mit Osteonekrose (Synonyme SONK oder Morbus Ahlbaeck), die Osteochondrosis dissecans und das Knochenmarkoedemsyndrom, zur 2. Gruppe das traumatologische oder mechanische Knochenmarkoedem. In der 3. Gruppe werden reaktive Knochenmarkoedeme zusammengefasst wie bei Gonarthrose, postoperative Knochenmarkoedeme und reaktive Oedeme bei Tumor oder tumoraehnlichen Erkrankungen. Der Nachweis eines Knochenmarkoedems gelingt mit der MRT sehr sensitiv, die rein morphologische MR-Information ist jedoch oft unspezifisch, sodass anamnestische und klinische Informationen fuer die sichere Zuordnung einer Erkrankung in den meisten Faellen notwendig sind. (orig.)

  4. Environmental enrichment promotes neural remodeling in newborn rats with hypoxic-ischemic brain damage

    Institute of Scientific and Technical Information of China (English)

    Chuanjun Liu; Yankui Guo; Yalu Li; Zhenying Yang

    2011-01-01

    We evaluated the effect of hypoxic-ischemic brain damage and treatment with early environmental enrichment intervention on development of newborn rats, as evaluated by light and electron microscopy and morphometry. Early intervention with environmental enrichment intelligence training attenuated brain edema and neuronal injury, promoted neuronal repair, and increased neuronal plasticity in the frontal lobe cortex of the newborn rats with hypoxic-ischemic brain damage.

  5. Evaluation of the Prevalence of Concomitant Idiopathic Cyclic Edema and Cellulite

    OpenAIRE

    de Godoy, José Maria Pereira; Godoy,Maria de Fátima Guerreiro

    2011-01-01

    The aim of this study was to evaluate the prevalence of concomitant idiopathic cyclic edema with Grade II and III cellulite. All patients treated for Grade II and III cellulite were evaluated for idiopathic cyclic edema in a retrospective, quantitative and cross-sectional study. The study was carried out at the Godoy Clinic in the period from 2006 to 2010. All patients with body mass indexes > 25, Grade I cellulite and other causes of edema were excluded. The diagnosis of idiopathic cyclic ed...

  6. Diagnosis and quantitative estimation of pulmonary congestion or edema by pulmonary CT numbers

    Energy Technology Data Exchange (ETDEWEB)

    Kato, Shiro; Nakamoto, Takaaki

    1987-12-01

    Pulmonary computed tomography (CT) was performed in 25 patients with left heart failure and 10 healthy persons to diagnose pulmonary congestion or edema associated with left heart failure. In an analysis of histogram for pulmonary CT numbers obtained from CT scans, CT numbers indicating pulmonary edema were defined as -650 to -750 H.U. This allowed pulmonary edema to be quantitatively estimated early when abnormal findings were not available on chest X-ray film or pulmonary circulation studies. Histograms for CT numbers could be displayed by colors on CT scans. (Namekawa, K.).

  7. Reexpansion pulmonary edema following a posttraumatic pneumothorax: a case report and review of the literature

    Directory of Open Access Journals (Sweden)

    Bechtold Barbara

    2011-09-01

    Full Text Available Abstract The reexpansion pulmonary edema is a rare, but life threatening complication of a pneumothorax. Early recognition and a fast symptom orientated therapy are necessary for a good outcome. Several cases after non traumatic pneumothoraces are reported. We describe a patient who presented with a post-traumatic right pneumothorax. After the insertion of a chest tube he developed a reexpansion pulmonary edema, which had to be treated by an intubation. Additionally, a review of the literature regarding case reports of reexpansion pulmonary edema is presented.

  8. Microperimetry Findings of a Patient with Macular Edema Secondary to Retinitis Pigmentosa

    Directory of Open Access Journals (Sweden)

    Cem Ozgonul

    2013-08-01

    Full Text Available Sixty-nine year old male patient with a diagnosis of retinitis pigmentosa admitted to our clinic. In ophthalmologic examination fundoscopy was compatible with retinitis pigmentosa. For evaluation of macular edema, optical coherence tomography and microperimetry were performed to examine the structure and function of the macula. Chronic macular edema findings were obtained with optical coherence tomography. By microperimetry, mean retinal sensitivity in the central 20 degrees of both eyes was measured 8-10 decibels. The aim of this study is, to emphasize the importance of microperimetry for the evaluation of retinal function in a patient with macular edema secondary to retinitis pigmentosa.

