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Sample records for alkalosis

  1. Alkalosis

    Science.gov (United States)

    ... causes you to breathe faster ( hyperventilate ) Aspirin poisoning Metabolic alkalosis is caused by too much bicarbonate in the ... alkalosis and show whether it is respiratory or metabolic alkalosis. Other tests may be needed to determine the ...

  2. [Alkalosis].

    Science.gov (United States)

    Kościelska, Malgorzata; Mieczkowski, Mariusz

    2013-01-01

    An elevation of arterial blood pH called alkalosis remains an underestimated condition in hospitalized patients. Serious alkalosis can be associated with high risk of death. The disorder can be caused by increased concentration of bicarbonate (metabolic alkalosis) or decreased concentration of carbon dioxide (respiratory alkalosis). In most cases of metabolic alkalosis it is generated by vomiting or diuretic use, whereas respiratory alkalosis is provoked by hyperventilation associated with respiratory or neurological disorder. Maintenance of metabolic alkalosis is possible only in patients with impaired renal base excretion which is most often produced by hypochloremia. In both respiratory and metabolic alkaloses treatment depends on the underlying factor. In hyperventilation syndrome is based on behavioral therapy. In most cases of metabolic alkalosis the administration of sodium and potassium chloride forms a substantial part of therapy.

  3. Respiratory alkalosis

    Science.gov (United States)

    ... a condition marked by a low level of carbon dioxide in the blood due to breathing excessively. ... aimed at the condition that causes respiratory alkalosis. Breathing ... dioxide -- sometimes helps reduce symptoms when anxiety is the ...

  4. Metabolic alkalosis.

    Science.gov (United States)

    Khanna, A; Kurtzman, N A

    2006-01-01

    Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation mainly in the proximal tubule and bicarbonate generation predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na-H antiporter and to a smaller extent by the H-ATPase. The principal factors affecting HCO 3 reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na delivery and reabsorption, aldosterone, arterial pH, and arterial pCO2. To generate metabolic alkalosis, either a gain of base or a loss of acid, must occur. The loss of acid may be via the GI tract or by the kidney. Excess base may be gained by oral or parenteral HCO 3 administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate (GFR), volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelma's Syndromes. The effects of metabolic alkalosis on the body are varied and include effects on the central nervous system, myocardium, skeletal muscle, and the liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors promoting alkalosis and in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.

  5. Approach to metabolic alkalosis.

    Science.gov (United States)

    Soifer, Jennifer T; Kim, Hyung T

    2014-05-01

    Metabolic alkalosis is a common disorder, accounting for half of all acid-base disturbances in hospitalized patients. It is the result of an increase in bicarbonate production, a decrease in bicarbonate excretion, or a loss of hydrogen ions. Most causes of metabolic alkalosis can be divided into 4 categories: chloride depletion alkalosis, mineralocorticoid excess syndromes, apparent mineralocorticoid excess syndromes, and excess alkali administration. Treatment is usually supportive and based on cause of the alkalosis. Copyright © 2014 Elsevier Inc. All rights reserved.

  6. Transplacental metabolic alkalosis.

    Science.gov (United States)

    Schimert, Patrik; Bernet-Buettiker, Vera; Rutishauser, Christoph; Schams, Mohammed; Frey, Bernhard

    2007-12-01

    We present a newborn with hypochloraemic metabolic alkalosis due to severe metabolic alkalosis of his mother. Hypoventilation as a leading symptom resolved quickly with treatment but may be life-threatening if not detected. In this case, the mother had a probable eating disorder. Little is known about transplacentally acquired electrolyte disorders in this setting. In the absence of symptoms, most of the cases might be undetected. The usual neonatal outcome of anorexia and/or bulimia nervosa in pregnancy is a lower birthweight and a lower risk for instrumental delivery.

  7. It is chloride depletion alkalosis, not contraction alkalosis.

    Science.gov (United States)

    Luke, Robert G; Galla, John H

    2012-02-01

    Maintenance of metabolic alkalosis generated by chloride depletion is often attributed to volume contraction. In balance and clearance studies in rats and humans, we showed that chloride repletion in the face of persisting alkali loading, volume contraction, and potassium and sodium depletion completely corrects alkalosis by a renal mechanism. Nephron segment studies strongly suggest the corrective response is orchestrated in the collecting duct, which has several transporters integral to acid-base regulation, the most important of which is pendrin, a luminal Cl/HCO(3)(-) exchanger. Chloride depletion alkalosis should replace the notion of contraction alkalosis.

  8. Severe metabolic alkalosis in pregnancy

    Science.gov (United States)

    Frise, Charlotte; Noori, Muna

    2013-01-01

    Summary Metabolic alkalosis is uncommon in pregnancy and is most often the result of severe vomiting. If this is present at the time of delivery, transient metabolic derangement in the fetus can occur, potentially requiring additional organ support. A 22-year-old woman is described, who presented at 37 weeks gestation with a severe metabolic alkalosis, vomiting and acute renal and hepatic impairment. The investigations, management options and maternal and fetal outcome are described. PMID:27708709

  9. A Quick Reference on Respiratory Alkalosis.

    Science.gov (United States)

    Johnson, Rebecca A

    2017-03-01

    Respiratory alkalosis, or primary hypocapnia, occurs when alveolar ventilation exceeds that required to eliminate the carbon dioxide produced by tissues. Concurrent decreases in Paco 2 , increases in pH, and compensatory decreases in blood HCO 3 - levels are associated with respiratory alkalosis. Respiratory alkalosis can be acute or chronic, with metabolic compensation initially consisting of cellular uptake of HCO 3 - and buffering by intracellular phosphates and proteins. Chronic respiratory alkalosis results in longer-lasting decreases in renal reabsorption of HCO 3 - ; the arterial pH can approach near-normal values. Copyright © 2016 Elsevier Inc. All rights reserved.

  10. Metabolic alkalosis after pediatric cardiac surgery.

    Science.gov (United States)

    van Thiel, Robert J; Koopman, Sofie R; Takkenberg, Johanna J M; Ten Harkel, Arend Derk Jan; Bogers, Ad J J C

    2005-08-01

    To determine occurrence, causes and associated mortality of postoperative metabolic alkalosis in pediatric cardiac surgery. We retrospectively analyzed clinical and biochemical variables of 186 consecutive cardiac operations other than ductal ligations on children less than 2 years old during the years 1999 and 2000. Metabolic alkalosis was defined as a pH>7.48 corrected for PCO2, with a base excess > or =5 on two or more consecutive measurements during an 8h period. Median age was 15 weeks [range 2 days-95 weeks] and median weight 4.5 kg [range 2.1-15.7 kg]. In 157 cases, cardiopulmonary bypass was used. In 92 [49%] procedures, metabolic alkalosis occurred with the highest corrected pH 24.3h after operation. Multivariate regression analysis associated age [Pmetabolic alkalosis. Of the surgical procedures the arterial switch for transposition of the great arteries [n=19] was strongly associated with metabolic alkalosis [100%, Palkalosis: those who experienced alkalosis had been hemodiluted to a greater extent [P=0.007]. Nearly 95% of patients experienced some increase in bicarbonate, but patients with metabolic alkalosis experienced more than those without [5.9 versus 3.5 mmol/l, Pmetabolic alkalosis. Metabolic alkalosis has a high incidence after pediatric cardiac surgery, strongly associated with younger age, cardiopulmonary bypass, preoperative ductal dependency and perioperative hemodilution. Early recognition allows for timely therapeutic intervention.

  11. Diagnosis and management of metabolic alkalosis.

    Science.gov (United States)

    Pahari, D K; Kazmi, W; Raman, G; Biswas, Sobhan

    2006-11-01

    Elevated pH and elevated plasma bicarbonate level above normal characterise metabolic alkalosis. When bicarbonate is elevated pCO2 must also be elevated to maintain pH to its normal range. Therefore with metabolic alkalosis, the compensation is to decrease alveolar ventilation, and increase pCO2. The causes of metabolic alkalosis are gastro-intestinal hydrogen and chloride loss and due to renal cause. For metabolic alkalosis to continue both generation and maintenance of high levels of bicarbonate are necessary. The diagnosis of metabolic alkalosis is established by noting pH, serum bicarbonate (elevated) and pCO2 (compensatory) elevation. To establish the causes it is necessary to determine intravascular volume, supine and standing blood pressure and renin angiotension alolosterone axis. In chloride responsive alkalosis in which the conditions are extracellular volume depletion, hypokalaemia and hypochloraemia correction of intravascular volume with sodium chloride is needed. In severe metabolic alkalosis of any cause dilute hydrochloric acid (0.1 N HCl) may be infused intravenously but haemolysis may be a complication. In emergency situation with severe hypokalaemia dialysis with higher K+, Cl- and low HCO3- bath will be appropriate.

  12. A Quick Reference on Metabolic Alkalosis.

    Science.gov (United States)

    Foy, Daniel S; de Morais, Helio Autran

    2017-03-01

    Metabolic alkalemia is characterized by an increase in bicarbonate concentration and base excess, an increase in pH, and a compensatory increase in carbon dioxide pressure. This article outlines indications for analysis, reference ranges, causes, and clinical signs of metabolic alkalosis. Algorithms for evaluation of patients with acid-base disorders and metabolic alkalosis are included. Copyright © 2016 Elsevier Inc. All rights reserved.

  13. Severe metabolic alkalosis in a hemodialysis patient.

    Science.gov (United States)

    Huber, Lu; Gennari, F John

    2011-07-01

    We present a patient with end-stage kidney disease receiving hemodialysis therapy who developed severe metabolic alkalosis secondary to vomiting. This case illustrates the important differences in pathogenesis, diagnosis, and management of this common acid-base disorder in patients without kidney function. The diagnostic approach and management strategy for metabolic alkalosis are discussed, highlighting the special issues to be considered in dialysis patients. Copyright © 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  14. Baking soda induced severe metabolic alkalosis in a haemodialysis patient.

    Science.gov (United States)

    Solak, Yalcin; Turkmen, Kultigin; Atalay, Huseyin; Turk, Suleyman

    2009-08-01

    Metabolic alkalosis is a rare occurence in hemodialysis population compared to metabolic acidosis unless some precipitating factors such as nasogastric suction, vomiting and alkali ingestion or infusion are present. When metabolic alkalosis develops, it may cause serious clinical consequences among them are sleep apnea, resistent hypertension, dysrhythmia and seizures. Here, we present a 54-year-old female hemodialysis patient who developed a severe metabolic alkalosis due to baking soda ingestion to relieve dyspepsia. She had sleep apnea, volume overload and uncontrolled hypertension due to metabolic alkalosis. Metabolic alkalosis was corrected and the patient's clinical condition was relieved with negative-bicarbonate hemodialysis.

  15. Magnesium Oxide Induced Metabolic Alkalosis in Cattle

    Science.gov (United States)

    Ogilvie, T.H.; Butler, D.G.; Gartley, C.J.; Dohoo, I.R.

    1983-01-01

    A study was designed to compare the metabolic alkalosis produced in cattle from the use of an antacid (magnesium oxide) and a saline cathartic (magnesium sulphate). Six, mature, normal cattle were treated orally with a magnesium oxide (MgO) product and one week later given a comparable cathartic dose of magnesium sulphate (MgSO4). The mean percent dry matter content of the cattle feces changed significantly (Pmetabolic alkalosis as determined by base excess values. The base excess values remained elevated for 24 hours in the MgO treated group compared to only 12 hours after MgSO4 administration. Following MgO administration, mean hydrogen ion concentration (pH), bicarbonate ion concentration ([HCO3-]) and base excess were 7.44, 33.3 mmol/L and +8.0 respectively compared to 7.38, 27 mmol/L and +3.0 after MgSO4. Since the oral use of MgO in normal cattle causes a greater and more prolonged metabolic alkalosis compared to MgSO4, MgO is contraindicated as a cathartic in normal cattle or in cattle with abomasal abnormalities characterized by pyloric obstruction and metabolic alkalosis. PMID:6883181

  16. Extreme metabolic alkalosis with fludrocortisone therapy.

    Science.gov (United States)

    Burns, A.; Brown, T. M.; Semple, P.

    1983-01-01

    We present an unusual case of extreme metabolic alkalosis resulting from severe hypokalaemia caused by unmonitored fludrocortisone therapy. Biochemical aspects of the disorder are discussed, as is the successful treatment with diuretics and potassium replacement. Some dangers of this therapy and necessary precautions are emphasized. PMID:6622340

  17. Severe metabolic alkalosis: a case report.

    Science.gov (United States)

    Javaheri, S; Nardell, E A

    1981-01-01

    A 45-year-old man who was admitted with nausea, vomiting, and abdominal pain was found to have severe metabolic alkalosis, with a PaCO2 of 11.4kPa (85.5 mm Hg), PaO2 of 5.8 kPa (43.5 mm Hg), pH of 7.61, and plasma bicarbonate concentration of 82.0 mmol/l. He was treated with oxygen, intravenous physiological saline, and phenytoin and improved within 48 hours. Radiographs showed gastric outlet obstruction secondary to peptic ulcer, which was treated by surgery. Though sever, the rise in carbon dioxide concentration in this patient was probably lifesaving. The PaCO2 was therefore allowed to fall gradually as the alkalosis was treated. The return of both PaCO2 and plasma bicarbonate values to normal in parallel suggests that hypoventilation compensated for the metabolic alkalosis and emphasises the importance of conservative treatment in cases of metabolic alkalosis. PMID:6794744

  18. [Infant metabolic alkalosis of dietetic origin].

    Science.gov (United States)

    Mesa Medina, O; González, J León; García Nieto, V; Romero Ramírez, S; Marrero Pérez, C

    2009-04-01

    Cases of metabolic alkalosis are divided into susceptible or resistant to treatment with sodium chloride, depending on the response to it. The resistant cases present with high urinary excretion of chloride, and are secondary to tubular disease or use of diuretics. Included among the sensitive cases are, vomiting, cystic fibrosis and low intake. Two infants were fed with "almond milk" and showed clinical symptoms of dehydration and failure to thrive. Hypochloraemic and hypokalaemic metabolic alkasosis was seen in both cases, which responded satisfactorily to water and electrolyte replacement. After ruling out vomiting, ingestion of drugs, tubular disease, and cystic fibrosis, the diagnosis was low intake, due to poor contribution of Na+ and Cl(-) provided by the "almond milk". This deficit induces an increase in proximal tubular reabsorption of H(-)CO3 and in parts of the distal nephron, an increase in reabsorption of Na+ and Cl(-) which are exchanged with K+ and H+, which can give rise to a hypochloraemic alkalosis and hypokalaemia. Secondary hypothyroidism was found in one case, apparently due to the lack of iodine in the almond milk, and disorders of the myelination characterized by optic neuritis and hearing loss. These disorders were resolved when feeding with human formula was established.

  19. Respiratory compensation to a primary metabolic alkalosis in humans.

    Science.gov (United States)

    Feldman, Mark; Alvarez, Naiara M; Trevino, Michael; Weinstein, Gary L

    2012-11-01

    There is limited and disparate information about the extent of the respiratory compensation (hypoventilation) that occurs in response to a primary metabolic alkalosis in humans. Our aim was to examine the influence of the plasma bicarbonate concentration, the plasma base excess, and the arterial pH on the arterial carbon dioxide tension in 52 adult patients with primary metabolic alkalosis, mostly due to diuretic use or vomiting. Linear regression analysis was used to correlate degrees of alkalosis with arterial carbon dioxide tensions. In this alkalotic cohort, whose arterial plasma bicarbonate averaged 31.6 mEq/l, plasma base excess averaged 7.8 mEq/l, and pH averaged 7.48, both plasma bicarbonate and base excess correlated closely with arterial carbon dioxide tensions (r = 0.97 and 0.96, respectively; p metabolic alkalosis than has been reported in prior smaller studies.

  20. Hypocapnic but Not Metabolic Alkalosis Impairs Alveolar Fluid Reabsorption

    Science.gov (United States)

    Myrianthefs, Pavlos M.; Briva, Arturo; Lecuona, Emilia; Dumasius, Vidas; Rutschman, David H.; Ridge, Karen M.; Baltopoulos, George J.; Sznajder, Jacob Iasha

    2005-01-01

    Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema. PMID:15764729

  1. Metabolic alkalosis in adults with stable cystic fibrosis.

    Science.gov (United States)

    Al-Ghimlas, Fahad; Faughnan, Marie E; Tullis, Elizabeth

    2012-01-01

    The frequency of metabolic alkalosis among adults with stable severe CF-lung disease is unknown. Retrospective chart review. Fourteen CF and 6 COPD (controls) patients were included. FEV1 was similar between the two groups. PaO2 was significantly higher in the COPD (mean ± 2 SD is 72.0 ± 6.8 mmHg,) than in the CF group (56.1 ± 4.1 mmHg). The frequency of metabolic alkalosis in CF patients (12/14, 86%) was significantly greater (p=0.04) than in the COPD group (2/6, 33%). Mixed respiratory acidosis and metabolic alkalosis was evident in 4 CF and 1 COPD patients. Primary metabolic alkalosis was observed in 8 CF and none of the COPD patients. One COPD patient had respiratory and metabolic alkalosis. Metabolic alkalosis is more frequent in stable patients with CF lung disease than in COPD patients. This might be due to defective CFTR function with abnormal electrolyte transport within the kidney and/ or gastrointestinal tract.

  2. Chloride losing diarrhoea and metabolic alkalosis in an infant with cystic fibrosis.

    Science.gov (United States)

    Hochman, H I; Feins, N R; Rubin, R; Gould, J

    1976-01-01

    A case of hypochloraemic metabolic alkalosis in an infant with chloride losing ileostomy drainage and cystic fibrosis is described. It is speculated that intestinal loss of chloride played a major role in the development of metabolic alkalosis. PMID:938082

  3. Multiple myeloma with hypercalcemia and chloride resistant metabolic alkalosis.

    Science.gov (United States)

    Alshayeb, Hala; Patel, Vikul; Naseer, Adnan; Mangold, Therese A; Wall, Barry M

    2011-10-01

    This report describes a novel presentation of chloride resistant metabolic alkalosis in a patient with hypercalcemia related to Multiple Myeloma (MM). A 51-year-old male with newly diagnosed MM presented with widespread skeletal involvement, calcium (Ca(+2)) of 18 mg/dL, phosphorous (PO4) of 6 mg/dL, serum bicarbonate (HCO3) of 37 mEq/L, and serum creatinine (Cr) of 2.6 mg/dL Other causes of metabolic alkalosis such as vomiting, diuretics, alkali ingestion, mineralocorticoid excess and hypokalemia were excluded. Hypercalcemia and metabolic alkalosis were only partially corrected after rehydration, calcitonin and steroids. Subsequent treatment with zoledronic acid resulted in resolution of hypercalcemia and correction of metabolic alkalosis.The chloride resistant component of metabolic alkalosis was most likely related to extensive release of Ca(+2), carbonate and phosphate from bone by activated osteoclasts with inhibited osteoblastic activity. The additional reduction in glomerular filtration rate due to MM, contributed to a triad mimicking Calcium-Alkali syndrome.

  4. Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease.

    Science.gov (United States)

    Bear, R.; Goldstein, M.; Phillipson, E.; Ho, M.; Hammeke, M.; Feldman, R.; Handelsman, S.; Halperin, M.

    1977-01-01

    Eleven instances of a mixed acid-base disorder consisting of chronic respiratory acidosis and metabolic alkalosis were recognized in eight patients with chronic obstructive lung disease and carbon dioxide retention. Correction of the metabolic alkalosis led to substantial improvement in blood gas values and clinical symptoms. Patients with mixed chronic respiratory acidosis and metabolic alkalosis constitute a common subgroup of patients with chronic obstructive lung disease and carbon dioxide retention; these patients benefit from correction of the metabolic alkalosis. PMID:21028

  5. Metabolic alkalosis, recovery and sprint performance.

    Science.gov (United States)

    Siegler, J C; McNaughton, L R; Midgley, A W; Keatley, S; Hillman, A

    2010-11-01

    Pre-exercise alkalosis and an active recovery improve the physiological state of recovery through slightly different mechanisms (e. g. directly increasing extracellular bicarbonate (HCO3 (-)) vs. increasing blood flow), and combining the two conditions may provide even greater influence on blood acid-base recovery from high-intensity exercise. Nine subjects completed four trials (Placebo Active ( PLAC A), sodium bicarbonate (NaHCO3) Active ( BICARB A), Placebo Passive ( PLAC P) and NaHCO3 Passive ( BICARB P)), each consisting of three, 30-s maximal efforts with a three min recovery between each effort. Pre-exercisealkalosis was evident in both NaHCO3 conditions, as pH and HCO3 (-) were significantly higher than both Placebo conditions (pH: 7.46 ± 0.04 vs. 7.39 ± 0.02; HCO3 (-): 28.8 ± 1.9 vs. 23.2 ± 1.4  mmol·L (-1); p<0.001). In terms of performance, significant interactions were observed for average speed (p<0.05), with higher speeds evident in the BICARB A condition (3.9 ± 0.3 vs. 3.7 ± 0.4  m·s (-1)). Total distance covered was different (p=0.05), with post hoc differences evident between the BICARB A and PLAC P conditions (368 ± 33 vs. 364 ± 35 m). These data suggest that successive 30-s high intensity performance may be improved when coupled with NaHCO3 supplementation.

  6. A patient with foot ulcer and severe metabolic alkalosis.

    Science.gov (United States)

    John, Ruby Samuel; Simoes, Sonia; Reddi, Alluru S

    2012-01-01

    We report a case of triple acid-base disorder with metabolic alkalosis as the primary disorder in a 65-year-old man due to ingestion and application to leg ulcers of baking soda (calcium bicarbonate). The blood pH was 7.65 with hypochloremia, hypokalemia, and prerenal azotemia. He was treated with isotonic saline with K replacement, and the patient improved without any adverse clinical consequences. We discuss the causes, mechanisms, and management of Cl-responsive (depletion) metabolic alkalosis.

  7. Girl with hypokaliemia and metabolic alkalosis: a case report

    Directory of Open Access Journals (Sweden)

    Ksenja Marguč Kirn

    2013-04-01

    Conclusions: In cases of unexplained hypokalemia and metabolic alkalosis associated with a normal or low blood pressure a tubulopathy, e.g., Gitelman syndrome, must be excluded. The identification and recognition of correct diagnosis is extremely important since a proper treatment can reduce the risk of life-threatening events, e.g. arrhythmias.

  8. Acetazolamide in critically ill neonates and children with metabolic alkalosis.

    Science.gov (United States)

    Andrews, Megan G; Johnson, Peter N; Lammers, Erin M; Harrison, Donald L; Miller, Jamie L

    2013-09-01

    Acetazolamide is an option for hypochloremic metabolic alkalosis, but there are limited reports in children. To describe the acetazolamide regimen and outcomes in critically ill children with metabolic alkalosis. This was a descriptive, retrospective study of patients metabolic alkalosis (ie, pH > 7.45 and bicarbonate [HCO3] > 26 mEq/L). Patients receiving other treatments for metabolic alkalosis within 24 hours of acetazolamide were excluded. The primary objective was to identify the mean dose and duration of acetazolamide. Secondary objectives were to determine the number of patients with treatment success (ie, serum HCO3 22-26 mEq/L) and occurrence of adverse events. Thirty-four patients were included for analysis, the median age was 0.25 years (range = 0.05-12 years). The acetazolamide regimen included a mean dose of 4.98 ± 1.14 mg/kg for a mean number of 6.1 ± 5.3 (range = 3-24) doses. The majority (70.6%) received acetazolamide every 8 hours. Treatment success was achieved in 10 (29.4%) patients. Statistically significant differences were noted between the pre-acetazolamide and post-acetazolamide pH and HCO3, 7.51 ± 0.05 versus 7.37 ± 0.05 (P metabolic alkalosis in children with and without cardiac disease. Acetazolamide treatment resulted in improved HCO3, but the majority of patients did not achieve our definition of treatment success. Future studies should elucidate the optimal acetazolamide regimen.

  9. Evaporation of free water causes concentrational alkalosis in vitro.

    Science.gov (United States)

    Lindner, Gregor; Doberer, Daniel; Schwarz, Christoph; Schneeweiss, Bruno; Funk, Georg-Christian

    2014-04-01

    The development of metabolic alkalosis was described recently in patients with hypernatremia. However, the causes for this remain unknown. The current study serves to clarify whether metabolic alkalosis develops in vitro after removal of free water from plasma and whether this can be predicted by a mathematical model. Ten serum samples of healthy humans were dehydrated by 29 % by vacuum centrifugation corresponding to an increase of the contained concentrations by 41 %. Constant partial pressure of carbon dioxide at 40 mmHg was simulated by mathematical correction of pH [pH(40)]. Metabolic acid-base state was assessed by Gilfix' base excess subsets. Changes of acid-base state were predicted by the physical-chemical model according to Watson. Evaporation increased serum sodium from 141 (140-142) to 200 (197-203) mmol/L, i.e., severe hypernatremia developed. Acid-base analyses before and after serum concentration showed metabolic alkalosis with alkalemia: pH(40): 7.43 (7.41 to 7.45) vs 7.53 (7.51 to 7.55), p = 0.0051; base excess: 1.9 (0.7 to 3.6) vs 10.0 (8.2 to 11.8), p = 0.0051; base excess of free water: 0.0 (- 0.2 to 0.3) vs 17.7 (16.8 to 18.6), p = 0.0051. The acidifying effects of evaporation, including hyperalbuminemic acidosis, were beneath the alkalinizing ones. Measured and predicted acid-base changes due to serum evaporation agreed well. Evaporation of water from serum causes concentrational alkalosis in vitro, with good agreement between measured and predicted acid-base values. At least part of the metabolic alkalosis accompanying hypernatremia is independent of renal function.

  10. Severe metabolic alkalosis due to pyloric obstruction: case presentation, evaluation, and management.

    Science.gov (United States)

    McCauley, Meredith; Gunawardane, Manjula; Cowan, Mark J

    2006-12-01

    A 46-year-old man presented to the emergency room with severe metabolic alkalosis, hypokalemia, and respiratory failure requiring intubation and mechanical ventilation. The cause of his acid-base disorder was initially unclear. Although alkalosis is common in the intensive care unit, metabolic alkalosis of this severity is unusual, carries a very high mortality rate, and requires careful attention to the pathophysiology and differential diagnosis to effectively evaluate and treat the patient. A central concept in the diagnosis of metabolic alkalosis is distinguishing chloride responsive and chloride nonresponsive states. Further studies are then guided by the history and physical examination in most cases. By using a systematic approach to the differential diagnosis, we were able to determine that a high-grade gastric outlet obstruction was the cause of the patients' alkalosis and to offer effective therapy for his condition. A literature review and algorithm for the diagnosis and management of metabolic alkalosis are also presented.

  11. Metabolic alkalosis induced by plasmapheresis in a patient with systemic lupus erythematosus.

    Science.gov (United States)

    Choi, M. Y.; Lee, J. D.; Lee, S. H.; Park, I. S.; Woo, J. Y.; Choi, E. J.; Chang, Y. S.; Bang, B. K.

    1993-01-01

    We report a patient with systemic lupus erythematosus (SLE), who had developed metabolic alkalosis during plasmapheresis. The metabolic alkalosis could be promptly corrected by reducing the amount of citrate load. The development of metabolic alkalosis can be explained by the citrate load during plasmapheresis. Careful monitoring of acid base status is mandatory in patients with limited renal function and the reduction of citrate load may be advisable in plasmapheresis. PMID:8240751

  12. Acetazolamide Therapy for Metabolic Alkalosis in Pediatric Intensive Care Patients.

    Science.gov (United States)

    López, Carolina; Alcaraz, Andrés José; Toledo, Blanca; Cortejoso, Lucía; Gil-Ruiz, Maite Augusta

    2016-12-01

    Patients in PICUs frequently present hypochloremic metabolic alkalosis secondary to loop diuretic treatment, especially those undergoing cardiac surgery. This study evaluates the effectiveness of acetazolamide therapy for metabolic alkalosis in PICU patients. Retrospective, observational study. A tertiary care children's hospital PICU. Children receiving at least a 2-day course of enteral acetazolamide. None. Demographic variables, diuretic treatment and doses of acetazolamide, urine output, serum electrolytes, urea and creatinine, acid-base excess, pH, and use of mechanical ventilation during treatment were collected. Patients were studied according to their pathology (postoperative cardiac surgery, decompensated heart failure, or respiratory disease). A total of 78 episodes in 58 patients were identified: 48 were carried out in cardiac postoperative patients, 22 in decompensated heart failure, and eight in respiratory patients. All patients received loop diuretics. A decrease in pH and PCO2 in the first 72 hours, a decrease in serum HCO3 (mean, 4.65 ± 4.83; p metabolic alkalosis secondary to diuretic therapy. Cardiac postoperative patients present a significant increase in urine output after acetazolamide treatment.

  13. Acetazolamide therapy for metabolic alkalosis in critically ill pediatric patients.

    Science.gov (United States)

    Bar, Amir; Cies, Jeff; Stapleton, Kathleen; Tauber, Danna; Chopra, Arun; Shore, Paul M

    2015-02-01

    Despite a paucity of supporting literature, acetazolamide is commonly used in critically ill children with metabolic alkalosis (elevated plasma bicarbonate [pHco-3] and pH). The objective of this study was to assess the change in 18 hours after initiation of acetazolamide therapy. Retrospective study. PICU of an urban, tertiary-care children's hospital. Mechanically ventilated children (≤ 17 yr) with metabolic alkalosis (pHco-3 ≥ 35 mmol/L). None. Of 153 consecutively screened patients, 61 patients (29 female patients) were enrolled: 18 cardiac patients (after congenital heart disease repair) and 43 noncardiac patients. The cardiac patients were younger than the noncardiac patients (median [interquartile range] age, 0.6 mo [0.3-2.5 mo] vs 7.4 mo [2.8-39.9 mo]; p metabolic alkalosis in critically ill children with congenital heart disease. Further study is required to determine why these cardiac patients respond differently to acetazolamide than noncardiac patients and whether this response impacts important clinical outcomes, for example, weaning mechanical ventilation.

  14. Alkalosis in Critically Ill Patients with Severe Sepsis and Septic Shock.

    Science.gov (United States)

    Kreü, Simon; Jazrawi, Allan; Miller, Jan; Baigi, Amir; Chew, Michelle

    2017-01-01

    Although metabolic alkalosis is a common occurrence in intensive care units (ICUs), no study has evaluated its prevalence or outcomes in patients with severe sepsis or septic shock. This is a retrospective cohort study of critically ill patients suffering from severe sepsis and septic shock admitted to the ICUs of Halmstad and Varberg County hospitals. From 910 patient records, 627 patients met the inclusion criteria. We investigated the relationship between metabolic alkalosis and mortality. Further, we studied the relationship between metabolic alkalosis and ICU length of stay (LOS). Metabolic alkalosis was associated with decreased 30-day and 12-month mortalities. This effect was however lost when a multivariate analysis was conducted, correcting for age, gender, pH on admission, base excess (BE) on admission, Simplified Acute Physiology Score III (SAPS III) and acute kidney injury (AKI). We then analyzed for any dose-response effect between the severity of metabolic alkalosis and mortality and found no relationship. Bivariate analysis showed that metabolic alkalosis had a significant effect on the length of ICU stay. When adjusting for age, sex, pH at admission, BE at admission, SAPS III and AKI in a multivariate analysis, metabolic alkalosis significantly contributed to prolonged ICU length of stay. In two separate sensitivity analyses pure metabolic alkalosis and late metabolic alkalosis (time of onset >48 hours) were the only significant predictor of increased ICU length of stay. Metabolic alkalosis did not have any effect on 30-day and 12-month mortalities after adjusting for age, sex, SAPS III-score, pH and BE on admission and AKI in a multivariate analysis. The presence of metabolic alkalosis was independently associated with an increased ICU length of stay.

  15. Incidence, nature, and etiology of metabolic alkalosis in dogs and cats.

    Science.gov (United States)

    Ha, Y-S; Hopper, K; Epstein, S E

    2013-01-01

    The incidence and causes of metabolic alkalosis in dogs and cats have not been fully investigated. To describe the incidence, nature, and etiology of metabolic alkalosis in dogs and cats undergoing blood gas analysis at a veterinary teaching hospital. Dogs and cats at a veterinary medical teaching hospital. Acid-base and electrolyte results for dogs and cats measured during a 13-month period were retrospectively collected from a computer database. Only the first measured (venous or arterial) blood gas analyzed in a single hospitalization period was included. Animals with a base excess above the reference range for the species were included. A total of 1,805 dogs and cats were included. Of these, 349 (19%) were identified as having an increased standardized base excess, 319 dogs and 30 cats. The mixed acid-base disorder of metabolic alkalosis with respiratory acidosis was the most common abnormality identified in both dogs and cats. Hypokalemia and hypochloremia were more common in animals with metabolic alkalosis compared to animals without metabolic alkalosis. The 4 most commonly identified underlying diseases were respiratory disease, gastrointestinal tract obstruction, furosemide administration, and renal disease. Metabolic alkalosis was less common than metabolic acidosis in the same population of animals. Evidence of contraction alkalosis was present in many patients in this study. Hypokalemia and hypochloremia were more frequent in patients with metabolic alkalosis and suggest the importance of evaluation of acid-base status in conjunction with serum electrolyte concentrations. Copyright © 2013 by the American College of Veterinary Internal Medicine.

  16. Metabolic alkalosis after using enhanced water to dilute powdered formula.

    Science.gov (United States)

    Eby, Anne Kathryn

    2009-01-01

    In this case study report of an infant with metabolic alkalosis, the healthcare team worked to discover the cause of the illness. They found that well-meaning parents had diluted their newborn's powdered formula with electrolyte-enhanced water. Electrolyte balance in the newborn is reviewed in this article, along with information about enhanced waters. It is essential that nurses working with new families be aware that heavily advertised enhanced waters could be used unknowingly by parents for their newborns, and that the consequences could be dire.

  17. Life-threatening metabolic alkalosis in Pendred syndrome.

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    Kandasamy, Narayanan; Fugazzola, Laura; Evans, Mark; Chatterjee, Krishna; Karet, Fiona

    2011-07-01

    Pendred syndrome, a combination of sensorineural deafness, impaired organification of iodide in the thyroid and goitre, results from biallelic defects in pendrin (encoded by SLC26A4), which transports chloride and iodide in the inner ear and thyroid respectively. Recently, pendrin has also been identified in the kidneys, where it is found in the apical plasma membrane of non-α-type intercalated cells of the cortical collecting duct. Here, it functions as a chloride-bicarbonate exchanger, capable of secreting bicarbonate into the urine. Despite this function, patients with Pendred syndrome have not been reported to develop any significant acid-base disturbances, except a single previous reported case of metabolic alkalosis in the context of Pendred syndrome in a child started on a diuretic. We describe a 46-year-old female with sensorineural deafness and hypothyroidism, who presented with severe hypokalaemic metabolic alkalosis during inter-current illnesses on two occasions, and who was found to be homozygous for a loss-of-function mutation (V138F) in SLC26A4. Her acid-base status and electrolytes were unremarkable when she was well. This case illustrates that, although pendrin is not usually required to maintain acid-base homeostasis under ambient condition, loss of renal bicarbonate excretion by pendrin during a metabolic alkalotic challenge may contribute to life-threatening acid-base disturbances in patients with Pendred syndrome.

  18. Acute respiratory acidosis and alkalosis – A modern quantitative interpretation

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    Andraž Stožer

    2014-03-01

    Full Text Available Background: Three different approaches for assessing the acid-base status of a patient exist, i.e. the Boston, Copenhagen, and Stewart´s approach, and they employ different parameters to assess a given acid-base disturbance. Students, researchers, and clinicians are getting confused by heated debates about which of these performs best and by the fact that during their curricula, they typically get acquainted with one of the approaches only, which prevents them to understand sources employing other approaches and to critically evaluate the advantages and drawbacks of each approach. In this paper, the authors introduce and define the basic parameters characterizing each of the approaches and point out differences and similarities between them. Special attention is devoted to how the different approaches assess the degree of change in the concentration of plasma bicarbonate that occurs during primary respiratory changes; proper understanding of these is necessary to correctly interpret chronic respiratory and metabolic acid-base changes.Conclusion: During acute respiratory acidosis the concentration of bicarbonate rises and during acute respiratory alkalosis it falls, depending on the buffering strength of non-bicarbonate buffers. During acute respiratory acid-base disturbances, buffer base (employed by the Copenhagen approach, apparent and effective strong ion difference, as well as strong ion gap (employed by the Stewart approach remain unchanged; the anion gap (employed by the Boston and Copenhagen approach falls during acute respiratory acidosis and rises during acute respiratory alkalosis.

  19. Cortical GABAergic neurons are more severely impaired by alkalosis than acidosis.

    Science.gov (United States)

    Zhang, Shuyan; Sun, Piyun; Sun, Zhongren; Zhang, Jingyu; Zhou, Jinlong; Gu, Yingli

    2013-12-05

    Acid-base imbalance in various metabolic disturbances leads to human brain dysfunction. Compared with acidosis, the patients suffered from alkalosis demonstrate more severe neurological signs that are difficultly corrected. We hypothesize a causative process that the nerve cells in the brain are more vulnerable to alkalosis than acidosis. The vulnerability of GABAergic neurons to alkalosis versus acidosis was compared by analyzing their functional changes in response to the extracellular high pH and low pH. The neuronal and synaptic functions were recorded by whole-cell recordings in the cortical slices. The elevation or attenuation of extracellular pH impaired these GABAergic neurons in terms of their capability to produce spikes, their responsiveness to excitatory synaptic inputs and their outputs via inhibitory synapses. Importantly, the dysfunction of these active properties appeared severer in alkalosis than acidosis. The severer impairment of cortical GABAergic neurons in alkalosis patients leads to more critical neural excitotoxicity, so that alkalosis-induced brain dysfunction is difficultly corrected, compared to acidosis. The vulnerability of cortical GABAergic neurons to high pH is likely a basis of severe clinical outcomes in alkalosis versus acidosis.

  20. Fluconazole and acetazolamide in the treatment of ectopic Cushing's syndrome with severe metabolic alkalosis.

    Science.gov (United States)

    Schwetz, Verena; Aberer, Felix; Stiegler, Claudia; R Pieber, Thomas; Obermayer-Pietsch, Barbara; Pilz, Stefan

    2015-01-01

    Cushing's syndrome (CS) due to ectopic ACTH production accounts for about 10% of all types of CS and is frequently associated with metabolic alkalosis. Treatment of CS involves surgical resection and/or medical therapy to control hypercortisolism. We present the case of an 80-year-old woman affected by CS due to an unknown cause. The patient had severe metabolic alkalosis with refractory hypokalemia. To treat the underlying CS, fluconazole was initiated due to unavailability of ketoconazole. In spite of markedly decreasing cortisol levels, metabolic alkalosis persisted. Treatment of metabolic alkalosis with acetazolamide was thus initiated and pH levels successfully lowered. This case report shows that hypercortisolism can be effectively treated with fluconazole in cases where ketoconazole is unavailable or not tolerated and that persistent severe metabolic alkalosis caused by glucocorticoid excess can be safely and successfully treated with acetazolamide. Hypercortisolism can be effectively treated with fluconazole where ketoconazole is unavailable or not tolerated.Glucocorticoid excess can cause severe metabolic alkalosis.Persistent severe metabolic alkalosis can be safely and successfully treated with acetazolamide.

  1. Cerebrospinal fluid ionic regulation, cerebral blood flow, and glucose use during chronic metabolic alkalosis

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    Schroeck, H.K.; Kuschinsky, W. (Univ. of Bonn (Germany, F.R.))

    1989-10-01

    Chronic metabolic alkalosis was induced in rats by combining a low K+ diet with a 0.2 M NaHCO3 solution as drinking fluid for either 15 or 27 days. Local cerebral blood flow and local cerebral glucose utilization were measured in 31 different structures of the brain in conscious animals by means of the iodo-(14C)antipyrine and 2-(14C)deoxy-D-glucose method. The treatment induced moderate (15 days, base excess (BE) 16 mM) to severe (27 days, BE 25 mM) hypochloremic metabolic alkalosis and K+ depletion. During moderate metabolic alkalosis no change in cerebral glucose utilization and blood flow was detectable in most brain structures when compared with controls. Cerebrospinal fluid (CSF) K+ and H+ concentrations were significantly decreased. During severe hypochloremic alkalosis, cerebral blood flow was decreased by 19% and cerebral glucose utilization by 24% when compared with the control values. The decrease in cerebral blood flow during severe metabolic alkalosis is attributed mainly to the decreased cerebral metabolism and to a lesser extent to a further decrease of the CSF H+ concentration. CSF K+ concentration was not further decreased. The results show an unaltered cerebral blood flow and glucose utilization together with a decrease in CSF H+ and K+ concentrations at moderate metabolic alkalosis and a decrease in cerebral blood flow and glucose utilization together with a further decreased CSF H+ concentration at severe metabolic alkalosis.

  2. Metabolic alkalosis during immobilization in monkeys (M. nemestrina)

    Science.gov (United States)

    Young, D. R.; Yeh, I.; Swenson, R. S.

    1983-01-01

    The systemic and renal acid-base response of monkeys during ten weeks of immobilization was studied. By three weeks of immobilization, arterial pH and bicarbonate concentrations were elevated (chronic metabolic alkalosis). Net urinary acid excretion increased in immobilized animals. Urinary bicarbonate excretion decreased during the first three weeks of immobilization, and then returned to control levels. Sustained increases in urinary ammonium excretion were seen throughout the time duration of immobilization. Neither potassium depletion nor hypokalemia was observed. Most parameters returned promptly to the normal range during the first week of recovery. Factors tentatively associated with changes in acid-base status of monkeys include contraction of extracellular fluid volume, retention of bicarbonate, increased acid excretion, and possible participation of extrarenal buffers.

  3. Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis.

    Science.gov (United States)

    Li, Kai; Xu, Yuan

    2015-01-01

    Metabolic alkalosis commonly results from excessive hydrochloric acid (HCl), potassium (K(+)) and water (H2O) loss from the stomach or through the urine. The plasma anion gap increases in non-hypoproteinemic metabolic alkalosis due to an increased negative charge equivalent on albumin and the free ionized calcium (Ca(++)) content of plasma decreases. The mean citrate load in all patients was 8740±7027 mg from 6937±6603 mL of transfused blood products. The citrate load was significantly higher in patients with alkalosis (9164±4870 vs. 7809±3967, P metabolism causes intracellular acidosis. As a result of intracellular acidosis compensation, decompensated metabolic alkalosis + respiratory acidosis and electrolyte imbalance may develop, blood transfusions may result in certain complications.

  4. Glucose Utilization and Production by the Dog Kidney In Vivo in Metabolic Acidosis and Alkalosis

    Science.gov (United States)

    Costello, J.; Scott, J. M.; Wilson, P.; Bourke, E.

    1973-01-01

    Using D-[1-14C]glucose as a tracer, renal glucose utilization and production was measured in chronic metabolic acidosis and alkalosis in dog kidney in vivo. In six experiments in acidosis, mean total renal glucose production was 4.447±1.655 SE μmol/min and glucose utilization was 4.187±0.576 SE μmol/min. In five alkalotic experiments it was found that mean total glucose production was 12.227±2.026 SE μmol/min and glucose utilization was 18.186±2.054 SE μmol/min. Renal glucose utilization and production are therefore significantly higher in alkalosis than in acidosis in vivo. Since glucose production is maximal under conditions when glutamine extraction is minimal (i.e. alkalosis), it is apparent that in alkalosis glutamine is not a major precursor of glucose. PMID:4685085

  5. Perioperative Concerns for Profound Metabolic Alkalosis During Kidney Transplantation: A Case Report.

    Science.gov (United States)

    Choi, Jung Ju; Kim, Yong Beom; Kim, Hong Soon; Lee, Kyung Cheon; Jo, Youn Yi

    2016-11-01

    Profound metabolic alkalosis is an uncommon consideration for the anesthetic management of kidney transplantation. Serum total carbon dioxide content and complex electrolyte abnormalities might be important diagnostic clues for the presence of metabolic alkalosis in the absence of arterial blood gas analysis. A 34-year-old female visited Gachon University Gil Medical Center, Incheon, South Korea during year 2015. She experienced aggravated renal function due to chronic hypokalemia and severe hypochloremic metabolic alkalosis, induced by laxative abuse, and underwent ABO incompatible kidney transplantation. Serum total carbon dioxide content remained high (about 60 mEq/L) over eight months of monthly follow-up prior to kidney transplantation. The authors described their anesthetic experience of profound metabolic alkalosis with complex electrolyte abnormalities and provided a review of relevant literature.

  6. The effect of metabolic alkalosis on the ventilatory response in healthy subjects

    NARCIS (Netherlands)

    Mos-Oppersma, Eline; Doorduin, Jonne; van der Hoeven, J.G.; Veltink, Petrus H.; van Hees, H.W.H.; Heunks, L.M.A.

    Background Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma

  7. Ectopic adrenocorticotropic hormone syndrome presenting as hypokalemic metabolic alkalosis and hypertension

    Directory of Open Access Journals (Sweden)

    Mansoor C Abdulla

    2016-01-01

    Full Text Available The ectopic adrenocorticotropic hormone (ACTH syndrome is an uncommon cause of hypercortisolism, which should be considered in patients with hypokalemic metabolic alkalosis and hypertension in the context of lung neoplasm. We report a 60-year-old male patient with severe hypertension, metabolic alkalosis, and hypokalemia as the initial manifestations of an ACTH-secreting small cell lung carcinoma. Ectopic Cushing's syndrome should always be ruled out in patients with severe hypertension and hypokalemia.

  8. [Effect of hypocapnia/alkalosis on the fluid filtration rate in isolated and perfused rabbit lungs].

    Science.gov (United States)

    Urich, Daniela; Trejo, Humberto; Pezzulo, Alejandro; Caraballo, Juan Carlos; Gutiérrez, Jeydith; Castro, Ignacio; Sánchez-de León, Roberto

    2008-06-01

    Hypocapnia/alkalosis is a consequence of several lung and metabolic pathologies. The aim of this study was to determine whether the increase of fluid filtration rate (FFR) that occurs during Hypocapnia/alkalosis circumstances is determined by hypocapnia, alkalosis or both. 7 groups were formed (N=36) using isolated rabbit lungs. Group 1: Control (PCO2 6%, pH: 7.35-7.45); Group 2 (n=6): Hypocapnia/Alkalosis (CO2 1%, pH: 7.9); Group 3 (n=6): Hypocapnia/Normo-pH (CO2 1% pH 7.35-7.45), Group 4 (n=6) Normocapnia/Alcalosis (CO2 6%, pH: 7.9). Fenoterol, papaverine and hydrocortisone were added to Groups 5, 6 and 7 (n=4) respectively, all under Normocapnia/Alkalosis. FFR and Pulmonary Arterial Pressure (Pap) were considerably higher in group 2 than in control (FFR: 1.92g/min +/- 0.6 vs 0.0 g/min +/- 0.006). A strong influence exerted by pH was observed when Group 3 and group 4 were compared (FFR: 0.02 g/min +/- 0.009 vs 2.3 g/min +/- 0.9) and (Pap: 13.5 cmH2O +/- 1.4 vs 90 cmH2O +/- 15). A reduced effect was observed in groups 5 and 6 (papaverine and hydrocorisone) and a totally abolished effect was observed in group 7 (fenoterol) (FFR: 0.001 +/- 0.0003 mL/min and Pap: 14 +/- 0.8 cmH2O). Pulmonary edema induced by Hypocapnia/alkalosis is a consequence of alkalosis and not of hypocapnia. This effect could be due to inflammatory damage in the lung parenchyma and alkalosis-mediated vasoconstriction.

  9. [Hypernatremic alkalosis. Possible counterpart of hyperchloremic acidosis in intensive care patients?].

    Science.gov (United States)

    Hofmann-Kiefer, K F; Chappell, D; Jacob, M; Schülke, A; Conzen, P; Rehm, M

    2009-12-01

    With broad acceptance of Stewart's acid-base model "hyperchloremic acidosis" is regarded as an independent form of metabolic disorder. It is unknown whether hypernatremia plays a corresponding role with respect to the development of alkalosis. A total of 201 artificially ventilated, critically ill patients were monitored for hypernatremic episodes. Inclusion criterion was a serum sodium concentration above 145 mmol/l. In 20 patients a total of 78 periods of elevated plasma sodium levels lasting at least 24 h were observed. In 86% of these cases sodium and chloride concentrations were simultaneously increased. The development of alkalosis correlated with the strong ion difference (r=0.80, pmetabolic alkalosis regularly occurred and a correlation between serum sodium concentration and base excess could be verified (r=0.66, p=0.03). Alkalosis occurred in 84.8% of cases where the strong on difference exceeded 39 mmol/l. From the available data hypernatremic alkalosis could not be defined as an independent metabolic disorder. In would seem more appropriate to use the term "strong ion alkalosis" in this context.

  10. Correction of metabolic alkalosis by the kidney after isometric expansion of extracellular fluid

    Science.gov (United States)

    Cohen, Jordan J.

    1968-01-01

    Metabolic alkalosis was induced in dogs by administering ethacrynic acid and sustained by feeding a chloride-deficient diet. At the height of the alkalosis extracellular fluid was expanded “isometrically,” i.e., with an infusion that duplicated plasma sodium, chloride, and bicarbonate concentrations. Correction of metabolic alkalosis promptly followed such expansion and was attributed to the selective retention by the kidneys of chloride from the administered solution. Since plasma chloride concentration was not increased as an immediate consequence of the infusion, it is concluded that the change in renal tubular function that led to the selective retention of chloride must have been mediated by factors independent of filtrate chloride concentration. A decrease in circulating mineralocorticoid level, as a consequence of volume expansion, does not seem to account for this change in tubular function since identical studies in dogs receiving excessive amounts of 11-deoxycorticosterone acetate during the day of infusion yielded similar findings. Moreover, no other consequence of volume expansion appears to be sufficient to cause this change in tubular function in the absence of metabolic alkalosis; when the alkalosis was corrected with hydrochloric acid before infusion, isometric expansion of extracellular volume did not induce selective chloride retention. We suggest that isometric expansion during metabolic alkalosis causes a decrease in proximal sodium reabsorption that relinquishes filtrate to a more distal site in the nephron and that this site may retain chloride preferentially when hypochloremia or chloride deficiency is present. Images PMID:5645861

  11. Metabolic alkalosis in children: Study of patients admitted to pediatrics center1

    Directory of Open Access Journals (Sweden)

    2000-07-01

    Full Text Available Metabolic alkalosis is characterized by high HCO3- as it is seen in chronic respiratory acidosis, but PH differentiates the two disorders. There is no characteristic symptom or sign. Orthostatic hypotension may be encountered. Weakness and hyporeflexia occur if serum K+ is markerdly low. Tetany and neuromuscular irritability occur rarely. We report the results of retrospective data analysis of metabolic alkalosis in 15463 patients hospitalized Pediatric Medical Center in Tehran during years 1995-1997. We found 50 cases of metabolic alkalosis (rate of 0.32 percent. 64 precent male and 36 percent female. Most of them had growth failure (40% were bellow 3 percentile of height by age, 44% bellow 5 percentile of weight by height. More than 60 percent had hypokalemia, hypocloremia and hyponatremia. The most common cause of Metabolic alkalosis was cystic fibrosis and pyloric stenosis. Fifty percent of cystic fibrosis patients and Bartter cases had metabolic alkalosis. Metabolic alkalosis should be considered in every pediatric patient presented with projectile vomitting.