  9. Acute Hemorrhagic Edema of Infancy: A Case Report Case Report¬

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    Hakan Turan

    2011-04-01

    Full Text Available Introduction: Acute hemorrhagic edema of infancy is a rare subtype of leukocytoclastic vasculitis. It is characterized by target-like hemorrhagic plaques with edema. Lesions are localized to face and distal extremities. It usually heals spontaneously without any sequelae.Case Report: Herein, an 8-month-old girl infant with acute hemorrhagic edema of infancy was presented. Conclusion: Both dermatologists and pediatricians must be familiar with this rare type of leukocytoclastic vasculitis. We believe that this familiarity will eliminate unnecessary treatment and anxiety about the disease (Journal of Current Pediatrics 2011; 9: 50-2

  10. Darapladib, a lipoprotein-associated phospholipase A2 inhibitor, in diabetic macular edema

    DEFF Research Database (Denmark)

    Staurenghi, Giovanni; Ye, Li; Magee, Mindy H;

    2015-01-01

    PURPOSE: To investigate the potential of lipoprotein-associated phospholipase A2 inhibition as a novel mechanism to reduce edema and improve vision in center-involved diabetic macular edema (DME). DESIGN: Prospective, multicenter, randomized, double-masked, placebo-controlled phase IIa study...... (AEs) and nonocular AEs were similar between treatment groups. CONCLUSIONS: Once-daily oral darapladib administered for 3 months demonstrated modest improvements in vision and macular edema that warrant additional investigation of this novel lipoprotein-associated phospholipase A2 inhibitory mechanism...

  11. Remitting seronegative symmetrical synovitis with pitting edema (RS3PE syndrome

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    Neslihan Gokcen

    2017-03-01

    Full Text Available Remitting seronegative symmetrical synovitis with pitting edema is a rare rheumatological disorder that presents with symmetrical hand and/or foot edema resembling rheumatoid arthritis. It is generally seen in male patients in older age, but atypical cases in different age groups have been documented. Although no clear mechanism has been described, certain genetic and environmental factors have been suggested for etiopathogenesis. Medical treatment is mainly focused on glucocorticoid therapy. This article aims to discuss the Remitting seronegative symmetrical synovitis with pitting edema syndrome and to review the current literature. [Cukurova Med J 2017; 42(1.000: 147-154

  12. Increasing recognition of dermatomyositis with subcutaneous edema - is this a poorer prognostic marker?

    Science.gov (United States)

    Tu, Jenny; McLean-Tooke, Andrew; Junckerstorff, Reimar

    2014-01-15

    Subcutaneous edema as a presenting feature of dermatomyositis has infrequently been described and is thought to signify a more aggressive disease course. We report a case involving a 38-year-old man who presented with significant subcutaneous edema involving his neck and upper body; he later developed clinical features and biopsy results consistent with dermatomyositis. Only sixteen previous cases of dermatomyositis with subcutaneous edema involving adults have been published in the literature and we aim to review disease progression, prognosis, and optimal treatment of the condition.

  13. Negative Pressure Pulmonary Edema Following use of Laryngeal Mask Airway (LMA

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    Yesim Bayraktar

    2013-06-01

    Full Text Available Negative pressure pulmonary edema (NPPE following upper airway obstruction is a non-cardiogenic pulmonary edema. The first cause in the etiology of NPPE is developed laryngospasm after intubation or extubation, while the other causes are epiglotitis, croup, hiccups, foreign body aspiration, pharyngeal hematoma and oropharyngeal tumors.The Late diagnosis and treatment causes high morbidity and mortality. The protection of the airway and maintainance of arterial oxygenation will be life saving.In this article we aimed to report  a case of negative pressure pulmonary edema, resolved succesfully after treatment, following use of laryngeal mask airway (LMA.

  14. Loss of wwox expression in zebrafish embryos causes edema and alters Ca2+ dynamics

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    Yusuke Tsuruwaka

    2015-01-01

    Full Text Available We investigated the role of the WW domain-containing oxidoreductase (wwox gene in the embryonic development of zebrafish, with particular emphasis on intracellular Ca2+ dynamics because Ca2+ is an important intracellular messenger. Comparisons between zebrafish wwox and human WWOX sequences identified highly conserved domain structures. wwox was expressed in developing heart tissues in the zebrafish embryo. Moreover, wwox knockdown induced pericardial edema with similarities to conditions observed in human breast cancer. The wwox knockdown embryos with the edema died within a week. High Ca2+ levels were observed at the boundary between the edema and yolk in wwox knockdown embryos.

  15. Updates on the Clinical Trials in Diabetic Macular Edema.

    Science.gov (United States)

    Demirel, Sibel; Argo, Colby; Agarwal, Aniruddha; Parriott, Jacob; Sepah, Yasir Jamal; Do, Diana V; Nguyen, Quan Dong

    2016-01-01

    In this era of evidence-based medicine, significant progress has been made in the field of pharmacotherapeutics for the management of diabetic macular edema (DME). A. number of landmark clinical trials have provided strong evidence of the safety and efficacy of agents such as anti-vascular endothelial growth factors for the treatment of DME. Decades of clinical research, ranging from the early treatment of diabetic retinopathy study to the present-day randomized clinical trials (RCTs) testing novel agents, have shifted the goal of therapy from preventing vision loss to ensuring a maximum visual gain. Systematic study designs have provided robust data with an attempt to optimize the treatment regimens including the choice of the agent and timing of therapy. However, due to a number of challenges in the management of DME with approved agents, further studies are needed. For the purpose of this review, an extensive database search in English language was performed to identify prospective, RCTs testing pharmacological agents for DME. In order to acquaint the reader with the most relevant data from these clinical trials, this review focuses on pharmacological agents that are currently approved or have widespread applications in the management of DME. An update on clinical trials presently underway for DME has also been provided.

  16. Acute Pulmonary Edema in Patients with Cushing’s Syndrome

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    Mitra Niafar

    2015-01-01

    Full Text Available IntroductionDyspnea refers to difficulty in breathing, and short and shallow breaths. This sign is seen in numerous diseases due to pulmonary, cardiac, metabolic and neurological causes. Among cardiac causes, heart failure is considered the main cause of dyspnea.Cardiac failure is a clinical syndrome associated with a set of symptoms (dyspnea, and fatigue and signs (edema and rales. Common causes of cardiac failure include: myocardial infarction, ischemic heart disease, hypertension, valvular heart diseases, and cardiomyopathy. Among uncommon causes of heart failure, endocrine disorders such as Cushing’s syndrome can be cited. Cushing’s syndrome can present itself in less common forms such as dyspnea due to heart failure. Cushing’s syndrome’s cardiovascular complications usually occur due to hypertension, end organ damage such as left ventricular heart failure, diastolic and ischemic myocardial heart failure, which are rather seen in chronic cases of the disease and are often irreversible.Transient heart failure in patients with Cushing’s syndrome, due to adrenal adenoma, has been reported in a number of patients. In this case report, a patient is introduced who presented to emergency department with severe dyspnea (FC III, and was ultimately diagnosed with Cushing’s syndrome after work up. Three months after treatment of Cushing’s syndrome, dramatic improvement was observed in this patient’s cardiac function.

  17. Fast axonal transport in early experimental disc edema.

    Science.gov (United States)

    Radius, R L; Anderson, D R

    1980-02-01

    Previous work has documented impairment of slow axonal transport in papilledema, but the abnormalities in rapid transport were less certain. Therefore fast axonal transport was studied in 19 primate eyes subjected to ocular hypotony for 6 to 72 hr following surgical fistulization of the anterior chamber. Mild, irregular alterations in fast axonal transport were detected only after nerve head swelling was apparent. These changes in fast transport mechanisms in cases of nerve head edema occur after, and may be secondary to, impaired slow axoplasmic flow and the resultant axonal swelling. Furthermore, since prolonged complete interruption of axonal transport is theoretically inconsistent with the continued normal neuron function characteristic of papilledema and, moreover, since previous data shows a "slowdown" rather than complete blockade of axonal transport in papilledema, it is likely that in eyes with papilledema there does not exist a complete flock of axonal transport. Therefore we hypothesize that the swelling results when slow axoplasmic flow is locally slowed down but not totally stopped, with the axon distention producing secondary mild, irregular changes in fast axonal transport.

  18. Three plasma metabolite signatures for diagnosing high altitude pulmonary edema

    Science.gov (United States)

    Guo, Li; Tan, Guangguo; Liu, Ping; Li, Huijie; Tang, Lulu; Huang, Lan; Ren, Qian

    2015-10-01

    High-altitude pulmonary edema (HAPE) is a potentially fatal condition, occurring at altitudes greater than 3,000 m and affecting rapidly ascending, non-acclimatized healthy individuals. However, the lack of biomarkers for this disease still constitutes a bottleneck in the clinical diagnosis. Here, ultra-high performance liquid chromatography coupled with Q-TOF mass spectrometry was applied to study plasma metabolite profiling from 57 HAPE and 57 control subjects. 14 differential plasma metabolites responsible for the discrimination between the two groups from discovery set (35 HAPE subjects and 35 healthy controls) were identified. Furthermore, 3 of the 14 metabolites (C8-ceramide, sphingosine and glutamine) were selected as candidate diagnostic biomarkers for HAPE using metabolic pathway impact analysis. The feasibility of using the combination of these three biomarkers for HAPE was evaluated, where the area under the receiver operating characteristic curve (AUC) was 0.981 and 0.942 in the discovery set and the validation set (22 HAPE subjects and 22 healthy controls), respectively. Taken together, these results suggested that this composite plasma metabolite signature may be used in HAPE diagnosis, especially after further investigation and verification with larger samples.