  12. Metabolic alkalosis in children: Study of patients admitted to pediatrics center

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    Sobhani A

    2001-07-01

    Full Text Available Metabolic alkalosis is characterized by high HCO3- as it is seen in chronic respiratory acidosis, but PH differentiates the two disorders. There is no characteristic symptom or sign. Orthostatic hypotension may be encountered. Weakness and hyporeflexia occur if serum K+ is markerdly low. Tetany and neuromuscular irritability occur rarely. We report the results of retrospective data analysis of metabolic alkalosis in 15463 patients hospitalized Pediatric Medical Center in Tehran during years 1995-1997. We found 50 cases of metabolic alkalosis (rate of 0.32 percent. 64 precent male and 36 percent female. Most of them had growth failure (40% were bellow 3 percentile of height by age, 44% bellow 5 percentile of weight by height. More than 60 percent had hypokalemia, hypocloremia and hyponatremia. The most common cause of Metabolic alkalosis was cystic fibrosis and pyloric stenosis. Fifty percent of cystic fibrosis patients and Bartter cases had metabolic alkalosis. Metabolic alkalosis should be considered in every pediatric patient presented with projectile vomitting.

  13. Severe metabolic alkalosis due to baking soda ingestion: case reports of two patients with unsuspected antacid overdose.

    Science.gov (United States)

    Fitzgibbons, L J; Snoey, E R

    1999-01-01

    Oral ingestion of baking soda (sodium bicarbonate) has been used for decades as a home remedy for acid indigestion. Excessive bicarbonate ingestion places patients at risk for a variety of metabolic derangements including metabolic alkalosis, hypokalemia, hypernatremia, and even hypoxia. The clinical presentation is highly variable but can include seizures, dysrhythmias, and cardiopulmonary arrest. We present two cases of severe metabolic alkalosis in patients with unsuspected antacid overdose. The presentation and pathophysiology of antacid-related metabolic alkalosis is reviewed.

  14. Injectable ammonium chloride used enterally for the treatment of persistent metabolic alkalosis in three pediatric patients.

    Science.gov (United States)

    Mathew, Jennie T; Bio, Laura L

    2012-01-01

    Enteral administration of injectable ammonium chloride may offer an effective method for the treatment of persistent metabolic alkalosis, without the adverse effects associated with the intravenous route. This case series describes 3 pediatric patients who received ammonium chloride enterally for the treatment of persistent metabolic alkalosis. The patients were a 2-month-old female infant, a 6-week-old male infant, and a 3-year-old male toddler. Four to 18 doses of ammonium chloride were administered enterally (range, 3-144 mEq/dose). Two of the 3 patients achieved resolution of metabolic alkalosis with ammonium chloride, while 1 patient's condition was refractory to treatment. Resolution of metabolic alkalosis occurred at 4 and 8 days, which required a total weight-based dose of 10.7 mEq/kg and 18 mEq/kg, respectively. No adverse effects were recorded. The use of ammonium chloride injection administered enterally was a safe and effective option in 2 of the 3 pediatric patients with persistent metabolic alkalosis.

  15. Metabolic alkalosis from unsuspected ingestion: use of urine pH and anion gap.

    Science.gov (United States)

    Yi, Joo-Hark; Han, Sang-Woong; Song, June-Seok; Kim, Ho-Jung

    2012-04-01

    Underlying causes of metabolic alkalosis may be evident from history, evaluation of effective circulatory volume, and measurement of urine chloride concentration. However, identification of causes may be difficult for certain conditions associated with clandestine behaviors, such as surreptitious vomiting, use of drugs or herbal supplements with mineralocorticoid activity, abuse of laxatives or diuretics, and long-term use of alkalis. In these circumstances, clinicians often are bewildered by unexplained metabolic alkalosis from an incomplete history or persistent deception by the patient, leading to misdiagnosis and poor outcome. We present a case of severe metabolic alkalosis and hypokalemia with a borderline urine chloride concentration in an alcoholic patient treated with a thiazide. The cause of the patient's metabolic alkalosis eventually was linked to surreptitious ingestion of baking soda. This case highlights the necessity of a high index of suspicion for the diverse clandestine behaviors that can cause metabolic alkalosis and the usefulness of urine pH and anion gap in its differential diagnosis. Copyright © 2012 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  16. Treatment of severe metabolic alkalosis in a patient with congestive heart failure.

    Science.gov (United States)

    Peixoto, Aldo J; Alpern, Robert J

    2013-05-01

    Metabolic alkalosis, isolated or in combination with another abnormality, is the most common acid-base disorder in patients with congestive heart failure. In most cases, it is a result of diuretic therapy, which causes activation of the renin-angiotensin system, chloride depletion, increased distal sodium delivery, hypokalemia, and increased urine acidification, all of which contribute to bicarbonate retention. In addition, the disease state itself results in neurohormonal activation (renin-angiotensin system, sympathetic nervous system, and endothelin) that further amplifies the tendency toward alkalosis. Treatment of metabolic alkalosis is based on the elimination of generation and maintenance factors, chloride and potassium repletion, enhancement of renal bicarbonate excretion (such as acetazolamide), direct titration of the base excess (hydrochloric acid), or, if accompanied by kidney failure, low-bicarbonate dialysis. In congestive heart failure, appropriate management of circulatory failure and use of an aldosterone antagonist in the diuretic regimen are integral to treatment. Published by Elsevier Inc.

  17. Acetazolamide for the management of chronic metabolic alkalosis in neonates and infants.

    Science.gov (United States)

    Tam, Bonnie; Chhay, Annie; Yen, Lilly; Tesoriero, Linda; Ramanathan, Rangasamy; Seri, Istvan; Friedlich, Philippe S

    2014-01-01

    In this study, we evaluated the efficacy and safety of acetazolamide in the management of chronic metabolic alkalosis in neonates and infants with chronic respiratory insufficiency. A retrospective chart review of 90 patients treated with acetazolamide between 2006 and 2007 admitted to the neonatal intensive care unit was performed. Blood gases and electrolytes obtained at baseline and by 24 hours after acetazolamide administration were compared. Compared with baseline and after 24 hours of acetazolamide, mean measured serum bicarbonate (29.5±3.7 vs. 26.9±3.8 mEq/L, Pmetabolic alkalosis in neonates and infants with chronic respiratory insufficiency needs further study.

  18. Metabolic alkalosis with multiple salt unbalance: an atypical onset of cystic fibrosis in a child

    Directory of Open Access Journals (Sweden)

    Dimitri Poddighe

    2017-12-01

    Full Text Available Dehydration with multiple salt abnormalities is frequently encountered in the paediatric emergency department, during acute illnesses complicated by loss of body fluids. Metabolic alkalosis is not a common finding in dehydrated children. The presence of unusual electrolyte unbalance, such as metabolic alkalosis, hyponatremia, hypochloremia and hypokalemia, without evidence of renal tubular defects, is named as pseudo-Bartter syndrome. It can occur in several clinical settings and, in infancy, it is described as a potential complication of cystic fibrosis. We report a case of pseudo-Bartter syndrome representing the onset of cystic fibrosis in childhood.

  19. The use of dilute hydrochloric acid and cimetidine to reverse severe metabolic alkalosis.

    Science.gov (United States)

    Rowlands, B. J.; Tindall, S. F.; Elliott, D. J.

    1978-01-01

    Two cases of severe metabolic alkalosis associated with gastric hypersecretion were successfully treated with dilute hydrochloric acid and a histamine H2-receptor antagonist given by intravenous infusion. This combined therapy with electrolyte replacement and suppression of gastric secretion is valuable in the control of this serious metabolic abnormality when conventional treatment is unsuccessful or contraindicated. PMID:634873

  20. Hypernatremia and metabolic alkalosis as a consequence of the therapeutic misuse of baking soda.

    Science.gov (United States)

    Fuchs, S; Listernick, R

    1987-12-01

    When used appropriately, baking soda (sodium bicarbonate, USP) is a nontoxic, readily available, multipurpose product found in many households. We report an infant who presented with hypernatremia and metabolic alkalosis due to the addition of baking soda to her water. This case represents the possible dangerous use of a common household product in infants owing to the lack of proper warning labels.

  1. Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low Plasma Bicarbonate Using the Urine Anion Gap.

    Science.gov (United States)

    Batlle, Daniel; Chin-Theodorou, Jamie; Tucker, Bryan M

    2017-09-01

    Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is a finding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratory alkalosis and mixed metabolic acidosis and chronic respiratory alkalosis. Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy. Proper diagnosis of the cause of hypobicarbonatemia requires integration of the laboratory values, arterial blood gas, and clinical history. The information derived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as a surrogate marker of urine ammonium excretion, in the evaluation of a patient with low plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urine acid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap) to evaluate urine acidification are discussed. Copyright © 2017 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  2. Acidosis-Induced Hypochloremic Alkalosis in Diabetic Ketoacidosis Confirmed by The Modified Base Excess Method.

    Science.gov (United States)

    Yasuda, Keigo; Hayashi, Makoto; Murayama, Masanori; Yamakita, Noriyoshi

    2016-06-01

    Diabetic ketoacidosis (DKA) is associated with a metabolic alkalosis, which is thought to be due to vomiting. However, alkalosis can occur in DKA without vomiting. We retrospectively reviewed the acid-base disturbances in DKA admissions without vomiting. We included admissions of the patients with blood glucose and beta-hydroxybutyrate (βOHB) levels > 250 mg/dL and > 1.0 mmol/L, respectively. Admissions without vomiting were classified into a group with a βOHB > 3.0 mmol/L (DKA group) and a group with βOHB of 1.0-3.0 mmol/L (pre-DKA group). The acid-base status was analyzed by the modified base excess (BE) method. BE effects were calculated by changes in sodium (BE free water, [BEFW]), and chloride (BECl). Positive and negative values for each parameter suggested alkalosis and acidosis, respectively. Forty-five included admissions were divided into DKA (n = 34) and pre-DKA (n =11) groups. Sodium-corrected chloride level and the chloride/sodium ratio were significantly lower in the DKA group than in the pre-DKA group. In both groups, BEFW values were modestly negative. The mean BECl values were positive in both groups, but significantly higher in the DKA group. The alkalinizing effects by hypochloremia diminished the base deficit in the DKA group by approximately 25%. The BECl value significantly correlated with serum total ketone levels (r = 0.66; P alkalosis in DKA without vomiting. This suggests the direct participation of serum ketoacids in the pathogenesis of hypochloremic alkalosis.

  3. Comparison of Arginine Hydrochloride and Acetazolamide for the Correction of Metabolic Alkalosis in Pediatric Patients.

    Science.gov (United States)

    Heble, Daniel E; Oschman, Alexandra; Sandritter, Tracy L

    Metabolic alkalosis is a common acid-base disturbance occurring in critically ill pediatric patients. Acetazolamide and arginine hydrochloride are pharmacologic agents used at our institution for patients refractory to first-line therapy or those unable to tolerate fluid replacement. The objective of this retrospective review was to determine if a course of arginine hydrochloride or acetazolamide was more effective at correcting metabolic alkalosis within a 24-hour period. Patients included received a course of acetazolamide or arginine hydrochloride for metabolic alkalosis with a repeat metabolic panel 18-30 hours after treatment initiation. Exclusion criteria consisted of previous treatment with either drug within 24 hours or a documented metabolic disorder. Efficacy was determined by proportion of patients achieving resolution of metabolic alkalosis (treatment success: serum CO2 96 mmol/L). Additionally, mean change in serum bicarbonate and chloride concentrations was assessed. Thirty-four patients met inclusion criteria, 19 patients received acetazolamide and 15 patients received arginine hydrochloride. Treatment success was similar in patients receiving acetazolamide and arginine hydrochloride (37% vs. 7%, P = 0.053). Correction of serum bicarbonate was observed in more patients treated with acetazolamide (42% vs. 7%, P = 0.047). Both groups had a similar increase in mean serum chloride concentration (5.7 ± 5.3 vs. 4.4 ± 4.4 mmol/L, P = 0.458). Mean decrease in serum bicarbonate concentration was equivalent between groups (5.6 ± 5.2 vs. 2.8 ± 4.7, mmol/L, P = 0.110). Acetazolamide and arginine hydrochloride appear to be equally effective in correcting metabolic alkalosis in critically ill pediatric patients.

  4. Transient metabolic alkalosis during early reperfusion abolishes helium preconditioning against myocardial infarction: restoration of cardioprotection by cyclosporin A in rabbits.

    Science.gov (United States)

    Pagel, Paul S; Krolikowski, John G

    2009-04-01

    Intracellular acidosis during early reperfusion after coronary artery occlusion was recently linked to cardioprotection resulting from myocardial ischemic postconditioning. We tested the hypotheses that transient alkalosis during early reperfusion abolishes helium preconditioning and that the mitochondrial permeability transition pore inhibitor cyclosporin A (CsA) restores the cardioprotective effects of helium during alkalosis in vivo. Rabbits (n = 36) instrumented for hemodynamics measurement were subjected to a 30-min left anterior descending coronary artery occlusion and 3-h reperfusion. The rabbits received 0.9% saline (control) or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture before left anterior descending coronary artery occlusion in the absence or presence of transient alkalosis (pH = 7.5) produced by administration of IV sodium bicarbonate (10 mEq) 2 min before reperfusion. Other rabbits preconditioned with helium received CsA (5 mg/kg) in the presence of alkalosis or CsA alone. Helium reduced myocardial infarct size (25% +/- 4% of left ventricular area at risk; P Alkalosis during early reperfusion did not alter infarct size alone (46% +/- 2%), but this intervention abolished helium-induced cardioprotection (45% +/- 3%). CsA restored reductions in infarct size produced by helium preconditioning in the presence of alkalosis (28% +/- 6%; P alkalosis during early reperfusion abolishes helium preconditioning in rabbits. CsA restored helium-induced cardioprotection during alkalosis, suggesting that helium preconditioning inhibits mitochondrial permeability transition pore formation by maintaining intracellular acidosis during early reperfusion.

  5. Retrospective Review of Hydrochloric Acid Infusion for the Treatment of Metabolic Alkalosis in Surgical Intensive Care Unit Patients.

    Science.gov (United States)

    Guffey, Jason D; Haas, Curtis E; Crowley, Amber; Connor, Kathryn A; Kaufman, David C

    2018-01-01

    Older reports of use of hydrochloric acid (HCl) infusions for treatment of metabolic alkalosis document variable dosing strategies and risk. This study sought to characterize use of HCl infusions in surgical intensive care unit patients for the treatment of metabolic alkalosis. This retrospective review included patients who received a HCl infusion for >8 hours. The primary end point was to evaluate the utility of common acid-base equations for predicting HCl dose requirements. Secondary end points evaluated adverse effects, efficacy, duration of therapy, and total HCl dose needed to correct metabolic alkalosis. Data on demographics, potential causes of metabolic alkalosis, fluid volume, and duration of diuretics as well as laboratory data were collected. A total of 30 patients were included, and the average HCl infusion rate was 10.5 ± 3.7 mEq/h for an average of 29 ± 14.6 hours. Metabolic alkalosis was primarily diuretic-induced (n = 26). Efficacy was characterized by reduction in the median total serum CO 2 from 34 to 27 mM/L ( P metabolic alkalosis, and no serious adverse events were seen. In this clinical setting, the baseline chloride ion deficit and SIDa were not useful for prediction of total HCl dose requirement, and serial monitoring of response is recommended.

  6. [Dehydration and metabolic alkalosis: an unusual presentation of cystic fibrosis in an infant].

    Science.gov (United States)

    Aranzamendi, Roberto J; Breitman, Fanny; Asciutto, Carolina; Delgado, Norma; Castaños, Claudio

    2008-10-01

    Cystic fibrosis (CF) may present during neonatal period with classic clinic symptoms related to the disease. The severity of the disease is multifactorial, one of the factors depends on the level of activity of the CFTR protein, which is related with the mutation type that affects the patient. An infant is presented who developed recurrent episodes of vomiting, anorexia, weight loss, dehydration and electrolyte abnormalities, such as metabolic alkalosis, hyponatremia, hypokalemia and hypochloremia. CF was diagnosed after the third episode showing an unusual and not very publicized presentation of the disease. Mutations !F 508 and 2789+5G-A were found. CF should be considered in patients of any age, but particularly in infants, presenting with anorexia, vomiting, failure to thrive, that are associated with recurrent episodes of hyponatremic hypochloremic, dehydration with metabolic alkalosis unexplained by other causes, even in the absence of respiratory or gastrointestinal symptoms or failure to thrive.

  7. Hyponatremic Chloride-depletion Metabolic Alkalosis Successfully Treated with High Cation-gap Amino Acid.

    Science.gov (United States)

    Ryuge, Akihiro; Matsui, Katsuomi; Shibagaki, Yugo

    2016-01-01

    Chloride (Cl)-depletion alkalosis (CDA) develops due to the loss of Cl-rich body fluid, i.e., vomiting or diuretics use, and is typically treated with a chloride-rich solution such as normal saline (NS). Although NS is one of the most utilized Cl-rich solutions, high cation-gap amino acid (HCG-AA) predominantly comprises Cl and less sodium, making HCG-AA more efficient in correcting CDA. We herein report a case of CDA with chronic hyponatremia after frequent vomiting, which was successfully treated with HCG-AA without overcorrecting hyponatremia or causing hypervolemia. HCG-AA may be more beneficial than NS for treating hyponatremic or hypervolemic metabolic alkalosis.

  8. Severe metabolic alkalosis and recurrent acute on chronic kidney injury in a patient with Crohn's disease.

    Science.gov (United States)

    Jacobi, Johannes; Schnellhardt, Susanne; Opgenoorth, Mirian; Amann, Kerstin U; Küttner, Axel; Schmid, Axel; Eckardt, Kai-Uwe; Hilgers, Karl F

    2010-04-18

    Diarrhea is common in patients with Crohn's disease and may be accompanied by acid base disorders, most commonly metabolic acidosis due to intestinal loss of bicarbonate. Here, we present a case of severe metabolic alkalosis in a young patient suffering from M. Crohn. The patient had undergone multiple resections of the intestine and suffered from chronic kidney disease. He was now referred to our clinic for recurrent acute kidney injury, the nature of which was pre-renal due to profound volume depletion. Renal failure was associated with marked hypochloremic metabolic alkalosis which only responded to high volume repletion and high dose blockade of gastric hypersecretion. Intestinal failure with stomal fluid losses of up to 5.7 litres per day required port implantation to commence parenteral nutrition. Fluid and electrolyte replacement rapidly improved renal function and acid base homeostasis. This case highlights the important role of gastrointestinal function to maintain acid base status in patients with Crohn's disease.

  9. Hypokalemic metabolic alkalosis caused by surreptitious vomiting: report of four cases.

    Science.gov (United States)

    Richardson, R. M.; Forbath, N.; Karanicolas, S.

    1983-01-01

    Four women, aged 22 to 40 years, presented with severe hypokalemia and metabolic alkalosis. Three had related neuromuscular symptoms. All four patients denied vomiting or diuretic ingestion, and a diagnosis of Bartter's syndrome was entertained. A diagnosis of surreptitious vomiting was suspected from the characteristic urine electrolyte pattern: high values for sodium and potassium, and a chloride concentration of less than 5 mmol/l. Three patients excreted sodium and potassium primarily with bicarbonate and had an alkaline urine; the fourth patient excreted these cations primarily with an organic anion and had an acid urine (pH 5.5). Since self-induced vomiting may be a common method of weight reduction in young women, recognition of this characteristic urine electrolyte pattern will assist in the rapid diagnosis of hypokalemia and metabolic alkalosis of obscure cause. PMID:6861055

  10. Changes in bone sodium and carbonate in metabolic acidosis and alkalosis in the dog

    Science.gov (United States)

    Burnell, James M.

    1971-01-01

    Metabolic acidosis and alkalosis were produced in adult dogs over 5- to 10-day periods. Midtibial cortical bone was analyzed for calcium, sodium, phosphorus, and carbonate. In acidosis bone CO3/Ca decreased 9.5% and bone Na/Ca decreased 6.3%. In alkalosis bone CO3/Ca increased 3.1% and bone Na/Ca increased 3.0%. Previous attempts to account for changes in net acid balance by summation of extra- and intracellular acid-base changes have uniformly resulted in about 40-60% of acid gained or lost being “unaccounted for.” If it is assumed that changes in tibial cortex reflect changes in the entire skeletal system, changes in bone CO3= are sufficiently large to account for the “unaccounted for” acid change without postulating changes in cellular metabolic acid production. PMID:5540172

  11. Hypercalcemia-Induced Hypokalemic Metabolic Alkalosis in a Multiple Myeloma Patient: The Risk of Furosemide Use.

    Science.gov (United States)

    Reiser, Ira W; Ali, Slamat; Gotlieb, Vladimir; Spitalewitz, Samuel

    2015-01-01

    Hypercalcemia is often seen in patients with malignancies, and in the past treatment for this has traditionally included loop diuretics. Clinically, patients with hypercalcemia frequently present with polyuria and volume contraction which may be further exacerbated by diuretic therapy. In the lab, hypercalcemia has been shown to activate the calcium-sensing receptor in the thick ascending limb of Henle and inactivate the 2 chloride sodium potassium co-transporter and induce a hypokalemic metabolic alkalosis, an effect similar to that of the loop diuretic furosemide. We now report what may well be the first clinical correlate of this laboratory finding in a patient who developed a hypokalemic metabolic alkalosis as a consequence of severe hypercalcemia due to multiple myeloma and whose metabolic derangement was corrected without the use of a loop diuretic which may have exacerbated the electrolyte abnormalities.

  12. Baking soda pica: a case of hypokalemic metabolic alkalosis and rhabdomyolysis in pregnancy.

    Science.gov (United States)

    Grotegut, Chad A; Dandolu, Vani; Katari, Sunita; Whiteman, Valerie E; Geifman-Holtzman, Ossie; Teitelman, Melissa

    2006-02-01

    We report a case of baking soda pica in a woman at 31 weeks of pregnancy causing severe hypokalemic metabolic alkalosis and rhabdomyolysis. A multigravida at 31 weeks of gestation presented with weakness and muscle pain. She was found to have severe hypokalemic metabolic alkalosis and rhabdomyolysis, with elevation in serum transaminases and hypertension. We initially thought the patient had an atypical presentation of preeclampsia until it was realized that she was ingesting 1 full box of baking soda (454 g sodium bicarbonate) per day. Symptoms and abnormal laboratory findings resolved with discontinuation of the patient's pica practices. Pica is a common but often overlooked practice that can potentially lead to life-threatening disorders. A thorough evaluation of a patient's dietary intake is extremely important, especially in the setting of atypical presentations of disease in pregnancy.

  13. Acidosis, but Not Alkalosis, Affects Anaerobic Metabolism and Performance in a 4-km Time Trial.

    Science.gov (United States)

    Correia-Oliveira, Carlos Rafaell; Lopes-Silva, João Paulo; Bertuzzi, Romulo; McConell, Glenn K; Bishop, David John; Lima-Silva, Adriano Eduardo; Kiss, Maria Augusta Peduti Dal'molin

    2017-09-01

    This study aimed to determine the effect of preexercise metabolic acidosis and alkalosis on power output (PO) and aerobic and anaerobic energy expenditure during a 4-km cycling time trial (TT). Eleven recreationally trained cyclists (V˙O2peak 54.1 ± 9.3 mL·kg·min) performed a 4-km TT 100 min after ingesting in a double-blind matter 0.15 g·kg of body mass of ammonium chloride (NH4Cl, acidosis), 0.3 g·kg of sodium bicarbonate (NaHCO3, alkalosis), or 0.15 g·kg of CaCO3 (placebo). A preliminary study (n = 7) was conducted to establish the optimal doses to promote the desirable preexercise blood pH alterations without gastrointestinal distress. Data for PO, aerobic and anaerobic energy expenditure, and blood and respiratory parameters were averaged for each 1 km and compared between conditions using two-way repeated-measures ANOVA (condition and distance factors). Gastrointestinal discomfort was analyzed qualitatively. Compared with placebo (pH 7.37 ± 0.02, [HCO3]: 27.5 ± 2.6 mmol·L), the NaHCO3 ingestion resulted in a preexercise blood alkalosis (pH +0.06 ± 0.04, [HCO3]: +4.4 ± 2.0 mmol·L, P 0.05). Minimal gastrointestinal distress was noted in all conditions. Preexercise acidosis, but not alkalosis, affects anaerobic metabolism and PO during a 4-km cycling TT.

  14. Acetazolamide improves oxygenation in patients with respiratory failure and metabolic alkalosis.

    Science.gov (United States)

    Gulsvik, Ragnhild; Skjørten, Ingunn; Undhjem, Kenneth; Holø, Lars; Frostad, Anne; Saure, Eirunn Waatevik; Lejlic, Vasvija; Humerfelt, Sjur; Hansen, Gunnar; Bruun Wyller, Torgeir

    2013-10-01

    Coexistent respiratory failure and metabolic alkalosis is a common finding. Acidotic diuretics cause a fall in pH that may stimulate respiration. The purpose of the study was to evaluate the effectiveness of short-term treatment with acetazolamide for combined respiratory failure and metabolic alkalosis. A randomised, placebo-controlled and double-blind parallel group trial where oral acetazolamide 250 mg three times a day for 5 days were administered to patients hospitalised for respiratory failure because of a pulmonary disease (Pa O2 ≤ 8 kPa and/or Pa CO2 ≥ 7 kPa) who had concurrent metabolic alkalosis [base excess (BE) ≥ 8 mmol/L]. Pa O2 after 5 days was the primary effect variable. Secondary effect variables were Pa CO2 , BE and pH on day 5, and the total number of days in hospital. Of 70 patients enrolled (35 in each group), data from 54 were analysed per protocol, while last observation carried forward was used for the remaining 16. During the 5-day treatment, Pa O2 increased on average 0.81 kPa in the placebo group and 1.41 kPa in the acetazolamide group. After adjustment for baseline skewness, the difference was statistically significant (adjusted mean difference 0.55 kPa, 95% confidence interval 0.03-1.06). Pa CO2 decreased in both groups, but the difference was not statistically significant. As expected, pH and BE decreased markedly in the acetazolamide group. Acetazolamide may constitute a useful adjuvant treatment mainly to be considered in selected patients with respiratory failure combined with prominent metabolic alkalosis or where non-invasive ventilation is insufficient or infeasible. © 2013 John Wiley & Sons Ltd.

  15. Rapid correction of metabolic alkalosis in hypertrophic pyloric stenosis with intravenous cimetidine: preliminary results.

    Science.gov (United States)

    Banieghbal, Behrouz

    2009-03-01

    Pyloromyotomy has been the treatment of choice for hypertrophic pyloric stenosis (HPS) for the past century. In most HPS cases, there is mild metabolic alkalosis, which requires intravenous fluid resuscitation with 5% dextrose/normal saline for 1-2 days. However, in some cases, due to a delay in diagnosis, alkalosis becomes severe and a much longer resuscitation period (5-10 days) is required to normalize serum pH. Metabolic alkalosis of HPS results from excessive vomiting of hydrochloric acid; and therefore if its production is reduced, serum pH can be normalized faster. In this study, the use of intravenous cimetidine (CM) in a small number of infants with HPS is presented. Over a 28-month period, 32 HPS cases, including a sub-group of 17 infants (aged 7-9 weeks) with arterial pH >7.60, were admitted to a tertiary referral unit. Four infants in this sub-group were treated with standard resuscitation fluids for 4 days prior to intravenous CM, while 12 infants received CM immediately. Intravenous CM (10 mg/kg) was given at twice daily until arterial pH was less than 7.50. In one case, intravenous omeprazole at 0.1 mg/kg was given instead of CM. In all 17 cases, CM treatment or omeprazole therapy (for 12-48 h) reduced pH to less than 7.50, thus allowing for Ramstedt pyloromyotomy the same day. These patients were allowed oral feeding on the following day and were discharged at 1-3 post-operative days. No complications due to CM (or omperazole) treatment were observed. Intravenous CM administration can rapidly normalize severe metabolic alkalosis in HPS patients. As a result, pyloromyotomy can be performed sooner reducing both hospital stay and costs.

  16. Metabolic alkalosis secondary to baking soda treatment of a diaper rash.

    Science.gov (United States)

    Gonzalez, J; Hogg, R J

    1981-06-01

    A 4-month-old infant was seen with hypokalemic metabolic alkalosis that was associated with prior application of liberal amounts of sodium bicarbonate (baking soda) to a diaper rash. After exclusion of other etiologies of the infant's acid-base disturbance, a complete resolution occurred following discontinuation of the baking soda applications. This case report provides a reminder of the significant side effects that may result from the excessive use of a seemingly harmless household substance.

  17. Acetazolamide therapy for hypochloremic metabolic alkalosis in pediatric patients with heart disease.

    Science.gov (United States)

    Moffett, Brady S; Moffett, Tiffany I; Dickerson, Heather A

    2007-01-01

    Pediatric patients with heart disease are often treated with high doses of diuretics, which can lead to hypochloremic metabolic alkalosis. There are no data in children regarding the efficacy and safety of acetazolamide to treat hypochloremic metabolic alkalosis. Patients from January 2004 to June 2005 who received acetazolamide were identified. Inclusion criteria were: age less than 18 years, being a cardiology patient, diuretics use, and had received a 3-day course of acetazolamide. Demographic information was collected along with serum electrolytes, serum creatinine/blood urea nitrogen, urine output, pH, acid-base excess, concurrent medications, cardiac lesion/surgery, and incidence of adverse effects. Efficacy of acetazolamide was determined by comparing variables before and after the 3-day course. Statistical comparisons were made using Student's t-test. A total of 28 patients were identified, 7 of whom received oral acetazolamide, 21 intravenous acetazolamide. Patients were a median of 2.5 (range, 0.3-20) months of age, and 57% (17/28) were female. Seventy-one percent of the cohort received acetazolamide after cardiac surgery. There was no significant difference in any electrolyte, blood urea nitrogen, or serum creatinine from baseline, except for serum bicarbonate, which decreased (36.2 +/- 4.6 vs. 30.9 +/- 4.5 mmol/L, P metabolic alkalosis.

  18. Differential effect of metabolic alkalosis and hypoxia on high-intensity cycling performance.

    Science.gov (United States)

    Flinn, Samantha; Herbert, Kathryn; Graham, Kenneth; Siegler, Jason C

    2014-10-01

    The purpose of this study was to investigate the effects of sodium bicarbonate (NaHCO3) ingestion and acute hypoxic exposure on repeated bouts of high-intensity cycling to task failure. Twelve subjects completed 4 separate intermittent cycling bouts cycling bouts to task failure (120% peak power output for 30-second interspersed with 30-second active recovery) under the following conditions: normoxia (FIO2% at 20.93%) alkalosis (NA), normoxia placebo (NP), hypoxia (FIO2% at 14.7%) alkalosis (HA), and hypoxia placebo (HP). For the NA and HA trials, the buffer solution (0.3 g·kg of NaHCO3) was dispensed into gelatin capsules and consumed over 90 minutes with 1 L of water. Whole-blood acid-base findings demonstrated metabolic alkalosis in both NA and HA before exercise (HCO3: 32.8 ± 1.8 mmol·L). Time to task failure was significantly impaired in the hypoxic conditions (NA: 199.1 ± 62.3 seconds, NP: 183.8 ± 45.0 seconds, HA: 127.8 ± 27.9 seconds, HP: 133.3 ± 28.7 seconds; p metabolic acidosis during intermittent high-intensity cycling to task failure. In application, the use of hypoxia and NaHCO3 concurrently to improve performance under these conditions does not seem warranted.

  19. Effectiveness of acetazolamide for reversal of metabolic alkalosis in weaning COPD patients from mechanical ventilation.

    Science.gov (United States)

    Faisy, Christophe; Mokline, Amel; Sanchez, Olivier; Tadié, Jean-Marc; Fagon, Jean-Yves

    2010-05-01

    To evaluate the effects of a single daily dose of acetazolamide (ACET) on metabolic alkalosis and respiratory parameters in weaning chronic obstructive pulmonary disease (COPD) patients from invasive mechanical ventilation. Case-control study. An 18-bed intensive care unit (ICU) in a university hospital. Twenty-six intubated COPD patients with mixed metabolic alkalosis (serum bicarbonate >26 mmol/l and arterial pH >or=7.38) were compared with a historical control group (n = 26) matched for serum bicarbonate, arterial pH, age, and severity of illness at admission to ICU. ACET administration (500 mg intravenously) was monitored daily according to arterial blood gas analysis from readiness to wean until extubation. ACET was administered 4 (1-11) days throughout the weaning period. Patients with ACET treatment significantly decreased their serum bicarbonate (p = 0.01 versus baseline) and arterial blood pH (p metabolic alkalosis but has no benefit in terms of improving PaCO(2) or respiratory parameters in weaning COPD patients from mechanical ventilation.

  20. Metabolic alkalosis due to feeding chicks in breeding Adélie penguins Pygoscelis adeliae under natural conditions.

    Science.gov (United States)

    Sakamoto, Kentaro Q; Sato, Katsufumi; Kato, Akiko; Fukui, Daisuke; Bando, Gen; Naito, Yasuhiko; Habara, Yoshiaki; Ishizuka, Mayumi; Fujita, Shoichi

    2010-01-01

    Prolonged abnormal vomiting causes metabolic alkalosis. Many seabirds are known to feed their chicks by regurgitation. We hypothesized that metabolic alkalosis occurs in seabirds even under natural conditions during the breeding season. Adélie penguins Pygoscelis adeliae feed their chicks by regurgitating food for 50-60 d until the chicks fledge. In this study, the concentrations of Cl(-), HCO(3)(-), Na+, K+, pH, and PCO2 in the blood of breeding Adélie penguins were measured throughout the chick-rearing season. The pH of penguin venous blood shifted from 7.54 in the guarding period to 7.47 in the crèche period. Decreasing Cl(-) and increasing HCO(3)(-) blood concentrations in parents were associated with increasing mass of their brood in the guarding period, the early phase of the rearing season, indicating that regurgitating to feed chicks causes loss of gastric acid and results in relative metabolic alkalosis. The inverse trend was observed during the crèche period, the latter phase of the rearing season, when parents spent more time at sea and have fewer opportunities for gastric acid loss. This was assumed to be the recovery phase. These results indicate that regurgitation might cause metabolic alkalosis in breeding Adélie penguins. To our knowledge, this is the first report to indicate that seabirds exhibit metabolic alkalosis due to regurgitation to feed chicks under natural conditions.

  1. Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport.

    Science.gov (United States)

    Gennari, F John

    2011-10-01

    Metabolic alkalosis is a unique acid-base disorder because it can be induced and sustained by functional alterations in renal ion transport. This review summarizes more than 50 years of research into the pathophysiologic processes causing this disorder. The evidence reviewed supports the hypothesis that virtually all forms of metabolic alkalosis are sustained by enhanced collecting duct hydrogen ion secretion, induced by stimulation of sodium uptake through the epithelial sodium channel (ENaC). Enhanced collecting duct hydrogen ion secretion in metabolic alkalosis occurs most commonly secondary to changes in ion transport earlier along the nephron, but also can occur as the result of primary stimulation of ENaC. In both these settings, potassium secretion is stimulated, and abnormal potassium losses cause depletion of body potassium stores. Potassium depletion has a key role in sustaining metabolic alkalosis by stimulating renal hydrogen ion secretion, enhancing renal ammonium production and excretion, and downregulating sodium reabsorption in the loop of Henle and early distal tubule. A new classification of the causes of metabolic alkalosis is proposed based on these pathophysiologic events rather than response to treatment. Copyright © 2011 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  2. Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician's Challenge.

    Science.gov (United States)

    Ijaz, Mohsin; Abbas, Naeem; Lvovsky, Dmitry

    2015-01-01

    Metabolic alkalosis secondary to citrate toxicity from plasma exchange is very uncommon in patients with normal renal function. In patients with advanced renal disease this can be a fatal event. We describe a case of middle-aged woman with Goodpasture's syndrome treated with plasma exchange who developed severe metabolic alkalosis. High citrate load in plasma exchange fluid is the underlying etiology. Citrate metabolism generates bicarbonate and once its level exceeds the excretory capacity of kidneys, the severe metabolic alkalosis ensues. Our patient presented with generalized weakness, fever, and oliguria and developed rapidly progressive renal failure. Patient had positive serology for antineutrophilic cytoplasmic antibodies myeloperoxidase (ANCA-MPO) and anti-glomerular basement membrane antibodies (anti-GBM). Renal biopsy showed diffuse necrotizing and crescentic glomerulonephritis with linear glomerular basement membrane staining. Patient did not respond to intravenous steroids. Plasma exchange was started with fresh frozen plasma but patient developed severe metabolic alkalosis. This metabolic alkalosis normalized with cessation of plasma exchange and initiation of low bicarbonate hemodialysis. ANCA-MPO and anti-GBM antibodies levels normalized within 2 weeks and remained undetectable at 3 months. Patient still required maintenance hemodialysis.

  3. Gitelman's syndrome with vomiting manifested by severe metabolic alkalosis and progressive renal insufficiency.

    Science.gov (United States)

    Lee, Jong-Ho; Lee, Jeonghwan; Han, Jin Suk

    2013-11-01

    Gitelman's syndrome is an autosomal recessive salt-losing tubulopathy showing hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis and hyperreninemic hyperaldosteronism. This syndrome is caused by mutations in the SLC12A3 gene that encodes sodium-chloride cotransporter expressed at the apical membrane of renal distal convoluted tubule. Symptoms and renal outcomes of Gitelman's syndrome are, in general, mild and benign, and renal insufficiency from Gitelman's syndrome associated with long-standing hypokalemia and volume depletion is extremely rare. Herein, we report a 27-year-old male patient with Gitelman's syndrome who manifested renal failure, hypokalemia, severe metabolic alkalosis and altered mentality. About one year ago, the patient had been transferred to Seoul National University Hospital, because of unsolved hypokalemia, and was diagnosed as Gitelman's syndrome by clinical features and genetic analysis of the SLC12A3 gene. The patient carries a missense mutation at one allele of SLC12A3 gene (c.781C>T, p.Arg261Cys). His mother is also heterozygous for the same mutation and she had a history of hypokalemia. On this admission, the patient had recurrent bouts of vomiting induced by psychiatric eating disorder and showed severe volume depletion with hypotension, azotemia and metabolic alkalosis. Intense hydration therapy and emergency hemodialysis transiently improved his fluid-electrolyte imbalance and renal function. However, renal dysfunction progressively deteriorated despite the medical treatment. Our findings suggest that even in Gitelman's syndrome, constant monitoring for volume status and other comorbid conditions should be employed to prevent progressive renal injury.

  4. [Cardiac arrest in chronic metabolic alkalosis due to sodium bicarbonate abuse].

    Science.gov (United States)

    Niewiński, Grzegorz; Korta, Teresa; Debowska, Małgorzata; Kosiński, Cezary; Kubik, Tomasz; Romanik, Wojciech; Kański, Andrzej

    2008-01-01

    Moderate metabolic alkalosis has not been considered as a life-threatening situation by many authors, but when it persists and pH increases above 7.65, the situation may become critical. We present a case of a 61-yr-old alcoholic male patient, who had been consuming approximately 200 g of sodium bicarbonate daily for twenty years, due to persisitent heartburn and abdominal pains. The patient was admitted to the ITU after home cardiac arrest and resuscitation. On admission he was unconscious and in respiratory distress, with a GCS of 5. Blood gases revealed that his pH was 7.64, HCO3 44 mmol L(-1), K+ 2.4 mmol L(-1)l, Cl- 44 mmol L(-1), and lactate concentration over 15 mmol L(-1). He was treated with controlled hypercapnia, up to a PaCO2 of 63 mm Hg, sedation, and administration of a large amount of chloride (864 mmol during the first day). The patient regained consciousness after 48 h, was extubated and transferred to the internal medicine department where he died 3 days later. Chronic alkali abuse can lead to various metabolic disturbances, neurologic disturbances and cardiovascular compromise. In the described case, the exact cause of cardiac arrest remained unknown, but may have been caused by alkalosis combined with hypoxia, hypokalemia and poor general condition. The extreme metabolic alkalosis (pH 7.8) could also have been enhanced by the administration of i.v. sodium bicarbonate during resuscitation. The treatment of choice in such cases should consist of vigorous chloride containing fluid resuscitation, ammonium chloride and hemodialysis.

  5. Treatment of metabolic alkalosis during continuous renal replacement therapy with regional citrate anticoagulation.

    Science.gov (United States)

    Kindgen-Milles, D; Amman, J; Kleinekofort, W; Morgera, S

    2008-04-01

    The use of citrate as an anticoagulant in continuous renal replacement therapy is an effective method to achieve regional anticoagulation of the extracorporeal blood circuit and to avoid systemic anticoagulation. This allows bleeding complications to be reduced and filter life time to be prolonged. However, citrate enters the systemic circulation and is metabolized in the liver to bicarbonate, causing metabolic alkalosis in some patients. In this case report, we discuss therapeutic interventions to control the acid-base status and to restore normal pH during continuous citrate hemodialysis.

  6. [Self-treatment with baking soda can lead to severe metabolic alkalosis].

    Science.gov (United States)

    Jensen, Sara; Skriver, Signe

    2014-12-15

    This case report describes a 66-year-old man, previously healthy besides mild hypertension. He ingested a self-made folk remedy consisting of baking soda and water against acid reflux in dosages that resulted in severe metabolic alkalosis (pH 7.8). Diagnosing and treating MA is easy and cheap, but if the condition is not treated, consequences can be severe. The challenge is to uncover patients' use of non prescription medications and folk remedies in the diagnostic process. Having this information it is possible to prevent MA in both high- and low-risk patients.

  7. Treatment of Severe Metabolic Alkalosis with Continuous Renal Replacement Therapy: Bicarbonate Kinetic Equations of Clinical Value.

    Science.gov (United States)

    Yessayan, Lenar; Yee, Jerry; Frinak, Stan; Kwon, David; Szamosfalvi, Balazs

    2015-01-01

    Concomitant severe metabolic alkalosis, hypernatremia, and kidney failure pose a therapeutic challenge. Hemodialysis to correct azotemia and abnormal electrolytes results in rapid correction of serum sodium, bicarbonate, and urea but presents a risk for dialysis disequilibrium and brain edema. We describe a patient with Zollinger-Ellison syndrome with persistent encephalopathy, severe metabolic alkalosis (highest bicarbonate 81 mEq/L), hypernatremia (sodium 157 mEq/L), and kidney failure despite 30 hours of intravenous crystalloids and proton pump inhibitor. We used continuous renal replacement therapy (RRT) with delivered hourly urea clearance of ~3 L/hour (24 hour sustained low efficiency dialysis with regional citrate anticoagulation protocol at blood flow rate 60 ml/min and dialysate flow rate 400 ml/min). To mitigate a pronounced decrease in plasma osmolality while removing urea from this hypernatremic patient, dialysate sodium was set to start at 155 mEq/L then at 150 mEq/L after 6 hours. Serum bicarbonate, urea, and sodium were slowly corrected over 26 hours. This case demonstrates how to regulate and predict the systemic bicarbonate level using single pool kinetic modeling during convective or diffusive RRT. Kinetic modeling provides a valuable tool for systemic blood pH control in future combined use of extracorporeal CO2 removal and continuous RRT systems.

  8. Severe metabolic alkalosis and recurrent acute on chronic kidney injury in a patient with Crohn's disease

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    Schmid Axel

    2010-04-01

    Full Text Available Abstract Background Diarrhea is common in patients with Crohn's disease and may be accompanied by acid base disorders, most commonly metabolic acidosis due to intestinal loss of bicarbonate. Case Presentation Here, we present a case of severe metabolic alkalosis in a young patient suffering from M. Crohn. The patient had undergone multiple resections of the intestine and suffered from chronic kidney disease. He was now referred to our clinic for recurrent acute kidney injury, the nature of which was pre-renal due to profound volume depletion. Renal failure was associated with marked hypochloremic metabolic alkalosis which only responded to high volume repletion and high dose blockade of gastric hypersecretion. Intestinal failure with stomal fluid losses of up to 5.7 litres per day required port implantation to commence parenteral nutrition. Fluid and electrolyte replacement rapidly improved renal function and acid base homeostasis. Conclusions This case highlights the important role of gastrointestinal function to maintain acid base status in patients with Crohn's disease.

  9. Effects of respiratory alkalosis on human skeletal muscle metabolism at the onset of submaximal exercise

    Science.gov (United States)

    LeBlanc, P J; Parolin, M L; Jones, N L; Heigenhauser, G J F

    2002-01-01

    The purpose of this study was to examine the effects of respiratory alkalosis on human skeletal muscle metabolism at rest and during submaximal exercise. Subjects exercised on two occasions for 15 min at 55 % of their maximal oxygen uptake while either hyperventilating (R-Alk) or breathing normally (Con). Muscle biopsies were taken at rest and after 1 and 15 min of exercise. At rest, no effects on muscle metabolism were observed in response to R-Alk. In the first minute of exercise, there was a delayed activation of pyruvate dehydrogenase (PDH) in R-Alk compared with Con, resulting in a reduced rate of pyruvate oxidation. Also, glycogenolysis was higher in R-Alk compared with Con, which was attributed to a higher availability of the monoprotonated form of inorganic phosphate (Pi), resulting in an elevated rate of pyruvate production. The mismatch between pyruvate production and its oxidation resulted in net lactate accumulation. These effects were not seen after 15 min of exercise, with no further differences in muscle metabolism between conditions. The results from the present study suggest that respiratory alkalosis may play an important role in lactate accumulation during the transition from rest to exercise in acute hypoxic conditions, but that other factors mediate lactate accumulation during steady-state exercise. PMID:12356901

  10. The effect of metabolic alkalosis on the ventilatory response in healthy subjects.

    Science.gov (United States)

    Oppersma, E; Doorduin, J; van der Hoeven, J G; Veltink, P H; van Hees, H W H; Heunks, L M A

    2018-02-01

    Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma bicarbonate levels decrease respiratory drive and minute ventilation. In an intervention study in 10 healthy subjects the ventilatory response using a hypercapnic ventilatory response (HCVR) test was assessed, before and after administration of high dose sodium bicarbonate. Total dose of sodiumbicarbonate was 1000 ml 8.4% in 3 days. Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO 2 pressure during the HCVR test, RR, V t , Pdi, EAdi and V E increased. The clinical ratio ΔV E /ΔP et CO 2 remained unchanged, but Pdi, EAdi and V E were significantly lower after bicarbonate administration for similar levels of inspired CO 2 . This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO 2 . Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

  11. Respiratory alkalosis and metabolic acidosis in a child treated with sulthiame.

    Science.gov (United States)

    Weissbach, Avichai; Tirosh, Irit; Scheuerman, Oded; Hoffer, Vered; Garty, Ben Zion

    2010-10-01

    To report on severe acid-base disturbance in a child with symptomatic epilepsy treated with sulthiame. A 9.5-year-old boy with chronic generalized tonic-clonic seizures was treated with carbamazepine and valproic acid. Because of poor seizure control, sulthiame was added to the treatment. Two months later, he presented at the emergency department with severe weakness, headache, dizziness, dyspnea, anorexia, and confusional state. Arterial blood gas analysis showed mixed respiratory alkalosis with high anion gap metabolic acidosis. Sulthiame-induced acid-base disturbance was suspected. The drug was withheld for the first 24 hours and then restarted at a reduced dosage. The arterial blood gases gradually normalized, the confusion disappeared, and the patient was discharged home.Three months later, 4 weeks after an increase in sulthiame dosage, the patient was once again admitted with the same clinical picture. Improvement was noted after the drug dosage was reduced. This is the first report of mixed respiratory alkalosis and metabolic acidosis in a child treated with sulthiame. Monitoring of the acid-base status should be considered in patients treated with sulthiame.

  12. Acute Hypocalcemia and Metabolic Alkalosis in Children on Cation-Exchange Resin Therapy

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    Aadil Kakajiwala

    2017-01-01

    Full Text Available Background. Sodium polystyrene sulfonate (SPS is a chelating agent used for the treatment of hyperkalemia. SPS has a wide range of exchange capacity requiring close monitoring of serum electrolytes. We observed two patients who developed acute hypocalcemia and increased metabolic alkalosis after initiating SPS therapy. We report these cases to draw attention to the potential risk of this medication in pediatric patients. Case Diagnosis/Treatment. Two children with chronic kidney disease on dialysis were started on SPS for hyperkalemia. Within a week after initiation of the medication, both patients developed hypocalcemia on routine labs without overt clinical manifestations. The hypocalcemia was rapidly corrected with oral supplementation and discontinuation of SPS. Conclusions. Severe hypocalcemia can develop after SPS therapy. The metabolic alkalosis in these patients associated with the hypocalcemia put them at increased risk for complications. Hence, careful attention must be paid to the state of calcium metabolism in all patients receiving SPS. Often calcium supplementation is required to maintain normal calcium levels.

  13. Acetazolamide-mediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients.

    NARCIS (Netherlands)

    Moviat, M.; Pickkers, P.; Voort, P.H. van der; Hoeven, J.G. van der

    2006-01-01

    INTRODUCTION: Metabolic alkalosis is a commonly encountered acid-base derangement in the intensive care unit. Treatment with the carbonic anhydrase inhibitor acetazolamide is indicated in selected cases. According to the quantitative approach described by Stewart, correction of serum pH due to

  14. Anesthetic Management of a Patient with Sustained Severe Metabolic Alkalosis and Electrolyte Abnormalities Caused by Ingestion of Baking Soda

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    Jose Soliz

    2014-01-01

    Full Text Available The use of alternative medicine is prevalent worldwide. However, its effect on intraoperative anesthetic care is underreported. We report the anesthetic management of a patient who underwent an extensive head and neck cancer surgery and presented with a severe intraoperative metabolic alkalosis from the long term ingestion of baking soda and other herbal remedies.

  15. Anesthetic management of a patient with sustained severe metabolic alkalosis and electrolyte abnormalities caused by ingestion of baking soda.

    Science.gov (United States)

    Soliz, Jose; Lim, Jeffrey; Zheng, Gang

    2014-01-01

    The use of alternative medicine is prevalent worldwide. However, its effect on intraoperative anesthetic care is underreported. We report the anesthetic management of a patient who underwent an extensive head and neck cancer surgery and presented with a severe intraoperative metabolic alkalosis from the long term ingestion of baking soda and other herbal remedies.