  19. Craniotomia descompressiva bifrontal no tratamento do edema cerebral grave

    Directory of Open Access Journals (Sweden)

    Walter C. Pereira

    1977-06-01

    Full Text Available São apresentados os resultados obtidos com craniotomia descompressiva bifrontal ampla em 12 doentes com edema cerebral grave e irreversível com os métodos convencionais de tratamento, provocado em 10 por traumatismo crânio-encefálico. Todos os pacientes apresentavam quadro neurológico muito grave, com sinais de comprometimento do tronco cerebral superior. Angiografia caro-tídea bilateral foi praticada sistematicamente, tanto no pré como no pós-operatório, constituindo-se no fator decisivo para a indicação cirúrgica. Seis (50% dos doentes sobreviveram, apresentando 5 (41,6% recuperação neurológica e psíquica praticamente totais. Levando em conta estes resultados, consideramos esta técnica cirúrgica o melhor recurso de tratamento em tais casos, máxime se indicada precocemente. São necessários, contudo, cuidados pós-operatórios especiais com estes pacientes, que devem, sempre que possível, ser mantidos em unidade de terapia intensiva, em virtude da grande incidência de complicações, mormente respiratórias.

  20. Proanthocyanidin to prevent formation of the reexpansion pulmonary edema

    Directory of Open Access Journals (Sweden)

    Akay Cemal

    2009-07-01

    Full Text Available Abstract Background We aimed to investigate the preventive effect of Proanthocyanidine (PC in the prevention of RPE formation. Methods Subjects were divided into four groups each containing 10 rats. In the Control Group (CG: RPE wasn't performed. Then subjects were followed up for three days and they were sacrificed after the follow up period. Samplings were made from tissues for measurement of biochemical and histopathologic parameters. In the Second Group (PCG: The same protocol as CG was applied, except the administration of PC to the subjects. In the third RPE Group (RPEG: Again the same protocol as CG was applied, but as a difference, RPE was performed. In the Treatment Group (TG: The same protocol as RPEG was applied except the administration of PC to the subjects. Results In RPEG group, the most important histopathological finding was severe pulmonary edema with alveolar damage and acute inflammatory cells. These findings were less in the TG group. RPE caused increased MDA levels, and decreased GPx, SOD and CAT activity significantly in lung tissue. Conclusion PC decreased MDA levels. Oxidative stress plays an important role in pathophysiology of RPE and PC treatment was shown to be useful to prevent formation of RPE.

  1. Microcystic macular edema detection in retina OCT images

    Science.gov (United States)

    Swingle, Emily K.; Lang, Andrew; Carass, Aaron; Ying, Howard S.; Calabresi, Peter A.; Prince, Jerry L.

    2014-03-01

    Optical coherence tomography (OCT) is a powerful imaging tool that is particularly useful for exploring retinal abnormalities in ophthalmological diseases. Recently, it has been used to track changes in the eye associated with neurological diseases such as multiple sclerosis (MS) where certain tissue layer thicknesses have been associated with disease progression. A small percentage of MS patients also exhibit what has been called microcystic macular edema (MME), where uid collections that are thought to be pseudocysts appear in the inner nuclear layer. Very little is known about the cause of this condition so it is important to be able to identify precisely where these pseudocysts occur within the retina. This identi cation would be an important rst step towards furthering our understanding. In this work, we present a detection algorithm to nd these pseudocysts and to report on their spatial distribution. Our approach uses a random forest classi er trained on manual segmentation data to classify each voxel as pseudocyst or not. Despite having a small sample size of ve subjects, the algorithm correctly identi es 84.6% of pseudocysts as compared to manual delineation. Finally, using our method, we show that the spatial distribution of pseudocysts within the macula are generally contained within an annulus around the fovea.

  2. Diabetic Macular Edema: From Old Concepts to New Therapeutic Avenues.

    Science.gov (United States)

    Mansour, Ahmad M; Pulido, Jose S; Arevalo, J Fernando

    2015-01-01

    Diabetic macular edema (DME) is a significant cause of blindness in the working population and is currently challenging to treat. Current interventions include focal laser or intravitreal injections. This article outlines a new treatment protocol based on the theory that peripheral ischemia is the precursor to angiogenesis, which will ultimately gather its momentum at the fovea. Extreme peripheral light laser panretinal photocoagulation (PRP) back to the equator reduces excessive production of the vascular endothelial growth factor (VEGF) in the eye. This decreases VEGF-induced DME and provides long-term protection against the development of neovascularization. Initial exacerbation of DME often accompanies PRP. Therefore, injections of anti-VEGF agents (with or without dexamethasone implants) initially can forestall worsening of DME and prevent loss of vision. However, on the other hand, applying peripheral PRP and intraocular injections can induce posterior vitreous detachment (PVD). This could help release vitreomacular adhesions (VMA) and vitreomacular traction (VMT), thereby decreasing DME severity and improving the response to intravitreal injections. In the current approach, peripheral retinal photocoagulation should stop the drive for VEGF release; moreover, laser ablation should produce secondary, accidental, and beneficial PVD. This approach precludes focal laser therapy and paves the path for prolonged intervals between anti-VEGF therapy.