  16. A 3-year old girl with seizures, hypokalemia and metabolic alkalosis.

    Science.gov (United States)

    Harnisch, E; Leertouwer, T; Cransberg, K; Kist-van Holthe, J E

    2010-11-26

    A 3-year-old girl presented to the emergency department with seizures, low-grade fever and vomiting. She had tachycardia and a slow capillary refill. Blood pressure could not be measured. Because of suspected sepsis and/or meningo-encephalitis, broad spectrum antibiotics and antiviral medication were given together, along with volume expansion and anticonvulsive therapy. A few hours later, after a second seizure, the blood pressure was extremely high (156/116 mm Hg). The girl was treated with anticonvulsants and intravenous antihypertensive agents. MRI of the brain showed signs of posterior reversible encephalopathy syndrome. Cultures of blood and cerebrospinal fluid remained sterile. Further investigation into the cause of the malignant hypertension revealed hypokalemia, metabolic alkalosis and extremely high plasma renin activity, caused by a rare renal abnormality: bilateral renal segmental hypoplasia or Ask-Upmark kidneys.

  17. Acid extrusion via blood-brain barrier causes brain alkalosis and seizures after neonatal asphyxia.

    Science.gov (United States)

    Helmy, Mohamed M; Ruusuvuori, Eva; Watkins, Paul V; Voipio, Juha; Kanold, Patrick O; Kaila, Kai

    2012-11-01

    Birth asphyxia is often associated with a high seizure burden that is predictive of poor neurodevelopmental outcome. The mechanisms underlying birth asphyxia seizures are unknown. Using an animal model of birth asphyxia based on 6-day-old rat pups, we have recently shown that the seizure burden is linked to an increase in brain extracellular pH that consists of the recovery from the asphyxia-induced acidosis, and of a subsequent plateau level well above normal extracellular pH. In the present study, two-photon imaging of intracellular pH in neocortical neurons in vivo showed that pH changes also underwent a biphasic acid-alkaline response, resulting in an alkaline plateau level. The mean alkaline overshoot was strongly suppressed by a graded restoration of normocapnia after asphyxia. The parallel post-asphyxia increase in extra- and intracellular pH levels indicated a net loss of acid equivalents from brain tissue that was not attributable to a disruption of the blood-brain barrier, as demonstrated by a lack of increased sodium fluorescein extravasation into the brain, and by the electrophysiological characteristics of the blood-brain barrier. Indeed, electrode recordings of pH in the brain and trunk demonstrated a net efflux of acid equivalents from the brain across the blood-brain barrier, which was abolished by the Na/H exchange inhibitor, N-methyl-isobutyl amiloride. Pharmacological inhibition of Na/H exchange also suppressed the seizure activity associated with the brain-specific alkalosis. Our findings show that the post-asphyxia seizures are attributable to an enhanced Na/H exchange-dependent net extrusion of acid equivalents across the blood-brain barrier and to consequent brain alkalosis. These results suggest targeting of blood-brain barrier-mediated pH regulation as a novel approach in the prevention and therapy of neonatal seizures.

  18. Rare F311L CFTR gene mutation in a child presented with recurrent electrolyte abnormalities and metabolic alkalosis: case report.

    Science.gov (United States)

    Lumpaopong, Adisorn; Thirakhupt, Prapaipim; Srisuwan, Konggrapun; Chulamokha, Yupapin

    2009-05-01

    Delta F508 mutation is recognized as the most common genotype of cystic fibrosis (CF) however, there are small numbers of CF patients having Delta F508/F311L. In the present study, the authors report a 2-year-old Thai boy, originating from North India, presenting with recurrent episodes of febrile illness, hyponatremia, hypokalemia, and metabolic alkalosis since 4 months of age. He was transferred to our hospital for further investigation. Blood chemistry revealed the following serum electrolytes, sodium 122, potassium 3.69, chloride 79.7, and bicarbonate 33.8 mEq/L, and the following urine electrolytes, sodium metabolic alkalosis improved DNA sequencing analysis of his blood demonstrates compound mutation for Delta F508 and F311L in CFTR gene. In conclusion, the authors report a rare case of CF with Delta F508/F311L genotype presented with recurrent hyponatremia and metabolic alkalosis. Awareness of electrolyte abnormalities during febrile illness, proper genetic counseling, and long-term follow up are necessary in this patient.

  19. Metabolism of Glutamine by the Intact Functioning Kidney of the Dog STUDIES IN METABOLIC ACIDOSIS AND ALKALOSIS

    Science.gov (United States)

    Pitts, R. F.; Pilkington, L. A.; MacLeod, M. B.; Leal-Pinto, E.

    1972-01-01

    The renal conversion of glutamine to glucose and its oxidation to CO2 were compared in dogs in chronic metabolic acidosis and alkalosis. These studies were performed at normal endogenous levels of glutamine utilizing glutamine-34C (uniformly labeled) as a tracer. It was observed in five experiments in acidosis that mean renal extraction of glutamine by one kidney amounted to 27.7 μmoles/min. Of this quantity, 5.34 μmoles/min was converted to glucose, and 17.5 μmoles/min was oxidized to CO2. Acidotic animals excreted an average of 41 μmoles/min of ammonia in the urine formed by one kidney. In contrast, in five experiments in alkalosis, mean renal extraction of glutamine amounted to 8.04 μmoles/min. Of this quantity, 0.92 μmole/min was converted to glucose, and 4.99 μmoles/min was oxidized to CO2. Alkalotic animals excreted an average of 3.23 μmoles/min of ammonia in the urine. We conclude that renal gluconeogenesis is not rate limiting for the production and excretion of ammonia in either acidosis or alkalosis. Since 40% of total CO2 production is derived from oxidation of glutamine by the acidotic kidney and 14% by the alkalotic kidney, it is apparent that renal energy sources change with acid-base state and that glutamine constitutes a major metabolic fuel in acidosis. Images PMID:5011100

  20. The effect of metabolic alkalosis on central and peripheral mechanisms associated with exercise-induced muscle fatigue in humans.

    Science.gov (United States)

    Siegler, Jason C; Marshall, Paul

    2015-04-20

    What is the central question of this study? Does metabolic alkalosis affect central and peripheral mechanisms associated with exercise-induced muscle fatigue in humans? What is the main finding and its importance? Inducing metabolic alkalosis before exercise preserved voluntary activation, but not muscle excitation, after a 2 min maximal voluntary contraction (MVC) followed by ischaemia. An effect of pH was also observed in maximal rates of torque development, where alkalosis mitigated the reduction in maximal rates of torque development after the initial 2 min MVC. For the first time, these results demonstrate a differential effect of pH on voluntary activation as well as maximal rates of torque development after sustained, maximal voluntary knee extension in humans. The increased concentration of protons during fatiguing exercise may contribute to increased activation of group III and IV afferents and subsequently reduced central drive, but this has yet to be confirmed in exercising humans. Here, we determined whether inducing metabolic alkalosis differentially affects descending central drive after fatiguing exercise and whether this effect may, in part, be explained by attenuating group III and IV afferent firing. Eleven men performed a maximal 2 min voluntary knee extension (MVC) followed by a 2 min rest and subsequent 1 min MVC with an occlusive cuff either in placebo [PLA; 0.3 g (kg body weight)(-1) calcium carbonate] or alkalosis conditions [ALK; 0.3 g (kg body weight)(-1) sodium bicarbonate]. Femoral nerve stimulation was applied before exercise, after the 2 min MVC and at 40-60 s intervals throughout the remainder of the protocol to explore central and peripheral mechanisms associated with reductions in maximal force and rate of torque development. Although voluntary activation declined to a similar extent after the 2 min MVC, during the ischaemic period voluntary activation was higher during ALK (PLA, 57 ± 8%; ALK, 76 ± 5%). Maximal

  1. Metabolic alkalosis reduces exercise-induced acidosis and potassium accumulation in human skeletal muscle interstitium

    Science.gov (United States)

    Street, Darrin; Nielsen, Jens-Jung; Bangsbo, Jens; Juel, Carsten

    2005-01-01

    Skeletal muscle releases potassium during activity. Interstitial potassium accumulation is important for muscle function and the development of fatigue resulting from exercise. In the present study we used sodium citrate ingestion as a tool to investigate the relationship between interstitial H+ concentration and K+ accumulation during exercise. Seven healthy subjects performed one-legged knee-extensor exercise on two separate days with and without sodium citrate ingestion. Interstitial H+ and K+ concentrations were measured with the microdialysis technique. Citrate ingestion reduced the plasma H+ concentration and increased the plasma HCO3− concentration. Citrate had no effect on interstitial H+ at rest. The increase in interstitial H+ concentration during intense exercise was significantly lower (P alkalosis) compared to the control experiment (8.0 ± 0.9 versus 11.0 ± 2 mm) and interstitial K+ concentration remained lower during the rest of the exercise period. The present study demonstrated a link between interstitial H+ and K+ accumulation, which may be through the ATP-sensitive K+ channels (KATP channels), which are sensitive to changes in H+. PMID:15860529

  2. Reversed electrogenic sodium bicarbonate cotransporter 1 is the major acid loader during recovery from cytosolic alkalosis in mouse cortical astrocytes.

    Science.gov (United States)

    Theparambil, Shefeeq M; Naoshin, Zinnia; Thyssen, Anne; Deitmer, Joachim W

    2015-08-15

    The regulation of H(+) i from cytosolic alkalosis has generally been attributed to the activity of Cl(-) -coupled acid loaders/base extruders in most cell types, including brain cells. The present study demonstrates that outwardly-directed sodium bicarbonate cotransport via electrogenic sodium bicarbonate cotransporter 1 (NBCe1) mediates the major fraction of H(+) i regulation from cytosolic alkalosis in mouse cortical astrocytes. Cl(-) -coupled acid-loading transporters play only a minor role in the regulation of H(+) i from alkalosis in mouse cortical astrocytes. NBCe1-mediated H(+) i regulation from alkalosis was dominant, with the support of intracellular carbonic anhydrase II, even when the intra- and extracellular [HCO3 (-) ] was very low (sodium bicarbonate cotransporter 1 (NBCe1) and for carbonic anhydrase (CA) isoform II. An acute cytosolic alkalosis was induced by the removal of either CO2 /HCO3 (-) or butyric acid, and the subsequent acid loading was analysed by monitoring changes in cytosolic H(+) or Na(+) using ion-sensitive fluorescent dyes. We have identified that NBCe1 reverses during alkalosis and contributes more than 70% to the rate of recovery from alkalosis by extruding Na(+) and HCO3 (-) . After CA inhibition or in CAII-knockout (KO) cells, the rate of recovery was reduced by 40%, and even by 70% in the nominal absence of CO2 /HCO3 (-) . Increasing the extracellular K(+) concentration modulated the rate of acid loading in wild-type cells, but not in NBCe1-KO cells. Removing chloride had only a minor effect on the recovery from alkalosis. Reversal of NBCe1 by reducing pH/[HCO3 (-) ] was demonstrated in astrocytes and in Xenopus oocytes, in which human NBCe1 was heterologously expressed. The results obtained suggest that reversed NBCe1, supported by CAII activity, plays a major role in acid-loading cortical astrocytes to support recovery from cytosolic alkalosis. © 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.

  3. Severe Uncompensated Metabolic Alkalosis due to Plasma Exchange in a Patient with Pulmonary-Renal Syndrome: A Clinician’s Challenge

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    Mohsin Ijaz

    2015-01-01

    Full Text Available Metabolic alkalosis secondary to citrate toxicity from plasma exchange is very uncommon in patients with normal renal function. In patients with advanced renal disease this can be a fatal event. We describe a case of middle-aged woman with Goodpasture’s syndrome treated with plasma exchange who developed severe metabolic alkalosis. High citrate load in plasma exchange fluid is the underlying etiology. Citrate metabolism generates bicarbonate and once its level exceeds the excretory capacity of kidneys, the severe metabolic alkalosis ensues. Our patient presented with generalized weakness, fever, and oliguria and developed rapidly progressive renal failure. Patient had positive serology for antineutrophilic cytoplasmic antibodies myeloperoxidase (ANCA-MPO and anti-glomerular basement membrane antibodies (anti-GBM. Renal biopsy showed diffuse necrotizing and crescentic glomerulonephritis with linear glomerular basement membrane staining. Patient did not respond to intravenous steroids. Plasma exchange was started with fresh frozen plasma but patient developed severe metabolic alkalosis. This metabolic alkalosis normalized with cessation of plasma exchange and initiation of low bicarbonate hemodialysis. ANCA-MPO and anti-GBM antibodies levels normalized within 2 weeks and remained undetectable at 3 months. Patient still required maintenance hemodialysis.

  4. Rising serum sodium levels are associated with a concurrent development of metabolic alkalosis in critically ill patients.

    Science.gov (United States)

    Lindner, Gregor; Schwarz, Christoph; Grüssing, Heidelinde; Kneidinger, Nikolaus; Fazekas, Andreas; Funk, Georg-Christian

    2013-03-01

    Changes in electrolyte homeostasis are important causes of acid-base disorders. While the effects of chloride are well studied, only little is known of the potential contributions of sodium to metabolic acid-base state. Thus, we investigated the effects of intensive care unit (ICU)-acquired hypernatremia on acid-base state. We included critically ill patients who developed hypernatremia, defined as a serum sodium concentration exceeding 149 mmol/L, after ICU admission in this retrospective study. Data on electrolyte and acid-base state in all included patients were gathered in order to analyze the effects of hypernatremia on metabolic acid-base state by use of the physical-chemical approach. A total of 51 patients were included in the study. The time of rising serum sodium and hypernatremia was accompanied by metabolic alkalosis. A transient increase in total base excess (standard base excess from 0.1 to 5.5 mmol/L) paralleled by a transient increase in the base excess due to sodium (base excess sodium from 0.7 to 4.1 mmol/L) could be observed. The other determinants of metabolic acid-base state remained stable. The increase in base excess was accompanied by a slight increase in overall pH (from 7.392 to 7.429, standard base excess from 0.1 to 5.5 mmol/L). Hypernatremia is accompanied by metabolic alkalosis and an increase in pH. Given the high prevalence of hypernatremia, especially in critically ill patients, hypernatremic alkalosis should be part of the differential diagnosis of metabolic acid-base disorders.

  5. Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs.

    Science.gov (United States)

    Hetenyi, G; Paradis, H; Kucharczyk, J

    1988-02-01

    The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8-1 g.kg-1.day-1NH4Cl over 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 +/- 0.013, 7.40 +/- 0.024, and 7.51 +/- 0.015 in normal dogs, and 7.22 +/- 0.025, 7.42 +/- 0.009, and 7.49 +/- 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 +/- 0.88, 22.0 +/- 0.80, and 32.4 +/- 1.88 mequiv. in normal dogs, and 12.3 +/- 1.30, 22.6 +/- 0.66, and 35.0 +/- 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid-base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH (r = 0.69, p less than 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid-base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid-base status.(ABSTRACT TRUNCATED AT 250 WORDS)

  6. Effect of acetazolamide on post-NIV metabolic alkalosis in acute exacerbated COPD patients.

    Science.gov (United States)

    Fontana, V; Santinelli, S; Internullo, M; Marinelli, P; Sardo, L; Alessandrini, G; Borgognoni, L; Ferrazza, A M; Bonini, M; Palange, P

    2016-01-01

    Non-invasive ventilation (NIV) is an effective treatment in patients with acute exacerbation of COPD (AECOPD). However, it may induce post-hypercapnic metabolic alkalosis (MA). This study aims to evaluate the effect of acetazolamide (ACET) in AECOPD patients treated with NIV. Eleven AECOPD patients, with hypercapnic respiratory failure and MA following NIV, were treated with ACET 500 mg for two consecutive days and compared to a matched control group. Patients and controls were non invasively ventilated in a bilevel positive airway pressure (BiPAP) mode to a standard maximal pressure target of 15-20 cmH2O. ACET intra-group analysis showed a significant improvement for PaCO2 (63.9 ± 9.8 vs. 54.9 ± 8.3 mmHg), HCO3- (43.5 ± 5.9 vs. 36.1 ± 5.4 mmol/L) and both arterial pH (7.46 ± 0.06 vs. 7.41 ± 0.06) and urinary pH (6.94 ± 0.77 vs 5.80 ± 0.82), already at day 1. No significant changes in endpoints considered were observed in the control group at any time-point. Inter-group analysis showed significant differences between changes in PaCO2 and HCO3- (delta), both at day 1 and 2. Furthermore, the length of NIV treatment was significantly reduced in the ACET group compared to controls (6 ± 8 vs. 19 ± 19 days). No adverse events were recorded in the ACET and control groups. ACET appears to be effective and safe in AECOPD patients with post-NIV MA.

  7. Induced alkalosis and caffeine supplementation: effects on 2,000-m rowing performance.

    Science.gov (United States)

    Carr, Amelia J; Gore, Christopher J; Dawson, Brian

    2011-10-01

    The purpose of this investigation was to determine the effect of ingested caffeine, sodium bicarbonate, and their combination on 2,000-m rowing performance, as well as on induced alkalosis (blood and urine pH and blood bicarbonate concentration [HCO3-]), blood lactate concentration ([La-]), gastrointestinal symptoms, and rating of perceived exertion (RPE). In a double-blind, crossover study, 8 well-trained rowers performed 2 baseline tests and 4 × 2,000-m rowing-ergometer tests after ingesting 6 mg/kg caffeine, 0.3 g/kg body mass (BM) sodium bicarbonate, both supplements combined, or a placebo. Capillary blood samples were collected at preingestion, pretest, and posttest time points. Pairwise comparisons were made between protocols, and differences were interpreted in relation to the likelihood of exceeding the smallest worthwhile-change thresholds for each variable. A likelihood of >75% was considered a substantial change. Caffeine supplementation elicited a substantial improvement in 2,000-m mean power, with mean (± SD) values of 354 ± 67 W vs. placebo with 346 ± 61 W. Pretest [HCO3-] reached 29.2 ± 2.9 mmol/L with caffeine + bicarbonate and 29.1 ± 1.9 mmol/L with bicarbonate. There were substantial increases in pretest [HCO3-] and pH and posttest urine pH after bicarbonate and caffeine + bicarbonate supplementation compared with placebo, but unclear performance effects. Rowers' performance in 2,000-m efforts can improve by ~2% with 6 mg/kg BM caffeine supplementation. When caffeine is combined with sodium bicarbonate, gastrointestinal symptoms may prevent performance enhancement, so further investigation of ingestion protocols that minimize side effects is required.

  8. Acetazolamide-mediated decrease in strong ion difference accounts for the correction of metabolic alkalosis in critically ill patients.

    Science.gov (United States)

    Moviat, Miriam; Pickkers, Peter; van der Voort, Peter H J; van der Hoeven, Johannes G

    2006-02-01

    Metabolic alkalosis is a commonly encountered acid-base derangement in the intensive care unit. Treatment with the carbonic anhydrase inhibitor acetazolamide is indicated in selected cases. According to the quantitative approach described by Stewart, correction of serum pH due to carbonic anhydrase inhibition in the proximal tubule cannot be explained by excretion of bicarbonate. Using the Stewart approach, we studied the mechanism of action of acetazolamide in critically ill patients with a metabolic alkalosis. Fifteen consecutive intensive care unit patients with metabolic alkalosis (pH > or = 7.48 and HCO3- > or = 28 mmol/l) were treated with a single administration of 500 mg acetazolamide intravenously. Serum levels of strong ions, creatinine, lactate, weak acids, pH and partial carbon dioxide tension were measured at 0, 12, 24, 48 and 72 hours. The main strong ions in urine and pH were measured at 0, 3, 6, 12, 24, 48 and 72 hours. Strong ion difference (SID), strong ion gap, sodium-chloride effect, and the urinary SID were calculated. Data (mean +/- standard error were analyzed by comparing baseline variables and time dependent changes by one way analysis of variance for repeated measures. After a single administration of acetazolamide, correction of serum pH (from 7.49 +/- 0.01 to 7.46 +/- 0.01; P = 0.001) was maximal at 24 hours and sustained during the period of observation. The parallel decrease in partial carbon dioxide tension was not significant (from 5.7 +/- 0.2 to 5.3 +/- 0.2 kPa; P = 0.08) and there was no significant change in total concentration of weak acids. Serum SID decreased significantly (from 41.5 +/- 1.3 to 38.0 +/- 1.0 mEq/l; P = 0.03) due to an increase in serum chloride (from 105 +/- 1.2 to 110 +/- 1.2 mmol/l; P metabolic alkalosis in critically ill patients by decreasing the serum SID. This effect is completely explained by the increased renal excretion ratio of sodium to chloride, resulting in an increase in serum chloride.

  9. A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs

    OpenAIRE

    Liu, Fan; Celi, Pietro; Chauhan, Surinder Singh; Cottrell, Jeremy James; Leury, Brian Joseph; Dunshea, Frank Rowland

    2017-01-01

    Objective Heat stress (HS) triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE) can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. Methods A total of 24 pigs were given either a control diet (17 IU/kg VE) or a high VE (200 IU/kg VE; HiVE) diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity) or HS (35°C, 35% to 45% humidity, 8...

  10. Effects of pre-exercise alkalosis on the decrease in VO2 at the end of all-out exercise.

    Science.gov (United States)

    Thomas, Claire; Delfour-Peyrethon, Rémi; Bishop, David J; Perrey, Stéphane; Leprêtre, Pierre-Marie; Dorel, Sylvain; Hanon, Christine

    2016-01-01

    This study determined the effects of pre-exercise sodium bicarbonate ingestion (ALK) on changes in oxygen uptake (VO2) at the end of a supramaximal exercise test (SXT). Eleven well-trained cyclists completed a 70-s all-out cycling effort, in double-blind trials, after oral ingestion of either 0.3 g kg(-1) of sodium bicarbonate (NaHCO3) or 0.2 g kg(-1) body mass of calcium carbonate (PLA). Blood samples were taken to assess changes in acid-base balance before the start of the supramaximal exercise, and 0, 5 and 8 min after the exercise; ventilatory parameters were also measured at rest and during the SXT. At the end of the PLA trial, which induced mild acidosis (blood pH = 7.20), subjects presented a significant decrease in VO2 (P metabolic alkalosis significantly prevented the exercise-induced decrease in VO2 in eleven well-trained participants (PLA:12.5 ± 2.1 % and ALK: 4.9 ± 0.9 %, P 0.05). Pre-exercise alkalosis counteracted the VO2 decrease related to mild acidosis, potentially as a result of changes in VE and in muscle acid-base status during the all-out supramaximal exercise.

  11. Respiratory alkalosis and primary hypocapnia in Labrador Retrievers participating in field trials in high-ambient-temperature conditions.

    Science.gov (United States)

    Steiss, Janet E; Wright, James C

    2008-10-01

    To determine whether Labrador Retrievers participating in field trials develop respiratory alkalosis and hypocapnia primarily in conditions of high ambient temperatures. 16 Labrador Retrievers. At each of 5 field trials, 5 to 10 dogs were monitored during a test (retrieval of birds over a variable distance on land [1,076 to 2,200 m]; 36 assessments); ambient temperatures ranged from 2.2 degrees to 29.4 degrees C. For each dog, rectal temperature was measured and a venous blood sample was collected in a heparinized syringe within 5 minutes of test completion. Blood samples were analyzed on site for Hct; pH; sodium, potassium, ionized calcium, glucose, lactate, bicarbonate, and total CO2 concentrations; and values of PvO2 and PvCO2. Scatterplots of each variable versus ambient temperature were reviewed. Regression analysis was used to evaluate the effect of ambient temperature ( 21 degrees C) on each variable. Compared with findings at ambient temperatures 21 degrees C; rectal temperature did not differ. Two dogs developed signs of heat stress in 1 test at an ambient temperature of 29 degrees C; their rectal temperatures were higher and PvCO2 values were lower than findings in other dogs. When running distances frequently encountered at field trials, healthy Labrador Retrievers developed hyperthermia regardless of ambient temperature. Dogs developed respiratory alkalosis and hypocapnia at ambient temperatures > 21 degrees C.

  12. Does metabolic alkalosis influence cerebral oxygenation in infantile hypertrophic pyloric stenosis?

    Science.gov (United States)

    Nissen, Matthias; Cernaianu, Grigore; Thränhardt, Rene; Vahdad, Mohammad R; Barenberg, Karin; Tröbs, Ralf-Bodo

    2017-05-15

    This pilot study focuses on regional tissue oxygenation (rSO 2 ) in patients with infantile hypertrophic pyloric stenosis in a perioperative setting. To investigate the influence of enhanced metabolic alkalosis (MA) on cerebral (c-rSO 2 ) and renal (r-rSO 2 ) tissue oxygenation, two-site near-infrared spectroscopy (NIRS) technology was applied. Perioperative c-rSO 2 , r-rSO 2 , capillary blood gases, and electrolytes from 12 infants were retrospectively compared before and after correction of MA at admission (T1), before surgery (T2), and after surgery (T3). Correction of MA was associated with an alteration of cerebral oxygenation without affecting renal oxygenation. When compared to T1, 5-min mean (± standard deviation) c-rSO 2 increased after correction of MA at T2 (72.74 ± 4.60% versus 77.89 ± 5.84%; P = 0.058), reaching significance at T3 (80.79 ± 5.29%; P = 0.003). Furthermore, relative 30-min c-rSO 2 values at first 3 h of metabolic compensation were significantly lowered compared with postsurgical states at 16 and 24 h. Cerebral oxygenation was positively correlated with levels of sodium (r = 0.37; P = 0.03) and inversely correlated with levels of bicarbonate (r = -0.34; P = 0.05) and base excess (r = -0.36; P = 0.04). Analysis of preoperative and postoperative cerebral and renal hypoxic burden yielded no differences. However, a negative correlation (r = -0.40; P = 0.03) regarding hematocrite and mean r-rSO 2 , indirectly indicative of an increased renal blood flow under hemodilution, was obtained. NIRS seems suitable for the detection of a transiently impaired cerebral oxygenation under state of pronounced MA in infants with infantile hypertrophic pyloric stenosis. Correction of MA led to normalization of c-rSO 2 . NIRS technology constitutes a promising tool for optimizing perioperative management, especially in the context of a possible diminished neurodevelopmental outcome after pyloromyotomy. Copyright © 2017 Elsevier

  13. Metabolic alkalosis in the rat. Evidence that reduced glomerular filtration rather than enhanced tubular bicarbonate reabsorption is responsible for maintaining the alkalotic state.

    Science.gov (United States)

    Cogan, M G; Liu, F Y

    1983-01-01

    Maintenance of chronic metabolic alkalosis might occur by a reduction in glomerular filtration rate (GFR) without increased bicarbonate reabsorption or, alternatively, by augmentation of bicarbonate reabsorption with a normal GFR. To differentiate these possibilities, free-flow micropuncture was performed in alkalotic Munich-Wistar rats with a glomerular ultrafiltrate total CO2 concentration of 46.5 +/- 0.9 mM (vs. 27.7 +/- 0.9 mM in controls). Alkalotic animals had a markedly reduced single nephron GFR compared with controls (27.4 +/- 1.5 vs. 51.6 +/- 1.6 nl/min) and consequently unchanged filtered load of bicarbonate. Absolute proximal bicarbonate reabsorption in alkalotic animals was similar to controls (981 +/- 49 vs. 1,081 +/- 57 pmol/min), despite a higher luminal bicarbonate concentration, contracted extracellular volume, and potassium depletion. When single nephron GFR during alkalosis was increased toward normal by isohydric volume expansion or in another group by isotonic bicarbonate loading, absolute proximal bicarbonate reabsorption was not substantially augmented and bicarbonaturia developed. To confirm that a fall in GFR occurs during metabolic alkalosis, additional clearance studies were performed. Awake rats were studied before and after induction of metabolic alkalosis associated with varying amounts of potassium and chloride depletion. In all cases, the rise in blood bicarbonate concentration was inversely proportional to a reduction in GFR; filtered bicarbonate load remained normal. In conclusion, a reduction in GFR is proposed as being critical for maintaining chronic metabolic alkalosis in the rat. Constancy of the filtered bicarbonate load allows normal rates of renal bicarbonate reabsorption to maintain the alkalotic state. Images PMID:6853706

  14. Citrate metabolism and its complications in non-massive blood transfusions: association with decompensated metabolic alkalosis+respiratory acidosis and serum electrolyte levels.

    Science.gov (United States)

    Bıçakçı, Zafer; Olcay, Lale

    2014-06-01

    Metabolic alkalosis, which is a non-massive blood transfusion complication, is not reported in the literature although metabolic alkalosis dependent on citrate metabolism is reported to be a massive blood transfusion complication. The aim of this study was to investigate the effect of elevated carbon dioxide production due to citrate metabolism and serum electrolyte imbalance in patients who received frequent non-massive blood transfusions. Fifteen inpatients who were diagnosed with different conditions and who received frequent blood transfusions (10-30 ml/kg/day) were prospectively evaluated. Patients who had initial metabolic alkalosis (bicarbonate>26 mmol/l), who needed at least one intensive blood transfusion in one-to-three days for a period of at least 15 days, and whose total transfusion amount did not fit the massive blood transfusion definition (metabolic alkalosis+respiratory acidosis developed as a result of citrate metabolism. There was a positive correlation between cumulative amount of citrate and the use of fresh frozen plasma, venous blood pH, ionized calcium, serum-blood gas sodium and mortality, whereas there was a negative correlation between cumulative amount of citrate and serum calcium levels, serum phosphorus levels and amount of urine chloride. In non-massive, but frequent blood transfusions, elevated carbon dioxide production due to citrate metabolism causes intracellular acidosis. As a result of intracellular acidosis compensation, decompensated metabolic alkalosis+respiratory acidosis and electrolyte imbalance may develop. This situation may contribute to the increase in mortality. In conclusion, it should be noted that non-massive, but frequent blood transfusions may result in certain complications. Copyright © 2014 Elsevier Ltd. All rights reserved.

  15. A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs.

    Science.gov (United States)

    Liu, Fan; Celi, Pietro; Chauhan, Surinder Singh; Cottrell, Jeremy James; Leury, Brian Joseph; Dunshea, Frank Rowland

    2018-02-01

    Heat stress (HS) triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE) can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. A total of 24 pigs were given either a control diet (17 IU/kg VE) or a high VE (200 IU/kg VE; HiVE) diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity) or HS (35°C, 35% to 45% humidity, 8 h daily) conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all pproducts (AOPP) in the heat-stressed pigs, suggesting HS triggers oxidative stress. The HiVE diet did not affect plasma BAP or AOPP. Only under TN conditions the HiVE diet reduced the plasma reactive oxygen metabolites (p<0.05 for diet× temperature). A short-term supplementation with 200 IU/kg VE partially alleviated respiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

  16. Respiratory alkalosis may impair the production of vitamin D and lead to significant morbidity, including the fibromyalgia syndrome.

    Science.gov (United States)

    Lewis, John M; Fontrier, Toinette H; Coley, J Lynn

    2017-05-01

    Hyperventilation caused by physical and/or psychological stress may lead to significant respiratory alkalosis and an elevated systemic pH. The alkalotic pH may in turn suppress the normal renal release of phosphate into the urine, thereby interrupting the endogenous production of 1,25-dihydroxyvitamin D (calcitriol). This could cause a shortfall in its normal production, leading to a variety of adverse consequences. It might partially explain the pathogenesis of acute mountain sickness, a treatable disease characterized by severe hyperventilation secondary to the hypoxia of high altitude exposure. Milder degrees of hyperventilation due to different forms of stress may produce other conditions which share characteristics with acute mountain sickness. One of these may be the fibromyalgia syndrome, a chronic painful disorder for which no satisfactory treatment exists. Should fibromyalgia and acute mountain sickness have a common etiology, may they also share a common form of treatment? Evidence is presented to support this hypothesis. Copyright © 2017 Elsevier Ltd. All rights reserved.

  17. Rare mutation in the SLC26A3 transporter causes life-long diarrhoea with metabolic alkalosis.

    Science.gov (United States)

    Abou Ziki, Maen D; Verjee, Mohamud A

    2015-01-07

    SLC26A3, a chloride/bicarbonate transporter mainly expressed in the intestines, plays a pivotal role in chloride absorption. We present a 23-year-old woman with a history of congenital chloride diarrhoea (CCD) and renal transplant who was admitted for rehydration and treatment of acute kidney injury after she presented with an acute diarrhoeal episode. Laboratory investigations confirmed metabolic alkalosis and severe hypochloraemia, consistent with her underlying CCD. This contrasts with most other forms of diarrhoea, which are normally associated with metabolic acidosis. Genetic testing was offered and revealed a homozygous non-sense mutation in SLC26A3 (Gly-187-Stop). This loss-of-function mutation results in bicarbonate retention in the blood and chloride loss into the intestinal lumen. Symptomatic management with daily NaCl and KCl oral syrups was supplemented with omeprazole therapy. The loss of her own kidneys is most likely due to crystal-induced nephropathy secondary to chronic volume contraction and chloride depletion. This case summarises the pathophysiology and management of CCD. 2015 BMJ Publishing Group Ltd.

  18. The differential effect of metabolic alkalosis on maximum force and rate of force development during repeated, high-intensity cycling.

    Science.gov (United States)

    Siegler, Jason C; Marshall, Paul W M; Raftry, Sean; Brooks, Cristy; Dowswell, Ben; Romero, Rick; Green, Simon

    2013-12-01

    The purpose of this investigation was to assess the influence of sodium bicarbonate supplementation on maximal force production, rate of force development (RFD), and muscle recruitment during repeated bouts of high-intensity cycling. Ten male and female (n = 10) subjects completed two fixed-cadence, high-intensity cycling trials. Each trial consisted of a series of 30-s efforts at 120% peak power output (maximum graded test) that were interspersed with 30-s recovery periods until task failure. Prior to each trial, subjects consumed 0.3 g/kg sodium bicarbonate (ALK) or placebo (PLA). Maximal voluntary contractions were performed immediately after each 30-s effort. Maximal force (F max) was calculated as the greatest force recorded over a 25-ms period throughout the entire contraction duration while maximal RFD (RFD max) was calculated as the greatest 10-ms average slope throughout that same contraction. F max declined similarly in both the ALK and PLA conditions, with baseline values (ALK: 1,226 ± 393 N; PLA: 1,222 ± 369 N) declining nearly 295 ± 54 N [95% confidence interval (CI) = 84-508 N; P alkalosis on maximum force vs. maximum rate of force development during a whole body fatiguing task.

  19. [Intraperitoneal irrigation for pseudomyxoma peritonei-a case of critical metabolic alkalosis precipitated by irrigation with 101 of sodium bicarbonate--].

    Science.gov (United States)

    Shirasaki, Reimi; Yamasaki, Saeko; Wakamatsu, Masaki; Mori, Yasuichiro; Hirano, Hiroko; Kaida, Takeshi; Machino, Asami

    2013-05-01

    Pseudomyxoma peritonei causes marked accumulation of jelly-like ascites in the peritoneal cavity. Removal of much mucinous ascites by irrigating the cavity appears to be an effective treatment. We describe a patient who underwent the irrigation with sodium bicarbonate solution and developed critical alkalemia. A 68-year-old woman with normal renal function was operated on for recurrent pseudomyxoma peritonei. Fol- lowing the excision of primary lesion, her intraperitoneal cavity was irrigated with 10 1 of 7% sodium bicarbonate in about 45 minutes. Thirty minutes after irrigation, blood gas analysis revealed severe metabolic alkalosis (pH 7.714, BE 25.6 mmol x l-1 ) with electrolyte disorder (Na 157.8 mmol x l-1 K 2.31mmol x l-1, Ca 0.73 mmol x l-1). Hypotension (130 beats x min -1) supervened 75 minutes later. Transferring to the ICU, she was given KC1 solution intravenously based on serial blood analysis while on mechanical ventilation. The next day acid-base disturbance returned spontaneously to normal (pH 7.45, BE 8.0mmol x l-1), leading to endotracheal extubation. Electrolyte imbalance was gradually resolved on 2nd POD and she was discharged from the ICU. Intraperitoneal irrigation with sodium bicarbonate requires special perioperative considerations for lifethreatening alkalemia, especially in a patient with renal impairment.

  20. Sodium acetate induces a metabolic alkalosis but not the increase in fatty acid oxidation observed following bicarbonate ingestion in humans.

    Science.gov (United States)

    Smith, Gordon I; Jeukendrup, Asker E; Ball, Derek

    2007-07-01

    We conducted this study to quantify the oxidation of exogenous acetate and to determine the effect of increased acetate availability upon fat and carbohydrate utilization in humans at rest. Eight healthy volunteers (6 males and 2 females) completed 2 separate trials, 7 d apart in a single-blind, randomized, crossover design. On each occasion, respiratory gas and arterialized venous blood samples were taken before and during 180 min following consumption of a drink containing either sodium acetate (NaAc) or NaHCO3 at a dose of 2 mmol/kg body mass. Labeled [1,2 -13C] NaAc was added to the NaAc drink to quantify acetate oxidation. Both sodium salts induced a mild metabolic alkalosis and increased energy expenditure (P bicarbonate trial. We determined that 80.1 +/- 2.3% of an exogenous source of acetate is oxidized in humans at rest. Whereas NaHCO3 ingestion increased fat oxidation, a similar response did not occur following NaAc ingestion despite the fact both sodium salts induced a similar increase in energy expenditure and shift in acid-base balance.

  1. A short-term supranutritional vitamin E supplementation alleviated respiratory alkalosis but did not reduce oxidative stress in heat stressed pigs

    Directory of Open Access Journals (Sweden)

    Fan Liu

    2018-02-01

    Full Text Available Objective Heat stress (HS triggers oxidative stress and respiratory alkalosis in pigs. The objective of this experiment was to study whether a short-term supranutritional amount of dietary vitamin E (VE can mitigate oxidative stress and respiratory alkalosis in heat-stressed pigs. Methods A total of 24 pigs were given either a control diet (17 IU/kg VE or a high VE (200 IU/kg VE; HiVE diet for 14 d, then exposed to thermoneutral (TN; 20°C, 45% humidity or HS (35°C, 35% to 45% humidity, 8 h daily conditions for 7 d. Respiration rate and rectal temperature were measured three times daily during the thermal exposure. Blood gas variables and oxidative stress markers were studied in blood samples collected on d 7. Results Although HiVE diet did not affect the elevated rectal temperature or respiration rate observed during HS, it alleviated (all p<0.05 for diet×temperature the loss of blood CO2 partial pressure and bicarbonate, as well as the increase in blood pH in the heat-stressed pigs. The HS reduced (p = 0.003 plasma biological antioxidant potential (BAP and tended to increase (p = 0.067 advanced oxidized protein products (AOPP in the heat-stressed pigs, suggesting HS triggers oxidative stress. The HiVE diet did not affect plasma BAP or AOPP. Only under TN conditions the HiVE diet reduced the plasma reactive oxygen metabolites (p<0.05 for diet× temperature. Conclusion A short-term supplementation with 200 IU/kg VE partially alleviated respiratory alkalosis but did not reduce oxidative stress in heat-stressed pigs.

  2. Acute Metabolic Alkalosis Enhances Response of C3H Mouse Mammary Tumors to the Weak Base Mitoxantrone

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    Natarajan Raghunand

    2001-01-01

    Full Text Available Uptake of weak acid and weak base chemotherapeutic drugs by tumors is greatly influenced by the tumor extracellular/interstitial pH (pHe, the intracellular pH (pHi maintained by the tumor cells, and by the ionization properties of the drug itself. The acid-outside plasmalemmal pH gradient in tumors acts to exclude weak base drugs like the anthracyclines, anthraquinones, and vinca alkaloids from the cells, leading to a substantial degree of “physiological drug resistance” in tumors. We have induced acute metabolic alkalosis in C3H tumor-bearing C3H/hen mice, by gavage and by intraperitoneal (i.p. administration of NaHCO3. 31P magnetic resonance spectroscopic measurements of 3-aminopropylphosphonate show increases of up to 0.6 pH units in tumor pHe, and 0.2 to 0.3 pH units in hind leg tissue pHe, within 2 hours of i.p. administration of NaHCO3. Theoretical calculations of mitoxantrone uptake into tumor and normal (hind leg tissue at the measured pH, and pHI values indicate that a gain in therapeutic index of up to 3.3-fold is possible with NaHCO3 pretreatment. Treatment of C3H tumor-bearing mice with 12 mg/kg mitoxantrone resulted in a tumor growth delay of 9 days, whereas combined NaHCO3mitoxantrone therapy resulted in an enhancement of the TGD to 16 days.

  3. Delay in onset of metabolic alkalosis during regional citrate anti-coagulation in continous renal replacement therapy with calcium-free replacement solution

    Directory of Open Access Journals (Sweden)

    See Kay

    2009-01-01

    Full Text Available Regional citrate anti-coagulation for continuous renal replacement therapy chelates calcium to produce the anti- coagulation effect. We hypothesise that a calcium-free replacement solution will require less citrate and produce fewer metabolic side effects. Fifty patients, in a Medical Intensive Care Unit of a tertiary teaching hospital (25 in each group, received continuous venovenous hemofiltration using either calcium-containing or calcium-free replacement solutions. Both groups had no significant differences in filter life, metabolic alkalosis, hypernatremia, hypocalcemia, and hypercalcemia. However, patients using calcium-containing solution developed metabolic alkalosis earlier, compared to patients using calcium-free solution (mean 24.6 hours,CI 0.8-48.4 vs. 37.2 hours, CI 9.4-65, P = 0.020. When calcium-containing replacement solution was used, more citrate was required (mean 280ml/h, CI 227.2-332.8 vs. 265ml/h, CI 203.4-326.6, P = 0.069, but less calcium was infused (mean 21.2 ml/h, CI 1.2-21.2 vs 51.6ml/h, CI 26.8-76.4, P ≤ 0.0001.

  4. Delay in onset of metabolic alkalosis during regional citrate anti-coagulation in continuous renal replacement therapy with calcium-free replacement solution.

    Science.gov (United States)

    See, Kay Choong; Lee, Margaret; Mukhopadhyay, Amartya

    2009-01-01

    Regional citrate anti-coagulation for continuous renal replacement therapy chelates calcium to produce the anti- coagulation effect. We hypothesise that a calcium-free replacement solution will require less citrate and produce fewer metabolic side effects. Fifty patients, in a Medical Intensive Care Unit of a tertiary teaching hospital (25 in each group), received continuous venovenous hemofiltration using either calcium-containing or calcium-free replacement solutions. Both groups had no significant differences in filter life, metabolic alkalosis, hypernatremia, hypocalcemia, and hypercalcemia. However, patients using calcium-containing solution developed metabolic alkalosis earlier, compared to patients using calcium-free solution (mean 24.6 hours,CI 0.8-48.4 vs. 37.2 hours, CI 9.4-65, P = 0.020). When calcium-containing replacement solution was used, more citrate was required (mean 280 ml/h, CI 227.2-332.8 vs. 265 ml/h, CI 203.4-326.6, P = 0.069), but less calcium was infused (mean 21.2 ml/h, CI 1.2-21.2 vs 51.6 ml/h, CI 26.8-76.4, P < or = 0.0001).

  5. Parallel adaptation of the rabbit renal cortical sodium/proton antiporter and sodium/bicarbonate cotransporter in metabolic acidosis and alkalosis.

    Science.gov (United States)

    Akiba, T; Rocco, V K; Warnock, D G

    1987-01-01

    Recent studies have shown that the bicarbonate reabsorptive capacity of the proximal tubule is increased in metabolic acidosis. For net bicarbonate reabsorption to be regulated, there may be changes in the rate of apical H+ secretion as well as in the basolateral base exit step. The present studies examined the rate of Na+/H+ exchange (acridine orange method) and Na+/HCO3 cotransport (22Na uptake) in apical and basolateral membranes prepared from the rabbit renal cortex by sucrose density gradient centrifugation. NH4Cl loading was used to produce acidosis (arterial pH, 7.27 +/- 0.03), and Cl-deficient diet with furosemide was used to produce alkalosis (arterial pH, 7.51 +/- 0.02). Maximal transport rate (Vmax) of Na+/H+ antiporter and Na+/HCO3 cotransporter were inversely related with plasma bicarbonate concentration from 6 to 39 mM. Furthermore, the maximal transport rates of both systems varied in parallel; when Vmax for the Na+/HCO3 cotransporter was plotted against Vmax for the Na+/H+ antiporter for each of the 24 groups of rabbits, the regression coefficient (r) was 0.648 (P less than 0.001). There was no effect of acidosis or alkalosis on affinity for Na+ of either transporter. We conclude that both apical and basolateral H+/HCO3 transporters adapt during acid-base disturbances, and that the maximal transport rates of both systems vary in parallel during such acid-base perturbations. PMID:3038953

  6. Downregulation of the Cl-/HCO3-Exchanger Pendrin in Kidneys of Mice with Cystic Fibrosis: Role in the Pathogenesis of Metabolic Alkalosis

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    Mujan Varasteh Kia

    2018-02-01

    Full Text Available Background/Aims: Patients with cystic fibrosis (CF are prone to the development of metabolic alkalosis; however, the pathogenesis of this life threatening derangement remains unknown. We hypothesized that altered acid base transport machinery in the kidney collecting duct underlies the mechanism of impaired bicarbonate elimination in the CF kidney. Methods: Balance studies in metabolic cages were performed in WT and CFTR knockout (CF mice with the intestinal rescue in response to bicarbonate loading or salt restriction, and the expression levels and cellular distribution of acid base and electrolyte transporters in the proximal tubule, collecting duct and small intestine were examined by western blots, northern blots and/or immunofluorescence labeling. Results: Baseline parameters, including acid-base and systemic vascular volume status were comparable in WT and CF mice, as determined by blood gas, kidney renin expression and urine chloride excretion. Compared with WT animals, CF mice demonstrated a significantly higher serum HCO3- concentration (22.63 in WT vs. 26.83 mEq/l in CF mice; n=4, p=0.013 and serum pH (7.33 in WT vs. 7.42 in CF mice; n=4, p=0.00792 and exhibited impaired kidney HCO3- excretion (urine pH 8.10 in WT vs. 7.35 in CF mice; n=7, p=0.00990 following a 3-day oral bicarbonate load. When subjected to salt restriction, CF mice developed a significantly higher serum HCO3- concentration vs. WT animals (29.26 mEq/L in CF mice vs. 26.72 in WT; n=5, p=0.0291. Immunofluorescence labeling demonstrated a profound reduction in the apical expression of the Cl-/HCO3- exchanger pendrin in cortical collecting duct cells and western and northern blots indicated diminished plasma membrane abundance and mRNA expression of pendrin in CF kidneys. Conclusions: We propose that patients with cystic fibrosis are prone to the development of metabolic alkalosis secondary to the inactivation of the bicarbonate secreting transporter pendrin, specifically

  7. Downregulation of the Cl-/HCO3-Exchanger Pendrin in Kidneys of Mice with Cystic Fibrosis: Role in the Pathogenesis of Metabolic Alkalosis.

    Science.gov (United States)

    Varasteh Kia, Mujan; Barone, Sharon; McDonough, Alicia A; Zahedi, Kamyar; Xu, Jie; Soleimani, Manoocher

    2018-01-01

    Patients with cystic fibrosis (CF) are prone to the development of metabolic alkalosis; however, the pathogenesis of this life threatening derangement remains unknown. We hypothesized that altered acid base transport machinery in the kidney collecting duct underlies the mechanism of impaired bicarbonate elimination in the CF kidney. Balance studies in metabolic cages were performed in WT and CFTR knockout (CF) mice with the intestinal rescue in response to bicarbonate loading or salt restriction, and the expression levels and cellular distribution of acid base and electrolyte transporters in the proximal tubule, collecting duct and small intestine were examined by western blots, northern blots and/or immunofluorescence labeling. Baseline parameters, including acid-base and systemic vascular volume status were comparable in WT and CF mice, as determined by blood gas, kidney renin expression and urine chloride excretion. Compared with WT animals, CF mice demonstrated a significantly higher serum HCO3- concentration (22.63 in WT vs. 26.83 mEq/l in CF mice; n=4, p=0.013) and serum pH (7.33 in WT vs. 7.42 in CF mice; n=4, p=0.00792) and exhibited impaired kidney HCO3- excretion (urine pH 8.10 in WT vs. 7.35 in CF mice; n=7, p=0.00990) following a 3-day oral bicarbonate load. When subjected to salt restriction, CF mice developed a significantly higher serum HCO3- concentration vs. WT animals (29.26 mEq/L in CF mice vs. 26.72 in WT; n=5, p=0.0291). Immunofluorescence labeling demonstrated a profound reduction in the apical expression of the Cl-/HCO3- exchanger pendrin in cortical collecting duct cells and western and northern blots indicated diminished plasma membrane abundance and mRNA expression of pendrin in CF kidneys. We propose that patients with cystic fibrosis are prone to the development of metabolic alkalosis secondary to the inactivation of the bicarbonate secreting transporter pendrin, specifically during volume depletion, which is a common occurrence in CF

  8. Effects of early administration of acetazolamide on the duration of mechanical ventilation in patients with chronic obstructive pulmonary disease or obesity-hypoventilation syndrome with metabolic alkalosis. A randomized trial.

    Science.gov (United States)

    Rialp Cervera, G; Raurich Puigdevall, J M; Morán Chorro, I; Martín Delgado, M C; Heras la Calle, G; Mas Serra, A; Vallverdú Perapoch, I

    2017-06-01

    Metabolic alkalosis (MA) inhibits respiratory drive and may delay weaning from mechanical ventilation (MV). MA is common in CO 2 -retainer patients that need MV. Acetazolamide (ACTZ) decreases serum bicarbonate concentration and stimulates respiratory drive. This study evaluated the effects of ACTZ on the duration of MV in patients with MA and COPD or obesity hypoventilation syndrome (OHS) intubated with acute respiratory failure. Multicenter, randomized, controlled, double-blind study, with COPD or OHS patients with MV 28 mmol/L and pH > 7.35. Test-treatment, ACTZ 500 mg or placebo, was daily administered if pH > 7.35 and bicarbonate >26 mmol/L. Clinical, respiratory and laboratory parameters were recorded. 47 patients (36 men) were randomized. There were no significant differences between groups in comorbidities, baseline characteristics or arterial blood gases at inclusion. The mean difference in the duration of MV between placebo and ACTZ group was 1.3 days (95%CI, -2.1-4.8; p = 0.44). Kaplan-Meier curves showed no differences in the duration of MV (Log-Rank p = 0.41). Between-group comparison of estimated marginal means (CI 95%) during MV were, respectively: PaCO 2 55 (51-59) vs 48 (47-50) mm Hg, p = 0.002; bicarbonate concentration 34 (32-35) vs 29 (28-30) mmol/L, p adverse effects with ACTZ administration. Among patients with MA and COPD or OHS, early treatment with ACTZ did not shorten significantly the duration of MV compared with placebo. clinical.trials.gov; NCT01499485; URL:.www.clinicaltrials.gov. Copyright © 2017 Elsevier Ltd. All rights reserved.

  9. [Acid-base homeostasis: metabolic acidosis and metabolic alkalosis].

    Science.gov (United States)

    Dussol, Bertrand

    2014-07-01

    Acid-base homeostasis ensured by the kidneys, which maintain the equilibrium between proton generation by cellular metabolism and proton excretion in urine. This requirement is lifesaving because of the protons' ability to bind to anionic proteins in the extracellular space, modifying their structure and functions. The kidneys also regenerate bicarbonates. The kidney is not the sole organ in charge of maintaining blood pH in a very narrow range; lungs are also involved since they allow a large amount of volatile acid generated by cellular respiration to be eliminated. Copyright © 2014 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.

  10. Hypoxia Silences Retrotrapezoid Nucleus Respiratory Chemoreceptors via Alkalosis

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    Basting, Tyler M.; Burke, Peter G.R.; Kanbar, Roy; Viar, Kenneth E.; Stornetta, Daniel S.; Stornetta, Ruth L.; Guyenet, Patrice G.

    2015-01-01

    In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exerting opposite effects on central respiratory chemoreceptors (CRCs). We tested this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nucleus (RTN), a putative CRC and chemoreflex integrator. Archaerhodopsin-(Arch)-transduced RTN neurons were reversibly silenced by light in anesthetized rats. We bilaterally transduced RTN and nearby C1 neurons with Arch (PRSx8-ArchT...

  11. Hypoxia Silences Retrotrapezoid Nucleus Respiratory Chemoreceptors via Alkalosis

    Science.gov (United States)

    Basting, Tyler M.; Burke, Peter G.R.; Kanbar, Roy; Viar, Kenneth E.; Stornetta, Daniel S.; Stornetta, Ruth L.

    2015-01-01

    In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exerting opposite effects on central respiratory chemoreceptors (CRCs). We tested this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nucleus (RTN), a putative CRC and chemoreflex integrator. Archaerhodopsin-(Arch)-transduced RTN neurons were reversibly silenced by light in anesthetized rats. We bilaterally transduced RTN and nearby C1 neurons with Arch (PRSx8-ArchT-EYFP-LVV) and measured the cardiorespiratory consequences of Arch activation (10 s) in conscious rats during normoxia, hypoxia, or hyperoxia. RTN photoinhibition reduced breathing equally during non-REM sleep and quiet wake. Compared with normoxia, the breathing frequency reduction (ΔfR) was larger in hyperoxia (65% FiO2), smaller in 15% FiO2, and absent in 12% FiO2. Tidal volume changes (ΔVT) followed the same trend. The effect of hypoxia on ΔfR was not arousal-dependent but was reversed by reacidifying the blood (acetazolamide; 3% FiCO2). ΔfR was highly correlated with arterial pH up to arterial pH (pHa) 7.5 with no frequency inhibition occurring above pHa 7.53. Blood pressure was minimally reduced suggesting that C1 neurons were very modestly inhibited. In conclusion, RTN neurons regulate eupneic breathing about equally during both sleep and wake. RTN neurons are the first putative CRCs demonstrably silenced by hypocapnic hypoxia in conscious mammals. RTN neurons are silent above pHa 7.5 and increasingly active below this value. During hyperoxia, RTN activation maintains breathing despite the inactivity of the carotid bodies. Finally, during hypocapnic hypoxia, carotid body stimulation increases breathing frequency via pathways that bypass RTN. PMID:25589748

  12. Metabolic alkalosis reduces exercise-induced acidosis and potassium accumulation in human skeletal muscle interstitium

    DEFF Research Database (Denmark)

    Street, D.; Nielsen, Jens Jung; Bangsbo, Jens

    2005-01-01

    Skeletal muscle releases potassium during activity. Interstitial potassium accumulation is important for muscle function and the development of fatigue resulting from exercise. In the present study we used sodium citrate ingestion as a tool to investigate the relationship between interstitial H+ ...

  13. Een geval van hypochloremische alkalose bij een pasgeborene

    NARCIS (Netherlands)

    van de Bor, M.; Ruys, J. H.; Kenter, G.; Zoethout, H. E.

    1984-01-01

    A full term neonate in which by accident a metabolic alkalosis was found, is described. The origin of the metabolic alkalosis was excessive vomiting by the mother during the days prior to delivery. The simplified form of the Henderson Hasselbalch equation is used to describe the factors responsible

  14. Respiration of Chemodenervated Goats in Acute Metabolic Acidosis,

    Science.gov (United States)

    1983-08-02

    metabolic ) alkalosis . Furthermore, the ventilatory responses to increase in PaCO2 produced by CO2 inhalation are shifted to lower values of PaCO2 in...the presence of metabolic acidosis, and to higher PaCO2 vaiues in metabolic alkalosis (Fencl et al. [1966]). The roles played by the carotid bodies (CB...and J.A. Broch (1969). Respiration and cerebral blood flow in metabolic acidosis and alkalosis in humans. J. Appl. Physiol. 27: 67-76. Gabel, R.A

  15. Newborn ventilatory response to maternal chronic hypercapnia.

    Science.gov (United States)

    DeLuca, L; Holzman, I; Gibbs, K

    2012-10-01

    This is a case of a neonate born with a respiratory acidosis with a compensatory metabolic alkalosis. This case demonstrates placental physiology of gas exchange as well as the blunted ventilatory response in the neonate from chronic hypercapnia.

  16. Generaliserede kramper som debutsymptom ved Gitelmans syndrom

    DEFF Research Database (Denmark)

    Hvelplund, Carolina; Jeppesen, Eva Mosfeldt; Mortensen, Henrik B

    2009-01-01

    Gitelman's syndrome is a rare autosomal recessive syndrome presenting with hypocalciuria, hypomagnesiemia and hypokalemic metabolic alkalosis. This case reports a patient admitted with generalized seizures with the above-mentioned biochemical abnormalities, thus representing a rare onset...

  17. Profile of acid-base disturbances in an intensive care unit of Fortaleza, Ceará, Brazil.

    Directory of Open Access Journals (Sweden)

    Renan Barbosa Rodrigues

    2014-09-01

    Full Text Available Introduction: Acid – base disturbances are entities caused by the deregulation of the concentration of bicarbonate ions, the concentration of hydrogen ions and the partial pressure of carbon dioxide in the blood. These disturbances modify most cell fuctions when present, jeopardizing the proper functioning of organs.Methods: Cross-sectional analytical study based upon data collected from medical files of patients in ICU as seen from August 1 to December 31, 2013 at the Dr. José Frota Institute in Fortaleza, Ceará. The variables studied were: age, sex, cause of ICU admission, pH, HCO3-, pO2, pCO2 , glomerular filtration rate ( GFR , serum potassium concentrarion, serum magnesium concentration, serum creatinine and hemoglobin levels.Results: The most frequent disorders were primary respiratory alkalosis with               33 ( 38,4 % cases, 30 ( 34,9 % of metabolic alkalosis, 13 ( 15.1% of metabolic acidosis,    7 ( 8,2% did not present acid-base disorders and respiratory acidosis           3 ( 3,5%. Patients admitted with TBI had respiratory alkalosis as the most common primary disorder, followed by metabolic alkalosis, 16 ( 47,0 % and 13 ( 38,2 % , respectively. The main disturbances were mixed respiratory alkalosis with metabolic alkalosis and respiratory alkalosis with metabolic alkalosis found in 15.12% of patients in each of these combinations. Conclusion:The importance  of a detailed evaluation of acid-base disturbances is necessary since these disorders lead to higher mortality rates, so it is necessary to establish the main types of disorders that are associated with a particular cause of hospitalization .

  18. Homespun remedy, homespun toxicity: baking soda ingestion for dyspepsia.

    Science.gov (United States)

    Ajbani, Keyur; Chansky, Michael E; Baumann, Brigitte M

    2011-04-01

    A 68-year-old man presented to the Emergency Department with a severe metabolic alkalosis after ingesting large quantities of baking soda to treat his dyspepsia. His underlying pulmonary disease and a progressively worsening mental status necessitated intubation for respiratory failure. Laboratory studies revealed a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis. The patient was successfully treated after cessation of the oral bicarbonate, initiation of intravenous hydration, and correction of electrolyte abnormalities. Copyright © 2011 Elsevier Inc. All rights reserved.

  19. Post-hypercapnia recovery in the dog: arterial blood acid-base equilibrium and glycolysis.

    Science.gov (United States)

    Saunier, C; Horsky, P; Hannhart, B; Garcia-Carmona, T; Hartemann, D

    1977-12-01

    Changes in acid-base equilibrium and blood lactate and pyruvate concentrations were studied during recovery (breathing room air) after three days hypercapnia (FICO2 = 0.10) in awake dogs. Fast return to FICO2 = 0 produced a slight alkalosis in arterial blood and an increase in lactate and pyruvate concentrations which seemed to be maximum at the 15th minute. These changes were inhibited by previous injection of acetazolamide (50 mg/kg body weight). During progressive return to FICO2 = 0, over 1 hour, the peak value of blood lactate and pyruvate was delayed until the end of that hour, at the same time as a slight blood alkalosis appeared. These phenomen are most probably explained by a stimulation, due to alkalosis, of glycolysis at the level of phosphofructokinase.

  20. Milk alkali syndrome induced by calcitriol and calcium bicarbonate in a patient with hypoparathyroidism

    Directory of Open Access Journals (Sweden)

    Eda Altun

    2013-01-01

    Full Text Available The milk-alkali syndrome (MAS was a common cause of hypercalcemia, metabolic alkalosis, and renal failure in the early 20 th century. This syndrome was first recognized secondary to treatment of peptic ulcer disease with milk and absorbable alkali. Its incidence fell after the introduction of H2-blocker and proton pump inhibitor. Persistent ingestion of calcium carbonate and vitamin D caused MAS. We report a patient presenting with a triad of hypercalcemia, metabolic alkalosis and renal failure secondary to treatment of idiopathic hypoparathyroidism.

  1. Bartter syndrome Type III and congenital anomalies of the kidney and urinary tract: an antenatal presentation

    NARCIS (Netherlands)

    Westland, R.; Hack, W.W.; van der Horst, H.J.; Uittenbogaard, L.B.; van Hagen, J.M.; van der Valk, P.; Kamsteeg, E.J.; Heuvel, L.P.W.J. van den; van Wijk, J.A.

    2012-01-01

    Bartter syndrome encompasses a variety of inheritable renal tubular transport disorders characterized by hypokalemia and hypochloremic metabolic alkalosis. Bartter syndrome Type III is caused by genetic alterations in the chloride channel kidney B (CLCNKB) gene and often presents in the first 2

  2. Liquorice-induced hypertension--a new understanding of an old disease: case report and brief review

    NARCIS (Netherlands)

    Heikens, J.; Fliers, E.; Endert, E.; Ackermans, M.; van Montfrans, G.

    1995-01-01

    The case is described of a 40-year-old female with severe hypertension and hypokalaemic metabolic alkalosis, due to prolonged liquorice ingestion. The pseudo-aldosterone-like effects of liquorice have always been attributed to glycyrrhizic acid, but its biochemical substrate has remained elusive. It

  3. Mechanistic Modeling of the Effects of Acidosis on Thrombin Generation

    Science.gov (United States)

    2015-08-01

    The damage control sequence and underlying logic. Surg Clin North Am 1997;77:761–77 5. Waters JH, Miller LR, Clack S, Kim JV. Cause of metabolic ...1002–9 10. Ramaker AJ, Meyer P, van der Meer J, Struys MM, Lisman T, van Oeveren W, Hendriks HG. Effects of acidosis, alkalosis , hyperthermia and

  4. Case Report

    African Journals Online (AJOL)

    fatigue and convulsions due to severe metabolic alkalosis or hypomagnesemia. Manifestations of GS are rarely apparent before the age of five, and the syndrome is usually diagnosed during adolescence or adulthood. Here we describe a case of GS presenting in infancy with hypokalemia and psychomotor retardation.

  5. Bicarbonate Concentration, Acid-Base Status, and Mortality in the Health, Aging, and Body Composition Study

    Science.gov (United States)

    Murphy, Rachel A.; Shlipak, Michael G.; Satterfield, Suzanne; Huston, Hunter K.; Sebastian, Anthony; Sellmeyer, Deborah E.; Patel, Kushang V.; Newman, Anne B.; Sarnak, Mark J.; Ix, Joachim H.; Fried, Linda F.

    2016-01-01

    Background and objectives Low serum bicarbonate associates with mortality in CKD. This study investigated the associations of bicarbonate and acid-base status with mortality in healthy older individuals. Design, setting, participants, & measurements We analyzed data from the Health, Aging, and Body Composition Study, a prospective study of well functioning black and white adults ages 70–79 years old from 1997. Participants with arterialized venous blood gas measurements (n=2287) were grouped into metabolic acidosis, 1.21 (95% CI, 1.01 to 1.46) for respiratory alkalosis, and 1.35 (95% CI, 1.08 to 1.69) for metabolic alkalosis categories. Respiratory acidosis did not associate with mortality. Conclusions In generally healthy older individuals, low serum bicarbonate associated with higher mortality independent of systemic pH and potential confounders. This association seemed to be present regardless of whether the cause of low bicarbonate was metabolic acidosis or respiratory alkalosis. Metabolic alkalosis also associated with higher mortality. PMID:26769766

  6. Acetazolamide: a second wind for a respiratory stimulant in the intensive care unit?

    Science.gov (United States)

    2012-01-01

    Patients with chronic obstructive pulmonary disease (COPD) are affected by episodes of respiratory exacerbations, some of which can be severe and may necessitate respiratory support. Prolonged invasive mechanical ventilation is associated with increased mortality rates. Persistent failure to discontinue invasive mechanical ventilation is a major issue in patients with COPD. Pure or mixed metabolic alkalosis is a common finding in the intensive care unit (ICU) and is associated with a worse outcome. In patients with COPD, the condition is called post-hypercapnic alkalosis and is a complication of mechanical ventilation. Reversal of metabolic alkalosis may facilitate weaning from mechanical ventilation of patients with COPD. Acetazolamide, a non-specific carbonic anhydrase inhibitor, is one of the drugs employed in the ICU to reverse metabolic alkalosis. The drug is relatively safe, undesirable effects being rare. The compartmentalization of the different isoforms of the carbonic anhydrase enzyme may, in part, explain the lack of evidence of the efficacy of acetazolamide as a respiratory stimulant. Recent findings suggest that the usually employed doses of acetazolamide in the ICU may be insufficient to significantly improve respiratory parameters in mechanically ventilated patients with COPD. Randomized controlled trials using adequate doses of acetazolamide are required to address this issue. PMID:22866939

  7. Hjertestopbehandling. Nyere aspekter af kardiopulmonal genoplivning

    DEFF Research Database (Denmark)

    Herlevsen, Per Ove; Andersen, H H; Jepsen, S

    1989-01-01

    compression and increase survival. Cardiac arrest results in anaerobic metabolism and combined metabolic and respiratory acidosis. On account of relatively low minute volume during external cardiac compression decrease in end-tidal carbon dioxide concentration is observed together with arterial alkalosis...

  8. A case of acquired Gitelman syndrome presenting as hypokalemic paralysis

    Directory of Open Access Journals (Sweden)

    M Kulkarni

    2015-01-01

    Full Text Available We report a case of a young female patient who presented with weakness of upper and lower limbs. On evaluation, she had hypokalemia, hypomagnesemia, metabolic alkalosis and hypocalciuria. Anti-Ro (SSA antibody was positive. She had an acquired Gitelman syndrome due to primary Sjögren′s syndrome (SS. SS presenting with features of Gitelman syndrome is very rare.

  9. Gitelman syndrome.

    NARCIS (Netherlands)

    Knoers, N.V.A.M.; Levtchenko, E.N.

    2008-01-01

    Gitelman syndrome (GS), also referred to as familial hypokalemia-hypomagnesemia, is characterized by hypokalemic metabolic alkalosis in combination with significant hypomagnesemia and low urinary calcium excretion. The prevalence is estimated at approximately 1:40,000 and accordingly, the prevalence

  10. Effect of acute metabolic acid/base shifts on the human airway calibre.

    NARCIS (Netherlands)

    Brijker, F.; Elshout, F.J.J. van den; Heijdra, Y.F.; Bosch, F.H.; Folgering, H.T.M.

    2001-01-01

    Acute metabolic alkalosis (NaHCO(3)), acidosis (NH(4)Cl), and placebo (NaCl) were induced in 15 healthy volunteers (12 females, median age 34 (range 24-56) years) in a double blind, placebo controlled study to evaluate the presence of the effects on airway calibre. Acid-base shifts were determined

  11. Mixed acid-base disorder secondary to topiramate use in traumatic brain injury

    Directory of Open Access Journals (Sweden)

    S Golla

    2016-01-01

    Full Text Available We report a case of a man with traumatic brain injury. He was started on to prophylactic topiramate which led to a mixed acid-base disorder. He had severe metabolic acidosis secondary to renal tubular acidification defect and respiratory alkalosis secondary to hyperventilation. Withdrawal of the offending drug led to the prompt resolution of the acid-base disturbance.

  12. Acid-base status determines the renal expression of Ca2+ and Mg2+ transport proteins.

    NARCIS (Netherlands)

    Nijenhuis, T.; Renkema, K.Y.R.; Hoenderop, J.G.J.; Bindels, R.J.M.

    2006-01-01

    Chronic metabolic acidosis results in renal Ca2+ and Mg2+ wasting, whereas chronic metabolic alkalosis is known to exert the reverse effects. It was hypothesized that these adaptations are mediated at least in part by the renal Ca2+ and Mg2+ transport proteins. The aim of this study, therefore, was

  13. Effects of acetazolamide and furosemide on ventilation and cerebral blood volume in normocapnic and hypercapnic patients with COPD.

    NARCIS (Netherlands)

    Ven, M.J.T. van de; Colier, W.N.J.M.; Sluijs, M.C. van der; Oeseburg, B.; Vis, P.; Folgering, H.T.M.

    2002-01-01

    STUDY OBJECTIVES: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (VI), mouth occlusion pressure (P(0.1)), and

  14. A patient with cystinosis presenting like bartter syndrome and review of literature.

    Science.gov (United States)

    Ertan, Pelin; Evrengul, Havva; Ozen, Serkan; Emre, Sinan

    2012-12-01

    Nephropathic cystinosis is an autosomal recessively inherited metabolic disorder presenting with metabolic acidosis, Fanconi syndrome and renal failure. We present a 6-year-old girl with severe growth failure, hyponatremia and hypokalemia. Her parents were 4(th) degree relatives. Two relatives were diagnosed as end stage renal failure. She also had persistant hypokalemic hypochloremic metabolic alkalosis. Her renal function was normal at presentation. She was thought to have Bartter syndrome with supporting findings of elevated levels of renin and aldosterone with normal blood pressure, and hyperplasia of juxtaglomerular apparatus. Her metabolic alkalosis did not resolve despite supportive treatment. At 6(th) month of follow-up proteinuria, glucosuria and deterioration of renal function developed. Diagnosis of cystinosis was made with slit lamp examination and leukocyte cystine levels. At 12(th) month of follow-up her metabolic alkalosis has converted to metabolic acidosis. In children presenting with persistant metabolic alkalosis, with family history of renal failure, and parental consanguinity, cystinosis should always be kept in mind as this disease is an important cause of end stage renal failure which may have features mimmicking Bartter syndrome.

  15. Gitelman syndrome : consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference

    NARCIS (Netherlands)

    Blanchard, Anne; Bockenhauer, Detlef; Bolignano, Davide; Calò, Lorenzo A; Cosyns, Etienne; Devuyst, Olivier; Ellison, David H; Karet Frankl, Fiona E; Knoers, Nine V A M; Konrad, Martin; Lin, Shih-Hua; Vargas-Poussou, Rosa

    Gitelman syndrome (GS) is a rare, salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. The disease is recessively inherited, caused by inactivating mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium-chloride

  16. Effect of urinary pH on the progression of urinary bladder tumours

    NARCIS (Netherlands)

    Lina, B.A.R.; Garderen-Hoetmer, A. van

    1999-01-01

    Systemic alkalosis has been postulated to enhance tumorigenesis, whereas systemic acidosis has been implicated to exert a favourable influence on tumour control and regression. In the present study the urinary pH was influenced by feeding acid-forming or base-forming diets, and the effect of

  17. [Pseudo-Bartter syndrome as manifestation of cystic fibrosis with DF508 mutation].

    Science.gov (United States)

    Galaviz-Ballesteros, María de Jesús; Acosta-Rodríguez-Bueno, Carlos Patricio; Consuelo-Sánchez, Alejandra; Franco-Álvarez, Isidro; Olalla-Mora, Odilo Iván; Vázquez-Frias, Rodrigo

    Pseudo Bartter syndrome (PBS) is defined as hypokalaemic hypochloraemic metabolic alkalosis in the absence of renal tubular pathology. Children with cystic fibrosis (CF) are at risk of developing electrolyte abnormalities and even PBS may occur. 5 months old female infant with a history of two events of dehydration with vomit, refusal to eat, chronic cough, polyuria, malnutrition, metabolic alkalosis, hypokalemia, hyponatremia, hypochloremia and acute renal failure. Chronic cough study was performed, discarding pulmonary tuberculosis, gastroesophageal reflux disease and impaired swallowing. PBS was diagnosed due to hypokalaemic hypochloraemic metabolic alkalosis in the absence of renal tubular pathology. CF was corroborated by electrolytes in sweat and through molecular analysis of the delta F508 mutation. This is one of the few reported cases linking PBS and this mutation. In patients with hyponatremic dehydration episodes with hypokalaemic hypochloraemic metabolic alkalosis, PBS should be considered as differential diagnosis. CF could be presented as PBS, mainly in patients younger than 2 years. Copyright © 2016 Hospital Infantil de México Federico Gómez. Publicado por Masson Doyma México S.A. All rights reserved.

  18. Influence of bicarbonate on ventilatory drive in healthy subjects

    NARCIS (Netherlands)

    Mos-Oppersma, Eline; Doorduin, Jonne; van der Hoeven, J.G.; Veltink, Peter; Heunks, Leo M.A.

    2016-01-01

    Background Acute hypoventilation results in CO2 retention and respiratory acidosis. Bicarbonate retention aims to restore pH level. However, after institution of mechanical ventilation metabolic alkalosis may develop, which could impair respiratory drive. Aim To investigate whether increased plasma

  19. Physiology of High-Altitude Acclimatization

    Indian Academy of Sciences (India)

    IAS Admin

    alkalosis due to HVR is offset by increased excretion of sodium and bicarbonate ions in the urine and retention of hydrogen ions. (shifting towards acidosis). Hormonal responses play very important regulatory functions during high altitude exposure. Under this, the role of renin– angiotensin–aldosterone axis as an important ...

  20. Case Report: Gitelman Syndrome as a Cause of Psychomotor ...

    African Journals Online (AJOL)

    Introduction: Gitelman syndrome (GS) is a very rare autosomal recessive tubulopathy due to loss-of-function or mutation in solute carrier family12, member 3 gene (SLC12A3 gene) encoding thiazide-sensitive NaCl co-transporter in the distal convoluted tubule, leading to hypokalemia, metabolic alkalosis, hypomagnesemia, ...

  1. Severe Milk-Alkali Syndrome in a Patient with Hypoparathyroidism Associated with 1,25(OH2D, Hydrochlorothiazide and Anthranoid Laxative Consumption

    Directory of Open Access Journals (Sweden)

    Lorenzo Morini

    2017-10-01

    Full Text Available Background: Milk-alkali syndrome is a life-threatening condition defined by the triad of hypercalcaemia, metabolic alkalosis and acute renal failure, and is associated with consumption of calcium and absorbable alkali. Methods: We report the case of a patient admitted to a step-down unit of a large hospital in Italy. Results: The patient was a 59-year-old woman with hypoparathyroidism and mild chronic kidney insufficiency, treated for a preceding episode of hypocalcaemia with high doses of calcitriol and calcium carbonate, who was also taking hydrochlorothiazide and unreported herbal anthranoid laxatives. The patient was admitted to hospital with severe hypercalcaemia, severe metabolic alkalosis and acute renal insufficiency. The patient was successfully treated with urgent dialysis, loop diuretics and calcitonin administration. Conclusions: This case underlines the need for caution when treating patients with impaired calcium metabolism regulation, and suggests that herbal anthranoid laxatives might act as triggers for milk-alkali syndrome..

  2. [Dynamics of bioelectric activity of the brain and erythrocyte ultrastructure after intravenous infusion of sodium bicarbonate to oncologic patients].

    Science.gov (United States)

    Davydova, I G; Kassil', V L; Raĭkhlin, N T; Filippova, N A

    1992-04-01

    23 patients with malignant tumors of different location and histogenesis were investigated. There were no metastases in 9 cases. 10 patients had metastases in regional areas and 4--distant. The results were compared with those obtained in 4 patients with nonmalignant diseases. EEG, blood gases, plasma acid--base balance and ultrastructure of erythrocytes were explored before and after intravenous infusion of 4.2% sodium bicarbonate solution. The metabolic alkalosis induced amelioration of EEG, which was changed basically, the condense of pre-membrane layer disappeared or decreased in erythrocytes, and disaggregation of erythrocytes took place in cancer patients vs those with nonmalignant tumors. The results confirm the suggestion of generalized intracellular acidosis in malignant tumor patients. This acidosis can be temporarily avoided or diminished artificially by blood alkalosis.

  3. GITELMAN SYNDROME AS A RARE CAUSE OF HYPOKALEMIA - CASE REPORT

    Directory of Open Access Journals (Sweden)

    Zorica Dimitrijević

    2014-09-01

    Full Text Available Gitelman syndrome is a rare autosomal recessive tubulopathy leading to hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria and low-to-normal blood pressure. Clinical signs are mostly secondary to chronic hypokalemia and include dizziness, fatigue, constipation and weakness. Patients can also present with muscle cramps, tetany and convulsions due to severe metabolic alkalosis or hypomagnesemia. Therefore, early recognition and treatment are important. Diagnosis of Gitelman syndrome is usually made incidentally during adolescence or early adulthood based on clinical and biochemical findings. In this paper we report a case of a young women with classic Gitelman syndrome. Treatment included magnesium and potassium salts and potassium saving diuretics. In general, the long-term prognosis of Gitelman syndrome is excellent. However, the severity of fatigue may seriously hamper some patients in their daily activities.

  4. Gitelman's syndrome: a rare presentation mimicking cauda equina syndrome.

    LENUS (Irish Health Repository)

    Quinlan, C S

    2012-02-01

    We describe a case of bilateral weakness of the lower limbs, sensory disturbance and intermittent urinary incontinence, secondary to untreated Gitelman\\'s syndrome, in a 42-year-old female who was referred with presumed cauda equina syndrome. On examination, the power of both legs was uniformly reduced, and the perianal and lower-limb sensation was altered. However, MRI of the lumbar spine was normal. Measurements of serum and urinary potassium were low and blood gas analysis revealed metabolic alkalosis. Her symptoms resolved following potassium replacement. We emphasise the importance of measurement of the plasma and urinary levels of electrolytes in the investigation of patients with paralysis of the lower limbs and suggest that they, together with blood gas analysis, allow the exclusion of unusual causes of muscle weakness resulting from metabolic disorders such as metabolic alkalosis.

  5. Congenital chloride diarrhea: late presentation

    Directory of Open Access Journals (Sweden)

    Al Bishi L

    2011-04-01

    Full Text Available Laila Al Bishi1, Mustafa Al Toonisi2Pediatric Department, North West Armed Forces Hospital, Tabuk, Kingdom of Saudi ArabiaAbstract: We report the case of a male infant who presented with diarrhea at 6 months of age. He was failing to thrive, and biochemical investigation revealed hypokalemic hypochloremic metabolic alkalosis. Diagnosis of congenital chloride diarrhea was suspected and confirmed by the stool chloride result. He was started on high-dose sodium chloride and potassium chloride to control the electrolyte imbalance. The disease was difficult to control for a year after diagnosis. Late presentation is associated with severe chronic electrolyte disturbances and high-dose replacement therapy.Keywords: congenital chloride diarrhea, hypokalemic hypochloremic metabolic alkalosis, high stool chloride

  6. Bartter Syndrome Type 1 Presenting as Nephrogenic Diabetes Insipidus

    Directory of Open Access Journals (Sweden)

    Gianluca Vergine

    2018-01-01

    Full Text Available Bartter syndrome (BS type 1 (OMIM #601678 is a hereditary salt-losing renal tubular disorder characterized by hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, polyuria, recurrent vomiting, and growth retardation. It is caused by loss-of-function mutations of the SLC12A1 gene, encoding the furosemide-sensitive Na-K-Cl cotransporter. Recently, a phenotypic variability has been observed in patients with genetically determined BS, including absence of nephrocalcinosis, hypokalemia, and/or metabolic alkalosis in the first year of life as well as persistent metabolic acidosis mimicking distal renal tubular acidosis. We report the case of a child with a genetically determined diagnosis of Bartter syndrome type 1 who presented with a phenotype of nephrogenic diabetes insipidus, with severe hypernatremia and urinary concentrating defect. In these atypical cases, molecular analysis is mandatory to define the diagnosis, in order to establish the correct clinical and therapeutic management.

  7. Classic Bartter syndrome: a rare cause of failure to thrive in a child.

    Science.gov (United States)

    Vieira, Helena; Mendes, Leonor; Mendes, Patricia; da Silva, José Esteves

    2012-06-28

    Bartter syndrome is a group of rare autosomal-recessive disorders caused by a defect in distal tubule transport of sodium and chloride. Blood gases and plasma electrolytes raise suspicion of this diagnosis and the definitive diagnosis is made by genetic study. Early treatment improves prognosis. The authors present the case of an 11-month-old child with early failure to thrive and severe regurgitation. Blood gases revealed hypochloraemic metabolic alkalosis, hyponatraemia and hypokalaemia. Blood pressure was normal and polyuria was documented. She began therapy with potassium chloride supplementation and indomethacin. There was clinical improvement and plasma potassium and bicarbonate normalised. The molecular study confirmed it was the classic form of Bartter syndrome. Despite being rare in clinical practice, which may lead to unnecessary medical investigation and diagnosis delay, in a child with failure to thrive, hypochloraemic metabolic alkalosis and hypokalaemia, this diagnosis must be considered.

  8. Blood pH and brain uptake of /sup 14/C-morphine

    Energy Technology Data Exchange (ETDEWEB)

    Schulman, D.S.; Kaufman, J.J.; Eisenstein, M.M.; Rapoport, S.I.

    1984-11-01

    /sup 14/C-Morphine was injected iv in control awake rats or in rats subjected to metabolic alkalosis or acidosis. Ten minutes later, radioactivity was determined within each of seven brain regions, after correction was made for intravascular tracer. In each region, parenchymal radioactivity was correlated positively and significantly (P less than 0.05) with arterial blood pH. Brain radioactivity was twofold to threefold greater in alkalotic rats (mean pH . 7.62) than in acidotic rats (mean pH . 7.16). The results are consistent with the pH-partition hypothesis for drug entry into the brain and indicate that morphine uptake can be increased by elevating the fraction of lipid-soluble uncharged morphine base in blood, by means of alkalosis. The observations may account for an exaggerated morphine-induced analgesia in alkalotic patients.

  9. Trichophytobezoar duodenal obstruction in New World camelids.

    Science.gov (United States)

    Sullivan, Eileen K; Callan, Robert J; Holt, Timothy N; Van Metre, David C

    2005-01-01

    To describe clinical findings, surgical treatment, and outcome associated with trichophytobezoar duodenal obstruction in New World camelids. Retrospective study. Alpacas (7) and 1 llama. Historical and clinical data were obtained from the medical records of New World camelids with a diagnosis of trichophytobezoar duodenal obstruction confirmed by surgical exploration or necropsy. Seven camelids were camelids with abdominal distension and hypochloremic metabolic alkalosis. Right paracostal celiotomy can be used for access to the descending duodenum and third gastric compartment for surgical relief of obstruction. Duodenal obstruction from bezoars should be considered in New World camelids <1year of age with abdominal distension and hypochloremic metabolic alkalosis. Surgical relief of the obstruction by right paracostal celiotomy has a good prognosis.

  10. Cystic fibrosis in three children with bronchopulmonary dysplasia.

    Science.gov (United States)

    Holmgren, N L; Faro, A; Gondor, M I; Orenstein, D M

    2001-06-01

    Cystic fibrosis (CF) and bronchopulmonary dysplasia (BPD) are two common causes of chronic lung disease in children. Patients with BPD or CF often have recurrent respiratory symptoms, failure to thrive, and/or metabolic alkalosis during infancy and childhood. Thus, recognizing the diagnosis of CF in an infant with BPD can be difficult. We present three infants with both BPD and CF. The infants shared a history of respiratory distress and prolonged oxygen requirements. All three also had difficulty gaining weight, even after pancreatic enzyme supplementation was instituted. Metabolic alkalosis was observed in two infants. Previous studies in children with CF suggest that early diagnosis may impact both lung health and nutritional status. A high index of suspicion is necessary for clinicians to identify these children early and intervene with appropriate therapy.

  11. Status epilepticus as the only presentation of the neonatal Bartter syndrome

    Directory of Open Access Journals (Sweden)

    Soumya Patra

    2012-01-01

    Full Text Available Bartter syndrome is a rare hereditary (autosomal recessive salt-losing tubulopathy characterized by hypokalemia, hypochloremia, metabolic alkalosis, and normal blood pressure with hyperreninemia, The underlying renal abnormality results in excessive urinary losses of sodium, chloride, and potassium. We report a case of a four-month-old infant with neonatal Bartter syndrome, who presented only with status epilepticus. To the best of our present knowledge, there is no reported case of Bartter syndrome who presented with status epilepticus.

  12. Effect of Six Days of Staging on Physiologic Adjustments and Acute Mountain Sickness During Ascent to 4300 Meters

    Science.gov (United States)

    2009-01-01

    semirecumbent position and breathed through a low-resistance breathing circuit connected to a breath-by-breath, open-circuit metabolic system (Vmax 229... metabolic pa- rameters and blood gas values, indicated that 6 d of staging at 2200 m induced ventilatory acclimatization. Resting ventila- tion, as...respiratory alkalosis due to hyperventilation that was partially compensated for by increased excretion of HCO3 to maintain a normal pH following

  13. An Unusual Cause of Hypokalemia in an Elderly Man with Hypertension

    Directory of Open Access Journals (Sweden)

    Hung-Chieh Wu

    2007-12-01

    Full Text Available Hypokalemia in the elderly usually results from gastrointestinal loss or the use of diuretics. However, primary aldosteronism should be considered in hypertensive patients with metabolic alkalosis and unexplained hypokalemia with hyperkaliuresis. We report a 63 year-old hypertensive man with such metabolic findings. The transtubular potassium concentration gradient and serum aldosterone level were higher than normal. Abdominal computed tomography showed bilaterally enlarged adrenal glands, and a nuclear medicine study supported the diagnosis of bilateral adrenal hyperplasia.

  14. The effect of pH and ADP on ammonia affinity for human glutamate dehydrogenases

    DEFF Research Database (Denmark)

    Zaganas, Ioannis; Pajecka, Kamilla; Nielsen, Camilla Wendel

    2013-01-01

    Glutamate dehydrogenase (GDH) uses ammonia to reversibly convert α-ketoglutarate to glutamate using NADP(H) and NAD(H) as cofactors. While GDH in most mammals is encoded by a single GLUD1 gene, humans and other primates have acquired a GLUD2 gene with distinct tissue expression profile. The two h...... of the kidney during systemic acidosis. The reverse could apply for conditions of local or systemic hyperammonemia or alkalosis....

  15. Electrolyte profile of pediatric patients with hypertrophic pyloric stenosis.

    Science.gov (United States)

    Tutay, Godfrey Jay; Capraro, Geoffrey; Spirko, Blake; Garb, Jane; Smithline, Howard

    2013-04-01

    Recent investigations have demonstrated that the classic hypochloremic, hypokalemic, metabolic alkalosis of hypertrophic pyloric stenosis (HPS) is not a common finding.Some have suggested a trend over time, but none has investigated factors contributing to laboratory derangement, such as duration of vomiting or patient age at presentation. We sought to determine the proportion of patients with HPS with normal and abnormal laboratory findings as a function of year of presentation, duration of vomiting, and patient age. This is a retrospective chart review of 205 patients younger than 6 months with operative diagnosis of HPS at a tertiary, regional pediatric center from 2000 to 2009. We examined the acid-base status and electrolyte levels (serum bicarbonate [CO2], serum potassium [K], and serum chloride [Cl]) at the time of the index visit to determine the proportion of normal, high, and low values for each as a function of year of presentation, duration of vomiting, and patient age. The proportion of HPS cases with normal CO2 was 62%; low serum CO2, 20%; and high CO2, 18%. The proportion with normal serum K was 57%; low K, 8%; and high K, 35%. The proportion with normal Cl was 69%; low Cl, 25%; and high Cl, 6%. Logistic regression analysis demonstrated that the prevalence of metabolic alkalosis increased across the decade, whereas the prevalence of metabolic acidosis decreased and that advancing age was associated with the presence of alkalosis. We observed that normal laboratory values are the most common finding in HPS and that metabolic alkalosis was found more commonly in the latter part of the decade and in older infants.

  16. Congenital chloride diarrhea: late presentation

    OpenAIRE

    Al Bishi, Laila; Mustafa,

    2011-01-01

    Laila Al Bishi1, Mustafa Al Toonisi2Pediatric Department, North West Armed Forces Hospital, Tabuk, Kingdom of Saudi ArabiaAbstract: We report the case of a male infant who presented with diarrhea at 6 months of age. He was failing to thrive, and biochemical investigation revealed hypokalemic hypochloremic metabolic alkalosis. Diagnosis of congenital chloride diarrhea was suspected and confirmed by the stool chloride result. He was started on high-dose sodium chloride and potassium chloride to...

  17. Bench-to-bedside review: Treating acid–base abnormalities in the intensive care unit – the role of renal replacement therapy

    OpenAIRE

    Naka, Toshio; Bellomo, Rinaldo

    2004-01-01

    Acid–base disorders are common in critically ill patients. Metabolic acid–base disorders are particularly common in patients who require acute renal replacement therapy. In these patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid–base status using the Stewart–Figge methodology shows that these patients have greater acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly secondary to hyperphosphatemia, hyperlactatemia, and the accu...

  18. A Clinical Approach to the Diagnosis of Acid-Base Disorders

    OpenAIRE

    Bear, Robert A.

    1986-01-01

    The ability to diagnose and manage acid-base disorders rapidly and effectively is essential to the care of critically ill patients. This article presents an approach to the diagnosis of pure and mixed acid-base disorders, metabolic or respiratory. The approach taken is based on using the law of mass-action equation as it applies to the bicarbonate buffer system (Henderson equation), using sub-classifications for diagnostic purposes of causes of metabolic acidosis and metabolic alkalosis, and ...

  19. Pathophysiological aspect of metabolic acid-base disorders

    Directory of Open Access Journals (Sweden)

    Nešović-Ostojić Jelena

    2016-01-01

    Full Text Available Maintaing the arterial pH values (in normal range of 7,35-7,45 is one of the main principles of homeostasis. Regulatory responses, including chemical buffering (extracellular, intracellular, sceletal, the regulation of pCO2 by the respiratory system, and the regulation of [HCO3-] by the kidneys, act in concert to maintain normal arterial pH value. The main extracellular chemical buffer is bicarbonate-carbonic acid buffer system. The kidneys contribute to the regulation of hydrogen (and bicarbonate in body fluids in two ways. Proximal tubules are important in bicarbonate reabsorption and distal tubules excrete hydrogen ion (as ammonium ion or titratable acid. There are four simple acid-base disorders: metabolic acidosis and metabolic alkalosis; respiratory acidosis and respiratory alkalosis. Metabolic acidosis can occur because of an increase in endogenous acid production (such as lactate and ketoacids, loss of bicarbonate (as in diarrhea, or accumulation of endogenous acids (as in renal failure. Metabolic acidosis can also be with high and normal (hyperchloremic metabolic acidosis anion gap. Renal tubular acidosis (RTA is a form of hyperchloremic metabolic acidosis which occurs when the renal damage primarily affects tubular function. The main problem in distal RTA is reduced H+ excretion in distal tubule. Type 2 RTA is also called proximal RTA because the main problem is greatly impaired reabsorption of bicarbonate in proximal tubule. Impaired cation exchange in distal tubule is the main problem in RTA type 4. Metabolic alkalosis occurs as a result of net gain of [HCO3-] or loss of nonvolatile acid from extracellular fluids. Metabolic alkalosis can be associated with reduced or increased extracellular volume.

  20. Unusual case of failure to thrive: Type III Bartter syndrome.

    Science.gov (United States)

    Agrawal, S; Subedi, K; Ray, P; Rayamajhi, A

    2016-09-01

    Bartter syndrome Type III is a rare autosomal recessive disorder resulting from an inherited defect in the thick ascending limb of the loop of henle of the nephrons in kidney. The typical clinical manifestations in childhood are failure to thrive and recurrent episodes of vomiting. Typical laboratory findings which help in the diagnosis are hypokalemic metabolic alkalosis, hypomagnesemia and hypercalciuria. We report a case of Type III Bartter syndrome not responding to repeated conventional treatment of failure to thrive.

  1. Metabolic effects of chronic ozone exposure on rats

    Energy Technology Data Exchange (ETDEWEB)

    Hathway, J.A.; Terrill, R.E.

    1962-01-01

    Rats were exposed to 0.8 to 1.5 ppm O/sub 3/ for 6 hr/day, 4 days/wk for 19 weeks. Lower titratable acidity after 91 days exposure and higher urine pH after 98 days exposure were observed. No significant differences in urine creatine, creatinine, uric acid/creatinine, or amino acid/creatinine were observed. pH differences suggest respiratory alkalosis, possibly due to subjectively noticed hyperventilation in exposed group.

  2. Reverse ventilation--perfusion mismatch

    Energy Technology Data Exchange (ETDEWEB)

    Palmaz, J.C.; Barnett, C.A.; Reich, S.B.; Krumpe, P.E.; Farrer, P.A.

    1984-01-01

    Patients having lobar airway obstruction or consolidation usually have decreases of both ventilation and perfusion on lung scans. We report three patients in whom hypoxic vasoconstriction was apparently incomplete, resulting in a ''reversed'' ventilation-perfusion mismatch. Perfusion of the hypoxic lobe on the radionuclide scan was associated with metabolic alkalosis, pulmonary venous and pulmonary arterial hypertension in these patients.

  3. Renal abnormalities in congenital chloride diarrhea

    International Nuclear Information System (INIS)

    Al-Hamad, Nadia M.; Al-Eisa, Amal A.

    2004-01-01

    Congenital chloride diarrhea CLD is a rare autosomal recessive disorder caused by a defect in the chloride/ bicarbonate exchange in the ileum and colon. It is characterized by watery diarrhea, abdominal distension, hypochloremic hypokalemic metabolic alkalosis with high fecal content of chloride >90 mmol/l. We report 3 patients with CLD associated with various renal abnormalities including chronic renal failure secondary to renal hypoplasia, nephrocalcinosis and congenital nephrotic syndrome. (author)

  4. The effect of acid-base balance on neostigmine antagonism of d-tubocurarine-induced neuromuscular blockade.

    Science.gov (United States)

    Miller, R D; Van Nyhuis, L S; Eger, E I; Way, W L

    1975-04-01

    d-Tubocurarine (dTc) was infused intravenously into 35 cats anesthetized with chloralose and urethane at a constant continuous rate to produce and maintain 90 per cent depression of twitch height of the anterior tibial muscle following supramaximal stimulation of the peroneal nerve. The mean infusion rates that produced 90 per cent depression were not significantly altered by respiratory acid-base changes. Metabolic alkalosis decreased (32.5 per cent) and metabolic acidosis increased (27.7 per cent) the required infusion rate of dTc. When pH and Paco2 were maintained at 7.37 and 38 torr, respectively, the addition of a bolus of neostigmine, 10.5 mug/kg, intravenously, to the continuing infusion of dTc produced 50 per cent antagonism of the dTc-depressed twitch. Respiratory alkalosis and metabolic acidosis did not alter the dose of neostigmine needed to produce 50 per cent antagonism. However, during respiratory acidosis (pH 7.13, Paco2 66 torr) and metabolic alkalosis (pH 7.59, Paco2 36 torr) 20.0 and 18.0 mug/kg neostigmine, respectively, were needed to produce 50 per cent antagonism. Still larger doses of neostigmine (75 mug/kg) could not completely antagonize the block unless pH and Paco2 were returned to 7.30-7.50 and 35-45 torr, respectively. It is concluded that respiratory acidosis and metabolic alkalosis limit and oppose antagonism of dTc by neostigmine.

  5. Atypical presentation of cystic fibrosis: Obese adolescent with hypertension and pseudo-Bartter’s syndrome

    Directory of Open Access Journals (Sweden)

    Sovtić Aleksandar

    2012-01-01

    Full Text Available Introduction. Infants with cystic fibrosis may fail to thrive despite recommended caloric intake because of electrolyte disurbances caused by salt depletion resulting in hypochloremic metabolic alkalosis or pseudo-Bartter's syndrome. In most patients reported symptoms began in infancy, but it may be an initial presentation of disease in a previously healthy adolescent. Case report. A 15-year-old boy was admitted for evaluation of recurrent episodes of malaise associated with dehydration and acute renal insufficiency. Laboratory analysis showed hypochloremic metabolic alkalosis with hyponatremia and hypokalemia. On admission the boy was obese, with body weight of 95.5 kg (> P97, height 174 cm (> P75, and body mass index of 31.2 kg/m2 (> P95. Physical examination was inconclusive. Blood pressure holter monitoring proved significant systolic hypertension. Routine urinalysis, protein and electrolyte levels in urine were normal. Plasma renin and aldosteron were normal. Sweat chloride concentration was 63 mmol/L. Genetic testing confirmed the diagnosis of cystic fibrosis. Conclusion. To our knowledge, this is the first reported case of atypical presentation of cystic fibrosis in an adolescent presented with pseudo-Bartter's syndrome and signs of obesity and hypertension. We suggest that every patient with hypochloremic metabolic alkalosis should be evaluated for cystic fibrosis.

  6. Potassium supplementation reduces cardiac and renal hypertrophy independent of blood pressure in DOCA/salt mice.

    Science.gov (United States)

    Wang, Qing; Domenighetti, Andrea A; Pedrazzini, Thierry; Burnier, Michel

    2005-09-01

    We have demonstrated previously that deoxycorticosterone acetate (DOCA)/salt induces cardiac hypertrophy and left ventricular dysfunction independent of blood pressure (BP) in 1-renin gene mice. Because these mice also develop hypokalemia and metabolic alkalosis caused by mineralocorticoid excess, we investigated whether correcting hypokalemia by dietary potassium supplementation would prevent the DOCA/salt-induced cardiac hypertrophy, cardiac dysfunction, and electrocardiographic changes in normotensive, 1-renin gene and hypertensive, 2-renin gene mice. All mice were studied after 5 weeks of DOCA and salt administration. Potassium was given by adding 0.4 or 0.6% KCl to the drinking water. Our results show that correction of hypokalemia and metabolic alkalosis prevents cardiac hypertrophy and normalizes cardiac function without affecting BP in normotensive, 1-renin gene mice. In hypertensive, 2-renin gene mice, potassium supplementation induces a significant decrease in BP. The decrease in BP and correction of kalemia are associated with a significant but partial correction of cardiac hypertrophy. In both group of mice, electrocardiographic alterations were measured after administration of DOCA/salt, which could be corrected by potassium supplementation. Thus, these results show that correction of hypokalemia and metabolic alkalosis does prevent the development of cardiac hypertrophy and normalizes cardiac function independent of BP in normotensive, 1-renin gene mice that receive excess mineralocorticoid and salt. In 2-renin gene, hypertensive mice, potassium supplementation also prevents the development of cardiac hypertrophy, but the effect cannot be separated from the decrease in BP.

  7. Effect of systemic pH on pHi and lactic acid generation in exhaustive forearm exercise

    International Nuclear Information System (INIS)

    Hood, V.L.; Schubert, C.; Keller, U.; Mueller, S.

    1988-01-01

    To investigate whether changes in systemic pH affect intracellular pH (pH i ), energy-rich phosphates, and lactic acid generation in muscle, eight normal volunteers performed exhaustive forearm exercise with arterial blood flow occluded for 2 min on three occasions. Subjects ingested 4 mmol/kg NH 4 Cl (acidosis; A) or NaHCO 3 (alkalosis; B) or nothing (control; C) 3 h before the exercise. Muscle pH i and phosphocreatine (PCr) content were measured with 31 P-nuclear magnetic resonance ( 31 P-NMR) spectroscopy during exercise and recovery. Lactate output during 0.5-7 min of recovery was calculated as deep venous-arterial concentration differences times forearm blood flow. Before exercise, blood pH and bicarbonate were lower in acidosis than alkalosis and intermediate in control. Lactic acid output during recovery was less with A than B and intermediate in C. PCr utilization and resynthesis were not affected by extracellular pH changes. pH i did not differ before exercise or at its end. Hence systemic acidosis inhibited and alkalosis stimulated lactic acid output. These findings suggest that systemic pH regulates cellular acid production, protecting muscle pH, at the expense of energy availability

  8. Drug-induced acid-base disorders.

    Science.gov (United States)

    Kitterer, Daniel; Schwab, Matthias; Alscher, M Dominik; Braun, Niko; Latus, Joerg

    2015-09-01

    The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal anti-inflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g., anesthetics, sedatives) or hyperventilation (e.g., salicylates, epinephrine, nicotine).

  9. Acid base imbalances in ill neonatal foals and their association with survival.

    Science.gov (United States)

    Viu, J; Armengou, L; Ríos, J; Cesarini, C; Jose-Cunilleras, E

    2017-01-01

    Acid-base imbalances observed in human paediatric patients are associated with outcome. Likewise, neonatal foals may have different acid-base imbalances associated with diagnosis or prognosis. To determine acid-base imbalances by the quantitative method in ill neonatal foals and assess their association with diagnosis and prognosis. Observational prospective clinical study. This study included 65 ill neonatal foals (32 septic, 33 nonseptic) admitted to an equine referral hospital from 2005 to 2011with acid-base parameters determined on admission and a control group of 33 healthy neonatal foals. Blood pH, pCO 2 , sodium, potassium, chloride, L-lactate, albumin and phosphate concentrations were determined. Bicarbonate, globulin, measured strong ion difference (SID m ), nonvolatile weak buffer concentrations (A tot ), base excess and its components were calculated. Analysis of covariance (ANCOVA) and multiple linear regression statistical analyses were performed. Results are summarised as mean ± s.d. for normally distributed variables and median [25-75th percentiles] for non-normally distributed ones. A total of 63% of ill foals had respiratory alkalosis and 58.5% had SID m acidosis. The combination of both alterations was detected in 21 of 65 ill foals and abnormal pH was found in 24 of 65. Compared with healthy foals, ill foals had significantly lower SID m (nonseptic 31.6 ± 6.3 [Pacid-base imbalances observed in ill foals were respiratory alkalosis, SID m acidosis or mixed respiratory alkalosis with strong ion acidosis. Increased venous pCO 2 and blood L-lactate concentration were associated with poor outcome. © 2015 EVJ Ltd.