  3. Pharmacologic therapies for diabetic retinopathy and diabetic macular edema.

    Science.gov (United States)

    Rechtman, Ehud; Harris, Alon; Garzozi, Hanna J; Ciulla, Thomas A

    2007-12-01

    Diabetic retinopathy (DR) and diabetic macular edema (DME) are leading causes of blindness in the working-aged population of most developed countries. The increasing number of persons with diabetes worldwide suggests that DR/DME will continue to be major contributors to vision loss and associated functional impairment for years to come. Early detection of retinopathy in persons with diabetes is critical in preventing visual loss, but current methods of screening fail to identify a sizable number of high-risk patients. The control of diabetes-associated metabolic abnormalities (ie, hyperglycemia, hyperlipidemia, and hypertension) is also important in preserving visual function, as these conditions have been identified as risk factors for both the development and progression of DR/DME. The non-pharmacologic interventions for DR/DME, laser photocoagulation and vitrectomy, only target advanced stages of disease. Several biochemical mechanisms, including increased vascular endothelial growth factor production, protein kinase C beta activation, oxidative stress, and accumulation of intracellular sorbitol and advanced glycosylation end products, may contribute to the vascular disruptions that characterize DR/DME. The inhibition of these pathways holds the promise of the intervention for diabetic retinopathy with higher success rate and also at earlier, non-sight-threatening stages.

  4. Management of acute cardiogenic pulmonary edema: a literature review.

    Science.gov (United States)

    Johnson, Jeremy M

    2009-01-01

    Acute cardiogenic pulmonary edema (CPE) is a pathology frequently seen in patients presenting to emergency departments (EDs) and can usually be attributed to preexisting cardiovascular disease. Heart failure alone accounts for more than 1 million hospital admissions annually and has one of the highest ED morbidity and mortality to date (). Historically, CPE has been managed by the treating clinician in a manner that is based largely on anecdotal evidence. Furosemide (Lasix), morphine, and nitroglycerin have historically been the baseline standard for drug therapy in CPE management. A lack of drastic improvement in the patient's condition over the course of the ED visit may reflect a management style that results in higher morbidity and mortality for CPE patients. Several recent articles provide evidence-based outcomes that suggest changing standard therapy along with the adjunctive use of other medications. These articles also describe treatment modalities that result in a marked improvement in the management of patients with CPE along with decreases in adverse outcomes and hospital length of stay. The goal of this article is to present a summary of the evidence regarding the management of CPE and discuss the implications for current practice.

  5. Epidemiological and clinical studies on aseptic meningitis in 377 cases, 3. A study on brain CT scan in acute phase

    Energy Technology Data Exchange (ETDEWEB)

    Nishimura, Masaaki; Kondo, Tomio; Takashima, Akira; Kono, Shinya; Yamashina, Manabu (Ogaki Shimin Hospital, Gifu (Japan))

    1984-02-01

    Brain CT scan performed in the acute phase of aseptic meningitis in 88 cases revealed abnormal findings in 5 consisting of 2 of cerebral edema, 2 of subdural hygroma and one of cerebral atrophy. Clinical findings showed no particular relation to the age, but cerebral edema was observed in the cases of possible cephalomeningitis diagnosed on the basis of accompanying convulsion and disturbance of consciousness. Abnormal findings were associated with 25% of symptoms diagnosed more than 4 days after onset.