  10. Severe hypernatremia and hyperchloremia in an elderly patient with IgG-kappa type

    Directory of Open Access Journals (Sweden)

    Berend K

    2013-12-01

    Full Text Available Kenrick BerendSt Elisabeth Hospital, Willemstad, CuraçaoImashuku et al1 describe a 77-year-old male patient with multiple myeloma who was admitted to the hospital after suffering a pelvic bone fracture due to a road traffic accident. Several days after admission the arterial blood gas showed a pH of 7.481; arterial carbon dioxide tension (PaCO2 of 28.2 mmHg; arterial oxygen tension (PaO2 of 84.0 mmHg; HCO3- of 20.8 mmol/L (normal; 23–31 mmol/L; and an anion gap of 8.9 mmol/L (normal;12 mmol/L. These data, as the authors concluded, were suggestive of metabolic acidosis. First, this is not true because a high pH and low PaCO2 confirm a respiratory alkalosis. Since the test was conducted days later we may expect a chronic respiratory alkalosis to be present, perhaps because of pain or a secondary pulmonary problem, as may be expected with a relatively low PaO2. In chronic respiratory alkalosis one would expect the HCO3- to decrease about 4 mmol/L with every 10 mmHg decrease of PaCO2.2 If the initial HCO3- had been about 25 mmol/L, the expected PaCO2 would be about 20.28 mmol/L, almost identical with the patient’s HCO3-.View original paper by Imashuku and colleagues.

  11. Reversible Hypokalemia and Bartter-Like Syndrome during Prolonged Systemic Therapy with Colistimethate Sodium in an Adult Patient.

    Science.gov (United States)

    Kamal Eldin, Tarek; Tosone, Grazia; Capuano, Alfredo; Orlando, Raffaele

    2017-12-01

    We present the case of a 58-year-old woman who developed hypokalaemia and metabolic alkalosis 2 weeks after therapy with colistimethate sodium for the treatment of chronic lower limb ulcer infection by extensively drug-resistant (XDR) Pseudomonas aeruginosa. The metabolic changes observed resembled Bartter syndrome, a group of congenital disorders affecting the distal segments of the renal tubules. The metabolic abnormalities reversed spontaneously 6 days after drug discontinuation. Acquired forms of Bartter syndrome have been reported during courses of antibiotic therapy; however, to our knowledge, this is the first documented case associated with colistimethate therapy in an adult.

  12. Gitelman’s syndrome presented with tetany: a case report

    Directory of Open Access Journals (Sweden)

    Md. Zahid Alam

    2012-01-01

    Full Text Available Gitelman’s syndrome is an autosomal recessive disorder caused by a defect of the thiazide-sensitive sodium chloride co-transporter at the distal tubule, characterized by hypomagnesemia, hypokalemic alkalosis and hypocalciuria. We report a case of Gitlman’s syndrome in a 44 years old female patient who presented with generalized muscle weakness and carpal spasm and characteristic electrolyte abnormalities. This condition is sometimes confused with Bartter’s syndrome. Ibrahim Med. Coll. J. 2012; 6(1: 34-36

  13. Gitelman syndrome associated with chondrocalcinosis: description of two cases

    Directory of Open Access Journals (Sweden)

    E. Filippucci

    2011-06-01

    Full Text Available Gitelman syndrome is a rare inherited tubulopathy, characterized by hypomagnesemia, hypokalemia, metabolic alkalosis, hypocalciuria and hyperreninemic hyperaldosteronism. The clinical spectrum is wide and includes: cramps, myalgies, muscle weakness, until episodes of carpo-podalic spasm, tetania, rabdomyolisis and paralysis. Some cases have been described in literature underlining the association of this condition with chondrocalcinosis, as a typical example of hypomagnesemia-induced crystal deposition disease. The therapy of Gitelman syndrome consists on the administration of defective electrolytes, althought not always effective. We describe two cases of Gitelman syndrome associated with chondrocalcinosis showing the wide range of presentation of this clinical condition.

  14. Hypercalcemic encephalopathy due to milk alkali syndrome and injection teriparatide

    Directory of Open Access Journals (Sweden)

    Sandeep Kharb

    2012-01-01

    Full Text Available An 82-year-old male, a known case of severe osteoporosis with vertebral fracture and prostatic carcinoma, was treated with gonadotropin releasing hormone analogue, calcium carbonate, cholecalciferol sachet and injection teriparatide. His diet consisted of milk and curd. He developed altered behavior and generalized weakness, and on investigation, hypercalcemia, hypokalemia, and metabolic alkalosis with low parathyroid hormone levels were detected. Injection teriparatide was stopped and he was managed with forced saline diuresis and injection zoledronic acid. He was diagnosed as a case of milk alkali syndrome in whom teriparatide and prolonged immobilization played a permissive role in the development of hypercalcemic encephalopathy.

  15. Gitelman′s syndrome: Rare presentation with growth retardation

    Directory of Open Access Journals (Sweden)

    A Gaur

    2014-01-01

    Full Text Available Gitelman′s syndrome is an autosomal recessive disorder characterized by hypokalemic metabolic alkalosis, hypokalemia, hypomagnesaemia, hypocalciuria, hyperreninemia and without hypertension. Gitelman′s syndrome is caused by mutations of the SLC12A3 gene, which encodes the Na/Cl co-transporter (NCCT in the distal convoluted tubule. Majority of cases manifest during adolescence or adulthood and growth retardation is not the common feature. We report a rare presentation of Gitelman′s syndrome in a four-year-old boy with growth retardation.

  16. HELLP syndrome in a pregnant patient with Gitelman syndrome

    Directory of Open Access Journals (Sweden)

    Minhyeok Lee

    2017-03-01

    Full Text Available Gitelman syndrome is characterized by hypokalemia, metabolic alkalosis, hypocalciuria, and hypomagnesemia. The clinical course of Gitelman syndrome in pregnant women remains unclear, but it is thought to be benign. We report here the first Korean case of atypical eclampsia in a 31-year-old who was diagnosed with Gitelman syndrome incidentally during an antenatal screening test. The patient did well during pregnancy despite significant hypokalemia. At 33 weeks’ gestation, the patient exhibited eclampsia, hemolysis, elevated liver enzymes, low platelets (HELLP syndrome, and renal insufficiency without significant hypertension or proteinuria. We explain this unusual clinical course through a review of the relevant literature.

  17. Unusual Presentation of the Conn's Syndrome: a Case Report

    Directory of Open Access Journals (Sweden)

    Maryam Al-Rajhi

    2011-11-01

    Full Text Available A 26 -year- old woman presented with rhabdomyolysis secondary to severe hypokalemia. Hypertension and metabolic alkalosis could lead to the suspicion of primary aldosteronism, which was confirmed by a decreased plasma rennin, elevated plasma aldosterone levels and high aldosterone/rennin ratio additionally. Additionally adrenal computed tomography showed an adrenal tumour. Blood pressure and hypokalemia returned to the normal level after adrenalectomy was performed. This case report highlights the need to be alert to the possibility of primary aldosteronism incidence in a patient presenting with rhabdomyolysis and hypertension caused by severe hypokalemia.

  18. Effects of a Taser: Conducted Energy Weapon on the Circulating Red-Blood-Cell Population and Other Factors in Sus scrofa

    Science.gov (United States)

    2013-03-30

    our study favoring either young or old RBCs being released from the spleen is unknown. Since alkalosis (rather than acidosis) tends to result in...204. 70. Waśkiewicz Z, Kłapcińska B, Sadowska-Krępa E, Czuba M, Kempa K, Kimsa E, Gerasimuk D. Acute metabolic responses to a 24-h ultra-marathon...cardiovascular, respiratory, and metabolic effects of a long duration electronic control device exposure in human volunteers. Forensic Sci Med Pathol. 2010;6

  19. Milk-Alkali syndrome induced by H1N1 influenza vaccine

    Directory of Open Access Journals (Sweden)

    Abdullah K Al-Hwiesh

    2017-01-01

    Full Text Available Milk-Alkali syndrome (MAS consists of a triad of hypercalcemia, metabolic alkalosis, and acute renal failure. We hereby report a 75-year-old Indian gentleman who presented to our emergency department with a history of generalized weakness and easy fatigability. Investigations were consistent with MAS secondary to calcium carbonate and calcitriol treatment to prevent osteoporosis, aggravated by H1N1 influenza vaccine. The patient was treated with hemodialysis and zoledronate. To our knowledge, this is the first reported case of such association in the literature.

  20. Hyponatremic-Hypertensive Syndrome in an 18-Month-Old Male Child

    Directory of Open Access Journals (Sweden)

    Dilek Yilmaz

    2016-04-01

    Full Text Available An eighteen-month-old boy presented with polyuria, polydipsia, hypertension, severe hyponatremia, metabolic alkalosis and nephrotic-range proteinuria. Hypertension was drug resistant. Renal artery angiogram revealed right renal artery occlusion. Nonfunctional right kidney was also detected on the nuclear renal scan. As percutaneous transluminal renal artery angioplasty was not appropriate for our patient, nephrectomy was performed. Right nephrectomy resulted in the resolution of all the symptoms. Rarity of hyponatremic hypertensive syndrome in children may project its under-recognition. We aimed to increase awareness of early diagnosis of HHS among polyuric, hypertensive and hyponatremic children in order to prevent renal damage and life-threatening complications.

  1. Anaesthetic management of a patient with Liddle's syndrome for emergency caesarean hysterectomy.

    LENUS (Irish Health Repository)

    Hayes, N E

    2012-02-01

    We describe the anaesthetic management of a patient with Liddle\\'s syndrome during caesarean section and emergency hysterectomy for placenta accreta associated with significant intrapartum haemorrhage. Liddle\\'s syndrome is a rare autosomal dominant disorder characterised by early onset arterial hypertension and hypokalaemic metabolic alkalosis. Additional issues were the presence of short stature, limb hypertonicity and preeclampsia. Initial management with a low-dose combined spinal-epidural technique was subsequently converted to general anaesthesia due to patient discomfort. The management of Liddle\\'s syndrome in the setting of neuraxial and general anaesthesia in a patient undergoing caesarean section is discussed.

  2. Anaesthetic management of a patient with Liddle's syndrome for emergency caesarean hysterectomy.

    LENUS (Irish Health Repository)

    Hayes, N E

    2011-04-01

    We describe the anaesthetic management of a patient with Liddle\\'s syndrome during caesarean section and emergency hysterectomy for placenta accreta associated with significant intrapartum haemorrhage. Liddle\\'s syndrome is a rare autosomal dominant disorder characterised by early onset arterial hypertension and hypokalaemic metabolic alkalosis. Additional issues were the presence of short stature, limb hypertonicity and preeclampsia. Initial management with a low-dose combined spinal-epidural technique was subsequently converted to general anaesthesia due to patient discomfort. The management of Liddle\\'s syndrome in the setting of neuraxial and general anaesthesia in a patient undergoing caesarean section is discussed.

  3. Teaching acid/base physiology in the laboratory

    DEFF Research Database (Denmark)

    Friis, Ulla G; Plovsing, Ronni; Hansen, Klaus

    2010-01-01

    Acid/base homeostasis is one of the most difficult subdisciplines of physiology for medical students to master. A different approach, where theory and practice are linked, might help students develop a deeper understanding of acid/base homeostasis. We therefore set out to develop a laboratory...... exercise in acid/base physiology that would provide students with unambiguous and reproducible data that clearly would illustrate the theory in practice. The laboratory exercise was developed to include both metabolic acidosis and respiratory alkalosis. Data were collected from 56 groups of medical...

  4. A case of Pseudo-Bartter syndrome

    Energy Technology Data Exchange (ETDEWEB)

    Yang, Ik; Choi, Bo Whan; Lee, Yul; Chung, Soo Young [College of Medicine, Hallym University, Seoul (Korea, Republic of)

    1994-10-15

    Pseudo-Bartter Syndrome is a rare medical disease of the kidney characterized by normal blood pressure, hypokalemic metabolic alkalosis, hyperreninemia and hyperaldosteronism with drug history of diuretics. We report US, CT and MRI findings of a patients with clinically proved Pseudo-Bartter syndrome. The patient was a 37 year old woman with a history of long term ingestion of the diuretics(furosemide) for 20 years. Renal US revealed hyperechoic renal medulla at both kidneys. The resistive index(RI), calculated from the duplex doppler waveform is 0.61. Unenhanced CT revealed faint high attenuation along the medulla. T1-weighted MRI revealed indistinct corticomedullary differentiation.

  5. [Disorders of the acid-base balance and the anion gap].

    Science.gov (United States)

    Kimmel, Martin; Alscher, Mark Dominik

    2016-10-01

    The regulation of the acid-base balance and pH is critical for the organism. The most important buffer system is CO 2 / HCO 3 - . The kidney controls systemic bicarbonate and therefore the metabolic regulation and the lung is relevant for respiratory regulation by an effective CO 2 elimination. There are four acid-base disorders with two metabolic and two respiratory disorders (acidosis and alkalosis). The anion gap enables a further workup of metabolic acidosis. © Georg Thieme Verlag KG Stuttgart · New York.

  6. Acid-Base and Electrolyte Disorders in Patients with and without Chronic Kidney Disease: An Update.

    Science.gov (United States)

    Dhondup, Tsering; Qian, Qi

    2017-12-01

    Kidneys play a pivotal role in the maintenance and regulation of acid-base and electrolyte homeostasis, which is the prerequisite for numerous metabolic processes and organ functions in the human body. Chronic kidney diseases compromise the regulatory functions, resulting in alterations in electrolyte and acid-base balance that can be life-threatening. In this review, we discuss the renal regulations of electrolyte and acid-base balance and several common disorders including metabolic acidosis, alkalosis, dysnatremia, dyskalemia, and dysmagnesemia. Common disorders in chronic kidney disease are also discussed. The most recent and relevant advances on pathophysiology, clinical characteristics, diagnosis, and management of these conditions have been incorporated.

  7. Cushing′s surgery: Role of the anesthesiologist

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    Rudin Domi

    2011-01-01

    Full Text Available Cushing′s syndrome is a clinical situation, caused by excessive glucocorticoid level, resulting in several features such as central obesity, supraclavicular fat, "moon face," "buffalo hump," hyperglycemia, metabolic alkalosis, hypokalemia, poor wound healing, easy bruising, hypertension, proximal muscle weakness, thin extremities, skin thinning, menstrual irregularities, and purple striae. In the perioperative period, the anesthesiologist must deal with difficult ventilation and intubation, hemodynamic disturbances, volume overload and hypokalemia, glucose intolerance, and diabetes, maintaining the blood cortisol level and preventing the glucocorticoid deficiency. This syndrome is quite rare and its features make these patients very difficult to the anesthesiologist.

  8. (/sup 11/C )-DMO for evaluation of regional tissue pH in patients with hemispheric infarction using positron emission tomography

    Energy Technology Data Exchange (ETDEWEB)

    Castaing, M.; Syrota, A.; Rougemont, D.; Berridge, M.; Chretien, L.; Baron, J.C.; Bousser, M.G.

    1983-06-01

    Changes in brain intracellular pH resulting from cerebral infarction were evaluated using the /sup 11/C-DMO (dimethyloxazolidine-dione) method, in 9 patients. A /sup 15/O/sub 2/-C/sup 15/O/sub 2/ study was performed the day following the DMO examination in order to obtain the values of cerebral blood flow, oxygen extraction and oxygen metabolic rate in the same regions-of-interest. The results emphasized the relationship between tissue alkalosis and luxury perfusion during recent infarction.

  9. 17-α-Hydroxylase deficiency: An unusual case with primary amenorrhea and hypertension

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    Sunil Kumar Kota

    2011-01-01

    Full Text Available A 14-year-old girl presented with acute onset quadriparesis and newly detected hypertension. Parental consanguinity, delayed puberty with normal stature form the additional information. Hypokalemia with metabolic alkalosis, low cortisol, high ACTH and FSH pointed to the possibility of CAH with 17α hydroxylase deficiency. 46XX karyotype and high progesterone supported this. Normalization of hypokalemia and hypertension with glucocorticoid treatment confirmed the diagnosis. In summary, the possibility of 17 OHD should be suspected in patients with hypokalemic myopathy, Hypertension and hypogonadism so that appropriate therapy can be implemented.

  10. Acid-base disturbance in patients with cirrhosis

    DEFF Research Database (Denmark)

    Henriksen, Jens H; Bendtsen, Flemming; Møller, Søren

    2015-01-01

    PURPOSE: Acid-base disturbances were investigated in patients with cirrhosis in relation to hemodynamic derangement to analyze the hyperventilatory effects and the metabolic compensation. METHODS: A total of 66 patients with cirrhosis and 44 controls were investigated during a hemodynamic study......, and effects of unidentified ions (all Pacid-base disturbances could not be identified. CONCLUSION: Hypocapnic alkalosis is related to disease severity and hyperdynamic systemic circulation in patients with cirrhosis. The metabolic compensation includes...... alterations in serum albumin and water retention that may result in a delicate acid-base balance in these patients....

  11. Hypokalemic paralysis and acid-base balance

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    Ivo Casagranda

    2006-10-01

    Full Text Available Three cases of hypokalemic paralysis are reported, presenting to the Emergency Department. The first is a patient with a hypokalemic periodic paralysis with a normal acid-base status, the second is a case of hypokalemic flaccid paralysis of all extremities with a normal anion gap metabolic acidosis, the last is a patient with a hypokalemic distal paralysis of right upper arm with metabolic alkalosis. Afterwards some pathophysiologic principles and the clinical aspects of hypokalemia are discussed and an appropriate approach to do in Emergency Department, to identify the hypokalemic paralysis etiologies in the Emergency Department, is presented, beginning from the evaluation of acid-base status.

  12. Hyperchloremia – Why and how

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    Glenn T. Nagami

    2016-07-01

    Full Text Available Hyperchloremia is a common electrolyte disorder that is associated with a diverse group of clinical conditions. The kidney plays an important role in the regulation of chloride concentration through a variety of transporters that are present along the nephron. Nevertheless, hyperchloremia can occur when water losses exceed sodium and chloride losses, when the capacity to handle excessive chloride is overwhelmed, or when the serum bicarbonate is low with a concomitant rise in chloride as occurs with a normal anion gap metabolic acidosis or respiratory alkalosis. The varied nature of the underlying causes of the hyperchloremia will, to a large extent, determine how to treat this electrolyte disturbance.

  13. Hypokalemic paralysis in a middle-aged female with classic Bartter syndrome.

    Science.gov (United States)

    Chiang, Wen-Fang; Lin, Shih-Hung; Chan, Jenq-Shyong; Lin, Shih-Hua

    2014-02-01

    Inherited classic Bartter syndrome (cBS) is an autosomal recessive renal tubular disorder resulting from inactivating mutations in the asolateral chloride channel (C1C-Kb) and usually presents in early infancy or childhood with mild to moderate hypokalemia. Profound hypokalemic paralysis in patients with cBS is extremely rare, especially in middle age. A 45-year-old Chinese female patient was referred for evaluation of chronic severe hypokalemia despite regular K+ supplementation (1 mmol/kg/d). She had had two episodes of muscle paralysis due to severe hypokalemia (K+ 1.9 - 2.1 mmol/l) in the past 3 years. She denied vomiting, diarrhea, or the use of laxatives or diuretics. Her blood pressure was normal. Biochemical studies showed hypokalemia (K+ 2.5 mmol/l) with renal potassium wasting, metabolic alkalosis (HCO3- 32 mmol/l), normomagnesemia (Mg2+ 0.8 mmol/l), hypercalciuria (calcium to creatinine ratio 0.5 mmol/mmol; normal paralysis and should be considered in adult patients with hypokalemia and metabolic alkalosis.

  14. Red cell function at extreme altitude on Mount Everest.

    Science.gov (United States)

    Winslow, R M; Samaja, M; West, J B

    1984-01-01

    As part of the American Medical Research Expedition to Everest in 1981, we measured hemoglobin concentration, red cell 2,3-diphosphoglycerate (2,3-DPG), Po2 at which hemoglobin is 50% saturated (P50), and acid-base status in expedition members at various altitudes. All measurements were made in expedition laboratories and, with the exception of samples from the South Col of Mt. Everest (8,050 m), within 2 h of blood collection. In vivo conditions were estimated from direct measurements of arterial blood gases and pH or inferred from base excess and alveolar PCO2. As expected, increased 2,3-DPG was associated with slightly increased P50, when expressed at pH 7.4. Because of respiratory alkalosis, however, the subjects' in vivo P50 at 6,300 m (27.6 Torr) was slightly less than at sea level (28.1 Torr). The estimated in vivo P50 was progressively lower at 8,050 m (24.9 Torr) and on the summit at 8,848 m (19.4 Torr in one subject). Our data suggest that, at extreme altitude, the blood O2 equilibrium curve shifts progressively leftward because of respiratory alkalosis. This left shift protects arterial O2 saturation at extreme altitude.

  15. RELATIONS BETWEEN SELECTED INDICATORS OF BLOOD AND MILK OF DAIRY COWS WITH METABOLIC DISORDERS

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    Jaroslav Kováčik

    2013-02-01

    Full Text Available The aim of this work was to monitor the relations between selected indicators of technological properties of milk and blood biochemical parameters of dairy cows with metabolic disorders. Thirty-two cows were chosen, which were divided into 3 groups: first group - cows with metabolic problems of acidosis, second group - cows with metabolic problems of alkalosis, third group - healthy cows. Blood, urine and milk samples were collected. Urea, total lipids, total proteins, glucose and calcium was determined in the blood serum. Pure acidobasic forms, pH and density of urine were determined. Proteins, lactose, non-fat-solids, somatic cells count, calcium, urea, titratable acidity, fermentability, rennetability and thermostability were determined in samples of milk. Significant negative dependences were observed in the group of cows with metabolic problems of acidosis between urea in blood and in milk (r = -0.694, P <0.05, between calcium in blood and in milk (r = -0.653, P <0, 05, and between calcium in milk and glucose in blood (r = -0.648, P <0.05. In the group of cows with alkalosis, statistically significant correlation between total lipids in blood and fat in milk was found (r = -0.879, P <0.05.

  16. Neuroblastoma Presenting with Acute Kidney Injury, Hyponatremic-Hypertensive-Like Syndrome and Nephrotic Proteinuria in a 10-Month-Old Child

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    Giovanni Maria Poggi

    2011-08-01

    Full Text Available Neuroblastoma is the most common extracranial solid tumor in childhood. Its presenting signs and symptoms may be highly variable, depending on the location of the primary tumor and its local or metastatic diffusion and, rarely, with paraneoplastic syndrome such as opsoclonus-myoclonus-ataxia syndrome and gastrointestinal disturbances, due to autoantibodies or to aberrant secretion of vasoactive intestinal peptide. Herein we describe a 10-month-old child with neuroblastoma presenting with a complex clinical picture characterized by acute kidney injury manifested by renal insufficiency and signs and symptoms of tubulointerstitial damage, with polyuria, polydipsia, glucosuria, aminoaciduria and hypochloremic metabolic alkalosis, and of glomerular damage with heavy proteinuria. Imaging study documented a suprarenal mass enveloping the aorta and its abdominal and renal ramifications and bilaterally renal veins. This clinical picture shows some analogies with the hyponatremic-hypertensive syndrome concerning the renovascular disease; however, in absence of systemic arterial hypertension, the heavy proteinuria and the polyuria could be explained by sectional increased intraglomerular pressure, due to local renal blood vessels constriction. Hypochloremic metabolic alkalosis probably developed because of local production of renin, responsible of renin-angiotensin-aldosterone system activation, but above all because of chloride loss through sweating. The long lasting dehydration, due to vomiting, sweating and polyuria, caused prolonged prerenal failure evolving in proximal tubular damage manifestations.

  17. Population pharmacodynamic modeling and simulation of the respiratory effect of acetazolamide in decompensated COPD patients.

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    Nicholas Heming

    Full Text Available Chronic obstructive pulmonary disease (COPD patients may develop metabolic alkalosis during weaning from mechanical ventilation. Acetazolamide is one of the treatments used to reverse metabolic alkalosis.619 time-respiratory (minute ventilation, tidal volume and respiratory rate and 207 time-PaCO2 observations were obtained from 68 invasively ventilated COPD patients. We modeled respiratory responses to acetazolamide in mechanically ventilated COPD patients and then simulated the effect of increased amounts of the drug.The effect of acetazolamide on minute ventilation and PaCO2 levels was analyzed using a nonlinear mixed effect model. The effect of different ventilatory modes was assessed on the model. Only slightly increased minute ventilation without decreased PaCO2 levels were observed in response to 250 to 500 mg of acetazolamide administered twice daily. Simulations indicated that higher acetazolamide dosage (>1000 mg daily was required to significantly increase minute ventilation (P0.75 L min(-1 in 60% of the population. The model also predicts that 45% of patients would have a decrease of PaCO2>5 mmHg with doses of 1000 mg per day.Simulations suggest that COPD patients might benefit from the respiratory stimulant effect after the administration of higher doses of acetazolamide.

  18. Gitelman syndrome combined with complete growth hormone deficiency

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    Se Ra Min

    2013-03-01

    Full Text Available Gitelman syndrome is a rare autosomal recessive hereditary salt-losing tubulopathy, that manifests as hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria. It is caused by mutations in the solute carrier family 12(sodium/chloride transporters, member 3 (SLC12A3 gene encoding the thiazide-sensitive sodium chloride cotransporter channel (NCCT in the distal convoluted tubule of the kidney. It is associated with muscle weakness, cramps, tetany, vomiting, diarrhea, abdominal pain, and growth retardation. The incidence of growth retardation, the exact cause of which is unknown, is lower than that of Bartter syndrome. Herein, we discuss the case of an overweight 12.9-year-old girl of short stature presenting with hypokalemic metabolic alkalosis. The patient, on the basis of detection of a heterozygous mutation in the SLC12A3 gene and poor growth hormone (GH responses in two provocative tests, was diagnosed with Gitelman syndrome combined with complete GH deficiency. GH treatment accompanied by magnesium oxide and potassium replacement was associated with a good clinical response.

  19. A Case of Hypercalcemia after Thyroidectomy

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    Katsarou Irini

    2016-12-01

    Full Text Available Total thyroidectomy is complicated by hypoparathyroidism in 1-3% of patients. Hypoparathyroidism is treated with oral calcium and vitamin-D supplements. Everyday use of calcium and vitamin D can lead sometimes to hypercalcemia. Ingestion of large amounts of calcium and absorbable alkali that cause hypercalcemia, various degrees of renal failure, and metabolic alkalosis, can be associated with a diagnosis of calcium-alkali syndrome. This syndrome was first identified as milkalkali syndrome, after treatment of peptic ulcer disease with milk and alkali which was widely adopted at the beginning of the 20th century. With the introduction of histamine-2 blockers and proton pump inhibitors, the occurrence of milk-alkali syndrome became rare; however, it has emerged recently as calcium-alkali syndrome because of the wide availability and increasing use of calcium carbonate, mostly for osteoporosis prevention. We present a female patient with hypoparathyroidism who presented with hypercalcemia and alkalosis as a result of treatment with calcium carbonate, vitamin D and thiazide diuretic. The patient was treated successfully by discontinuation of the above drugs, intravenous fluid administration and enhancement of calcium renal excretion. Hypercalcemia presenting as calcium-alkali syndrome is a diagnosis that requires a high index of suspicion in order to quickly identify the disorder and initiate appropriate therapy. It is important for clinicians to keep the syndrome on their list of differential diagnosis.

  20. Gitelman Syndrome in a School Boy Who Presented with Generalized Convulsion and Had a R642H/R642W Mutation in the SLC12A3 Gene

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    Shigeru Makino

    2014-01-01

    Full Text Available An 8-year-old Japanese boy presented with a generalized convulsion. He had hypokalemia (serum K 2.4 mEq/L, hypomagnesemia, and metabolic alkalosis (BE 5.7 mmol/L. In addition, his plasma renin activity was elevated. He was tentatively diagnosed with epilepsy on the basis of the electroencephalogram findings and was treated by potassium L-aspartate and carbamazepine to control the hypokalemia and seizure, respectively. However, a year later, the patient continued to have similar abnormal laboratory data. A presumptive diagnosis of Gitelman syndrome (GS was then made and the patient’s peripheral blood mononuclear cells were subjected to sequence analysis of the SLC12A3 gene, which encodes a thiazide-sensitive sodium-chloride cotransporter. The patient was found to have compound heterozygous mutations, namely, R642H inherited from his father and R642W inherited from his mother. Thus, if a patient shows persistent hypokalemia and metabolic alkalosis, GS must be considered, even if the patient exhibits atypical clinical symptoms.

  1. The effect of oral sodium acetate administration on plasma acetate concentration and acid-base state in horses

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    Lindinger Michael I

    2007-12-01

    Full Text Available Abstract Aim Sodium acetate (NaAcetate has received some attention as an alkalinizing agent and possible alternative energy source for the horse, however the effects of oral administration remain largely unknown. The present study used the physicochemical approach to characterize the changes in acid-base status occurring after oral NaAcetate/acetic acid (NAA administration in horses. Methods Jugular venous blood was sampled from 9 exercise-conditioned horses on 2 separate occasions, at rest and for 24 h following a competition exercise test (CET designed to simulate the speed and endurance test of 3-day event. Immediately after the CETs horses were allowed water ad libitum and either: 1 8 L of a hypertonic NaAcetate/acetic acid solution via nasogastric tube followed by a typical hay/grain meal (NAA trial; or 2 a hay/grain meal alone (Control trial. Results Oral NAA resulted in a profound plasma alkalosis marked by decreased plasma [H+] and increased plasma [TCO2] and [HCO3-] compared to Control. The primary contributor to the plasma alkalosis was an increased [SID], as a result of increased plasma [Na+] and decreased plasma [Cl-]. An increased [Atot], due to increased [PP] and a sustained increase in plasma [acetate], contributed a minor acidifying effect. Conclusion It is concluded that oral NaAcetate could be used as both an alkalinizing agent and an alternative energy source in the horse.

  2. Do over 200 million healthy altitude residents really suffer from chronic Acid-base disorders?

    Science.gov (United States)

    Zubieta-Calleja, Gustavo; Zubieta-Castillo, Gustavo; Zubieta-Calleja, Luis; Ardaya-Zubieta, Gustavo; Paulev, Poul-Erik

    2011-01-01

    As the oxygen tension of inspired air falls with increasing altitude in normal subjects, hyperventilation ensues. This acute respiratory alkalosis, induces increased renal excretion of bicarbonate, returning the pH back to normal, giving rise to compensated respiratory alkalosis or chronic hypocapnia. It seems a contradiction that so many normal people at high altitude should permanently live as chronic acid-base patients. Blood gas analyses of 1,865 subjects at 3,510 m, reported a P(a)CO(2) (arterial carbon dioxide tension ± SEM) = 29.4 ± 0.16 mmHg and pH = 7.40 ± 0.005. Base excess, calculated with the Van Slyke sea level equation, is -5 mM (milliMolar or mmol/l) as an average, suggesting chronic hypocapnia. THID, a new term replacing "Base Excess" is determined by titration to a pH of 7.40 at a P(a)CO(2) of 5.33 kPa (40 mmHg) at sea level, oxygen saturated and at 37°C blood temperature. Since our new modified Van Slyke equations operate with normal values for P(a)CO(2) at the actual altitude, a calculation of THID will always result in normal values-that is, zero.

  3. Hyperventilation and finger exercise increase venous-arterial Pco2 and pH differences.

    Science.gov (United States)

    Umeda, Akira; Kawasaki, Kazuteru; Abe, Tadashi; Watanabe, Maki; Ishizaka, Akitoshi; Okada, Yasumasa

    2008-11-01

    Since the invention of the pulse oximeter, physicians often or even routinely perform venous blood gas analysis (VBGA). However, it has not been generally agreed that the application of VBGA is practically meaningful in routine clinical situations such as in an ED. We measured venous-arterial Pco(2) difference ((v-a)Pco(2)) and arterial-venous pH difference ((a-v)pH), and analyzed the physiological factors that affect these differences in healthy volunteers and hyperventilation patients. In healthy volunteers, both (v-a)Pco(2) and (a-v)pH increased during finger exercise or hyperventilation in an intensity-dependent manner. Doppler echography indicated that increases in (v-a)Pco(2) and (a-v)pH during hyperventilation are induced by reduction of peripheral blood flow. Approximately 40% of patients with untreated respiratory alkalosis were found to be incorrectly diagnosed if based only on VBGA. It must be noted that VBGA may lead to overestimation of acidosis and to underestimation of respiratory alkalosis when extremities muscles are active or patients are hyperventilating. Physicians should keep these limitations in mind when conducting VBGA.

  4. Calcium Unresponsive Hypocalcemic Tetany: Gitelman Syndrome with Hypocalcemia

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    Madhav Desai

    2013-01-01

    Full Text Available Introduction. Gitelman’s syndrome (GS is autosomal recessive renal tubular disorder characterized by hypokalemia, hypomagnesemia, hypocalciuria, metabolic alkalosis, and hyperreninemic hyperaldosteronism. It is usually associated with normal serum calcium. We report a patient presented with hypocalcemic tetany, and evaluation showed Gitelman’s syndrome with hypocalcemia. Case Report. A 28-year-old woman presented with cramps of the arms, legs, fatigue, and carpal spasms of one week duration. She has history of similar episodes on and off for the past two years. Her blood pressure was 98/66 mmHg. Chvostek’s sign and Trousseau’s sign were positive. Evaluation showed hypokalemia, hypocalcemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Self-medication, diuretic use, laxative abuse, persistent vomiting, and diarrhoea were ruled out. Urinary prostaglandins and genetic testing could not be done because of nonavailability. To differentiate Gitelman syndrome from Bartter’s syndrome (BS, thiazide loading test was done. It showed blunted fractional chloride excretion. GS was confirmed and patient was treated with spironolactone along with magnesium, calcium, and potassium supplementation. Symptomatically, she improved and did not develop episodes of tetany again. Conclusion. In tetany patient along with serum calcium measurement, serum magnesium, serum potassium, and arterial blood gases should be measured. Even though hypocalcemia in Gitelman syndrome is rare, it still can occur.

  5. Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis

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    Javier Mata-Gómez

    2015-08-01

    Full Text Available BACKGROUND AND OBJECTIVES: Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH normalization, cerebrospinal fluid can keep a state of metabolic alkalosis. This circumstance, in addition to the residual effect of neuromuscular blocking agents, inhalant anesthetics and opioids could increase the risk of postoperative apnea after a general anesthesia.CASE REPORT: We present the successful management in 3 neonates in those a pyloromyotomy was carried out because they had presented congenital hypertrophic pyloric stenosis. This procedure was done under general anesthesia with orotracheal intubation and rapid sequence induction. Then, ultrasound-guided paravertebral block was performed as analgesic method without the need for administrating opioids within intraoperative period and keeping an appropriate analgesic level.CONCLUSIONS: Local anesthesia has demonstrated to be safe and effective in pediatric practice. We consider the ultrasound-guided paravertebral block with one dose as a possible alternative for other local techniques described, avoiding the use of opioids and neuromuscular blocking agents during general anesthesia, and reducing the risk of central apnea within postoperative period.

  6. Hippocampal electrical activity of adult rabbits during moderate passive hyperventilation

    International Nuclear Information System (INIS)

    Touchard, Francoise

    1982-01-01

    The effects of a moderate passive hyperventilation (HV) were studied in immobilized un-anesthetized rabbits. Hypocapnia (PCO 2 = 23.3 ± 2.8 mm Hg) and alkalosis (pH = 7.54 ± 0.07) were measured on arterial samples. PO 2 remained stable. The following results were obtained. From the onset of HV, the mean discharge rate (F) of the pyramidal cells (CA 1 ) was modified. Several types of cellular behaviours were defined according to whether F decreased (51 pc of the neurons), increased (39 pc) or remained stable (6 pc). The most marked effect was observed 15 min after HV onset when 87 pc of cells showed a discharge rate lower than in controls. Whatever F variations, the temporal organization of the action potentials remained unchanged in 71 pc of cases. The evoked response resulting from the stimulation of the commissural inputs corresponded with the activity of GABA inhibitory neurons (basket cells). The response threshold, amplitude and latency were not modified by HV. Only the facilitation process resulting from paired pulses was modified in its late stage. These results as well as those concerning unit activity do not support various assumption such as trouble of the neuronal energetic metabolism due to hypoxia, modification of ionic exchanges (Na + , K + , Ca ++ ), or variations of neurotransmitter concentrations (especially GABA). The effects observed could be ascribed to modifications of neuronal membrane resting potential resulting from direct action of CO 2 and alkalosis. (author) [fr

  7. Quantified pH imaging with hyperpolarized (13) C-bicarbonate.

    Science.gov (United States)

    Scholz, David Johannes; Janich, Martin A; Köllisch, Ulrich; Schulte, Rolf F; Ardenkjaer-Larsen, Jan H; Frank, Annette; Haase, Axel; Schwaiger, Markus; Menzel, Marion I

    2015-06-01

    Because pH plays a crucial role in several diseases, it is desirable to measure pH in vivo noninvasively and in a spatially localized manner. Spatial maps of pH were quantified in vitro, with a focus on method-based errors, and applied in vivo. In vitro and in vivo (13) C mapping were performed for various flip angles for bicarbonate (BiC) and CO2 with spectral-spatial excitation and spiral readout in healthy Lewis rats in five slices. Acute subcutaneous sterile inflammation was induced with Concanavalin A in the right leg of Buffalo rats. pH and proton images were measured 2 h after induction. After optimizing the signal to noise ratio of the hyperpolarized (13) C-bicarbonate, error estimation of the spectral-spatial excited spectrum reveals that the method covers the biologically relevant pH range of 6 to 8 with low pH error (< 0.2). Quantification of pH maps shows negligible impact of the residual bicarbonate signal. pH maps reflect the induction of acute metabolic alkalosis. Inflamed, infected regions exhibit lower pH. Hyperpolarized (13) C-bicarbonate pH mapping was shown to be sensitive in the biologically relevant pH range. The mapping of pH was applied to healthy in vivo organs and interpreted within inflammation and acute metabolic alkalosis models. © 2014 Wiley Periodicals, Inc.

  8. The Role of Sodium Bicarbonate in the Management of Some Toxic Ingestions

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    Aibek E. Mirrakhimov

    2017-01-01

    Full Text Available Adverse reactions to commonly prescribed medications and to substances of abuse may result in severe toxicity associated with increased morbidity and mortality. According to the Center for Disease Control, in 2013, at least 2113 human fatalities attributed to poisonings occurred in the United States of America. In this article, we review the data regarding the impact of systemic sodium bicarbonate administration in the management of certain poisonings including sodium channel blocker toxicities, salicylate overdose, and ingestion of some toxic alcohols and in various pharmacological toxicities. Based on the available literature and empiric experience, the administration of sodium bicarbonate appears to be beneficial in the management of a patient with the above-mentioned toxidromes. However, most of the available evidence originates from case reports, case series, and expert consensus recommendations. The potential mechanisms of sodium bicarbonate include high sodium load and the development of metabolic alkalosis with resultant decreased tissue penetration of the toxic substance with subsequent increased urinary excretion. While receiving sodium bicarbonate, patients must be monitored for the development of associated side effects including electrolyte abnormalities, the progression of metabolic alkalosis, volume overload, worsening respiratory status, and/or worsening metabolic acidosis. Patients with oliguric/anuric renal failure and advanced decompensated heart failure should not receive sodium bicarbonate.

  9. Out of Warburg effect: An effective cancer treatment targeting the tumor specific metabolism and dysregulated pH.

    Science.gov (United States)

    Schwartz, Laurent; Seyfried, Thomas; Alfarouk, Khalid O; Da Veiga Moreira, Jorgelindo; Fais, Stefano

    2017-04-01

    As stated by Otto Warburg nearly a century ago, cancer is a metabolic disease, a fermentation caused by malfunctioning mitochondria, resulting in increased anabolism and decreased catabolism. Treatment should, therefore, aim at restoring the energy yield. To decrease anabolism, glucose uptake should be reduced (ketogenic diet). To increase catabolism, the oxidative phosphorylation should be restored. Treatment with a combination of α-lipoic acid and hydroxycitrate has been shown to be effective in multiple animal models. This treatment, in combination with conventional chemotherapy, has yielded extremely encouraging results in glioblastoma, brain metastasis and lung cancer. Randomized trials are necessary to confirm these preliminary data. The major limitation is the fact that the combination of α-lipoic acid and hydroxycitrate can only be effective if the mitochondria are still present and/or functional. That may not be the case in the most aggressive tumors. The increased intracellular alkalosis is a strong mitogenic signal, which bypasses most inhibitory signals. Concomitant correction of this alkalosis may be a very effective treatment in case of mitochondrial failure. Copyright © 2017 Elsevier Ltd. All rights reserved.

  10. Alkali-treated titanium selectively regulating biological behaviors of bacteria, cancer cells and mesenchymal stem cells.

    Science.gov (United States)

    Li, Jinhua; Wang, Guifang; Wang, Donghui; Wu, Qianju; Jiang, Xinquan; Liu, Xuanyong

    2014-12-15

    Many attentions have been paid to the beneficial effect of alkali-treated titanium to bioactivity and osteogenic activity, but few to the other biological effect. In this work, hierarchical micro/nanopore films were prepared on titanium surface by acid etching and alkali treatment and their biological effects on bacteria, cancer cells and mesenchymal stem cells were investigated. Gram-positive Staphylococcus aureus, Gram-negative Escherichia coli, and human cholangiocarcinoma cell line RBE were used to investigate whether alkali-treated titanium can influence behaviors of bacteria and cancer cells. Responses of bone marrow mesenchymal stem cells (BMMSCs) to alkali-treated titanium were also subsequently investigated. The alkali-treated titanium can potently reduce bacterial adhesion, inhibit RBE and BMMSCs proliferation, while can better promote BMMSCs osteogenesis and angiogenesis than acid-etched titanium. The bacteriostatic ability of the alkali-treated titanium is proposed to result from the joint effect of micro/nanotopography and local pH increase at bacterium/material interface due to the hydrolysis of alkali (earth) metal titanate salts. The inhibitory action of cell proliferation is thought to be the effect of local pH increase at cell/material interface which causes the alkalosis of cells. This alkalosis model reported in this work will help to understand the biologic behaviors of various cells on alkali-treated titanium surface and design the intended biomedical applications. Copyright © 2014 Elsevier Inc. All rights reserved.

  11. Hypercapnea and Acidemia despite Hyperventilation following Endotracheal Intubation in a Case of Unknown Severe Salicylate Poisoning

    Directory of Open Access Journals (Sweden)

    Shannon M. Fernando

    2017-01-01

    Full Text Available Salicylates are common substances for deliberate self-harm. Acute salicylate toxicity is classically associated with an initial respiratory alkalosis, followed by an anion gap metabolic acidosis. The respiratory alkalosis is achieved through hyperventilation, driven by direct stimulation on the respiratory centers in the medulla and considered as a compensatory mechanism to avoid acidemia. However, in later stages of severe salicylate toxicity, patients become increasingly obtunded, with subsequent loss of airway reflexes, and therefore intubation may be necessary. Mechanical ventilation has been recommended against in acute salicylate poisoning, as it is believed to take away the compensatory hyperpnea and tachypnea. Despite the intuitive physiological basis for this recommendation, there is a paucity of evidence to support it. We describe a case of a 59-year-old male presenting with decreased level of consciousness and no known history of ingestion. He was intubated and experienced profound hypercarbia and acidemia despite mechanical ventilation with high minute ventilation and tidal volumes. This case illustrates the deleterious effects of intubation in severe salicylate toxicity.

  12. [Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis].

    Science.gov (United States)

    Mata-Gómez, Javier; Guerrero-Domínguez, Rosana; García-Santigosa, Marta; Ontanilla, Antonio

    2015-01-01

    Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH normalization, cerebrospinal fluid can keep a state of metabolic alkalosis. This circumstance, in addition to the residual effect of neuromuscular blocking agents, inhalant anesthetics and opioids could increase the risk of postoperative apnea after a general anesthesia. We present the successful management in 3 neonates in those a pyloromyotomy was carried out because they had presented congenital hypertrophic pyloric stenosis. This procedure was done under general anesthesia with orotracheal intubation and rapid sequence induction. Then, ultrasound-guided paravertebral block was performed as analgesic method without the need for administrating opioids within intraoperative period and keeping an appropriate analgesic level. Local anesthesia has demonstrated to be safe and effective in pediatric practice. We consider the ultrasound-guided paravertebral block with one dose as a possible alternative for other local techniques described, avoiding the use of opioids and neuromuscular blocking agents during general anesthesia, and reducing the risk of central apnea within postoperative period. Copyright © 2014 Sociedade Brasileira de Anestesiologia. Publicado por Elsevier Editora Ltda. All rights reserved.

  13. Ultrasound-guided paravertebral block for pyloromyotomy in 3 neonates with congenital hypertrophic pyloric stenosis.

    Science.gov (United States)

    Mata-Gómez, Javier; Guerrero-Domínguez, Rosana; García-Santigosa, Marta; Ontanilla, Antonio

    2015-01-01

    Hypertrophic pyloric stenosis is a relatively common affection of gastrointestinal tract in childhood that results in symptoms, such as projectile vomiting and metabolic disorders that imply a high risk of aspiration during anesthetic induction. In this way, the carrying out of a technique with general anesthesia and intravenous rapid sequence induction, preoxygenation and cricoid pressure are recommended. After the correction of systemic metabolic alkalosis and pH normalization, cerebrospinal fluid can keep a state of metabolic alkalosis. This circumstance, in addition to the residual effect of neuromuscular blocking agents, inhalant anesthetics and opioids could increase the risk of postoperative apnea after a general anesthesia. We present the successful management in 3 neonates in those a pyloromyotomy was carried out because they had presented congenital hypertrophic pyloric stenosis. This procedure was done under general anesthesia with orotracheal intubation and rapid sequence induction. Then, ultrasound-guided paravertebral block was performed as analgesic method without the need for administrating opioids within intraoperative period and keeping an appropriate analgesic level. Local anesthesia has demonstrated to be safe and effective in pediatric practice. We consider the ultrasound-guided paravertebral block with one dose as a possible alternative for other local techniques described, avoiding the use of opioids and neuromuscular blocking agents during general anesthesia, and reducing the risk of central apnea within postoperative period. Copyright © 2014 Sociedade Brasileira de Anestesiologia. Published by Elsevier Editora Ltda. All rights reserved.

  14. Clinical observations and acid-base imbalances in sheep during chronic copper poisoningAvaliação clínica e hemogasométrica de ovinos com intoxicação cúprica acumulativa

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    Clara Satsuk Mori

    2011-08-01

    Full Text Available Twelve male sheep were intoxicated with copper and four served as controls. When hemoglobinuria was first diagnosed, the poisoned sheep were randomly distributed into two groups: 4 untreated and 8 tetratiomolybdate-treated. Blood samples and clinical evaluation were performed daily, from the onset of poisoning until the 30th day. Analysis of packed cell volume, plasma free hemoglobin, and blood gas were made. Elevated heart rates and rectal temperature, and reduced respiratory and ruminal movement rates were recorded in the intoxicated group. The poisoned sheep developed mild alkalosis caused by bicarbonate retention, while a short-periodic increase of pCO2 occurred to compensate the ongoing alkalosis. Elevated degree of anemia was directly proportional to heart rate, while high degree of alkalosis was inversely proportional to respiratory rate. Further, there was an elevated positive relationship between plasma free hemoglobin and rectal temperature, and an increase in rectal temperature accompanied a reduced ruminal movement.Foram utilizados 16 cordeiros, sendo 12 submetidos à intoxicação cúprica e quatro animais controle. Quando foi verificada a presença de hemoglobinúria, os animais intoxicados foram aleatoriamente distribuídos em dois grupos, quatro animais não tratados e oito animais tratados com tetratiomolybidato de amônia. Foi realizado exame clínico e coleta de sangue diariamente desde o início da intoxicação até 30 dias após. Foram analisados o volume globular, concentração de hemoglobina plasmática e avaliação hemogasométrica. Nos animais intoxicados, foi observado elevação da freqüência cardíaca e da temperatura retal e redução da freqüência respiratória e dos movimentos ruminais. Os ovinos intoxicados desenvolveram alcalose moderada causada por retenção de bicarbonato seguido de um aumento pontual da pCO2 para compensar a alcalose em curso. Quanto maior o grau de anemia foi maior a freqüência card

  15. Effect of Acetazolamide vs Placebo on Duration of Invasive Mechanical Ventilation Among Patients With Chronic Obstructive Pulmonary Disease: A Randomized Clinical Trial.

    Science.gov (United States)

    Faisy, Christophe; Meziani, Ferhat; Planquette, Benjamin; Clavel, Marc; Gacouin, Arnaud; Bornstain, Caroline; Schneider, Francis; Duguet, Alexandre; Gibot, Sébastien; Lerolle, Nicolas; Ricard, Jean-Damien; Sanchez, Olivier; Djibre, Michel; Ricome, Jean-Louis; Rabbat, Antoine; Heming, Nicholas; Urien, Saïk; Esvan, Maxime; Katsahian, Sandrine

    2016-02-02

    Acetazolamide has been used for decades as a respiratory stimulant for patients with chronic obstructive pulmonary disease (COPD) and metabolic alkalosis, but no large randomized placebo-controlled trial is available to confirm this approach. To determine whether acetazolamide reduces mechanical ventilation duration in critically ill patients with COPD and metabolic alkalosis. The DIABOLO study, a randomized, double-blind, multicenter trial, was conducted from October 2011 through July 2014 in 15 intensive care units (ICUs) in France. A total of 382 patients with COPD who were expected to receive mechanical ventilation for more 24 hours were randomized to the acetazolamide or placebo group and 380 were included in an intention-to treat analysis. Acetazolamide (500-1000 mg, twice daily) vs placebo administered intravenously in cases of pure or mixed metabolic alkalosis, initiated within 48 hours of ICU admission and continued during the ICU stay for a maximum of 28 days. The primary outcome was the duration of invasive mechanical ventilation via endotracheal intubation or tracheotomy. Secondary outcomes included changes in arterial blood gas and respiratory parameters, weaning duration, adverse events, use of noninvasive ventilation after extubation, successful weaning, the duration of ICU stay, and in-ICU mortality. Among 382 randomized patients, 380 (mean age, 69 years; 272 men [71.6%]; 379 [99.7%] with endotracheal intubation) completed the study. For the acetazolamide group (n = 187), compared with the placebo group (n = 193), no significant between-group differences were found for median duration of mechanical ventilation (-16.0 hours; 95% CI, -36.5 to 4.0 hours; P = .17), duration of weaning off mechanical ventilation (-0.9 hours; 95% CI, -4.3 to 1.3 hours; P = .36), daily changes of minute-ventilation (-0.0 L/min; 95% CI, -0.2 to 0.2 L/min; P = .72), or partial carbon-dioxide pressure in arterial blood (-0.3 mm Hg; 95% CI, -0.8 to 0.2 mm

  16. [Meeting point Stewart. Buffer bases, base excess and strong ions].

    Science.gov (United States)

    Lang, W

    2007-04-01

    Development of a two-buffer model which simulates the acid-base properties of blood and allows comparison of the different acidbase concepts according to Stewart and to Siggaard-Andersen. The two-buffer model consisted of different aqueous solutions of bicarbonate/CO(2) (pCO(2), sCO(2), pK(1)), HEPES buffer (A(tot), pK(a)) and electrolytes. These were used to calculate the pH from the independent variables according to Stewart - strong ion difference (SID), pCO(2) and total concentration of the weak acids (A(tot)) - from which all other dependent variables (cHCO(3)(-), cA(-), BB, BE) were obtained and compared with the measured values. The normal pH (7.408) was calculated from the normal values for SID (48 mmol/l), pCO(2) (40 mmHg) and A(tot) (45.2 mmol/l) and agreed perfectly with the measured value (7.409+/-0.001). This was also valid for all calculated and measured pH values when the SID was varied: non-respiratory alkalosis ( upward arrow) or acidosis ( downward arrow), pCO(2):respiratory acidosis ( upward arrow) or alkalosis ( downward arrow) and A(tot):hyperproteinemic acidosis ( upward arrow) or hypoproteinemic alkalosis ( downward arrow) were varied and the sum of the buffer bases (BB) was always equal to the SID. All changes and hence BE were also equal, providing that A(tot) was normal. This was not the case, however, if A(tot) was outside the normal range, when BE was then the difference from the normal BB at the respective reference point. Whereas the deviation of the measured pCO(2) was acceptable (1.74+/-0.86 mmHg), this was not the case for the SID (-6.18+/-3.58 mmol/l) calculated from the measured ion concentrations (Na, K, Ca, Cl). Despite controversial discussions, both concepts are much closer than might be expected. Whereas in the Stewart approach the focus of analysis is on plasma, with the Siggaard-Andersen approach it is on blood. Hence, a combined analysis of the blood gases (pH, pCO(2), pO(2), sO(2), cHb, BE) and of the strong ion gap (SIG

  17. Effect of hypoxaemia on water and sodium homeostatic hormones and renal function

    DEFF Research Database (Denmark)

    Olsen, Niels Vidiendal

    1995-01-01

    , a hypoxic ventilatory response produces hypocapnia and respiratory alkalosis. Acute hypoxaemia depresses aldosterone secretion secondary to a direct effect on adrenal cells. Also plasma renin is decreased in resting hypoxaemic conditions, but the mechanism remains unknown. These hormonal changes may have...... decreases during hypercapnic hypoxaemia. Renal clearance studies in humans after 24-48 hours in altitude hypoxia (4,350 m) demonstrate that glomerular and tubular function is only slightly changed in spite of marked depression of the renin-aldosterone system and increased plasma levels of norepinephrine...... and bicarbonate in the proximal tubules secondary to the associated hyperventilation and hypocapnia. After 6 hours, sodium and water excretion is normalized or even depressed, dependent on the severity of acute mountain sickness. In view of the prompt increase in sodium and water excretion found during short...

  18. A Case Report of Multiple Endocrine Neoplasia Type IIa Associated with Cushing Syndrome

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    Sh. Borzouei

    2013-10-01

    Full Text Available Introduction: Multiple endocrine neoplasia type IIa (MEN IIa is an autosomal dominant syn-drome characterized bypheochromocytoma ,medullary thyroid carcinoma and hyperparathy-roidism. Pheochromocytoma approximately occurs in 50% of patients with MEN IIa. This tumor has the capacity to produce ACTH ectopically and becomes manifest like Cushing syndrome,although it is very rare. Case Report: We report a 26-year-old woman patient with severe muscle weakness, skin le-sions in extremity, hypertension, new onset diabetes and in the laboratory data hypokalemia, metabolic alkalosis, high serum level of cortisol, metanephrine, normetanephrine, calcitonin and bilateral adrenal mass in computed tomography as the first clinical manifestations of an ACTH-secreting pheochromocytoma. Conclusion: In the patients with hypertension, new onset diabetes and hypokalemia Cushing syndrome and pheochromocytoma should always be ruled out. (Sci J Hamadan Univ Med Sci 2013; 20 (3:260-265

  19. A Case of Paraneoplastic Cushing Syndrome Presenting as Hyperglycemic Hyperosmolar Nonketotic Syndrome

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    Christina E. Brzezniak

    2017-04-01

    Full Text Available Carcinoid tumors are neuroendocrine tumors that mainly arise in the gastrointestinal tract, lungs, and bronchi. Bronchopulmonary carcinoids have been associated with Cushing syndrome, which results from ectopic adrenocorticotrophic hormone (ACTH secretion. We report the case of a 65-year-old man, a colonel in the US Air Force, with metastatic bronchopulmonary carcinoid tumors treated on a clinical trial who was hospitalized for complaints of increasing thirst, polydipsia, polyuria, weakness, and visual changes. Decompensated hyperglycemia suggested a diagnosis of hyperglycemic hyperosmolar nonketotic syndrome (HHNS. Additional findings, which included hypokalemia, hypernatremia, hypertension, metabolic alkalosis, moon facies, and striae, raised a red flag for an ectopic ACTH syndrome. Elevated ACTH levels confirmed Cushing syndrome. Treatment with a fluid replacement and insulin drip resulted in immediate symptomatic improvement. Cushing syndrome should be considered in carcinoid patients with physical stigmata such as moon facies and striae. HHNS may be the presenting clinical feature in patients with impaired glucose metabolism.

  20. Sporadic hypothyroidism-related hypokalemic paralysis: Diagnosis in a resource-poor setting

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    Nadasha Kadeeja

    2017-01-01

    Full Text Available Hypothyroidism and distal renal tubular acidosis causing hypokalemic paralysis (HP have been described only in four female patients. HP as the initial manifestation of uncomplicated diabetes has been reported only in three young males. We report two middle-aged patients presenting with gradual-onset areflexic quadriparesis and neck flop, associated with urinary potassium losses, and recovering over 3 days. The male patient with alcohol abuse had urine pH >5.5 and hyperchloremic metabolic acidosis due to renal tubular acidosis and hypothyroidism. The second, a hypertensive female, had metabolic alkalosis, hypomagnesemia, and diabetes mellitus diagnosed at admission. Both these patients improved with intravenous and oral potassium supplementation.

  1. Rare presentation of pancreatitis secondary to intussusception of duodenal duplication cyst, a pediatric case report

    Directory of Open Access Journals (Sweden)

    Valentina Shakhnovich

    2014-12-01

    Full Text Available Duodenal duplication cysts are rare congenital malformations of which there is limited literature in the pediatric population. The most common presentation in symptomatic patients is abdominal pain and pancreatitis. We present a case of a 14 year old female that presented with emesis, abdominal pain, weight loss, and admission biochemical profile concerning for acute pancreatitis in conjunction with severe hypochloremic, hypokalemic metabolic alkalosis. Further imaging was highly suggestive of duodeno-duodenal intussusception causing obstruction of the pancreatic duct. Patient was taken emergently to the operating room for exploration. Patient underwent laparoscopic assisted reduction of intussusception and resection of duodenal duplication cyst. Patient tolerated the surgery well, and was able to be discharged home in stable condition soon after. There have been no cases reported in the literature that describe pancreatitis secondary to intussusception of duodenal duplication cyst. When diagnosed early, these patients can be safely managed laparoscopically even in emergent settings.

  2. Inherited renal tubular defects with hypokalemia

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    Muthukrishnan J

    2009-01-01

    Full Text Available Bartter′s and Gitelman′s syndrome are two ends of a spectrum of inherited renal tubular disorders that present with hypokalemic metabolic alkalosis of varying severity. Clinical features and associated calcium and magnesium ion abnormalities are used to diagnose these cases after excluding other commoner causes. We report on two cases, the first being a young boy, born of pregnancy complicated by polyhydramnios, who had classical dysmorphic features, polyuria, hypokalemia and hypercalciuria and was diagnosed as having Bartter′s syndrome. The second patient is a lady who had recurrent tetany as the only manifestation of Gitelman′s syndrome, which is an unusual presentation. Potassium replacement with supplementation of other deficient ions led to satisfactory clinical and biochemical response.

  3. Case Report: Cervical chondrocalcinosis as a complication of Gitelman syndrome [version 1; referees: 2 approved

    Directory of Open Access Journals (Sweden)

    Zahra Iqbal

    2016-05-01

    Full Text Available Gitelman syndrome is an inherited tubulopathy leading to a hypokalaemic metabolic alkalosis with hypomagnesaemia and hypocalciuria. Most cases are due to mutations in SLC12A3, encoding the apical thiazide sensitive co-transporter in the distal convoluted tubule. Musculoskeletal effects of Gitelman syndrome are common, including muscle weakness, tetany and cramps. Chronic hypomagnesaemia can lead to chondrocalcinosis, which often affects knees but can affect other joints. Here we present a case of Gitelman syndrome complicated by cervical chondrocalcinosis leading to neck pain and numbness of the fingers. Treatments directed at correcting both hypokalaemia and hypomagnesaemia were initiated and allowed conservative non-surgical management of the neck pain. Recognition of chondrocalcinosis is important and treatments must be individualised to correct the underlying hypomagnesaemia.

  4. An interesting case of primary hypoparathyroidism

    Directory of Open Access Journals (Sweden)

    D A Kirpalani

    2014-01-01

    Full Text Available Primary hypoparathyroidism can occur due to an activating mutation of calcium sensing receptor (CaSR. Most patients remain asymptomatic and therefore not diagnosed until adulthood. We present a 38-year-old lady who had a history of muscle cramps since 8 years. She presented with vomiting, abdomen pain and body ache, showed clinical evidence of hypovolemia, severe hypocalcemia, hypokalemia, hypomagnesemia, hyperphosphatemia and metabolic alkalosis. Her 24 h urinary phosphorus was low and 24 h urinary excretion of sodium, potassium and chloride were high. Her intact parathormone was on the lower side of the normal range. She improved once we had corrected her biochemical abnormalities. By excluding acquired causes of hypoparathyroidism, we are able to conclude that this may be a case of primary hypoparathyroidism due to activating mutation of CaSR.

  5. Nephropathic Cystinosis Mimicking Bartter Syndrome: a Novel Mutation.

    Science.gov (United States)

    Bastug, Funda; Nalcacioglu, Hulya; Ozaltin, Fatih; Korkmaz, Emine; Yel, Sibel

    2018-01-01

    Cystinosis is a rare autosomal recessive disorder resulting from defective lysosomal transport of cystine due to mutations in the cystinosin lysosomal cystine transporter (CTNS) gene. The clinical phenotype of nephropathic cystinosis is characterized by renal tubular Fanconi syndrome and development of end-stage renal disease during the first decade. Although metabolic acidosis is the classically prominent finding of the disease, a few cases may present with hypokalemic metabolic alkalosis mimicking Bartter syndrome. Bartter-like presentation may lead to delay in diagnosis and initiation of specific treatment for cystinosis. We report a case of a 6-year-old girl initially presenting with the features of Bartter syndrome that was diagnosed 2 years later with nephropathic cystinosis and a novel CTNS mutation.

  6. Hypercholermic metabolic alcalsosis as a presentation of cystic fibrosis: presentation of two cases = Alcalosis metabólica hipoclorémica como presentación de la fibrosis quística. Informe de dos casos

    Directory of Open Access Journals (Sweden)

    Olga Lucía Morales Múnera

    2013-07-01

    Full Text Available Introduction: We describe two cases of patients with hyperchloremic metabolic acidosis as an initial presentation of cystic fibrosis (CF or as part of a second CF exacerbation. Clinical Cases: Two patients, 6 and 9 months old, consulted for cough, fever, and dyspnea. The first had syndrome of recurrent bronchial obstruction, without a diagnosis of CF on admission. Both presented with difficulty breathing, dehydration, and malnutrition. Arterial blood gases showed metabolic acidosis, hypokalemia, and severe hypochloremia. Treatment with sodium chloride and potassium improved their electrolyte balance and acid-base status. They did not present with renal or gastrointestinal losses of chloride. CF and pseudo-Barter’s Syndrome were diagnosed. Conclusion: Metabolic alkalosis can present as an initial manifestation of CF in infants with recurrent bronchiolitis and short stature suspected of having CF: equally it can be an acute exacerbation in patients with known CF. Your recognition and treatment are an opportunity to decrease morbidity.

  7. The Effects in the Rat of Varying Intakes of Dietary Calcium, Phosphorus, and Hydrogen Ion on Hyperparathyroidism Due to Chronic Renal Failure

    Science.gov (United States)

    Kaye, Michael

    1974-01-01

    Renal failure of 4 wk duration in rats led to parathyroid enlargement, increased bone resorption, and decreased tubular reabsorption of phosphate by the remnant kidney. The degree of hyperparathyroidism was influenced by each of the three dietary factors investigated. In the first study increasing calcium intake reduced the size of the parathyroids by increasing calcium and reducing phosphate absorption. In the second study phosphate intake was linearly related to parathyroid gland size in the uremic animals and associated with rising plasma phosphate levels. In the last study acidosis led directly to increased bone resorption but small parathyroid glands associated with elevated ionized calcium levels. Alkalosis lowered the serum ionized calcium and led to parathyroid enlargement and the expected associated findings. It was shown that parathyroid weight reflected both metabolic activity as judged by amino acid uptake, and the content of immunoassayable parathyroid hormone. In all studies gland weight was inversely related to serum ionized calcium. PMID:4808640

  8. Amitraz poisoning: case report

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    Jaime Alexander Molina-Bolaños

    2017-10-01

    Full Text Available Amitraz is an insecticide compound used worldwide for controlling pests, especially in agricultural and livestock areas. However, amitraz poisoning in Colombia is rare. This article reports the case of an 18-year-old female patient who was admitted in the emergency service 3 hours after the intake of an unknown amount of Triatox® (amitraz. The patient presented with a depressed level of consciousness, respiratory distress, hypotension, bradycardia, myosis and metabolic acidosis compensated with respiratory alkalosis. Initial treatment was provided using life support measures in the emergency ward, and subsequent transfer and support in the intensive care unit. She was discharged 24 hours after admission. This case considers the clinical similarity between amitraz poisoning and poisoning caused by other more frequent toxic compounds such as carbamates, organophosphates and opioids, which require different management.

  9. Maintaining K+ balance on the low-Na+, high-K+ diet

    Science.gov (United States)

    Cornelius, Ryan J.; Wang, Bangchen; Wang-France, Jun

    2016-01-01

    A low-Na+, high-K+ diet (LNaHK) is considered a healthier alternative to the “Western” high-Na+ diet. Because the mechanism for K+ secretion involves Na+ reabsorptive exchange for secreted K+ in the distal nephron, it is not understood how K+ is eliminated with such low Na+ intake. Animals on a LNaHK diet produce an alkaline load, high urinary flows, and markedly elevated plasma ANG II and aldosterone levels to maintain their K+ balance. Recent studies have revealed a potential mechanism involving the actions of alkalosis, urinary flow, elevated ANG II, and aldosterone on two types of K+ channels, renal outer medullary K+ and large-conductance K+ channels, located in principal and intercalated cells. Here, we review these recent advances. PMID:26739887

  10. Opiate Withdrawal Complicated by Tetany and Cardiac Arrest

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    Irfanali R. Kugasia

    2014-01-01

    Full Text Available Patients with symptoms of opiate withdrawal, after the administration of opiate antagonist by paramedics, are a common presentation in the emergency department of hospitals. Though most of opiate withdrawal symptoms are benign, rarely they can become life threatening. This case highlights how a benign opiate withdrawal symptom of hyperventilation led to severe respiratory alkalosis that degenerated into tetany and cardiac arrest. Though this patient was successfully resuscitated, it is imperative that severe withdrawal symptoms are timely identified and immediate steps are taken to prevent catastrophes. An easier way to reverse the severe opiate withdrawal symptom would be with either low dose methadone or partial opiate agonists like buprenorphine. However, if severe acid-base disorder is identified, it would be safer to electively intubate these patients for better control of their respiratory and acid-base status.

  11. Persistent severe hypokalemia: Gitelman syndrome and differential diagnosis

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    Christine Zomer Dal Molin

    Full Text Available Abstract The main causes of hypokalemia are usually evident in the clinical history of patients, with previous episodes of vomiting, diarrhea or diuretic use. However, in some patients the cause of hypokalemia can become a challenge. In such cases, two major components of the investigation must be performed: assessment of urinary excretion potassium and the acid-base status. This article presents a case report of a patient with severe persistent hypokalemia, complementary laboratory tests indicated that's it was hypomagnesaemia and hypocalciuria associated with metabolic alkalosis, and increase of thyroid hormones. Thyrotoxic periodic paralysis was included in the differential diagnosis, but evolved into euthyroid state, persisting with severe hypokalemia, which led to be diagnosed as Gitelman syndrome.

  12. A Basic Therapy Gone Awry.

    Science.gov (United States)

    Galinko, Laura B; Hsu, Steven H; Gauran, Cosmin; Fingerhood, Michael L; Pastores, Stephen M; Halpern, Neil A; Chawla, Sanjay

    2017-11-01

    Baking soda (sodium bicarbonate) is a common household item that has gained popularity as an alternative cancer treatment. Some have speculated that alkali therapy neutralizes the extracellular acidity of tumor cells that promotes metastases. Internet blogs have touted alkali as a safe and natural alternative to chemotherapy that targets cancer cells without systemic effects. Sodium bicarbonate overdose is uncommon, with few reports of toxic effects in humans. The case described here is the first reported case of severe metabolic alkalosis related to topical use of sodium bicarbonate as a treatment for cancer. This case highlights how a seemingly benign and readily available product can have potentially lethal consequences. ©2017 American Association of Critical-Care Nurses.

  13. Acute toxicity from baking soda ingestion.

    Science.gov (United States)

    Thomas, S H; Stone, C K

    1994-01-01

    Sodium bicarbonate is an extremely well-known agent that historically has been used for a variety of medical conditions. Despite the widespread use of oral bicarbonate, little documented toxicity has occurred, and the emergency medicine literature contains no reports of toxicity caused by the ingestion of baking soda. Risks of acute and chronic oral bicarbonate ingestion include metabolic alkalosis, hypernatremia, hypertension, gastric rupture, hyporeninemia, hypokalemia, hypochloremia, intravascular volume depletion, and urinary alkalinization. Abrupt cessation of chronic excessive bicarbonate ingestion may result in hyperkalemia, hypoaldosteronism, volume contraction, and disruption of calcium and phosphorus metabolism. The case of a patient with three hospital admissions in 4 months, all the result of excessive oral intake of bicarbonate for symptomatic relief of dyspepsia is reported. Evaluation and treatment of patients with acute bicarbonate ingestion is discussed.

  14. Forty years abuse of baking soda, rhabdomyolysis, glomerulonephritis, hypertension leading to renal failure: a case report.

    Science.gov (United States)

    Forslund, Terje; Koistinen, Arvo; Anttinen, Jorma; Wagner, Bodo; Miettinen, Marja

    2008-01-01

    We present a patient who had ingested sodium bicarbonate for treatment of alcoholic dyspepsia during forty years at increasing doses. During the last year he had used more than 50 grams daily. He presented with metabolic alkalosis, epileptic convulsions, subdural hematoma, hypertension and rhabdomyolysis with end stage renal failure, for which he had to be given regular intermittent hemodialysis treatment. Untreated hypertension and glomerulonephritis was probably present prior to all these acute incidents. Examination of the kidney biopsy revealed mesangial proliferative glomerulonephritis and arterial wall thickening causing nephrosclerosis together with interstitial calcinosis. The combination of all these pathologic changes might be responsible for the development of progressive chronic renal failure ending up with the need for continuous intermittent hemodialysis treatment.

  15. A Case of Hyperemesis Gravidarum due to Gastric Cancer Masquerading as Preeclampsia

    Directory of Open Access Journals (Sweden)

    Daniel R. Hersh

    2011-12-01

    Full Text Available Nausea and vomiting are symptoms frequently seen in normal pregnancy. We report a patient with gastric carcinoma who presented with severe hyperemesis gravidarum that led to extreme volume depletion, hypertension, proteinuria, and acute renal failure. A 35-year-old woman (para 2-1-0-1 with a prenatal course significant for persistent nausea, vomiting, and poor weight gain presented at 36 weeks' gestation with elevated blood pressure (157/114 mm Hg, proteinuria (4+, hypochloremic metabolic alkalosis, and severe intravascular volume contraction. A presumptive diagnosis of severe preeclampsia was made, the patient was given intravenous MgSO4, and cesarean delivery was accomplished uneventfully. When significant emesis persisted in the postoperative period, esophagogastroduodenoscopy revealed an antral/prepyloric mass with a biopsy-proven poorly differentiated adenocarcinoma. To our knowledge, this is the first report of a case of hyperemesis gravidarum with gastric cancer masquerading as preeclampsia.

  16. Gitelman's syndrome in pregnancy: case report and review of the literature.

    LENUS (Irish Health Repository)

    McCarthy, Fergus P

    2012-01-31

    Gitelman\\'s syndrome (GS), a rare renal disorder, results in hypokalaemia, hypomagnesaemia, hypocalciuria and a metabolic alkalosis. It is unclear if an alteration in management is necessary or beneficial during pregnancy. A 32-year-old woman with GS was managed in her second pregnancy. Antenatally, the patient required 39 (principally day case) admissions to the hospital for intravenous (IV) therapy and received a cumulative total of 47 l of IV 0.9% saline solution, 47 doses of 20 mmol magnesium chloride and 46 doses of 80 mmol potassium chloride. She delivered a 2940-g female infant in excellent condition by caesarean section. We would suggest that close attention to maternal weight gain during pregnancy is an easily available clinical tool to assess adequacy of fluid and electrolyte repletion in this condition.

  17. Bilateral acute lupus pneumonitis in a case of rhupus syndrome

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    Supriya Sarkar

    2012-01-01

    Full Text Available Rhupus syndrome, the overlap of rheumatoid arthritis (RA and systemic lupus erythematosus (SLE, is an extremely uncommon condition. Organ damages found due to SLE are usually mild in rhupus. Lupus pneumonitis in rhupus syndrome has not been reported worldwide. We are reporting a 23-year-old female with bilateral symmetric erosive arthritis, oral ulcer, alopecia, polyserositis, anemia, leucopenia, positive RA-factor, anti nuclear antibody (ANA and anti ds-DNA. She presented with acute onset dyspnea, high fever, chest pain, tachycardia, tachypnea, hypoxia and respiratory alkalosis. High resolution computed tomography (HRCT-thorax showed bilateral, basal consolidation with air bronchogram. Repeated sputum and single broncho alveolar lavage (BAL fluid examination revealed no organism or Hemosiderin-laden macrophage. The diagnosis of rhupus was confirmed by combined manifestations of RA and SLE, and the diagnosis of acute lupus pneumonitis was established by clinico-radiological picture and by excluding other possibilities.

  18. Quantified pH imaging with hyperpolarized 13C‐bicarbonate

    DEFF Research Database (Denmark)

    Scholz, David Johannes; Janich, Martin A.; Köllisch, Ulrich

    2015-01-01

    for various flip angles for bicarbonate (BiC) and CO2 with spectral‐spatial excitation and spiral readout in healthy Lewis rats in five slices. Acute subcutaneous sterile inflammation was induced with Concanavalin A in the right leg of Buffalo rats. pH and proton images were measured 2 h after induction....... After optimizing the signal to noise ratio of the hyperpolarized 13C‐bicarbonate, error estimation of the spectral‐spatial excited spectrum reveals that the method covers the biologically relevant pH range of 6 to 8 with low pH error (... of the residual bicarbonate signal. pH maps reflect the induction of acute metabolic alkalosis. Inflamed, infected regions exhibit lower pH. Hyperpolarized 13C‐bicarbonate pH mapping was shown to be sensitive in the biologically relevant pH range. The mapping of pH was applied to healthy in vivo organs...

  19. in Critically Ill Patients: Success and Limits

    Directory of Open Access Journals (Sweden)

    Filippo Mariano

    2011-01-01

    Full Text Available Citrate anticoagulation has risen in interest so it is now a real alternative to heparin in the ICUs practice. Citrate provides a regional anticoagulation virtually restricted to extracorporeal circuit, where it acts by chelating ionized calcium. This issue is particularly true in patients ongoing CRRT, when the “continuous” systemic anticoagulation treatment is per se a relevant risk of bleeding. When compared with heparin most of studies with citrate reported a longer circuit survival, a lower rate of bleeding complications, and transfused packed red cell requirements. As anticoagulant for CRRT, the infusion of citrate is prolonged and it could potentially have some adverse effects. When citrate is metabolized to bicarbonate, metabolic alkalosis may occur, or for impaired metabolism citrate accumulation leads to acidosis. However, large studies with dedicated machines have indeed demonstrated that citrate anticoagulation is well tolerated, safe, and an easy to handle even in septic shock critically ill patients.

  20. Technetium-99m methoxyisobutylisonitrile localizes an ectopic ACTH-producing tumour: case report and review of the literature

    Energy Technology Data Exchange (ETDEWEB)

    Jacobsson, H. (Dept. of Diagnostic Radiology, Karolinska Hospital, Stockholm (Sweden)); Wallin, G. (Dept. of Surgery, Karolinska Hospital, Stockholm (Sweden)); Werner, S. (Dept. of Endocrinology and Diabetology, Karolinska Hospital, Stockholm (Sweden)); Larsson, S.A. (Dept. of Hospital Physics, Karolinska Hospital, Stockholm (Sweden))

    1994-06-01

    Extensive investigation including whole-body examinations with computed tomography and magnetic resonance imaging did not detect the suspected ectopic ACTH-producing tumour in a patient with advanced Cushing's syndrome and hypokalemic alkalosis. Gamma camera examination with technetium-99m methoxyisobutylisonitrile (MIBI) depicted the tumour, which was localized in the anterior neck and mediastinum. This was later verified by surgery. [sup 99m]Tc-MIBI is normally used for myocardial scintigraphy. Its accumulation is unspecific and merely reflects metabolic activity. Despite this, the present case shows that examination with this agent can provide important information with regard to tumour localization in a given situation, thereby serving as a complement to other imaging modalities. The current literature on [sup 99m]Tc-MIBI for tumour diagnosis is reviewed. (orig.)

  1. Catalytically and noncatalytically treated automobile exhaust: biological effects in rats

    Energy Technology Data Exchange (ETDEWEB)

    Cooper, G.P. (Univ. of Cincinnati); Lewkowski, J.P.; Hastings, L.; Malanchuk, M.

    1977-12-01

    Chronic exposure to catalytically treated or noncatalytically treated automobile exhaust significantly depressed the spontaneous locomotor activity (SLA) of rats. Exposure to H/sub 2/SO/sub 4/ alone or CO at comparable levels did not alter the SLA. Exposure to noncatalytically treated exhaust resulted in significant reductions in growth rate and food and water intake. However, these effects were not evident in the exposure to catalytically treated exhaust or in the control H/sub 2/SO/sub 4/ and CO exposures. Blood acid-base analyses indicated that exposure to either catalytically treated exhaust or H/sub 2/SO/sub 4/ elicits a metabolic alkalosis, while exposure to CO alone results in a metabolic acidosis. All acid-base parameters were within the normal range several weeks after the termination of exposure.

  2. Infantile variant of Bartter syndrome and sensorineural deafness: A new autosomal recessive disorder

    Energy Technology Data Exchange (ETDEWEB)

    Landau, D.; Shalev, H.; Carmi, Rivka; Ohaly, M. [Univ. of the Negev, Ashkelon (Israel)

    1995-12-04

    The infantile variant of Bartter syndrome (IBS) is usually associated with maternal polyhydramnios, premature birth, postnatal polyuria and hypokalemic hypochloremic metabolic alkalosis and a typical appearance. IBS is thought to be an autosomal recessive trait. Several congenital tubular defects are associated with sensorineural deafness (SND). However, an association between the IBS and SND has not been reported so far. Here we describe 5 children of an extended consanguineous Bedouin family with IBS and SND. In 3 of the cases, the typical electrolyte imbalance and facial appearance were detected neonatally. SND was detected as early as age 1 month, suggesting either coincidental homozygotization of 2 recessive genes or a pleiotropic effect of one autosomal recessive gene. This association suggests that evaluation of SND is warranted in every case of IBS. 35 refs., 2 figs., 2 tabs.

  3. Colorectal injury by compressed air--a report of 2 cases.

    Science.gov (United States)

    Suh, H. H.; Kim, Y. J.; Kim, S. K.

    1996-01-01

    We report two colorectal trauma patients whose rectosigmoid region was ruptured due to a jet of compressed air directed to their anus while they were playing practical jokes with their colleagues in their place of work. It was difficult to diagnose in one patient due to vague symptoms and signs and due to being stunned by a stroke of the compressed air. Both patients suffered from abdominal pain and distension, tension pneumoperitoneum and mild respiratory alkalosis. One patient was treated with primary two layer closure, and the other with primary two layer closure and sigmoid loop colostomy. Anorectal manometry and transanal ultrasonography checked 4 weeks after surgery, revealed normal anorectal function and anatomy. The postoperative courses were favorable without any wound infection or intraabdominal sepsis. PMID:8835767

  4. A new mutation in the gene encoding mitochondrial seryl-tRNA synthetase as a cause of HUPRA syndrome.

    Science.gov (United States)

    Rivera, Henry; Martín-Hernández, Elena; Delmiro, Aitor; García-Silva, María Teresa; Quijada-Fraile, Pilar; Muley, Rafael; Arenas, Joaquín; Martín, Miguel A; Martínez-Azorín, Francisco

    2013-09-13

    HUPRA syndrome is a rare mitochondrial disease characterized by hyperuricemia, pulmonary hypertension, renal failure in infancy and alkalosis. This syndrome was previously described in three patients with a homozygous mutation c.1169A > G (p.D390G) in SARS2, encoding the mitochondrial seryl-tRNA synthetase. Here we report the clinical and genetic findings in a girl and her brother. Both patients were clinically diagnosed with the HUPRA syndrome. Analysis of the pedigree identified a new homozygous mutation c.1205G > A (p.R402H) in SARS2 gene. This mutation is very rare in the population and it is located at the C-terminal globular domain of the homodimeric enzyme very close to p.D390G. Several data support that p.R402H mutation in SARS2 is a new cause of HUPRA syndrome.

  5. Mineralocorticoid hypertension: clinical and laboratory studies with special reference to selective percutaneous venography combined with aldosterone assay in the adrenal venous blood

    International Nuclear Information System (INIS)

    Wajchenberg, B.L.; Liberman, B.; Novaes, M.

    1977-01-01

    With the purpose of demonstrating the presence of hypertension, hypokalemia and alkalosis were studied. The presence of daily aldosteronism was verified in five patients; the sixth one presented no daily aldosteronism but an increase of 18-OH-DOCA production, an ACTH dependente mineralocorticoid. The presence of tumor (less than 0.9cm) could not be shown in two patients by bilateral selective adrenal venography. The aldosterone assay during catherization of adrenal vein of those patients permitted to determine the tumoral side. Attention must be given to the fact that the blood collection of adrenal vein must always be made during adrenal venography to demonstrate the presence of short unilateral tumor or bilateral disease [pt

  6. Clinical acid-base pathophysiology: disorders of plasma anion gap.

    Science.gov (United States)

    Moe, Orson W; Fuster, Daniel

    2003-12-01

    The plasma anion gap is a frequently used parameter in the clinical diagnosis of a variety of conditions. The commonest application of the anion gap is to classify cases of metabolic acidosis into those that do and those that do not leave unmeasured anions in the plasma. While this algorithm is useful in streamlining the diagnostic process, it should not be used solely in this fashion. The anion gap measures the difference between the unmeasured anions and unmeasured cations and thus conveys much more information to the clinician than just quantifying anions of strong acids. In this chapter, the significance of the anion gap is emphasized and several examples are given to illustrate a more analytic approach to using the clinical anion gap; these include disorders of low anion gap, respiratory alkalosis and pyroglutamic acidosis.

  7. Pseudo-Bartter’s syndrome in patients with cystic fibrosis: A case series and review of the literature

    Directory of Open Access Journals (Sweden)

    Vilotijević-Dautović Gordana

    2015-01-01

    Full Text Available Introduction. Pseudo-Bartter syndrome (PBS is characterized by hyponatremic, hypochloremic metabolic alkalosis that mimics Bartter syndrome but with no pathology in the renal tubules. We present five patients with cystic fibrosis (CF and PBS. Cases Outline. Four children aged between three and five-and-one-half months with previously diagnosed CF and one aged 17 months with previously undiagnosed disease, were hospitalized during the summer season, with severe dehydration, oliguria, apathy and adynamia. Additionally, one of them had an ileostomy due to meconium ileus after birth. All children were on a diet without additional salt intake. Laboratory analysis on admission showed hyponatremia (115-133 mmol/L, mean 122.4 mmol/L, high plasma renin activity (229-500 pg/ml, mean 324 pg/ml and metabolic alkalosis (pH 7.5-7.6, mean 7.56 in all the patients, and in four of them high blood level of aldosterone (74-560 pg/ml, mean 295.9 pg/ml, hypokalemia (2.3-2.8 mmol/L, mean 2.6 mmol/L, hypochloremia (59-71 mmol/L, mean 66 mmol/L and low urinary sodium (5-12 mmol/L, mean 9 mmol/L. After intravenous rehydration followed by additional use of sodium and chloride in mean dosis of 1.78 mmol/kg per day, all the patients made a complete recovery. With advice for additional use of salt in the mentioned amount, the patients were discharged from the hospital. Conclusion. PBS is one of CF complications, especially in infants and young children in situations accompanied by increased sweating and/or other causes of additional loss of sodium and chlorine. Sometimes, as was the case with one of our patients, PBS may be the initial presentation form of the disease.

  8. Na+/HCO3- Cotransporter NBCn2 Mediates HCO3- Reclamation in the Apical Membrane of Renal Proximal Tubules.

    Science.gov (United States)

    Guo, Yi-Min; Liu, Ying; Liu, Mei; Wang, Jin-Lin; Xie, Zhang-Dong; Chen, Kang-Jing; Wang, Deng-Ke; Occhipinti, Rossana; Boron, Walter F; Chen, Li-Ming

    2017-08-01

    The kidney maintains systemic acid-base balance by reclaiming from the renal tubule lumen virtually all HCO 3 - filtered in glomeruli and by secreting additional H + to titrate luminal buffers. For proximal tubules, which are responsible for about 80% of this activity, it is believed that HCO 3 - reclamation depends solely on H + secretion, mediated by the apical Na + /H + exchanger NHE 3 and the vacuolar proton pump. However, NHE3 and the proton pump cannot account for all HCO 3 - reclamation. Here, we investigated the potential contribution of two variants of the electroneutral Na + /HCO 3 - cotransporter NBCn2, the amino termini of which start with the amino acids MCDL (MCDL-NBCn2) and MEIK (MEIK-NBCn2). Western blot analysis and immunocytochemistry revealed that MEIK-NBCn2 predominantly localizes at the basolateral membrane of medullary thick ascending limbs in the rat kidney, whereas MCDL-NBCn2 localizes at the apical membrane of proximal tubules. Notably, NH 4 Cl-induced systemic metabolic acidosis or hypokalemic alkalosis downregulated the abundance of MCDL-NBCn2 and reciprocally upregulated NHE 3 Conversely, NaHCO 3 -induced metabolic alkalosis upregulated MCDL-NBCn2 and reciprocally downregulated NHE 3 We propose that the apical membrane of the proximal tubules has two distinct strategies for HCO 3 - reclamation: the conventional indirect pathway, in which NHE 3 and the proton pump secrete H + to titrate luminal HCO 3 - , and the novel direct pathway, in which NBCn2 removes HCO 3 - from the lumen. The reciprocal regulation of NBCn2 and NHE 3 under different physiologic conditions is consistent with our mathematical simulations, which suggest that HCO 3 - uptake and H + secretion have reciprocal efficiencies for HCO 3 - reclamation versus titration of luminal buffers. Copyright © 2017 by the American Society of Nephrology.

  9. Mixed acid-base disorders, hydroelectrolyte imbalance and lactate production in hypercapnic respiratory failure: the role of noninvasive ventilation.

    Directory of Open Access Journals (Sweden)

    Claudio Terzano

    Full Text Available BACKGROUND: Hypercapnic Chronic Obstructive Pulmonary Disease (COPD exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV when treating hypercapnic respiratory failure. METHODS: Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO(2 and PaCO(2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. RESULTS: Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7% mixed respiratory acidosis-metabolic alkalosis, 10/36 (27.8% respiratory acidosis and 3/5 (60% mixed respiratory-metabolic acidosis patients (p = 0.026, with durations of 45.1 ± 9.8, 36.2 ± 8.9 and 53.3 ± 4.1 hours, respectively (p = 0.016. The duration of ventilation was associated with higher blood lactate (p<0.001, lower pH (p = 0.016, lower serum sodium (p = 0.014 and lower chloride (p = 0.038. Hyponatremia without hypervolemic hypochloremia occurred in 11 respiratory acidosis patients. Hypovolemic hyponatremia with hypochloremia and hypokalemia occurred in 10 mixed respiratory acidosis-metabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. CONCLUSIONS: Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated.

  10. Mixed Acid-Base Disorders, Hydroelectrolyte Imbalance and Lactate Production in Hypercapnic Respiratory Failure: The Role of Noninvasive Ventilation

    Science.gov (United States)

    Terzano, Claudio; Di Stefano, Fabio; Conti, Vittoria; Di Nicola, Marta; Paone, Gregorino; Petroianni, Angelo; Ricci, Alberto

    2012-01-01

    Background Hypercapnic Chronic Obstructive Pulmonary Disease (COPD) exacerbation in patients with comorbidities and multidrug therapy is complicated by mixed acid-base, hydro-electrolyte and lactate disorders. Aim of this study was to determine the relationships of these disorders with the requirement for and duration of noninvasive ventilation (NIV) when treating hypercapnic respiratory failure. Methods Sixty-seven consecutive patients who were hospitalized for hypercapnic COPD exacerbation had their clinical condition, respiratory function, blood chemistry, arterial blood gases, blood lactate and volemic state assessed. Heart and respiratory rates, pH, PaO2 and PaCO2 and blood lactate were checked at the 1st, 2nd, 6th and 24th hours after starting NIV. Results Nine patients were transferred to the intensive care unit. NIV was performed in 11/17 (64.7%) mixed respiratory acidosis–metabolic alkalosis, 10/36 (27.8%) respiratory acidosis and 3/5 (60%) mixed respiratory-metabolic acidosis patients (p = 0.026), with durations of 45.1±9.8, 36.2±8.9 and 53.3±4.1 hours, respectively (p = 0.016). The duration of ventilation was associated with higher blood lactate (pmetabolic alkalosis patients, and euvolemic hypochloremia occurred in the other 7 patients with this mixed acid-base disorder. Conclusions Mixed acid-base and lactate disorders during hypercapnic COPD exacerbations predict the need for and longer duration of NIV. The combination of mixed acid-base disorders and hydro-electrolyte disturbances should be further investigated. PMID:22539963

  11. Experience of diagnosis and treatment of Gitelman syndrome

    Directory of Open Access Journals (Sweden)

    Shuo TIAN

    2017-12-01

    Full Text Available Objective To analyze the clinical characteristics and provide the experiences in diagnosis and treatment of 3 cases of Gitelman syndrome (GitS. Methods Three patients diagnosed as GitS were selected as the objects in Tangshan gongren Hospital from Aug. 2010 to Jan. 2017. Their clinical data were retrospectively analyzed and combined with the related literatures, and the clinical characteristics and treatment experiences of the disease were discussed. Results Of the 3 patients, 2 were teenager onset and another one was adult onset. The blood pressure of the 3 patients was normal, and the clinical features were as paroxysmal weakness, tetany, polyuria and nocturia increased. Laboratory tests revealed low potassium, low sodium, low chlorine, hypomagnesemia, occasionally hypocalcemia, high urinary potassium, metabolic alkalosis, urine Ca/Cr ≤0.2, plasma rennin activity increased significantly and plasma aldosterone was normal. Being eliminated symptoms and phenomena were the potassium intake inadequate, loss of potassium in digestive tract, taking potassium excretion drugs, primary aldosteronism and Cushing syndrome. etc. Patients got symptoms relief and serum potassium level rose to near normal level after receiving the combined potassium and magnesium supplement. Conclusions The clinical characteristics of GitS manifest as fatigue, tetany, normal blood pressure, hypokalemia, hypomagnesemia, metabolic alkalosis, plasma rennin activity increases significantly and plasma aldosterone rises or normal. Treatment with combined potassium and magnesium supplement may lead to a good prognosis, but hypomagnesemia is harder to correct. Kidney damage can be avoided by early diagnosis and treatment. DOI: 10.11855/j.issn.0577-7402.2017.12.13

  12. Anaerobic work and power output during cycle ergometer exercise: effects of bicarbonate loading.

    Science.gov (United States)

    McNaughton, L; Curtin, R; Goodman, G; Perry, D; Turner, B; Showell, C

    1991-01-01

    Eight trained male cyclists who competed regularly in track races, were studied under control, alkalotic (NaHCO3) and placebo (CaCO3) conditions in a laboratory setting to study the effect of orally induced metabolic alkalosis on 60 s anaerobic work and power output on a bicycle ergometer. Basal, pre- and post-exercise blood samples in the three conditions were analysed for pH, pCO2, pO2, bicarbonate, base excess and lactate. All blood gas measurements were within normal limits at basal levels. There were significant differences in the amount of work produced, and in the maximal power output produced by the cyclists in the experimental condition when compared to the control and placebo conditions (P less than 0.01). The post-exercise pH decreased in all three conditions (P less than 0.05) and post-exercise pCO2 increased significantly in the alkalosis trial (P less than 0.01). In the alkalotic condition, the pre-exercise base excess and HCO3- levels were both higher (P less than 0.05) than the basal levels, suggesting that the bicarbonate ingestion had a significant increase in the buffering ability of the blood. Post-exercise lactate levels were significantly higher (P less than 0.05) after the alkalotic trial when compared to the other two conditions, immediately post-exercise and for the next 3 min. Post-exercise lactate levels were higher than basal or pre-exercise levels (P less than 0.001). This was true immediately post-exercise and for the next 5 min. The results of this study suggest that NaHCO3 is an effective ergogenic aid when used for typically anaerobic exercise as used in this experiment. We feel that this ergogenic property is probably due to the accelerated efflux of H+ ions from the muscle tissue due to increased extracellular bicarbonate buffering.

  13. Clinical presentation of cystic fibrosis at the time of diagnosis: a multicenter study in a region without newborn screening.

    Science.gov (United States)

    Farahmand, Fatemeh; Khalili, Manijeh; Shahbaznejad, Leila; Hirbod-Mobarakeh, Armin; Najafi Sani, Mehri; Khodadad, Ahmad; Motamed, Farzaneh; Rezaei, Nima

    2013-01-01

    Cystic fibrosis is the most common inherited lethal disease, which could be frequently identified late in regions without newborn screening. There are dramatically better outcomes in the early diagnosis of cystic fibrosis patients. This study aimed to evaluate the spectrum of manifestations of cystic fibrosis at first admission leading to diagnosis. This study was performed in a multi-referral pediatrics center in Iran. Data of patients with cystic fibrosis at the time of diagnosis were recorded based on a checklist denoting demographic characteristics, clinical and laboratory features. All of the patients had two documented sweat chloride tests. One hundred and ninety seven patients with cystic fibrosis were enrolled in this study. Among them, 119 patients (74%) were less than six months and 34 patients (21%) were between 6 and 12 months of age. The most common clinical findings were failure to thrive, recurrent pulmonary infections, and steatorrhea in 178 (90%), 139 (71%), and 135 (69%) patients, respectively. The most common radiologic abnormality was hyperaeration. In patients with salty tasting skin, steatorrhea, metabolic alkalosis, radiologic findings, and liver function abnormalities, the mean age at the time of diagnosis was significantly low than in the subjects without these findings. This study suggests that some conditions such as failure to thrive, recurrent respiratory infections, steatorrhea, metabolic alkalosis, and salty tasting skin should be considered as clinical screening tools for cystic fibrosis, especially in regions with high rate of cystic fibrosis. In these regions, awareness and clinical suspicion of medical professionals are crucial for early diagnosis of cystic fibrosis patients in the pre-diagnostic period.

  14. Carbonic anhydrase 2-like and Na⁺-K⁺-ATPase α gene expression in medaka (Oryzias latipes) under carbonate alkalinity stress.

    Science.gov (United States)

    Yao, Zongli; Lai, Qifang; Hao, Zhuoran; Chen, Ling; Lin, Tingting; Zhou, Kai; Wang, Hui

    2015-12-01

    High carbonate alkalinity is one of the major stress factors for living organisms in saline-alkaline water areas. Acute and chronic effects of carbonate alkalinity on expression of two genes, carbonic anhydrase 2-like (CA2-like) and Na(+)-K(+)-ATPase α subunit (NKA-α) mRNA in medaka (Oryzias latipes) were evaluated to better understand the responses important for coping with a carbonate alkalinity stress. In the acute exposure experiment, the expression of CA2-like and NKA-α mRNA in the gill and kidney of medaka were examined from 0 h to 7 days exposed to 30.4 mM carbonate alkalinity water. Exposure to high carbonate alkalinity resulted in a transitory alkalosis, followed by a transient increase in gill and kidney CA2-like and NKA-α mRNA expression. In the chronic exposure experiment, the expression of these two genes was examined in the gill and kidney at 50 days post-exposure to six different carbonate alkalinity concentrations ranging from 1.5 to 30.4 mM. Gill and kidney CA2-like mRNA levels in 30.4 mM were approximately 10 and 30 times higher than that of the control (1.5 mM), respectively. Less differences were found in NKA-α expression in the 50-days exposure. The results indicate that when transferred to high carbonate alkalinity water, a transitory alkalosis may occur in medaka, followed by compensatory acid-base and ion regulatory responses. Thus, CA2-like and NKA-α are at least two of the important factors that contribute to the regulation of alkalinity stress.

  15. [Acid-base status in patients treated with peritoneal dialysis].

    Science.gov (United States)

    Katalinić, Lea; Blaslov, Kristina; Pasini, Eva; Kes, Petar; Bašić-Jukić, Nikolina

    2014-04-01

    When compared to hemodialysis, peritoneal dialysis is very simple yet low cost method of renal replacement therapy. Series of studies have shown its superiority in preserving residual renal function, postponing uremic complications, maintaining the acid-base balance and achieving better post-transplant outcome in patients treated with this method. Despite obvious advantages, its role in the treatment of chronic kidney disease is still not as important as it should be. Metabolic acidosis is an inevitable complication associated with progressive loss of kidney function. Its impact on mineral and muscle metabolism, residual renal function, allograft function and anemia is very complex but can be successfully managed. The aim of our study was to evaluate the efficiency in preserving the acid-base balance in patients undergoing peritoneal dialysis at Zagreb University Hospital Center. Twenty-eight patients were enrolled in the study. The mean time spent on the treatment was 32.39 ± 43.43 months. Only lactate-buffered peritoneal dialysis fluids were used in the treatment. Acid-base balance was completely maintained in 73.07% of patients; 11.54% of patients were found in the state of mild metabolic acidosis, and the same percentage of patients were in the state of mild metabolic alkalosis. In one patient, mixed alkalosis with respiratory and metabolic component was present. The results of this study showed that acid-base balance could be maintained successfully in patients undergoing peritoneal dialysis, even only with lactate-buffered solutions included in the treatment, although they were continuously proclaimed as inferior in comparison with bicarbonate-buffered ones. In well educated and informed patients who carefully use this method, accompanied by the attentive and thorough care of their physicians, this method can provide quality continuous replacement of lost renal function as well as better quality of life.

  16. Effect of acute acid-base disturbances on ErbB1/2 tyrosine phosphorylation in rabbit renal proximal tubules.

    Science.gov (United States)

    Skelton, Lara A; Boron, Walter F

    2013-12-15

    The renal proximal tubule (PT) is a major site for maintaining whole body pH homeostasis and is responsible for reabsorbing ∼80% of filtered HCO3(-), the major plasma buffer, into the blood. The PT adapts its rate of HCO3(-) reabsorption (JHCO3(-)) in response to acute acid-base disturbances. Our laboratory previously showed that single isolated perfused PTs adapt JHCO3(-) in response to isolated changes in basolateral (i.e., blood side) CO2 and HCO3(-) concentrations but, surprisingly, not to pH. The response to CO2 concentration can be blocked by the ErbB family tyrosine kinase inhibitor PD-168393. In the present study, we exposed enriched rabbit PT suspensions to five acute acid-base disturbances for 5 and 20 min using a panel of phosphotyrosine (pY)-specific antibodies to determine the influence of each disturbance on pan-pY, ErbB1-specific pY (four sites), and ErbB2-specific pY (two sites). We found that each acid-base treatment generated a distinct temporal pY pattern. For example, the summated responses of the individual ErbB1/2-pY sites to each disturbance showed that metabolic acidosis (normal CO2 concentration and reduced HCO3(-) concentration) produced a transient summated pY decrease (5 vs. 20 min), whereas metabolic alkalosis produced a transient increase. Respiratory acidosis (normal HCO3(-) concentration and elevated CO2 concentration) had little effect on summated pY at 5 min but produced an elevation at 20 min, whereas respiratory alkalosis produced a reduction at 20 min. Our data show that ErbB1 and ErbB2 in the PT respond to acute acid-base disturbances, consistent with the hypothesis that they are part of the signaling cascade.

  17. Analysis of Arterial Blood Gas Report in Chronic Kidney Diseases - Comparison between Bedside and Multistep Systematic Method.

    Science.gov (United States)

    Ghatak, Ishita; Dhat, Vaishali; Tilak, Mona A; Roy, Indranath

    2016-08-01

    Acid Base Disorders (ABDs) are commonly encountered in critically ill Chronic Kidney Disease (CKD) patients. Timely and correct analysis of Arterial Blood Gases (ABG) is critical for the diagnosis, treatment and prediction of outcome of the patients. The aim was to explore type and prevalence of ABDs in 31 critically ill CKD patients from a tertiary care hospital in Maharashtra, to compare two methods of analysis- bedside and systematic approaches and to clinically correlate the nature of ABDs in these patients. The initial ABG reports of 31 consecutive CKD patients were analysed by two methods. Medica Easy stat analyser was the equipment for analysis with Principle of potentiometry and ion selective electrode for pH and pCO2 and amperometry for pO2. Serum albumin was also measured by Bromocresol green dye binding method using liquixx albumin kit in Erba XL 300 autoanalyser. Chi-square test was used for statistical analysis using Epi Info version 3.5.4 and SPSS 14.0 softwares. The systematic method showed a significantly higher prevalence of mixed disorders (50%) compared to bedside method (12.9%). Most prevalent disorder by bedside method was metabolic acidosis in 15 cases (48.39%). By the systematic method, 3 reports were invalid. As a single category, most prevalent type was both simple respiratory alkalosis and mixed metabolic acidosis with respiratory alkalosis- 6 of 31 cases in each type (19.36% each). As a whole, metabolic acidosis (including both High Anion Gap Metabolic Acidosis or HAGMA and Non Anion Gap Metabolic Acidosis or NAGMA with 4 in each type) was most prevalent- 8 of 31(25.8%). Systematic approach was more effective in diagnosing mixed acid base disorders. By systematic method the findings of analysis in most cases could be correlated with the clinical condition and provisional diagnosis. Thus interpretation of ABDs by using stepwise approach could be useful to the clinicians in early diagnosis and management of the patients.