  6. Nanowired Drug Delivery Across the Blood-Brain Barrier in Central Nervous System Injury and Repair.

    Science.gov (United States)

    Sharma, Aruna; Menon, Preeti; Muresanu, Dafin F; Ozkizilcik, Asya; Tian, Z Ryan; Lafuente, José V; Sharma, Hari S

    2016-01-01

    The blood-brain barrier (BBB) is a physiological regulator of transport of essential items from blood to brain for the maintenance of homeostasis of the central nervous system (CNS) within narrow limits. The BBB is also responsible for export of harmful or metabolic products from brain to blood to keep the CNS fluid microenvironment healthy. However, noxious insults to the brain caused by trauma, ischemia or environmental/chemical toxins alter the BBB function to small as well as large molecules e.g., proteins. When proteins enter the CNS fluid microenvironment, development of brain edema occurs due to altered osmotic balance between blood and brain. On the other hand, almost all neurodegenerative diseases and traumatic insults to the CNS and subsequent BBB dysfunction lead to edema formation and cell injury. To treat these brain disorders suitable drug therapy reaching their brain targets is needed. However, due to edema formation or only a focal disruption of the BBB e.g., around brain tumors, many drugs are unable to reach their CNS targets in sufficient quantity. This results in poor therapeutic outcome. Thus, new technology such as nanodelivery is needed for drugs to reach their CNS targets and be effective. In this review, use of nanowires as a possible novel tool to enhance drug delivery into the CNS in various disease models is discussed based on our investigations. These data show that nanowired delivery of drugs may have superior neuroprotective ability to treat several CNS diseases effectively indicating their role in future therapeutic strategies.

  7. Cerebrolysin reduces blood-cerebrospinal fluid barrier permeability change, brain pathology, and functional deficits following traumatic brain injury in the rat.

    Science.gov (United States)

    Sharma, Hari Shanker; Zimmermann-Meinzingen, Sibilla; Johanson, Conrad E

    2010-06-01

    Traumatic brain injuries (TBIs) induce profound breakdown of the blood-brain and blood-cerebrospinal fluid barriers (BCSFB), brain pathology/edema, and sensory-motor disturbances. Because neurotrophic factors, such as brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), and glial cell-derived neurotrophic factor (GDNF), are neuroprotective in models of brain and spinal cord injuries, we hypothesized that a combination of neurotrophic factors would enhance neuroprotective efficacy. In the present investigation, we examined the effects of Cerebrolysin, a mixture of different neurotrophic factors (Ebewe Neuro Pharma, Austria) on the brain pathology and functional outcome in a rat model of TBI. TBI was produced under Equithesin (3 mL/kg, i.p.) anesthesia by making a longitudinal incision into the right parietal cerebral cortex. Untreated injured rats developed profound disruption of the blood-brain barrier (BBB) to proteins, edema/cell injury, and marked sensory-motor dysfunctions on rota-rod and grid-walking tests at 5 h TBI. Intracerebroventricular administration of Cerebrolysin (10 or 30 microL) either 5 min or 1 h after TBI significantly reduced leakage of Evans blue and radioiodine tracers across the BBB and BCSFB, and attenuated brain edema formation/neuronal damage in the cortex as well as underlying subcortical regions. Cerebrolysin-treated animals also had improved sensory-motor functions. However, administration of Cerebrolysin 2 h after TBI did not affect these parameters significantly. These observations in TBI demonstrate that early intervention with Cerebrolysin reduces BBB and BCSFB permeability changes, attenuates brain pathology and brain edema, and mitigates functional deficits. Taken together, our observations suggest that Cerebrolysin has potential therapeutic value in TBI.

  8. Edema pulmonar por presión negativa: a propósito de 3 casos Negative pressure pulmonary edema: 3 cases report

    Directory of Open Access Journals (Sweden)

    J. R. Ortiz-Gómez

    2006-08-01

    Full Text Available El edema agudo pulmonar por presión negativa es una complicación descrita desde 1977 tras la obstrucción de la vía aérea respiratoria, tanto en niños como en adultos. Aunque su etiopatogenia es multifactorial, destaca especialmente la excesiva presión intratorácica negativa causada por la inspiración forzada espontánea de un paciente con la glotis cerrada, que resulta en trasudación de líquido de los capilares pulmonares hacia el espacio alveolointersticial. El edema pulmonar resultante puede aparecer en pocos minutos tras la obstrucción de la vía aérea o de forma diferida al cabo de varias horas. Este cuadro clínico es potencialmente grave, pero habitualmente responde bien al tratamiento con oxigenoterapia, ventilación mecánica a presión positiva y diuréticos. Es importante el diagnóstico de sospecha para adecuar el tratamiento con presteza. Presentamos nuestra experiencia en 3 casos clínicos con edema agudo pulmonar por presión negativa.Negative pressure pulmonary edema is a complication, described since 1977, caused by upper airway obstruction in both children and adults. Although its aetiopathogeny is multifactorial, especially outstanding is excessive negative intrathoracic pressure caused by the forced spontaneous inspiration of a patient against a closed glottis, that causes high arteriole and capillary fluid pressures that favor transudation into the alveolar space The resulting pulmonary edema can appear a few minutes after the obstruction of the airway or in a deferred way after several hours. The clinical manifestations are potentially serious, but normally respond well to treatment with supplemental oxygen, positive pressure mechanical ventilation and diuretics. Diagnostic suspicion is important for acting promptly. We report three clinical cases with acute negative pressure pulmonary edema.