  18. Sodium bicarbonate-augmented stress thallium myocardial scintigraphy

    International Nuclear Information System (INIS)

    Sarin, Badal; Chugh, Pradeep Kumar; Kaushal, Dinesh; Soni, Nakse Lal; Sawroop, Kishan; Mondal, Anupam; Bhatnagar, Aseem

    2004-01-01

    It is well known that sodium bicarbonate in pharmacological doses induces transient alkalosis, causing intracellular transport of serum potassium. The aims of this study were (a) to investigate whether, in humans, myocardial thallium-201 uptake can be augmented by pretreatment with a single bolus of sodium bicarbonate at a pharmacological dose, (b) to verify general safety aspects of the intervention and (c) to evaluate the clinical implications of augmentation of 201 Tl uptake, if any. Routine exercise myocardial scintigraphy was performed twice in eight adult volunteers (five normal and three abnormal), once without intervention and the second time (within a week) following intravenous administration of sodium bicarbonate (88 mEq in 50 ml) as a slow bolus 1 h prior to the injection of 201 Tl. Conventional myocardial thallium study was compared with sodium bicarbonate interventional myocardial scintigraphy with respect to myocardial uptake (counts per minute per mCi injected dose), washout patterns in normal and abnormal myocardial segments, and overall clinical interpretation based on planar and single-photon emission tomographic (SPET) images. All patients remained asymptomatic after the intervention. A mean increase of 53% in myocardial uptake of thallium was noted in post-exercise acquisitions after the intervention, confirming uptake of the tracer via the potassium-hydrogen pump and its augmentation by transient alkalosis. The washout pattern remained unchanged. The visual quality of planar and SPET images improved significantly after the intervention. Out of the five abnormal myocardial segments identified in three cases, four showed significant filling-in after the intervention, causing the diagnosis to be upgraded from ''partial scar'' to ''ischaemia'', or from ''ischaemia'' to ''normal''. The overall scan impression changed in two out of three such cases. Sodium bicarbonate augmentation may have significant implications for stress-thallium scintigraphy

  19. Absence of transepithelial anion exchange by rabbit OMCD: Evidence against reversal of cell polarity

    Energy Technology Data Exchange (ETDEWEB)

    Hayashi, Matsuhiko; Schuster, V.L.; Stokes, J.B. (Univ. of Iowa College of Medicine, Iowa City (USA))

    1988-08-01

    In the rabbit cortical collecting duct (CCD), Cl tracer crosses the epithelium predominantly via an anion exchange system that operates in either a Cl-Cl or Cl-HCO{sub 3} exchange mode. In the present study, the authors used the {sup 36}Cl lumen-to-bath rate coefficient (K{sub Cl}, nm/s), a sensitive measurement of CCD transepithelial anion transport, to investigate the nature of Cl transport in the medullary collecting duct dissected from inner stripe, outer medulla (OMCD). The K{sub Cl} in OMCD perfused and bathed in HCO{sub 3}-Ringer solution was low and similar to that value observed in the CCD when anion exchange is inhibited and Cl permeates the epithelium by diffusion. To test the hypothesis that metabolic alkalosis could reverse the polarity of intercalated cells and thus induce an apical Cl-HCO{sub 3} exchanger in H{sup +}-secreting OMCD cells, they measured K{sub Cl} in OMCD from rabbits make alkalotic by deoxycorticosterone and furosemide. Although the base-line K{sub Cl} was slightly higher than in OMCD from control rabbits, the value was still far lower than the K{sub Cl} under comparable conditions in CCD. They conclude (1) Cl transport across the MCD by anion exchange is immeasurably low or nonexistent; (2) unlike the CCD, Cl transport in OMCD is not responsive to cAMP; and (3) metabolic alkalosis does not induce an apical anion exchanger in OMCD, i.e., does not cause epithelial polarity reversal.

  20. The use of the standard exercise test to establish the clinical significance of mild echocardiographic changes in a Thoroughbred poor performer : clinical communication

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    C. Meyer

    2004-06-01

    Full Text Available A 4-year-old Thoroughbred gelding racehorse was referred to the Onderstepoort Veterinary Academic Hospital (OVAH with a history of post-race distress and collapse. In the absence of any obvious abnormalities in the preceding diagnostic work-up, a standard exercise test was performed to determine an underlying cause for the post-race distress reported. In this particular case oxygen desaturation became evident at speeds as slow as 6 m/s, where PO2 was measured at 82.3 mm Hg. Similarly at a blood pH of 7.28, PCO2 had dropped to 30.0mm Hg indicating a combined metabolic acidosis and respiratory alkalosis. The cause of the distress was attributed to a severe hypoxia, with an associated hypocapnoea, confirmed on blood gas analyses, where PO2 levels obtained were as low as 56.6 mm Hg with a mean PCO2 level of 25.4 mm Hg during strenuous exercise. Arterial oxygenation returned to normal immediately after cessation of exercise to 106.44 mm Hg, while the hypocapnoeic alkalosis, PCO2 25.67 mm Hg, persisted until the animal's breathing normalized. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise. The combination of an aortic stenosis and a mitral valve insufficiency may have resulted in a condition similar to that described as high-altitude pulmonary oedema, with respiratory changes and compensation as for acute altitude disease. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise and substantiate the fact that an extensive diagnostic regime may be required to establish a cause for poor performance and that the standard exercise test remains an integral part of this work-up.

  1. Gitelman syndrome manifesting in early childhood and leading to delayed puberty: a case report

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    Raza Farhan

    2012-10-01

    Full Text Available Abstract Introduction Gitelman syndrome is an inherited autosomal recessive renal salt-wasting disorder. It presents with variable clinical symptoms including muscle weakness and fatigue, and the diagnosis is based on metabolic alkalosis, hypokalemia, hypomagnesemia and hypocalciuria. It is usually diagnosed incidentally in early adulthood. There are rare cases of Gitelman syndrome presenting in early childhood; however, to the best of our knowledge it has not previously been associated with delayed puberty. Case presentation A 17-year-old South Asian man with recurrent episodes of generalized muscle weakness, fatigue and cramps from the age of two years was admitted for further workup. Before the age of 12 years, the episodes had been mild, but they then got progressively worse. Other symptoms include polyuria, polydipsia, nocturia, paresthesia and occasional watery diarrhea. He also had a history of short stature, poor weight gain and delayed developmental landmarks. His family history was unremarkable except for the consanguineous marriage of his parents. An examination revealed a thin and lean man with blood pressure of 95/60mmHg. His height and weight were below the third percentile and his sexual development was at Tanner Stage II. Laboratory work revealed serum sodium of 124mmol/L, potassium 2.4mmol/L, calcium 6.5mmol/L and magnesium of 1.2mg/dL. His testosterone level was low (0.85ng/mL, normal for his age 2.67 to 10.12ng/mL with normal levels of luteinizing hormone and follicle-stimulating hormone. The sex hormone findings were attributed to delayed puberty. A 24-hour urinary analysis revealed decreased excretion of calcium (25.9mg/24 hours. Based on the findings of hypokalemic metabolic alkalosis without hypertension, severe hypomagnesemia and hypocalciuria, a diagnosis of Gitelman syndrome was made. Treatment was started with oral supplementation of potassium, magnesium and calcium along with spironolactone and liberal salt intake

  2. The role of acid-base imbalance in statin-induced myotoxicity.

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    Taha, Dhiaa A; De Moor, Cornelia H; Barrett, David A; Lee, Jong Bong; Gandhi, Raj D; Hoo, Chee Wei; Gershkovich, Pavel

    2016-08-01

    Disturbances in acid-base balance, such as acidosis and alkalosis, have potential to alter the pharmacologic and toxicologic outcomes of statin therapy. Statins are commonly prescribed for elderly patients who have multiple comorbidities such as diabetes mellitus, cardiovascular, and renal diseases. These patients are at risk of developing acid-base imbalance. In the present study, the effect of disturbances in acid-base balance on the interconversion of simvastatin and pravastatin between lactone and hydroxy acid forms have been investigated in physiological buffers, human plasma, and cell culture medium over pH ranging from 6.8-7.8. The effects of such interconversion on cellular uptake and myotoxicity of statins were assessed in vitro using C2C12 skeletal muscle cells under conditions relevant to acidosis, alkalosis, and physiological pH. Results indicate that the conversion of the lactone forms of simvastatin and pravastatin to the corresponding hydroxy acid is strongly pH dependent. At physiological and alkaline pH, substantial proportions of simvastatin lactone (SVL; ∼87% and 99%, respectively) and pravastatin lactone (PVL; ∼98% and 99%, respectively) were converted to the active hydroxy acid forms after 24 hours of incubation at 37°C. At acidic pH, conversion occurs to a lower extent, resulting in greater proportion of statin remaining in the more lipophilic lactone form. However, pH alteration did not influence the conversion of the hydroxy acid forms of simvastatin and pravastatin to the corresponding lactones. Furthermore, acidosis has been shown to hinder the metabolism of the lactone form of statins by inhibiting hepatic microsomal enzyme activities. Lipophilic SVL was found to be more cytotoxic to undifferentiated and differentiated skeletal muscle cells compared with more hydrophilic simvastatin hydroxy acid, PVL, and pravastatin hydroxy acid. Enhanced cytotoxicity of statins was observed under acidic conditions and is attributed to increased

  3. The acid-base effects of continuous hemofiltration with lactate or bicarbonate buffered replacement fluids.

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    Tan, H K; Uchino, S; Bellomo, R

    2003-06-01

    To evaluate, quantify and compare the effects of continuous veno-venous hemofiltration (CVVH) with lactate or bicarbonate-buffered replacement fluids on acid-base balance. Randomized double crossover study. Intensive Care Unit of Tertiary Medical Center. Eight patients with severe acute renal failure. Random allocation to either 2 hours of isovolemic lactate-buffered (treatment A) CVVH or 2 hours of bicarbonate-buffered (treatment B) CVVH with cross over and with same procedure repeated the following day (double cross over). Timed collections of arterial blood and ultrafiltrate (UF), measurement of blood and UF gases and lactate concentrations and calculation of buffer-base mass balance. At baseline, both groups of patients had a similar, slight metabolic alkalosis (pH: 7.45 vs. 7.45; BE 3.9 mEq/L for treatment A and 4.0 for treatment B) and a serum bicarbonate of 28.1 mmol/L for treatment A vs. 28.3 mmol/L for treatment B; all NS. This alkalosis was present despite slight hyperlactatemia in both groups (A: 2.4 mmol/L vs. B 2.8 mmol/; NS). Within 60 minutes of treatment, however, treatment A led to a significantly higher lactate concentration (3.9 vs 2.5 mmol/L; p = 0.0011), a significantly lower BE (2.3 vs 4.1 mEq/L; p = 0.0019) and a significantly lower bicarbonate concentration (26.7 vs. 28.3 mmol/L; p = 0.0038) in the presence of an unchanged PaCO2. These differences persisted during the study period. The UF of patients receiving treatment A contained more lactate (10.2 vs 2.9 mmol/L; p buffer-base balance of +20.4 mEq/h compared to -2.6 mEq/h for treatment B; p buffered replacement fluids induces iatrogenic hyperlactatemia. Such hyperlactatemia is associated with an acidifying effect despite a positive buffer-base balance.

  4. Functional and molecular characterization of transmembrane intracellular pH regulators in human dental pulp stem cells.

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    Chen, Gunng-Shinng; Lee, Shiao-Pieng; Huang, Shu-Fu; Chao, Shih-Chi; Chang, Chung-Yi; Wu, Gwo-Jang; Li, Chung-Hsing; Loh, Shih-Hurng

    2018-06-01

    Homeostasis of intracellular pH (pH i ) plays vital roles in many cell functions, such as proliferation, apoptosis, differentiation and metastasis. Thus far, Na + -H + exchanger (NHE), Na + -HCO 3 - co-transporter (NBC), Cl - /HCO 3 - exchanger (AE) and Cl - /OH - exchanger (CHE) have been identified to co-regulate pH i homeostasis. However, functional and biological pH i -regulators in human dental pulp stem cells (hDPSCs) have yet to be identified. Microspectrofluorimetry technique with pH-sensitive fluorescent dye, BCECF, was used to detect pH i changes. NH 4 Cl and Na + -acetate pre-pulse were used to induce intracellular acidosis and alkalosis, respectively. Isoforms of pH i -regulators were detected by Western blot technique. The resting pH i was no significant difference between that in HEPES-buffered (nominal HCO 3 - -free) solution or CO 2 /HCO 3 -buffered system (7.42 and 7.46, respectively). The pH i recovery following the induced-intracellular acidosis was blocked completely by removing [Na + ] o , while only slowed (-63%) by adding HOE694 (a NHE1 specific inhibitor) in HEPES-buffered solution. The pH i recovery was inhibited entirely by removing [Na + ] o , while adding HOE 694 pulse DIDS (an anion-transporter inhibitor) only slowed (-55%) the acid extrusion. Both in HEPES-buffered and CO 2 /HCO 3 -buffered system solution, the pH i recovery after induced-intracellular alkalosis was entirely blocked by removing [Cl - ] o . Western blot analysis showed the isoforms of pH i regulators, including NHE1/2, NBCe1/n1, AE1/2/3/4 and CHE in the hDPSCs. We demonstrate for the first time that resting pH i is significantly higher than 7.2 and meditates functionally by two Na + -dependent acid extruders (NHE and NBC), two Cl - -dependent acid loaders (CHE and AE) and one Na + -independent acid extruder(s) in hDPSCs. These findings provide novel insight for basic and clinical treatment of dentistry. Copyright © 2018 Elsevier Ltd. All rights reserved.

  5. Variability of Acid-Base Status in Acetate-Free Biofiltration 84% versus Bicarbonate Dialysis

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    Harzallah Kais

    2008-01-01

    Full Text Available The ultimate goal of hemodialysis (HD treatment is to achieve the highest level of efficacy in the presence of maximal clinical tolerance. With an aim to offer good hemodynamic stability, as observed during the acetate-free biofiltration 14% (AFB 14% to patients who are intolerant to bicarbonate dialysis (BD and with less cost, we have developed since June 1994, a new HD technique, namely AFB 84%. This study was carried out to analyze acid-base variations during the AFB 84% in comparison to BD in hemodynamically stable patients on regular HD. This was a prospective randomized crossover study carried out on 12 patients (6 males and 6 females for a total of 144 HD sessions (72 BD and 72 AFB 84%. Patients with decompensated cardiomyopathy, respiratory diseases or uncontrolled hypertension were not included in the trial. All the patients were treated with BD or AFB 84%; the latter is characterized by the absence of acetate in the dialysate and a complete correction of buffer balance by post-dilutional infusion of bicarbonate-based replacement solution. The comparison of pre-dialysis arterial acid-base and blood-gas parameters revealed no significant differences of pH, HCO 3 - and paCO 2 levels between the two techniques. Analysis of post-dialysis parameters showed that, among patients dialyzed with BD, there was over correction of metabolic acidosis with a tendency towards metabolic alkalosis. In contrast, in patients dialyzed with AFB 84%, we observed a significant improvement in pH and HCO 3 - levels but the increase in paCO2 level was not significant. A comparison of these parameters between the two techniques showed statistically significant difference in pH, HCO3 - and paCO2 levels, but not for paO2 level. AFB 84% can offer some important advantages with the complete absence of acetate from the substitution fluids, and permits a better correction of metabolic acidosis than BD, without causing alkalosis.

  6. Construction and validation of a decision tree for treating metabolic acidosis in calves with neonatal diarrhea

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    Trefz Florian M

    2012-12-01

    Full Text Available Abstract Background The aim of the present prospective study was to investigate whether a decision tree based on basic clinical signs could be used to determine the treatment of metabolic acidosis in calves successfully without expensive laboratory equipment. A total of 121 calves with a diagnosis of neonatal diarrhea admitted to a veterinary teaching hospital were included in the study. The dosages of sodium bicarbonate administered followed simple guidelines based on the results of a previous retrospective analysis. Calves that were neither dehydrated nor assumed to be acidemic received an oral electrolyte solution. In cases in which intravenous correction of acidosis and/or dehydration was deemed necessary, the provided amount of sodium bicarbonate ranged from 250 to 750 mmol (depending on alterations in posture and infusion volumes from 1 to 6.25 liters (depending on the degree of dehydration. Individual body weights of calves were disregarded. During the 24 hour study period the investigator was blinded to all laboratory findings. Results After being lifted, many calves were able to stand despite base excess levels below −20 mmol/l. Especially in those calves, metabolic acidosis was undercorrected with the provided amount of 500 mmol sodium bicarbonate, which was intended for calves standing insecurely. In 13 calves metabolic acidosis was not treated successfully as defined by an expected treatment failure or a measured base excess value below −5 mmol/l. By contrast, 24 hours after the initiation of therapy, a metabolic alkalosis was present in 55 calves (base excess levels above +5 mmol/l. However, the clinical status was not affected significantly by the metabolic alkalosis. Conclusions Assuming re-evaluation of the calf after 24 hours, the tested decision tree can be recommended for the use in field practice with minor modifications. Calves that stand insecurely and are not able to correct their position if pushed

  7. Hypoxia and Its Acid-Base Consequences: From Mountains to Malignancy.

    Science.gov (United States)

    Swenson, Erik R

    Hypoxia, depending upon its magnitude and circumstances, evokes a spectrum of mild to severe acid-base changes ranging from alkalosis to acidosis, which can alter many responses to hypoxia at both non-genomic and genomic levels, in part via altered hypoxia-inducible factor (HIF) metabolism. Healthy people at high altitude and persons hyperventilating to non-hypoxic stimuli can become alkalotic and alkalemic with arterial pH acutely rising as high as 7.7. Hypoxia-mediated respiratory alkalosis reduces sympathetic tone, blunts hypoxic pulmonary vasoconstriction and hypoxic cerebral vasodilation, and increases hemoglobin oxygen affinity. These effects and others can be salutary or counterproductive to tissue oxygen delivery and utilization, based upon magnitude of each effect and summation. With severe hypoxia either in the setting of profound arterial hemoglobin desaturation and reduced O2 content or poor perfusion (ischemia) at the global or local level, metabolic and hypercapnic acidosis develop along with considerable lactate formation and pH falling to below 6.8. Although conventionally considered to be injurious and deleterious to cell function and survival, both acidoses may be cytoprotective by various anti-inflammatory, antioxidant, and anti-apoptotic mechanisms which limit total hypoxic or ischemic-reperfusion injury. Attempts to correct acidosis by giving bicarbonate or other alkaline agents under these circumstances ahead of or concurrent with reoxygenation efforts may be ill advised. Better understanding of this so-called "pH paradox" or permissive acidosis may offer therapeutic possibilities. Rapidly growing cancers often outstrip their vascular supply compromising both oxygen and nutrient delivery and metabolic waste disposal, thus limiting their growth and metastatic potential. However, their excessive glycolysis and lactate formation may not necessarily represent oxygen insufficiency, but rather the Warburg effect-an attempt to provide a large amount

  8. Pattern of acid base abnormalities in critically ill patinets

    International Nuclear Information System (INIS)

    Ahmad, T.M.; Mehmood, A.; Malik, T.M.

    2015-01-01

    To find out the pattern of acid base abnormalities in critically ill patients in a tertiary care health facility. Study Design: A descriptive study. Place and Duration of Study: The study was carried out in the department of pathology, Combined Military Hospital Kharian from January 2013 to June 2013. Patients and Methods: Two hundred and fifty patients suffering from various diseases and presenting with exacerbation of their clinical conditions were studied. These patients were hospitalized and managed in acute care units of the hospital. Arterial blood gases were analysed to detect acid base status and their correlation with their clinical condition. Concomitant analysis of electrolytes was carried out. Tests related to concurrent illnesses e.g. renal and liver function tests, cardiac enzymes and plasma glucose were assayed by routine end point and kinetic methods. Standard reference materials were used to ensure internal quantify control of analyses. Results: Two hundred and fifteen patients out of 250 studied suffered from acid base disorders. Gender distribution showed a higher percentage of male patients and the mean age was 70.5 ± 17.4 years. Double acid base disorders were the commonest disorders (34%) followed by metabolic acidosis (30%). Anion gap was calculated to further stratify metabolic acidosis and cases of diabetic ketoacidosis were the commonest in this category (47%). Other simple acid base disorders were relatively less frequent. Delta bicarbonate was calculated to unmask the superimposition of respiratory alkalosis or acidosis with metabolic acidosis and metabolic alkalosis. Though triple acid base disorders were noted in a small percentage of cases (05%), but were found to be the most complicated and challenging. Mixed acid base disorders were associated with high mortality. Conclusion: A large number of critically ill patients manifested acid base abnormalities over the full spectrum of these disorders. Mixed acid base disorders were

  9. Avoiding Management Errors in Patients with Obesity Hypoventilation Syndrome.

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    Manthous, Constantine A; Mokhlesi, Babak

    2016-01-01

    The prevalence of obesity hypoventilation syndrome and obstructive sleep apnea are increasing rapidly in the United States in parallel with the obesity epidemic. As the pathogenesis of this chronic illness is better understood, effective evidence-based therapies are being deployed to reduce morbidity and mortality. Nevertheless, patients with obesity hypoventilation still fall prey to at least four avoidable types of therapeutic errors, especially at the time of hospitalization for respiratory or cardiovascular decompensation: (1) patients with obesity hypoventilation syndrome may develop acute hypercapnia in response to administration of excessive supplemental oxygen; (2) excessive diuresis for peripheral edema using a loop diuretic such as furosemide exacerbates metabolic alkalosis, thereby worsening daytime hypoventilation and hypoxemia; (3) excessive or premature pharmacological treatment of psychiatric illnesses can exacerbate sleep-disordered breathing and worsen hypercapnia, thereby exacerbating psychiatric symptoms; and (4) clinicians often erroneously diagnose obstructive lung disease in patients with obesity hypoventilation, thereby exposing them to unnecessary and potentially harmful medications, including β-agonists and corticosteroids. Just as literary descriptions of pickwickian syndrome have given way to greater understanding of the pathophysiology of obesity hypoventilation, clinicians might exercise caution to consider these potential pitfalls and thus avoid inflicting unintended and avoidable complications.

  10. Effect of altitude on brain intracellular pH and inorganic phosphate levels.

    Science.gov (United States)

    Shi, Xian-Feng; Carlson, Paul J; Kim, Tae-Suk; Sung, Young-Hoon; Hellem, Tracy L; Fiedler, Kristen K; Kim, Seong-Eun; Glaeser, Breanna; Wang, Kristina; Zuo, Chun S; Jeong, Eun-Kee; Renshaw, Perry F; Kondo, Douglas G

    2014-06-30

    Normal brain activity is associated with task-related pH changes. Although central nervous system syndromes associated with significant acidosis and alkalosis are well understood, the effects of less dramatic and chronic changes in brain pH are uncertain. One environmental factor known to alter brain pH is the extreme, acute change in altitude encountered by mountaineers. However, the effect of long-term exposure to moderate altitude has not been studied. The aim of this two-site study was to measure brain intracellular pH and phosphate-bearing metabolite levels at two altitudes in healthy volunteers, using phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS). Increased brain pH and reduced inorganic phosphate (Pi) levels were found in healthy subjects who were long-term residents of Salt Lake City, UT (4720ft/1438m), compared with residents of Belmont, MA (20ft/6m). Brain intracellular pH at the altitude of 4720ft was more alkaline than that observed near sea level. In addition, the ratio of inorganic phosphate to total phosphate signal also shifted toward lower values in the Salt Lake City region compared with the Belmont area. These results suggest that long-term residence at moderate altitude is associated with brain chemical changes. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  11. Bartter's Syndrome with Type 2 Diabetes Mellitus

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    Ting-Ting See

    2009-02-01

    Full Text Available We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patient's condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin, oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions.

  12. Necessity Of ABG Analysis In HPS

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    Kalantari M

    2005-06-01

    Full Text Available Background: The purpose of this study is to determine the incidence of electrolyte and ABG abnormalities in infants with HPS and also we evaluate other parameters of the study. ‎ Materials and Methods: This descriptive study covers 161 infants with HPS hospitalized in children Medical center of Tehran university underwent surgical repair from march 1996 to march 2002 . ‎ Results & Conclusion: The results indicated that Hypokalemic metabolic alkalosis had occurred in 40% of patients. ‎The sex ratio was 3/1 =M/F and the most time of presentation was between 15t and 5st week and the most presenting sign was vomiting. Clinical icter happened to be found in 15% of patients. The incidence of accompanying anomalies was 9% and olive sign was palpable in 40%. ‎The best way for evaluating and diagnosis was sonography. ‎The mean period to begin postoperative feeding was 30 hours' no complication related to option was reported after operation.

  13. Anticoagulation Strategies in Venovenous Hemodialysis in Critically Ill Patients: A Five-Year Evaluation in a Surgical Intensive Care Unit

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    Christoph Sponholz

    2014-01-01

    Full Text Available Renal failure is a common complication among critically ill patients. Timing, dosage, and mode of renal replacement (RRT are under debate, but also anticoagulation strategies and vascular access interfere with dialysis success. We present a retrospective, five-year evaluation of patients requiring RRT on a multidisciplinary 50-bed surgical intensive care unit of a university hospital with special regard to anticoagulation strategies and vascular access. Anticoagulation was preferably performed with unfractionated heparin or regional citrate application (RAC. Bleeding and suspected HIT-II were most common causes for RAC. In CVVHD mode filter life span was significantly longer under RAC compared to heparin or other anticoagulation strategies (P=0.001. Femoral vascular access was associated with reduced filter life span (P=0.012, especially under heparin anticoagulation (P=0.015. Patients on RAC had higher rates of metabolic alkalosis (P=0.001, required more transfusions (P=0.045, and showed higher illness severity measured by SOFA scores (P=0.001. RRT with unfractionated heparin represented the most common anticoagulation strategy in this study population. However, patients with bleeding risk and severe organ dysfunction were more likely placed on RAC. Citrate provided longer filter life spans regardless of vascular access site. Attention has to be paid to metabolic disturbances.

  14. A dangerous mixture

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    Anna Piva

    2014-03-01

    Full Text Available A 59-year old woman was admitted for fatigue and arm paresthesias with Trousseau sign. Her medical history included thyroidectomy and hypercholesterolemia recently treated with simvastatin. Laboratory tests showed severe hypokalemia and hypocalcemia, severe increase in muscle enzymes, metabolic alkalosis; low plasma renin activity, increased thyroid-stimulating hormone, normal free thyroxine, increased parathyroid hormone, decreased vitamin D3; alterations in electrolyte urinary excretion, cortisol and aldosterone were excluded. Hypothesizing a statin-related myopathy, simvastatin was suspended; the patient reported use of laxatives containing licorice. Electrolytes normalized with intravenous supplementation. Among many biochemical alterations, none stands out as a major cause for muscular and electrolyte disorders. All co-factors are inter-connected, starting with statin-induced myopathy, worsened by hypothyroidism, secondary hyperaldosteronism and vitamin D deficiency, leading to hypocalcemia and hypokalemia, perpetrating muscular and electrolyte disorders. The importance of considering clinical conditions as a whole emerges with multiple co-factors involved. Another issue concerns herbal products and their potential dangerous effects.

  15. Renal transplantation in a patient with Bartter syndrome and glomerulosclerosis

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    Se Eun Lee

    2011-01-01

    Full Text Available Bartter syndrome (BS is a clinically and genetically heterogeneous inherited renal tube disorder characterized by renal salt wasting, hypokalemic metabolic alkalosis and normotensive hyperreninemic hyperaldosteronism. There have been several case reports of BS complicated by focal segmental glomerulosclerosis (FSGS. Here, we have reported the case of a BS patient who developed FSGS and subsequent end-stage renal disease (ESRD and provided a brief literature review. The patient presented with classic BS at 3 months of age and developed proteinuria at 7 years. Renal biopsy performed at 11 years of age revealed a FSGS perihilar variant. Hemodialysis was initiated at 11 years of age, and kidney transplantation was performed at 16 years of age. The post-transplantation course has been uneventful for more than 3 years with complete disappearance of BS without the recurrence of FSGS. Genetic study revealed a homozygous p.Trp(TGG610Stop(TGA mutation in the CLCNKB gene. In summary, BS may be complicated by secondary FSGS due to the adaptive response to chronic salt-losing nephropathy, and FSGS may progress to ESRD in some patients. Renal transplantation in patients with BS and ESRD results in complete remission of BS.

  16. Milk alkali syndrome in an infant with chronic kidney disease

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    Kari JA

    2012-06-01

    Full Text Available Jameela A Kari, Sherif M El DesokyDepartment of Pediatrics and Pediatric Nephrology Unit, King Abdulaziz University, Jeddah, Kingdom of Saudi ArabiaAbstract: We report a case of milk alkali syndrome in a 15-month-old infant who had chronic kidney disease. His kidney function worsened, with creatinine raised from 1.11 mg/dL (98 µmol/L to 3.98 mg/dL (350.3 µmol/L, normal 0.4–1.0 mg/dL (35–91 µmol. He had hypercalcemia, serum calcium level 3.11 (normal 2.1–2.6 mmol/L, and metabolic alkalosis, HCO3 48.7 (normal 21–26 mmol/L. His kidney function returned to its base level and his calcium and bicarbonate levels normalized with adjustment of calcium carbonate and sodium bicarbonate doses. We report this case to highlight an unusual complication and to review the literature on milk alkali syndrome which is rare in children.Keywords: milk alkali syndrome, infants, chronic kidney disease

  17. Congenital Chloride Diarrhea: Diagnosis by Easy-Accessible Chloride Measurement in Feces

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    C. Gils

    2016-01-01

    Full Text Available Background. Congenital chloride diarrhea (CCD is an autosomal recessive disorder caused by mutations in the genes encoding the intestinal Cl−/HCO3- exchanger and is clinically characterized by watery, profound diarrhea, electrolyte disturbances, and metabolic alkalosis. The CCD diagnosis is based on the clinical symptoms and measurement of high chloride concentration in feces (>90 mmol/L and is confirmed by DNA testing. Untreated CCD is lethal, while long-term clinical outcome improves when treated correctly. Case Presentation. A 27-year-old woman had an emergency caesarian due to pain and discomfort in gestational week 36 + 4. The newborn boy had abdominal distension and yellow fluid per rectum. Therapy with intravenous glucose and sodium chloride decreased his stool frequency and improved his clinical condition. A suspicion of congenital chloride diarrhea was strongly supported using blood gas analyzer to measure an increased chloride concentration in the feces; the diagnosis was confirmed by DNA testing. Discussion. Measurement of chloride in feces using an ordinary blood gas analyzer can serve as a preliminary analysis when congenital chloride diarrhea is suspected. This measurement can be easily performed with a watery feces composition. An easy-accessible chloride measurement available will facilitate the diagnostics and support the initial treatment if CCD is suspected.

  18. Double knockout of pendrin and Na-Cl cotransporter (NCC) causes severe salt wasting, volume depletion, and renal failure

    Science.gov (United States)

    Soleimani, Manoocher; Barone, Sharon; Xu, Jie; Shull, Gary E.; Siddiqui, Faraz; Zahedi, Kamyar; Amlal, Hassane

    2012-01-01

    The Na-Cl cotransporter (NCC), which is the target of inhibition by thiazides, is located in close proximity to the chloride-absorbing transporter pendrin in the kidney distal nephron. Single deletion of pendrin or NCC does not cause salt wasting or excessive diuresis under basal conditions, raising the possibility that these transporters are predominantly active during salt depletion or in response to excess aldosterone. We hypothesized that pendrin and NCC compensate for loss of function of the other under basal conditions, thereby masking the role that each plays in salt absorption. To test our hypothesis, we generated pendrin/NCC double knockout (KO) mice by crossing pendrin KO mice with NCC KO mice. Pendrin/NCC double KO mice displayed severe salt wasting and sharp increase in urine output under basal conditions. As a result, animals developed profound volume depletion, renal failure, and metabolic alkalosis without hypokalemia, which were all corrected with salt replacement. We propose that the combined inhibition of pendrin and NCC can provide a strong diuretic regimen without causing hypokalemia for patients with fluid overload, including patients with congestive heart failure, nephrotic syndrome, diuretic resistance, or generalized edema. PMID:22847418

  19. Electrolyte and Acid-Base Disturbances in End-Stage Liver Disease: A Physiopathological Approach.

    Science.gov (United States)

    Jiménez, José Víctor; Carrillo-Pérez, Diego Luis; Rosado-Canto, Rodrigo; García-Juárez, Ignacio; Torre, Aldo; Kershenobich, David; Carrillo-Maravilla, Eduardo

    2017-08-01

    Electrolyte and acid-base disturbances are frequent in patients with end-stage liver disease; the underlying physiopathological mechanisms are often complex and represent a diagnostic and therapeutic challenge to the physician. Usually, these disorders do not develop in compensated cirrhotic patients, but with the onset of the classic complications of cirrhosis such as ascites, renal failure, spontaneous bacterial peritonitis and variceal bleeding, multiple electrolyte, and acid-base disturbances emerge. Hyponatremia parallels ascites formation and is a well-known trigger of hepatic encephalopathy; its management in this particular population poses a risky challenge due to the high susceptibility of cirrhotic patients to osmotic demyelination. Hypokalemia is common in the setting of cirrhosis: multiple potassium wasting mechanisms both inherent to the disease and resulting from its management make these patients particularly susceptible to potassium depletion even in the setting of normokalemia. Acid-base disturbances range from classical respiratory alkalosis to high anion gap metabolic acidosis, almost comprising the full acid-base spectrum. Because most electrolyte and acid-base disturbances are managed in terms of their underlying trigger factors, a systematic physiopathological approach to their diagnosis and treatment is required.

  20. Citrate Anticoagulation for CRRT in Children: Comparison with Heparin

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    Sara Nicole Fernández

    2014-01-01

    Full Text Available Regional anticoagulation with citrate is an alternative to heparin in continuous renal replacement therapies, which may prolong circuit lifetime and decrease hemorrhagic complications. A retrospective comparative cohort study based on a prospective observational registry was conducted including critically ill children undergoing CRRT. Efficacy, measured as circuit survival, and secondary effects of heparin and citrate were compared. 12 patients on CRRT with citrate anticoagulation and 24 patients with heparin anticoagulation were analyzed. Median citrate dose was 2.6 mmol/L. Median calcium dose was 0.16 mEq/kg/h. Median heparin dose was 15 UI/kg/h. Median circuit survival was 48 hours with citrate and 31 hours with heparin (P=0.028. 66.6% of patients treated with citrate developed mild metabolic alkalosis, which was directly related to citrate dose. There were no cases of citrate intoxication: median total calcium/ionic calcium index (CaT/I of 2.16 and a maximum CaT/I of 2.33, without metabolic acidosis. In the citrate group, 45.5% of patients developed hypochloremia and 27.3% hypomagnesemia. In the heparin group, 27.8% developed hypophosphatemia. Three patients were moved from heparin to citrate to control postoperatory bleeding. In conclusion citrate is a safe and effective anticoagulation method for CRRT in children and it achieves longer circuit survival than heparin.

  1. Pseudo-Bartter syndrome as the sole manifestation of cystic fibrosis in a child with 711+G>T/IVS8-5T mutation: a new face of an old disease.

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    Tinsa, Faten; Hadj Fredj, Sondes; Bel Hadj, Imen; Khalsi, Fatma; Abdelhak, Sonia; Boussetta, Khadija; Messaoud, Taieb

    2017-08-01

    Pseudo-Bartter syndrome (PBS) describes an uncommon complication of cystic fibrosis leading to hypochloraemic, hypokalaemic metabolic alkalosis. PBS as the sole manifestation of cystic fibrosis in children is extremely rare and has never been described in patients carrying 5T variant. We report a clinical, biochemical and genetic study of a four year-old boy presenting a pseudo-Bartter syndrome as the sole manifestation of cystic fibrosis. All 27 exons and the flanking intron regions of the CFTR gene were analysed by PCR and direct sequencing. Direct sequencing was also used to analyse TG m T n and M470V polymorphisms in the patient and his parents. Two sweat tests were abnormal with elevated chloride levels at 78 and 88 mmol/L. DNA sequencing revealed a heterozygous mutation 711+1 G>T and an IVS8-T5 allele. The mutation 711+1 G>T is in trans with the IVS8-T5-TG11 allele and the child carried M470/V470 genotype. To the best of our knowledge, the genotype 711+1 G>T /IVS8-5T found in our patient is described for the first time. The role of TG11-5T-V470 allele in cases of cystic fibrosis with PB syndrome remains to be determined.

  2. Dysfunctional breathing: a review of the literature and proposal for classification

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    Richard Boulding

    2016-09-01

    Full Text Available Dysfunctional breathing is a term describing breathing disorders where chronic changes in breathing pattern result in dyspnoea and other symptoms in the absence or in excess of the magnitude of physiological respiratory or cardiac disease. We reviewed the literature and propose a classification system for the common dysfunctional breathing patterns described. The literature was searched using the terms: dysfunctional breathing, hyperventilation, Nijmegen questionnaire and thoraco-abdominal asynchrony. We have summarised the presentation, assessment and treatment of dysfunctional breathing, and propose that the following system be used for classification. 1 Hyperventilation syndrome: associated with symptoms both related to respiratory alkalosis and independent of hypocapnia. 2 Periodic deep sighing: frequent sighing with an irregular breathing pattern. 3 Thoracic dominant breathing: can often manifest in somatic disease, if occurring without disease it may be considered dysfunctional and results in dyspnoea. 4 Forced abdominal expiration: these patients utilise inappropriate and excessive abdominal muscle contraction to aid expiration. 5 Thoraco-abdominal asynchrony: where there is delay between rib cage and abdominal contraction resulting in ineffective breathing mechanics. This review highlights the common abnormalities, current diagnostic methods and therapeutic implications in dysfunctional breathing. Future work should aim to further investigate the prevalence, clinical associations and treatment of these presentations.

  3. Renal acidification responses to respiratory acid-base disorders.

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    Madias, Nicolaos E

    2010-01-01

    Respiratory acid-base disorders are those abnormalities in acid-base equilibrium that are expressed as primary changes in the arterial carbon dioxide tension (PaCO2). An increase in PaCO2 (hypercapnia) acidifies body fluids and initiates the acid-base disturbance known as respiratory acidosis. By contrast, a decrease in PaCO2 (hypocapnia) alkalinizes body fluids and initiates the acid-base disturbance known as respiratory alkalosis. The impact on systemic acidity of these primary changes in PaCO2 is ameliorated by secondary, directional changes in plasma [HCO3¯] that occur in 2 stages. Acutely, hypercapnia or hypocapnia yields relatively small changes in plasma [HCO3¯] that originate virtually exclusively from titration of the body's nonbicarbonate buffers. During sustained hypercapnia or hypocapnia, much larger changes in plasma [HCO3¯] occur that reflect adjustments in renal acidification mechanisms. Consequently, the deviation of systemic acidity from normal is smaller in the chronic forms of these disorders. Here we provide an overview of the renal acidification responses to respiratory acid-base disorders. We also identify gaps in knowledge that require further research.

  4. Sleep disturbances in patients admitted to a step-down unit after ICU discharge: the role of mechanical ventilation.

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    Fanfulla, Francesco; Ceriana, Piero; D'Artavilla Lupo, Nadia; Trentin, Rossella; Frigerio, Francesco; Nava, Stefano

    2011-03-01

    Severe sleep disruption is a well-documented problem in mechanically ventilated, critically ill patients during their time in the intensive care unit (ICU), but little attention has been paid to the period when these patients become clinically stable and are transferred to a step-down unit (SDU). We monitored the 24-h sleep pattern in 2 groups of patients, one on mechanical ventilation and the other breathing spontaneously, admitted to our SDU to assess the presence of sleep abnormalities and their association with mechanical ventilation. Twenty-two patients admitted to an SDU underwent 24-h polysomnography with monitoring of noise and light. One patient did not complete the study. At night, 10 patients showed reduced sleep efficiency, 6 had reduced percentage of REM sleep, and 3 had reduced percentage of slow wave sleep (SWS). Sleep amount and quality did not differ between patients breathing spontaneously and those on mechanical ventilation. Clinical severity (SAPS(II) score) was significantly correlated with daytime total sleep time and efficiency (r = 0.51 and 0.5, P sleep quantity and quality; and higher PaO(2) was correlated with increased SWS (r = 0.49; P = 0.02). Patients admitted to an SDU after discharge from an ICU still have a wide range of sleep abnormalities. These abnormalities are mainly associated with a high severity score and alkalosis. Mechanical ventilation does not appear to be a primary cause of sleep impairment.

  5. [Gitelman's syndrome: an important differential diagnosis of hypokalemia].

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    Kurschat, C; Heering, P; Grabensee, B

    2003-05-30

    A 26-year-old woman presented with fatigue, muscle cramps and weakness. Since the age of 8 years she had moderate hypokalemia of unknown origin that was confirmed on multiple occasions. There was no family history of disease. Laboratory tests showed moderate to severe hypokalemia with a serum potassium concentration of 2.7 to 3.0 mmol/l, hypomagnesemia, metabolic alkalosis and pronounced stimulation of the renin-angiotensin-aldosterone system. Despite normal serum calcium levels, urinary calcium excretion was below the detection threshold. Increased natriuresis was observed after administration of furosemide, but not after administration of hydrochlorothiazide. This finding pointed to the presence of a non-functional thiazide-sensitive sodium/chloride cotransporter in the distal convoluted tubule, characteristic for Gitelman's syndrome. Genetic analysis confirmed the diagnosis of Gitelman's syndrome and documented two heterozygous mutations in the gene encoding the sodium/chloride cotransporter. The patient was treated with 160 mmol potassium and 30 mmol magnesium supplementation per day. Serum potassium was normalized and magnesium serum levels increased. Weakness and fatigue improved markedly. Gitelman's syndrome is an important differential diagnosis in the evaluation of the normotensive patient with hypokalemia.

  6. Effect of Modified Alkaline Supplementation on Syngenic Melanoma Growth in CB57/BL Mice.

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    Tommaso Azzarito

    Full Text Available Tumor extracellular acidity is a hallmark of malignant cancers. Thus, in this study we evaluated the effects of the oral administration of a commercially available water alkalizer (Basenpulver® (BP on tumor growth in a syngenic melanoma mouse model. The alkalizer was administered daily by oral gavage starting one week after tumor implantation in CB57/BL mice. Tumors were calipered and their acidity measured by in vivo MRI guided 31P MRS. Furthermore, urine pH was monitored for potential metabolic alkalosis. BP administration significantly reduced melanoma growth in mice; the optimal dose in terms of tolerability and efficacy was 8 g/l (p< 0.05. The in vivo results were supported by in vitro experiments, wherein BP-treated human and murine melanoma cell cultures exhibited a dose-dependent inhibition of tumor cell growth. This investigation provides the first proof of concept that systemic buffering can improve tumor control by itself and that this approach may represent a new strategy in prevention and/or treatment of cancers.

  7. Congenital chloride diarrhea: a review of twelve Arabian children

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    Elrefae F

    2013-06-01

    Full Text Available Fawaz Elrefae,1 Ahmed Farag Elhassanien,2 Hesham Abdel-Aziz Alghiaty3 1Pediatric Gastroenterology, Al-Adan Hospital, Kuwait; 2Faculty of Medicine, Elmansoura University, El Mansoura, El Dakahleya, Egypt; 3Faculty of Medicine, Benha University, Egypt Background: Congenital chloride diarrhea (CCD, a rare autosomal recessive disorder, is characterized by sustained watery diarrhea (due to defect of active Chloride/HCO3 exchange in the ileum and colon with high fecal chloride. Objective: To spotlight the common presentation of CCD for early management and prevention of complications. Subjects and methods: This is a retrospective case series study of patients diagnosed as CCD who were followed up in the pediatric department of Al-Adan Hospital, Kuwait. Results: Twelve patients diagnosed with CCD were born to consanguineous parents; had antenatal history of intrauterine growth retardation (IUGR; polyhydramnios; and distended hypoechoic fetal bowel; and presented with abdominal distension, hypotonia and muscle wasting. 90% of patients had maternal hypertension and 75% of patients had absence of normal meconium at birth. Our patients showed a decrease in serum sodium, potassium, chloride and urine chloride. Conclusion: A high level of suspicion for an early diagnosis of CCD should be considered for any infant presenting with chronic diarrhea, especially in the presence of consanguineous marriage, and the characteristic features in antenatal ultrasound. Thus, allowing for early investigations and appropriate management. Keywords: congenital chloride diarrhea, children, chronic diarrhea, metabolic alkalosis, prenatal diagnosis

  8. Hypercalcemia due to Milk –Alkali Syndrome and Fracture-induced Immobilization in an Adolescent Boy with Hypoparathyroidism

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    Henry, Rohan K.; Gafni, Rachel I.

    2016-01-01

    Background Hypercalcemia of immobilization, while rare, may occur in adolescent boys after fracture. Although not fully understood, the mechanism appears to be related to bone turnover uncoupling, in part mediated by upregulation of RANKL. Animal studies suggest that parathyroidectomy suppresses RANKL-stimulated osteoclastogenesis in immobilized bone. Thus, immobilization-induced hypercalcemia should be uncommon in patients with hypoparathyroidism. Methods/Results We present a 15-year-old boy with well-controlled hypoparathyroidism who developed hypercalcemia and milk-alkali syndrome 5 weeks after sustaining a severe tibia/fibula fracture requiring bedrest. Milk-alkali syndrome (hypercalcemia, alkalosis, and renal insufficiency) results from chronic excessive ingestion of calcium and absorbable alkali. Prior to fracture, our patient had not experienced hypercalcemia despite high doses of supplements, necessary during puberty. Supplements were discontinued and his biochemistries normalized with saline diuresis and a dose of pamidronate. Alkaline phosphatase, which was low at presentation, returned to normal 5 weeks later with remobilization. Conclusions Fracture and immobilization caused acute suppression of bone formation with persistent bone resorption in this rapidly growing adolescent; continuation of carbonate-containing calcium supplements resulted in the milk-alkali syndrome. Therefore, close monitoring of serum calcium with adjustments in supplementation are indicated in immobilized patients with hypoparathyroidism. PMID:27184240

  9. Hypercalcemia due to Milk-Alkali Syndrome and Fracture-Induced Immobilization in an Adolescent Boy with Hypoparathyroidism.

    Science.gov (United States)

    Henry, Rohan K; Gafni, Rachel I

    2016-01-01

    Hypercalcemia of immobilization, while rare, may occur in adolescent boys after fracture. Although not fully understood, the mechanism appears to be related to bone turnover uncoupling, in part mediated by upregulation of RANKL. Animal studies suggest that parathyroidectomy suppresses RANKL-stimulated osteoclastogenesis in immobilized bone. Thus, immobilization-induced hypercalcemia should be uncommon in patients with hypoparathyroidism. We present a 15-year-old boy with well-controlled hypoparathyroidism who developed hypercalcemia and milk-alkali syndrome 5 weeks after sustaining a severe tibia/fibula fracture requiring bedrest. Milk-alkali syndrome (hypercalcemia, alkalosis, and renal insufficiency) results from chronic excessive ingestion of calcium and absorbable alkali. Prior to fracture, our patient had not experienced hypercalcemia despite high doses of supplements, necessary during puberty. Supplements were discontinued and his biochemistries normalized with saline diuresis and a dose of pamidronate. Alkaline phosphatase, which was low at presentation, returned to normal 5 weeks later with remobilization. Fracture and immobilization caused acute suppression of bone formation with persistent bone resorption in this rapidly growing adolescent; continuation of carbonate-containing calcium supplements resulted in the milk-alkali syndrome. Therefore, close monitoring of serum calcium with adjustments in supplementation are indicated in immobilized patients with hypoparathyroidism. © 2016 S. Karger AG, Basel.

  10. EFEITOS DA SUPLEMENTAÇÃO DE BICARBONATO DE SÓDIO EM UM TESTE ERGOMÉTRICO DE ESFORÇO CRESCENTE EM HOMENS RECREACIONALMENTE ATIVOS

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    Everton Marcio Derisso

    2014-02-01

    Full Text Available The supplementation of sodium bicarbonate (NaHCO3 is being used as a way to induce blood alkalosis and increase the buffering chemical capacity. The literature shows a need for studies that use supplemental NaHCO3 at high intensities lasting more than 5 minutes. This study compares the effect of supplementation of NaHCO3 in speed corresponding to maximum working speed (vMAX and the respiratory compensation point (vRCP during an incremental treadmill test. We evaluate six recreationally active males (22.00 ± 2.00 years, 81.80 ± 9.90 kg, 1.81 ± 0.06 m and BMI 25 ± 2 kg/m2 and previously trained. The volunteers presented to the laboratory on two different days. They ingested 0.1 g/kg body weight of NaHCO3 (Group B or placebo with calcium carbonate (CaCO3 (Group P and performed an incremental test on a treadmill with 1km/h increments every 2 minutes until volitional exhaustion maximum. There was no significant difference in the velocities corresponding to vPCR and vMAX with supplementation of NaHCO3 and in any respiratory parameter. The ingestion of NaHCO3 at a concentration of 0.1 g/kg body weight does not improve performance in an incremental test on a treadmill.

  11. Hypersensitivity Reaction and Acute Respiratory Distress Syndrome in Pyrethroid Poisoning and Role of Steroid Therapy

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    Jisa George

    2015-06-01

    Full Text Available Background: Pyrethroids are generally of low toxicity to humans, but in suicidal poisonings which are usually associated with ingestion of high doses, they lead to severe systemic effects. Case Report: A 30-year old woman presented to emergency department with a history of intentional ingestion of about 15 mL of prallethrin around 3 days earlier. She complained of shortness of breath along with chest pain for the last 2 days. She reported no vomiting or stomach pain prior to presentation to hospital. On chest auscultation, breath sounds were mildly decreased in bilateral infrascapular areas with generalized crepitation. Arterial blood gas analysis revealed respiratory alkalosis. Chest X ray and computed tomography of thorax revealed widespread confluent areas of consolidation with interlobular septal thickening involving bilateral parahilar regions suggestive of acute respiratory distress syndrome (ARDS. The patient did not respond to broad spectrum antibiotic coverage, diuretics and oxygen inhalation. Intravenous methylprednisolone (2 mg/kg/day divided 6 hourly was started and slowly tapered off during the next days. The patient discharged after 3 weeks in good health. Discussion: As pyrethroids can affect sodium channels, the osmotic gradient of alveolar epithelium probably disrupts and therefore, alveolar infiltrations gradually spread over lungs. In addition, there is a possibility of hypersensitivity reactions to pyrethroids, which can cause progressive inflammation and involve respiratory tract in severe cases. Conclusion: Pyrethroid poisoning can lead to ARDS. Steroid therapy may help such patients tide over the pulmonary crisis.