  9. Costs and Quality of Life in Diabetic Macular Edema: Canadian Burden of Diabetic Macular Edema Observational Study (C-REALITY

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    John R. Gonder

    2014-01-01

    Full Text Available Purpose. To characterize the economic and quality of life burden of diabetic macular edema (DME in Canadian patients. Patients and Methods. 145 patients with DME were followed for 6 months with monthly telephone interviews and medical chart reviews at months 0, 3, and 6. Visual acuity in the worst-seeing eye was assessed at months 0 and 6. DME-related healthcare costs were determined over 6 months, and vision-related (National Eye Institute Visual Functioning Questionnaire and generic (EQ-5D quality of life was assessed at months 0, 3, and 6. Results. Mean age of patients was 63.7 years: 52% were male and 72% had bilateral DME. At baseline, visual acuity was categorized as normal/mild loss for 63.4% of patients, moderate loss for 10.4%, and severe loss/nearly blind for 26.2%. Mean 6-month DME-related costs/patient were as follows: all patients (n=135, $2,092; normal/mild loss (n=88, $1,776; moderate loss (n=13, $1,845; and severe loss/nearly blind (n=34, $3,007. Composite scores for vision-related quality of life declined with increasing visual acuity loss; generic quality of life scores were highest for moderate loss and lowest for severe loss/nearly blind. Conclusions. DME-related costs in the Canadian healthcare system are substantial. Costs increased and vision-related quality of life declined with increasing visual acuity severity.

  10. Sheehan's Syndrome with Edema in Optical Neural Sheaths: A Case Report

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    Mehtap Evran

    2013-04-01

    Full Text Available Sheehan syndrome is partial or complete hypophyseal insufficiency due to hypophyseal necrosis secondary to postpartum hemorrhage and hypovolemia. Clinical findings are cessation of lactation, secondary amenorrhea, loss of libido and hypophyseal reserve loss. Treatment is hormone replacement. Forty-four years old women admitted with somnolence, malaise, edema and blurred vision. Physical examination revealed edema and hypotension. She had massive bleeding during her birth 11 years old ago; therefore she had received blood transfusion and could not breast-feed then. She had amenorrhea when she admitted. She was diagnosed to be Sheehan syndrome while glucocorticoid and levothyroxine replacement was started. Hypophyseal and orbital magnetic resonance imaging revealed empty sella and edema in bilateral optical neural sheaths respectively. Empty sella may cause edema in optical neural sheaths by increasing pressure in subarachnoidal space. We present this case to point out this coincidence. [Cukurova Med J 2013; 38(2.000: 299-304

  11. Emergent balloon mitral valvotomy in pregnant women presenting with refractory pulmonary edema

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    N. Bouchahda

    2014-03-01

    Conclusion: During pregnancy, emergent BMV is safe and feasible in patients with symptomatic mitral stenosis and severe pulmonary edema. There is marked symptomatic relief, along with excellent maternal and fetal outcomes.

  12. Subclinical high altitude pulmonary edema:A clinical observation of 12 cases in Yushu

    Institute of Scientific and Technical Information of China (English)

    Li Shuzhi; Zheng Bihai; Wu Tianyi; Chen Huixing; Zhang Ming

    2013-01-01

    During the Yushu Earthquake on April 14,2010,a high incidence of acute high altitude illness was observed in the mountain rescuers,and 0.73 % of these patients suffered from high altitude pulmonary edema,of which 12 patients developed subclinical pulmonary edema and concomitantly contracted acute mountain sickness.Symptoms and signs were atypically high heart rate with high respiratory rate,striking cyanosis,and significantly low oxygen saturation,whereas no moist rates were heard on auscultation,and Chest X-ray showed peripheral with a patchy distribution of mottled infiltrations in one or both lung fields.We believe that subclinical high altitude pulmonary edema is an earliest stage of pulmonary edema at high altitude.The possible pathogenesis and the diagnosis were discussed.

  13. A Case of Re-Expansion Pulmonary Edema after Rapid Pleural Evacuation

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    SH Shahbazi

    2007-07-01

    Full Text Available Introduction & Objective: Pulmonary edema after chest tube insertion is a rare complication and is associated with high mortality. The cause of this phenomenon is not clear, although causes such as decrease in surfactant and inflammatory process have been defined. Early diagnosis and treatment decrease the mortality. This study introduces a case of re-expansion pulmonary edema after rapid pleural evacuation. Case: The case is a 4.5 y/o boy, a case of Tetralogy of Fallot, who developed respiratory distress after surgery (Total Correction in ICU of Namazi Hospital in 1385. Chest X ray showed pneumothorax of left lung. For the patient, chest tube was inserted and the symptoms improved. After few hours the patient developed tachypnea, tachycardia, and CXR showed pulmonary edema of left lung. Appropriate treatment was done for the patient and his condition improved. Conclusion: Pulmonary edema after sudden evacuation of pleura is a rare phenomenon and early diagnosis decreases the mortality.

  14. Emergent Unilateral Renal Artery Stenting for Treatment of Flash Pulmonary Edema: Fact or Fiction?

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    Asaad Akbar Khan

    2015-01-01

    Full Text Available Flash pulmonary edema is characteristically sudden in onset with rapid resolution once appropriate therapy has been instituted (Messerli et al., 2011. Acute increase of left ventricular (LV end diastolic pressure is the usual cause of sudden decompensated cardiac failure in this patient population. Presence of bilateral renal artery stenosis or unilateral stenosis in combination with a single functional kidney in the susceptible cohort is usually blamed for this condition. We describe a patient who presented with flash pulmonary edema in the setting of normal coronary arteries. Our case is distinct as our patient developed flash pulmonary edema secondary to unilateral renal artery stenosis in the presence of bilateral functioning kidneys. Percutaneous stent implantation in the affected renal artery resulted in rapid resolution of pulmonary edema.

  15. Emergent Unilateral Renal Artery Stenting for Treatment of Flash Pulmonary Edema: Fact or Fiction?

    Science.gov (United States)

    Khan, Asaad Akbar; McFadden, Eugene Patrick

    2015-01-01

    Flash pulmonary edema is characteristically sudden in onset with rapid resolution once appropriate therapy has been instituted (Messerli et al., 2011). Acute increase of left ventricular (LV) end diastolic pressure is the usual cause of sudden decompensated cardiac failure in this patient population. Presence of bilateral renal artery stenosis or unilateral stenosis in combination with a single functional kidney in the susceptible cohort is usually blamed for this condition. We describe a patient who presented with flash pulmonary edema in the setting of normal coronary arteries. Our case is distinct as our patient developed flash pulmonary edema secondary to unilateral renal artery stenosis in the presence of bilateral functioning kidneys. Percutaneous stent implantation in the affected renal artery resulted in rapid resolution of pulmonary edema. PMID:25793128

  16. 神经源性肺水肿%Neurogenic pulmonary edema

    Institute of Scientific and Technical Information of China (English)

    孙若鹏; 赵翠芬

    2008-01-01

    @@ Neurogenic pulmonary edema (NPE) is a type of pulmonary edema that occurs secondary to central nervous sytem (CNS) damage, namely centrogenic pulmonary edema or cerebrogenic pulmonary edema[1,2] NPE is clinically characterized by acute dyspnea and progressive hypoxemia, while tachycardia, hypertension and tachypnea are only nonspecific symptoms in early phase. Early diagnosis of NPE is difficult since chest X-ray shows no remarkable sign or only increased hazy lung markings in early stage[3]. Diagnosis can be made definitely in the late stage of NPE according to the following manifestation : paleness, clamminess, feeling of impending death, rales, frothy pink sputum, hypoxemia and bilateral widespread infiltration on chest roentgenography. However, successful rescue rate is very low and mortality rate could reach as high as 90% at this stage[4-6].

  17. Etiology and treatment of the inflammatory causes of cystoid macular edema.

    Science.gov (United States)

    Cho, Hyung; Madu, Assumpta

    2009-01-01

    Cystoid macular edema in its various forms can be considered one of the leading causes of central vision loss in the developed world. It occurs in a wide variety of pathologic conditions and represents the final common pathway of several basic processes. Therapeutic approaches to cystoid macular edema depend on a clear understanding of its contributing pathophysiologic mechanisms. This review will discuss the mechanism of ocular inflammation in cystoid macular edema with a particular focus on the inflammatory causes: post-operative, uveitic, and after laser procedures. A variety of pharmacologic agents targeting inflammatory molecules have been shown to reduce macular edema and improve visual function. However, the long-term efficacy and safety of most new therapies have yet to be established in controlled clinical trials.

  18. Etiology and treatment of the inflammatory causes of cystoid macular edema

    Science.gov (United States)

    Cho, Hyung; Madu, Assumpta

    2009-01-01

    Cystoid macular edema in its various forms can be considered one of the leading causes of central vision loss in the developed world. It occurs in a wide variety of pathologic conditions and represents the final common pathway of several basic processes. Therapeutic approaches to cystoid macular edema depend on a clear understanding of its contributing pathophysiologic mechanisms. This review will discuss the mechanism of ocular inflammation in cystoid macular edema with a particular focus on the inflammator