  12. Proximal duodenoileal anastomosis for treatment of small intestinal obstruction and volvulus in a green iguana (Iguana iguana).

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    Wills, Sarah; Beaufrère, Hugues; Watrous, Gwyneth; Oblak, Michelle L; Smith, Dale A

    2016-11-01

    CASE DESCRIPTION A 13-year-old female green iguana (Iguana iguana) was examined because of a 6-day history of vomiting, anorexia, and lethargy and a 4-day history of decreased fecal and urate output. CLINICAL FINDINGS Physical examination revealed a distended abdomen, signs of depression, pallor, tachycardia, harsh lung sounds, and vomiting. Abdominal radiographs revealed gas distention of the stomach and small intestine with fluid lines evident on the lateral view. Plasma biochemical analysis indicated hypochloremic metabolic alkalosis, hyperglycemia, and hyperuricemia. TREATMENT AND OUTCOME Exploratory laparotomy confirmed a diagnosis of small intestinal entrapment and 170° volvulus involving approximately 80% (20 to 30 cm) of the small intestine. The portion of the small intestine extending from the middle portion of the duodenum to the caudal extent of the ileum was resected, and end-to-end anastomosis of the remaining small intestine was performed. The iguana recovered without apparent complications and was reportedly doing well 1 year after surgery. CLINICAL RELEVANCE Findings suggested that iguanas, as hindgut fermenters, may tolerate > 70% resection of the small intestine with a good outcome and no clinical evidence of residual gastrointestinal dysfunction.

  13. Differences in Hematological Traits between High- and Low-Altitude Lizards (Genus Phrynocephalus.

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    Songsong Lu

    Full Text Available Phrynocephalus erythrurus (Lacertilia: Agamidae is considered to be the highest living reptile in the world (about 4500-5000 m above sea level, whereas Phrynocephalus przewalskii inhabits low altitudes (about 1000-1500 m above sea level. Here, we report the differences in hematological traits between these two different Phrynocephalus species. Compared with P. przewalskii, the results indicated that P. erythrurus own higher oxygen carrying capacity by increasing red blood cell count (RBC, hemoglobin concentration ([Hb] and hematocrit (Hct and these elevations could promote oxygen carrying capacity without disadvantage of high viscosity. The lower partial pressure of oxygen in arterial blood (PaO2 of P. erythrurus did not cause the secondary alkalosis, which may be attributed to an efficient pulmonary system for oxygen (O2 loading. The elevated blood-O2 affinity in P. erythrurus may be achieved by increasing intrinsic O2 affinity of isoHbs and balancing the independent effects of potential heterotropic ligands. We detected one α-globin gene and three β-globin genes with 1 and 33 amino acid substitutions between these two species, respectively. Molecular dynamics simulation results showed that amino acids substitutions in β-globin chains could lead to the elimination of hydrogen bonds in T-state Hb models of P. erythrurus. Based on the present data, we suggest that P. erythrurus have evolved an efficient oxygen transport system under the unremitting hypobaric hypoxia.

  14. Association between serum bicarbonate and pH with depression, cognition and sleep quality in hemodialysis patients.

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    Afsar, Baris; Elsurer, Rengin

    2015-07-01

    Metabolic acidosis is a common feature in chronic renal failure patients, worsening progressively as renal function declines. There are conflicting data in hemodialysis (HD) patients with regard to acidosis, alkalosis and mortality. In HD patients, cognitive impairment, depression, sleep disorders and impaired quality of life are very common. Besides, these conditions are related with increased morbidity and mortality. However, no previous study investigated the relationship between pH, venous bicarbonate and anion gap with depression, sleep problems and cognitive function in HD patients. In this study we investigated these relationships. In total, 65 HD patients were included. The demographic parameters and laboratory parameters including bicarbonate, pH and anion gap was measured for all patients. Depressive symptoms, sleep quality and cognitive function, were measured by Beck depression inventory, The Pittsburgh Sleep Quality Index and by Mini Mental State Examination, respectively. We found that, sleep quality but not cognitive function or depression was independently related with venous pH and bicarbonate. Anion gap has no independent relationship with sleep quality, cognitive function and depression. In conclusion, metabolic acidosis and bicarbonate levels were independently related with sleep quality in HD patients. However, there was no association between metabolic acidosis and bicarbonate levels with cognitive function and depression.

  15. Unusual Complication of Multidrug Resistant Tuberculosis

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    Prerna Sharma

    2017-01-01

    Full Text Available Introduction. Capreomycin is a second-line drug often used for multidrug-resistant tuberculosis which can result in nephrotoxic effects similar to other aminoglycosides. We describe a case of capreomycin induced Bartter-like syndrome with hypocalcemic tetany. Case Report. 23-year-old female patient presented with carpopedal spasms and tingling sensations in hands. Patient was being treated with capreomycin for two months for tuberculosis. On further investigation, hypocalcemia, hyponatremia, hypomagnesemia, hypokalemia, and hypochloremic metabolic alkalosis were noted. Vitamin D and serum PTH levels were within normal limits. Hypercalciuria was confirmed by urine calcium/creatinine ratio. Calcium, potassium, and magnesium supplementation was given and capreomycin was discontinued. Electrolytes normalized in two days after cessation of capreomycin with no further abnormalities on repeat investigations. Discussion. Aminoglycosides can result in renal tubular dysfunction leading to Fanconi syndrome, Bartter syndrome, and distal tubular acidosis. Impaired mitochondrial function in the tubular cells has been hypothesized as the possible cause of these tubulopathies. Acquired Bartter-like syndrome phenotypically resembles autosomal dominant type 5 Bartter syndrome. Treatment consists of correction of electrolyte abnormalities, indomethacin, and potassium-sparing diuretics. Prompt diagnosis and treatment of severe dyselectrolytemia are warranted in patients on aminoglycoside therapy.

  16. Using phosphate supplementation to reverse hypophosphatemia and phosphate depletion in neurological disease and disturbance.

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    Håglin, Lena

    2016-06-01

    Hypophosphatemia (HP) with or without intracellular depletion of inorganic phosphate (Pi) and adenosine triphosphate has been associated with central and peripheral nervous system complications and can be observed in various diseases and conditions related to respiratory alkalosis, alcoholism (alcohol withdrawal), diabetic ketoacidosis, malnutrition, obesity, and parenteral and enteral nutrition. In addition, HP may explain serious muscular, neurological, and haematological disorders and may cause peripheral neuropathy with paresthesias and metabolic encephalopathy, resulting in confusion and seizures. The neuropathy may be improved quickly after proper phosphate replacement. Phosphate depletion has been corrected using potassium-phosphate infusion, a treatment that can restore consciousness. In severe ataxia and tetra paresis, complete recovery can occur after adequate replacement of phosphate. Patients with multiple risk factors, often with a chronic disease and severe HP that contribute to phosphate depletion, are at risk for neurologic alterations. To predict both risk and optimal phosphate replenishment requires assessing the nutritional status and risk for re-feeding hypophosphatemia. The strategy for correcting HP depends on the severity of the underlying disease and the goal for re-establishing a phosphate balance to limit the consequences of phosphate depletion.

  17. Hypophosphatemia. From retrospective analysis to the analysis of the potential role of phosphatemia in panic disorders

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    Alessandro Riccardi

    2010-09-01

    Full Text Available The detection of a low serum phosphate level is not unusual in an Emergency Department, especially in clinical conditions linked to hyperventilation and subsequent respiratory alkalosis, asthma, sepsis, severe pain, anxiety. Symptoms of hypophosphatemia are typically not specific when the imbalance is not particularly severe, but if hyphophosphatemia does not resolve rhabdomyolisis, hemolysis, decreased tissue oxygenation and respiratory failure can be observed. Only recently some authors have pointed out that the level of serum phosphate in patient with anxiety and panic disorders can give information on the severity of the attacks as well on the clinical course of the disease. In a retrospective analysis on 599 case of hypophosphatemia observed in our ED, the percentage of case of panic disorders was particularly high among patients with lower phosphatemia. Therefore, we decided to examine this aspect closely, assessing if the determination of serum phosphate could be useful in the management of panic attacks at first approach in emergency room. Our observation are consistent with the statement that hypophosphatemia is one of the main clinical aspect of panic attack, and strongly support the hypothesis that hypophosphatemia correlates with the most severe symptoms of panic attack and should be itself considered as one of the most important aspect of this syndrome. Serum phosphate levels appear to mirror its clinical course, and can be used in the clinical setting of an Emergency Department, for the confirmation of a diagnosis of anxiety-panic disorder and as marker of the response to therapy

  18. Is CO2 gas unsufflator necessary for laparoscopic training in animals?

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    Tiraboshi Ricardo Brianezi

    2003-01-01

    Full Text Available OBJECTIVE: To verify the efficacy and safety of compressed air to produce pneumoperitoneum for laparoscopic surgery in pigs for a training program of residence. METHODS: Dalland pigs weighing 15-17kg underwent general anethesia and mechanical ventilation. They were divided in 3 groups: A - (38 the pneumoperitnoneum was established with an automatic CO2 insufflator, B - (7 as in A except the CO2 gas was changed by compressed air, and C - (11 abdomen insufflation was obtained with compressed air directly from hospital pipe network system. Intra-abdominal pressure in all groups was kept between 12 and 15 mmHg. The laparoscopic procedures performed were distributed proportionally among groups: 20 bilateral nephrectomy, 20 dismembered pyeloplasty and 16 partial nephrectomy. Arterial blood sampling for gasometry was obtained before and 2h after establishment of pneumoperitoneum in 5 pigs of group C. RESULTS: The cost of 25 4,5kg CO2 container used in group A was R$ 3,150.00 (U$ 1,050.00. The mean length time of surgeries in groups A, B and C were respectively: 181±30min, 196±39min e 210±47min (p>0.05. Respiratory alkalosis occurred in 3 out of 5 pigs of group C. No animal exhibited signs of gas embolism or died during surgery. CONCLUSION: The use of compressed air for laparoscopy in pigs was safe, reduced costs and did not require the use of an automatic gas insufflator.

  19. The importance of the ionic product for water to understand the physiology of the acid-base balance in humans.

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    Adeva-Andany, María M; Carneiro-Freire, Natalia; Donapetry-García, Cristóbal; Rañal-Muíño, Eva; López-Pereiro, Yosua

    2014-01-01

    Human plasma is an aqueous solution that has to abide by chemical rules such as the principle of electrical neutrality and the constancy of the ionic product for water. These rules define the acid-base balance in the human body. According to the electroneutrality principle, plasma has to be electrically neutral and the sum of its cations equals the sum of its anions. In addition, the ionic product for water has to be constant. Therefore, the plasma concentration of hydrogen ions depends on the plasma ionic composition. Variations in the concentration of plasma ions that alter the relative proportion of anions and cations predictably lead to a change in the plasma concentration of hydrogen ions by driving adaptive adjustments in water ionization that allow plasma electroneutrality while maintaining constant the ionic product for water. The accumulation of plasma anions out of proportion of cations induces an electrical imbalance compensated by a fall of hydroxide ions that brings about a rise in hydrogen ions (acidosis). By contrast, the deficiency of chloride relative to sodium generates plasma alkalosis by increasing hydroxide ions. The adjustment of plasma bicarbonate concentration to these changes is an important compensatory mechanism that protects plasma pH from severe deviations.

  20. Physiologic and Pharmacokinetic Changes in Pregnancy

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    Maged eCostantine

    2014-04-01

    Full Text Available Physiologic changes in pregnancy induce profound alterations to the pharmacokinetic properties of many medications. These changes affect distribution, absorption, metabolism, and excretion of drugs, and thus may impact their pharmacodynamic properties during pregnancy. Pregnant women undergo several adaptations in many organ systems. Some adaptations are secondary to hormonal changes in pregnancy, while others occur to support the gravid woman and her developing fetus. Some of the changes in maternal physiology during pregnancy include, for example, increased maternal fat and total body water, decreased plasma protein concentrations, especially albumin, increased maternal blood volume, cardiac output and blood flow to the kidneys and uteroplacental unit, and decreased blood pressure. The maternal blood volume expansion occurs at a larger proportion than the increase in red blood cell mass, which results in physiologic anemia and hemodilution. Other physiologic changes include increased tidal volume, partially compensated respiratory alkalosis, delayed gastric emptying and gastrointestinal motility, and altered activity of hepatic drug metabolizing enzymes. Understating these changes and their profound impact on the pharmacokinetic properties of drugs in pregnancy is essential to optimize maternal and fetal health.

  1. Rare exonic deletions implicate the synaptic organizer Gephyrin (GPHN) in risk for autism, schizophrenia and seizures.

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    Lionel, Anath C; Vaags, Andrea K; Sato, Daisuke; Gazzellone, Matthew J; Mitchell, Elyse B; Chen, Hong Yang; Costain, Gregory; Walker, Susan; Egger, Gerald; Thiruvahindrapuram, Bhooma; Merico, Daniele; Prasad, Aparna; Anagnostou, Evdokia; Fombonne, Eric; Zwaigenbaum, Lonnie; Roberts, Wendy; Szatmari, Peter; Fernandez, Bridget A; Georgieva, Lyudmila; Brzustowicz, Linda M; Roetzer, Katharina; Kaschnitz, Wolfgang; Vincent, John B; Windpassinger, Christian; Marshall, Christian R; Trifiletti, Rosario R; Kirmani, Salman; Kirov, George; Petek, Erwin; Hodge, Jennelle C; Bassett, Anne S; Scherer, Stephen W

    2013-05-15

    The GPHN gene codes for gephyrin, a key scaffolding protein in the neuronal postsynaptic membrane, responsible for the clustering and localization of glycine and GABA receptors at inhibitory synapses. Gephyrin has well-established functional links with several synaptic proteins that have been implicated in genetic risk for neurodevelopmental disorders such as autism spectrum disorder (ASD), schizophrenia and epilepsy including the neuroligins (NLGN2, NLGN4), the neurexins (NRXN1, NRXN2, NRXN3) and collybistin (ARHGEF9). Moreover, temporal lobe epilepsy has been linked to abnormally spliced GPHN mRNA lacking exons encoding the G-domain of the gephyrin protein, potentially arising due to cellular stress associated with epileptogenesis such as temperature and alkalosis. Here, we present clinical and genomic characterization of six unrelated subjects, with a range of neurodevelopmental diagnoses including ASD, schizophrenia or seizures, who possess rare de novo or inherited hemizygous microdeletions overlapping exons of GPHN at chromosome 14q23.3. The region of common overlap across the deletions encompasses exons 3-5, corresponding to the G-domain of the gephyrin protein. These findings, together with previous reports of homozygous GPHN mutations in connection with autosomal recessive molybdenum cofactor deficiency, will aid in clinical genetic interpretation of the GPHN mutation spectrum. Our data also add to the accumulating evidence implicating neuronal synaptic gene products as key molecular factors underlying the etiologies of a diverse range of neurodevelopmental conditions.

  2. Concentrations of prealbumin and some appetite-controlling hormones in pregnancies associated with hyperemesis gravidarium.

    Science.gov (United States)

    Ozturk, Gulfer; Ozgu-Erdinc, A Seval; Ucar, Fatma; Ginis, Zeynep; Erden, Gonul; Danisman, Nuri

    2017-03-01

    Background Hyperemesis gravidarum, which affects 0.3-2.3% of pregnancies, is defined as excessive vomiting during pregnancy and usually starts in week 4 or 5 of gestation. Symptoms include weight loss, dehydration, ketonaemia, ketonuria, fasting acidosis, alkalosis due to hydrochloric acid loss and hypokalaemia and its exact cause is unknown. The present study was undertaken to investigate the relationship between prealbumin, ghrelin, nesfatin-1 and obestatin concentrations in pregnancies associated with hyperemesis gravidarum. Methods A total of 40 pregnant females with hyperemesis gravidarum and 38 pregnant females without hyperemesis gravidarum as controls were included in this study. Serum concentrations of prealbumin, ghrelin, obestatin and nesfatin-1 were measured. Results There were no significant differences in age, gestational week, gravidity and parity between the two groups. Body mass index was significantly lower in cases than in controls. Serum ghrelin and prealbumin concentrations were significantly lower in cases than in controls ( P  hyperemesis gravidarum. Conclusions Decreased serum concentrations of ghrelin and prealbumin in patients with hyperemesis gravidarum are independent of body mass index. Based on our results, we believe that ghrelin may be considered to play a role in the aetiopathogenesis of hyperemesis gravidarum and that hyperemesis gravidarum may result in disruption of the relationship between nesfatin-1 and ghrelin. In addition, we believe that the measurement of serum prealbumin may be used for assessing nutritional status in pregnancy.

  3. Secretin stimulates HCO3(-) and acetate efflux but not Na+/HCO3(-) uptake in rat pancreatic ducts

    DEFF Research Database (Denmark)

    Novak, I; Christoffersen, B C

    2001-01-01

    to be important in HCO3(-) -transporting epithelia. pHi was measured with BCECF in freshly isolated intralobular ducts. A reduction in extracellular Na+ concentration or application of HOE 694 (1 microM) decreased pHi by 0.1 to 0.6 pH units, demonstrating Na+/H+ exchanger activity. A reduction in extracellular Cl......- concentration or addition of H2DIDS (10 microM) increased pHi by 0.1 to 0.5 pH units, demonstrating Cl-/ HCO(3)- (OH ) exchanger activity. In experimental acidosis, extracellular HCO3(-)/CO2 buffer did not increase the rate of pHi recovery, indicating that provision of HCO3(-) by the Na+/HCO3(-) cotransporter...... was not apparent. Most importantly, Na+/HCO3(-) cotransport was not stimulated by secretin (1 nM). In contrast, in experimental alkalosis the pHi recovery was increased in HCO3(-)/CO2 buffer, possibly due to Na+/HCO3(-) cotransport in the efflux mode. Secretin (1 nM) and carbachol (1 microM) stimulated HCO3...

  4. Po2 temperature blood factor for blood gas apparatus.

    Science.gov (United States)

    Teisseire, B P; Hérigault, R A; Teisseire, L J; Laurent, D N

    1984-01-01

    PO2 temperature formulae supplied by manufacturers on automatic blood gas apparatus, PO2 corr. = PO2 37 degrees C X 10F X delta T were studied and compared to the experimental determination of the delta log PO2/delta T ratio (Hérigault et al. [10]). Acid-base status at 37 degrees C appeared to have a measurable influence on the PO2 temperature factor; alkalosis increased the delta log PO2/delta T ratio, and the contrary was found for acidosis in comparison with normal acid-base status at 37 degrees C. For the same PO2, measured at 37 degrees C, all the proposed formulae of commercial blood gas automatic apparatus did not give the same temperature corrected PO2. The observed difference between the corrected PO2 may be important and greater than the precision of the initial measurement. To correct the measured PO2 for temperature, a relationship between delta log PO2/delta T and PO2 is proposed, between PO2 zero and PO2 180 mmHg, which takes into account measured pH and PO2 values at 37 degrees C:delta log PO2/delta T = [(-0.35 pH + 0.658) X 10(-4) X PO2] + 0.035.

  5. The physiological stress response to high-intensity sprint exercise following the ingestion of sodium bicarbonate.

    Science.gov (United States)

    Peart, Daniel J; Kirk, Richard J; Hillman, Angela R; Madden, Leigh A; Siegler, Jason C; Vince, Rebecca V

    2013-01-01

    The purpose of this study was to investigate the effects of pre-exercise alkalosis on the physiological stress response to high-intensity exercise. Seven physically active males (age 22 ± 3 years, height 1.82 ± 0.06 m, mass 81.3 ± 8.4 kg and peak power output 300 ± 22 W) performed a repeated sprint cycle exercise following a dose of 0.3 g kg(-1) body mass of sodium bicarbonate (NaHCO(3)) (BICARB), or a placebo of 0.045 g kg(-1) body mass of sodium chloride (PLAC). Monocyte-expressed heat shock protein 72 (HSP72) and plasma thiobarbituric acid reactive substances (TBARS) were significantly attenuated in BICARB compared to PLAC (p = 0.04 and p = 0.039, respectively), however total anti-oxidant capacity, the ratio of oxidised to total glutathione, cortisol, interleukin 6 and interleukin 8 were not significantly induced by the exercise. In conclusion, monocyte-expressed HSP72 is significantly increased following high-intensity anaerobic exercise, and its attenuation following such exercise with the ingestion of NaHCO(3) is unlikely to be due to a decreased oxidative stress.

  6. The Importance of the Ionic Product for Water to Understand the Physiology of the Acid-Base Balance in Humans

    Directory of Open Access Journals (Sweden)

    María M. Adeva-Andany

    2014-01-01

    Full Text Available Human plasma is an aqueous solution that has to abide by chemical rules such as the principle of electrical neutrality and the constancy of the ionic product for water. These rules define the acid-base balance in the human body. According to the electroneutrality principle, plasma has to be electrically neutral and the sum of its cations equals the sum of its anions. In addition, the ionic product for water has to be constant. Therefore, the plasma concentration of hydrogen ions depends on the plasma ionic composition. Variations in the concentration of plasma ions that alter the relative proportion of anions and cations predictably lead to a change in the plasma concentration of hydrogen ions by driving adaptive adjustments in water ionization that allow plasma electroneutrality while maintaining constant the ionic product for water. The accumulation of plasma anions out of proportion of cations induces an electrical imbalance compensated by a fall of hydroxide ions that brings about a rise in hydrogen ions (acidosis. By contrast, the deficiency of chloride relative to sodium generates plasma alkalosis by increasing hydroxide ions. The adjustment of plasma bicarbonate concentration to these changes is an important compensatory mechanism that protects plasma pH from severe deviations.

  7. Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

    Science.gov (United States)

    Adeva-Andany, María M.; Fernández-Fernández, Carlos; Mouriño-Bayolo, David; Castro-Quintela, Elvira; Domínguez-Montero, Alberto

    2014-01-01

    Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated. PMID:25405229

  8. The importance of genetic counseling and genetic screening: a case report of a 16-year-old boy with resistant hypertension and severe hypokalemia.

    Science.gov (United States)

    Kuang, Ze-Min; Wang, Ying; Wang, Jia-Jie; Liu, Jing-Hua; Zeng, Rong; Zhou, Qi; Yu, Zhen-Qiu; Jiang, Long

    2017-03-01

    Liddle's syndrome, an autosomal dominant form of monogenic hypertension, is characterized by salt-sensitive hypertension with early penetrance, hypokalemia, metabolic alkalosis, suppression of plasma rennin activity and aldosterone secretion, and a clear-cut response to epithelial sodium channel blockers but not spironolactone therapy. Here, we describe the case of a 16-year-old boy patient with resistant hypertension (maintain 170-180/100-110 mm Hg after administration four kinds of antiypertensive drugs) and severe hypokalemia. After a series of checks, we exclude primary aldosteronism and renal artery stenosis and other diseases. Finally, the Liddle syndrome was diagnosed because of the DNA sequencing found that the proband's mother and himself had mutations P616L (c.1847 C>T) in the SCNN1B gene. Liddle syndrome should be considered as a cause of hypertension in children or adolescents particularly with suppressed renin activity. Early diagnosis and appropriately tailored treatment avoid complications of long-term unrecognized or inappropriately managed hypertension. Genetic testing has made it possible to make accurate diagnoses and develop tailored therapies for mutation carriers. The role of genetic testing and genetic counseling in establishing the early diagnosis of Liddle's syndrome is important. Copyright © 2017 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.

  9. The V-ATPase is expressed in the choroid plexus and mediates cAMP-induced intracellular pH alterations

    DEFF Research Database (Denmark)

    Christensen, Henriette L; Păunescu, Teodor G; Matchkov, Vladimir

    2017-01-01

    The cerebrospinal fluid (CSF) pH influences brain interstitial pH and, therefore, brain function. We hypothesized that the choroid plexus epithelium (CPE) expresses the vacuolar H(+)-ATPase (V-ATPase) as an acid extrusion mechanism in the luminal membrane to counteract detrimental elevations in CSF...... fraction in the luminal microvillus area. The vesicles did not translocate to the luminal membrane in two in vivo models of hypocapnia-induced alkalosis. The Na(+)-independent intracellular pH (pHi) recovery from acidification was studied in freshly isolated clusters of CPECs. At extracellular pH (pHo) 7.......4, the cells failed to display significant concanamycin A-sensitive pHi recovery (i.e., V-ATPase activity). The recovery rate in the absence of Na(+) amounted to Hi recovery rate observed in the presence of Na(+) Recovery of pHi was faster at pHo 7.8 and was abolished at pHo 7.0. The concanamycin...

  10. Monitoring of interstitial buffer systems using micro-dialysis and infrared spectrometry

    Science.gov (United States)

    Heise, H. M.; Cocchieri, L.; Vahlsing, T.; Ihrig, D.; Elm, J.

    2017-02-01

    Nowadays, continuous sensing systems are important point-of-care devices for the hospital and personalized patient technology. FTIR-spectrometers have been successfully employed for the development of bed-side systems. In-vivo applications for critically ill patients can be envisaged for analytes and parameters, which are of interest for intensive care such as lactate, urea, pCO2 and pH. The human body maintains the blood pH around 7.4, but for severe pH level changes acidosis or alkalosis can lead to serious health problems. Three different buffer systems exist based on bicarbonate, phosphate and proteins; for the most important bicarbonate and phosphate systems infrared transmission spectra were recorded. By using the CO2 and HCO3 - bands of the bicarbonate spectra, the pH of the harvested biofluid can be predicted using the Henderson-Hasselbalch equation. Furthermore, we studied the solubility of CO2 in aqueous solutions using gas mixtures of N2 and CO2 with known composition within partial pressures of CO2 as relevant for invivo conditions. Thus, values of pCO2 up to 150 mm Hg (200 hPa) with distilled water and a Ringer solution, which is an isotonic electrolyte solution used for medical infusion, were measured at 25 °C and 37 °C (normal body temperature).

  11. Antenatal Bartter Syndrome: A Review

    Directory of Open Access Journals (Sweden)

    Y. Ramesh Bhat

    2012-01-01

    Full Text Available Antenatal Bartter syndrome (ABS is a rare autosomal recessive renal tubular disorder. The defective chloride transport in the loop of Henle leads to fetal polyuria resulting in severe hydramnios and premature delivery. Early onset, unexplained maternal polyhydramnios often challenges the treating obstetrician. Increasing polyhydramnios without apparent fetal or placental abnormalities should lead to the suspicion of this entity. Biochemical analysis of amniotic fluid is suggested as elevated chloride level is usually diagnostic. Awareness, early recognition, maternal treatment with indomethacin, and amniocentesis allow the pregnancy to continue. Affected neonates are usually born premature, have postnatal polyuria, vomiting, failure to thrive, hypercalciuria, and subsequently nephrocalcinosis. Hypokalemia, metabolic alkalosis, secondary hyperaldosteronism and hyperreninaemia are other characteristic features. Volume depletion due to excessive salt and water loss on long term stimulates renin-angiotensin-aldosterone system resulting in juxtaglomerular hyperplasia. Clinical features and electrolyte abnormalities may also depend on the subtype of the syndrome. Prenatal diagnosis and timely indomethacin administration prevent electrolyte imbalance, restitute normal growth, and improve activity. In this paper, authors present classification, pathophysiology, clinical manifestations, laboratory findings, complications, and prognosis of ABS.

  12. Nephrocalcinosis and Placental Findings in Neonatal Bartter Syndrome

    Directory of Open Access Journals (Sweden)

    Hidehiko Maruyama

    2013-05-01

    Full Text Available Neonatal Bartter syndrome (NBS is an inherited renal tubular disorder associated with hypokalemic alkalosis. Here we report a case of genetically diagnosed NBS. Polyhydramnios was noted at 26 weeks. A boy was born at 31 weeks and 1 day, weighed 1344 g, and had an Apgar score of 8/8. We initiated indomethacin (IND at a dose of 0.2 mg/kg/d on day 31, and increased it to approximately 3 mg/kg/d. However, his urinary calcium (Ca levels remained unchanged. At 4 months of age, nephrocalcinosis was detected by ultrasound. The placenta weighed 700 g (+2.7 standard deviations. Although the proportion of terminal villi was consistent with the gestational age, many of them exhibited poorly dilated capillaries. Hemosiderin pigment was seen throughout the amniochorionic connective tissue and along about 50% of the trophoblast basement membrane (TBM. Von Kossa stain revealed the corresponding area of mineralization along the TBM. In our opinion, urinary Ca levels were high and did not change after IND initiation, indicating that nephrocalcinosis may be inevitable. Enhanced inflow of maternal plasma through the basement membrane would cause Ca deposition, given that the same finding was obtained in the case with polyhydramnios. The same mechanism would also explain the hemosiderin pigment distribution.

  13. Novel molecular variants of the Na-Cl cotransporter gene are responsible for Gitelman syndrome

    Energy Technology Data Exchange (ETDEWEB)

    Mastroianni, N.; De Fusco, M.; Casari, G. [Univsersita` di Milano (Italy)] [and others

    1996-11-01

    A hereditary defect of the distal tubule accounts for the clinical features of Gitelman syndrome (GS), an autosomal recessive disease characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. Recently, we cloned the cDNA coding for the human Na-Cl thiazide-sensitive cotransporter (TSC; also known as {open_quotes}NCCT{close_quotes} or {open_quotes}SLC12A3{close_quotes}) as a possible candidate for GS, and Simon et al., independently, described rotation in patients with GS. Now, we show 12 additional mutations consistent with a loss of function of the Na-Cl cotransporter in GS. Two missense replacements, R09W and P349L, are common to both studies and could represent ancient mutations. The other mutations include three deletions, two insertions, and six missense mutations. When all mutations from both studies are considered, missense mutations seem to be more frequently localized within the intracellular domains of the molecule, rather than in transmembrane or extracellular domains. One family, previously reported as a GS form with dominant inheritance, has proved to be recessive, with the affected child being a compound heterozygote. A highly informative intragenic tetranucleotide marker, useful for molecular diagnostic studies, has been identified at the acceptor splice site of exon 9. 12 refs., 3 figs., 2 tabs.

  14. [Hypertrophic Pyloric Stenosis - Five-Year Retrospective Analysis].

    Science.gov (United States)

    Bašković, M; Župančić, B; Lesjak, N; Vukasović, I

    2016-04-01

    Although the etiology of the disease has not yet been fully clarified in the 21st century, clinical significance of the disease is huge because it is frequent in the neonatal period compared with other diseases. Today, owing to advanced diagnostic possibilities, hypertrophic pyloric stenosis is easily distinguished from other differential diagnoses that are manifested by vomiting as the main symptom. At Department of Pediatric Surgery, Zagreb Children’s Hospital, efforts have been invested to successfully manage this and a number of other conditions that affect newborns. We retrospectively analyzed data on 40 hospitalized children retrieved from the hospital information system for the 2010-2015 period and present them as a basis for the respective algorithms and future research. Reviewing a range of parameters, we have come to some concrete conclusions. On average, the disease started manifesting on 28th day after birth; 63% of the children developed metabolic alkalosis. Thickness of the muscle wall verified by ultrasound ranged from 3.1 mm to 7 mm. Surgery was performed seven days after hospitalization and correction of metabolic condition. The average duration of surgery was 48 minutes. The mean length of hospital stay was 11.64 days, of which 2 days in the intensive care unit. Complications occurred in two patients.

  15. Effect of Intravenously Administered Crystalloid Solutions on Acid-Base Balance in Domestic Animals.

    Science.gov (United States)

    Muir, W

    2017-09-01

    Intravenous fluid therapy can alter plasma acid-base balance. The Stewart approach to acid-base balance is uniquely suited to identify and quantify the effects of the cationic and anionic constituents of crystalloid solutions on plasma pH. The plasma strong ion difference (SID) and weak acid concentrations are similar to those of the administered fluid, more so at higher administration rates and with larger volumes. A crystalloid's in vivo effects on plasma pH are described by 3 general rules: SID > [HCO3-] increases plasma pH (alkalosis); SID solutions has little to no effect on plasma pH because of their low titratable acidity. Appreciation of IV fluid composition and an understanding of basic physicochemical principles provide therapeutically valuable insights about how and why fluid therapy can produce and correct alterations of plasma acid-base equilibrium. The ideal balanced crystalloid should (1) contain species-specific concentrations of key electrolytes (Na + , Cl - , K + , Ca ++ , Mg ++ ), particularly Na + and Cl - ; (2) maintain or normalize acid-base balance (provide an appropriate SID); and (3) be isosmotic and isotonic (not induce inappropriate fluid shifts) with normal plasma. Copyright © 2017 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.

  16. The physiological challenges of the 1952 Copenhagen poliomyelitis epidemic and a renaissance in clinical respiratory physiology

    Science.gov (United States)

    West, John B.

    2005-01-01

    The 1952 Copenhagen poliomyelitis epidemic provided extraordinary challenges in applied physiology. Over 300 patients developed respiratory paralysis within a few weeks, and the ventilator facilities at the infectious disease hospital were completely overwhelmed. The heroic solution was to call upon 200 medical students to provide round-the-clock manual ventilation using a rubber bag attached to a tracheostomy tube. Some patients were ventilated in this way for several weeks. A second challenge was to understand the gas exchange and acid-base status of these patients. At the onset of the epidemic, the only measurement routinely available in the hospital was the carbon dioxide concentration in the blood, and the high values were initially misinterpreted as a mysterious “alkalosis.” However, pH measurements were quickly instituted, the PCO2 was shown to be high, and modern clinical respiratory acid-base physiology was born. Taking a broader view, the problems highlighted by the epidemic underscored the gap between recent advances made by physiologists and their application to the clinical environment. However, the 1950s ushered in a renaissance in clinical respiratory physiology. In 1950 the coverage of respiratory physiology in textbooks was often woefully inadequate, but the decade saw major advances in topics such as mechanics and gas exchange. An important development was the translation of the new knowledge from departments of physiology to the clinical setting. In many respects, this period was therefore the beginning of modern clinical respiratory physiology. PMID:16020437

  17. [Acid-base equilibrium and spinal fluid enzyme activity in newborn infants with pathology of the nervous system].

    Science.gov (United States)

    Tammpere, A Ia; Kaasik, A A; Tal'vik, T A; Paiu, A Iu

    1985-01-01

    The acid-base balance of the blood and cerebrospinal fluid was studied in 90 babies born in asphyxia in order to use these data in assessing the damage to the nervous system. Analysis revealed the hypoxic nature of the cerebral affection which was manifested by anaerobic glycolysis of the cerebral tissue and arterial hypoxemia. The degree of acidosis detected in the cerebrospinal fluid correlated with the severity of the nervous system damage. Children with the lethal outcome presented deeompensated respiratory acidosis, in the cerebrospinal fluid whereas children with severe neurological pathology had alkalosis. It is concluded that alkolosis is induced by an intensified catabolism of the nervous system proteins which leads to the accumulation of ammoniac compounds. The same children showed pulmonary hyperventilation leading to respiratory acidocis which was not related to pulmonary pathology. The latter points to the hypoxic impairment of the respiratory centre. At the same time, a considerable increase in the activity of the glycolytic enzymes was observed; the activity of glutamate oxalacetate transaminase increased 5-fold, the activity of lactate dehydrogenase rose two-fold.

  18. Mineralocorticoid hypertension

    Directory of Open Access Journals (Sweden)

    Vishal Gupta

    2011-01-01

    Full Text Available Hypertension affects about 10 - 25% of the population and is an important risk factor for cardiovascular and renal disease. The renin-angiotensin system is frequently implicated in the pathophysiology of hypertension, be it primary or secondary. The prevalence of primary aldosteronism increases with the severity of hypertension, from 2% in patients with grade 1 hypertension to 20% among resistant hypertensives. Mineralcorticoid hypertension includes a spectrum of disorders ranging from renin-producing pathologies (renin-secreting tumors, malignant hypertension, coarctation of aorta, aldosterone-producing pathologies (primary aldosteronism - Conns syndrome, familial hyperaldosteronism 1, 2, and 3, non-aldosterone mineralocorticoid producing pathologies (apparent mineralocorticoid excess syndrome, Liddle syndrome, deoxycorticosterone-secreting tumors, ectopic adrenocorticotropic hormones (ACTH syndrome, congenitalvadrenal hyperplasia, and drugs with mineraocorticoid activity (locorice, carbenoxole therapy to glucocorticoid receptor resistance syndromes. Clinical presentation includes hypertension with varying severity, hypokalemia, and alkalosis. Ratio of plasma aldosterone concentraion to plasma renin activity remains the best screening tool. Bilateral adrenal venous sampling is the best diagnostic test coupled with a CT scan. Treatment is either surgical (adrenelectomy for unilateral adrenal disease versus medical therapy for idiopathic, ambiguous, or bilateral disease. Medical therapy focuses on blood pressure control and correction of hypokalemia using a combination of anti-hypertensives (calcium channel blockers, angiotensin converting enzyme inhibitors, or angiotensin receptor blockers and potassium-raising therapies (mineralcorticoid receptor antagonist or potassium sparing diuretics. Direct aldosterone synthetase antagonists represent a promising future therapy.

  19. The Measurement of Maximal (Anaerobic Power Output on a Cycle Ergometer: A Critical Review

    Directory of Open Access Journals (Sweden)

    Tarak Driss

    2013-01-01

    Full Text Available The interests and limits of the different methods and protocols of maximal (anaerobic power ( assessment are reviewed: single all-out tests versus force-velocity tests, isokinetic ergometers versus friction-loaded ergometers, measure of during the acceleration phase or at peak velocity. The effects of training, athletic practice, diet and pharmacological substances upon the production of maximal mechanical power are not discussed in this review mainly focused on the technical (ergometer, crank length, toe clips, methodological (protocols and biological factors (muscle volume, muscle fiber type, age, gender, growth, temperature, chronobiology and fatigue limiting in cycling. Although the validity of the Wingate test is questionable, a large part of the review is dedicated to this test which is currently the all-out cycling test the most often used. The biomechanical characteristics specific of maximal and high speed cycling, the bioenergetics of the all-out cycling exercises and the influence of biochemical factors (acidosis and alkalosis, phosphate ions… are recalled at the beginning of the paper. The basic knowledge concerning the consequences of the force-velocity relationship upon power output, the biomechanics of sub-maximal cycling exercises and the study on the force-velocity relationship in cycling by Dickinson in 1928 are presented in Appendices.

  20. Pseudoaldosteronism due to the concurrent use of two herbal medicines containing glycyrrhizin: interaction of glycyrrhizin with angiotensin-converting enzyme inhibitor.

    Science.gov (United States)

    Iida, Rinako; Otsuka, Yasushi; Matsumoto, Kei; Kuriyama, Satoru; Hosoya, Tatsuo

    2006-06-01

    A 77-year-old man with a history of hypertension and hyperuricemia was admitted to our hospital complaining of limb weakness, persistent constipation, and worsening hypertension. He had been taking a Chinese herbal remedy for allergic rhinitis for the past 10 years, together with an angiotensin-converting enzyme inhibitor (ACE-I; enalapril, 20 mg daily). After the dosage of enalapril had been reduced to 10 mg daily about 1(1/2) years before the current admission, he had developed persistent constipation. Therefore, he had started taking another traditional Chinese herbal remedy, a laxative, for the constipation, about 4 months prior to this hospitalization. Laboratory data on admission demonstrated marked metabolic alkalosis with severe hypokalemia associated with urinary wasting of potassium and chloride. A diagnosis of pseudoaldosteronism was made based upon his past history of exposure to various traditional Chinese medicines containing glycyrrhizin. Discontinuation of the Chinese remedies and supplementation of potassium successfully normalized the electrolyte imbalance and relieved all symptoms within a short time. The present case describes the occurrence of pseudoaldosteronism induced by a patient taking two traditional Chinese herbs, both containing glycyrrhizin, resulting in an overdose of this causative chemical agent. The development of pseudoaldosteronism appeared to be of particular interest with regard to the interaction of the renin-angiotensin-aldosterone (RAA) system with glycyrrhizin, in which an ACE-I retarded the development of pseudoaldosteronism.

  1. Liddle Syndrome: Review of the Literature and Description of a New Case

    Directory of Open Access Journals (Sweden)

    Martina Tetti

    2018-03-01

    Full Text Available Liddle syndrome is an inherited form of low-renin hypertension, transmitted with an autosomal dominant pattern. The molecular basis of Liddle syndrome resides in germline mutations of the SCNN1A, SCNN1B and SCNN1G genes, encoding the α, β, and γ-subunits of the epithelial Na+ channel (ENaC, respectively. To date, 31 different causative mutations have been reported in 72 families from four continents. The majority of the substitutions cause an increased expression of the channel at the distal nephron apical membrane, with subsequent enhanced renal sodium reabsorption. The most common clinical presentation of the disease is early onset hypertension, hypokalemia, metabolic alkalosis, suppressed plasma renin activity and low plasma aldosterone. Consequently, treatment of Liddle syndrome is based on the administration of ENaC blockers, amiloride and triamterene. Herein, we discuss the genetic basis, clinical presentation, diagnosis and treatment of Liddle syndrome. Finally, we report a new case in an Italian family, caused by a SCNN1B p.Pro618Leu substitution.

  2. Vertebral Subluxation Repair in a Pet Goat.

    Science.gov (United States)

    Nannarone, Sara; Bellezza, Enrico; Moens, Yves P; Larenza Menzies, Paula

    2017-01-01

    To describe the perioperative management, including surgery, anesthesia, metabolic derangements, and physiotherapy, in a goat referred for paraparesis secondary to a road traffic accident. Case report. 2-year-old mixed breed dwarf 44 kg female pet goat. Clinical examination showed symptoms of early compensatory stages of shock, paraparesis with hyperextension of the thoracic limbs, pain on palpation of the thoracolumbar spine, increased patellar reflexes of both pelvic limbs without superficial sensitivity, but preserved deep pain sensation. These signs suggested a spinal cord injury with upper motor neuron syndrome and an anatomic localization between the third thoracic and third lumbar vertebrae. Radiographic examination revealed a thoracolumbar vertebral subluxation. Vertebral stabilization was achieved with the application of pins in the vertebral bodies stabilized by an interconnecting bridge of polymethylmethacrylate, a technique commonly adopted in companion animals. Surgery and recovery from anesthesia were uneventful, but 3 days later ruminal atony and subsequent bloating occurred. This was associated with metabolic derangements (metabolic alkalosis), decreased mentation, and marked tachypnea that responded to medical treatment. From day 3 post-surgery, the goat underwent physiotherapy with manual and active exercises during the rehabilitation period of 21 days duration. The injury in this goat was successfully managed using vertebral stabilization similar to that used in dogs and cats. Extensive postoperative physiotherapeutic support contributed to the complete recovery of the animal. © 2016 The American College of Veterinary Surgeons.

  3. Apparent mineralocorticoid excess: time of manifestation and complications despite treatment.

    Science.gov (United States)

    Knops, Noël B B; Monnens, Leo A; Lenders, Jacques W; Levtchenko, Elena N

    2011-06-01

    Here we describe the case of a patient followed from birth because of a positive family history for apparent mineralocorticoid excess (AME) in an older brother. The patient, a girl, had normal serum electrolyte and blood pressure measurements in the first months after birth. Not until the age of 11 months did she develop anorexia and failure to thrive in combination with hypertension, hypokalemia, and metabolic alkalosis, which are consistent with the diagnosis of AME. This diagnosis was confirmed by mutation analysis of the HSD11B2 gene (C1228T). Treatment with amiloride and furosemide electrolyte disturbances normalized her blood pressure. At the age of 19 years she unexpectedly suffered a stroke. Additional investigations revealed no accepted risk factor for stroke. We discuss the possible underlying mechanisms for the delayed manifestation of hypertension and electrolyte disturbances in AME, propose an additional explanation for the stroke in this patient, and advise treatment with a mineralocorticoid receptor antagonist to reduce stroke risk in patients with AME.

  4. [Eating disorder or gastrointestinal disease? Massive weight loss and abdominal complaints in a 13-year-old girl].

    Science.gov (United States)

    Teising, S; Buchholtz, A; Layer, P; Keller, J

    2014-09-01

    In a 13-year-old girl regurgitation, constipation and postprandial abdominal pain developed, with decreased nutrient uptake and severe weight loss (BMI 12,6) following a gastroenteritis 2 years before. An eating disorder had been strongly suspected but this diagnosis was not accepted by the family. Initial investigations including physical investigation, elaborate laboratory tests and imaging techniques showed normal results, but we found transit disturbances and hypotensive motility of the upper gastrointestinal tract. Therapy and course of disease: During prokinetic treatment the girl was asymptomatic for about 9 months, but then the symptoms recurred and no longer responded to drug treatment. Feeding via a jejunal tube because of severe malnutrition was not tolerated either. Refractory vomiting and life-threatening hypokalemia and alkalosis occurred. Imaging techniques now showed marked dilatation of the proximal duodenum. Laparotomy was performed because a Wilkie's syndrome was suspected. However, during the operation mesenterial malrotation was found with adhesive fixation of the distal ileum in the upper left abdomen and compression of the proximal jejunum. The malrotation had been possible because the proximal colon was hypermobile. Following correction of the anatomical situation and retroperitoneal fixation of the colon, oral nutrition was well tolerated. The girl gained weight and remained symptom-free. Not only eating disorders but also defined gastroenterological disturbances may cause weight loss and abdominal symptoms in adolescent girls, even in patients with suggestive symptoms and without pathological findings with routine diagnostics. © Georg Thieme Verlag KG Stuttgart · New York.

  5. The effects of fluorocitrate on renal glutamine, lactate, alanine, and oxygen metabolism in the dog.

    Science.gov (United States)

    Fine, A

    1989-06-01

    Acid-base status is considered the major factor controlling renal NH4+ production from glutamine, with maximal values found in chronic acidosis. However, metabolic inhibitors have been shown to increase NH4+ production without acid-base change; the mechanism for this increase is unclear. Fluorocitrate was administered to dogs with chronic metabolic alkalosis. Following fluorocitrate total renal NH4+ production rose from 32 +/- 5 to 104 +/- 15 mumol/(min.100 mL glomerular filtration rate (GFR] (p less than 0.01) and glutamine extraction rose from 26 +/- 8 to 65 +/- 8 mumol/(min.100 mL GFR) (p less than 0.01). These values approximate maximal values found in chronic acidosis. Lactate utilization fell from 165 +/- 19 to 99 +/- 7 mumol/(min.100 mL GFR) following fluorocitrate (p less than 0.01). Citrate extraction fell to zero and alanine production rose from 27 +/- 4 to 46 +/- 7 mumol/(min.100 mL GFR) (p less than 0.01). Oxygen consumption remained unchanged following fluorocitrate, 584 +/- 29 vs. 549 +/- 29 mumol/(min.100 mL GFR). These results demonstrate that in the presence of metabolic inhibition in the kidney, ATP production remains constant. This is achieved by increased utilization of one substrate, glutamine, when the ATP production from other substrates is reduced. Thus the necessity to maintain constant ATP production appears to modulate renal NH4+ production.

  6. Differences in Hematological Traits between High- and Low-Altitude Lizards (Genus Phrynocephalus).

    Science.gov (United States)

    Lu, Songsong; Xin, Ying; Tang, Xiaolong; Yue, Feng; Wang, Huihui; Bai, Yucheng; Niu, Yonggang; Chen, Qiang

    2015-01-01

    Phrynocephalus erythrurus (Lacertilia: Agamidae) is considered to be the highest living reptile in the world (about 4500-5000 m above sea level), whereas Phrynocephalus przewalskii inhabits low altitudes (about 1000-1500 m above sea level). Here, we report the differences in hematological traits between these two different Phrynocephalus species. Compared with P. przewalskii, the results indicated that P. erythrurus own higher oxygen carrying capacity by increasing red blood cell count (RBC), hemoglobin concentration ([Hb]) and hematocrit (Hct) and these elevations could promote oxygen carrying capacity without disadvantage of high viscosity. The lower partial pressure of oxygen in arterial blood (PaO2) of P. erythrurus did not cause the secondary alkalosis, which may be attributed to an efficient pulmonary system for oxygen (O2) loading. The elevated blood-O2 affinity in P. erythrurus may be achieved by increasing intrinsic O2 affinity of isoHbs and balancing the independent effects of potential heterotropic ligands. We detected one α-globin gene and three β-globin genes with 1 and 33 amino acid substitutions between these two species, respectively. Molecular dynamics simulation results showed that amino acids substitutions in β-globin chains could lead to the elimination of hydrogen bonds in T-state Hb models of P. erythrurus. Based on the present data, we suggest that P. erythrurus have evolved an efficient oxygen transport system under the unremitting hypobaric hypoxia.

  7. Determinação de eletrólitos, gases sanguíneos, osmolalidade, hematócrito, hemoglobina, base titulável e anion gap no sangue venoso de equinos destreinados submetidos a exercício máximo e submáximo em esteira rolante Determination of electrolytes, hemogasometry, osmalility, hematocrit, hemoglobin, base concentration, and anion gap in detrained equines submitted a maximum and submaximum exercise on treadmill

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    M.A.G. Silva

    2009-10-01

    Base, SatvO2, and PvO2. So, maximum exercises can lead equines to present metabolic acidosis with respiratory alkalosis as response, hypercalemia and increase in hematocrit and hemoglobin, values. Submaximum exercises can present hypochloremic metabolic alkalosis but no alterations in the hydroelectrolitic balance.

  8. The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder O papel da hiperventilação: a hipocapnia no patomecanismo do distúrbio de pânico

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    Andras Sikter

    2007-12-01

    Full Text Available OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. METHOD: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. DISCUSSION: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2 when the latent (metabolic acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation and catecholamine sensitivity begins to increase. CONCLUSION: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.OBJETIVO: Os autores apresentam um modelo de transtorno do pânico que se baseia nos efeitos da hiperventilação aguda e crônica, característicos do subtipo respiratório de transtorno do pânico. O modelo é generalizado a partir desses efeitos. Ele integra três características da hiperventilação: a hiperventilação é uma resposta fisiológica à hipercapnia; a hiperventilação pode induzir ataques de pânico; a hiperventila

  9. Effect of continuous hemofiltration on internal environment and survival rate of severe heatstroke dogs with shock

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    Guang-ming CHEN

    2011-08-01

    Full Text Available Objective To explore the effect of continuous hemofiltration(CHF on internal environment and survival rate of severe heatstroke dogs with shock.Methods Sixteen healthy male dogs were randomly divided into heatshock group(HS group,n=8 and continuous hemofiltration group(CHF group,n=8.Severe heatstroke model was established by applying high temperature to whole body,and then the animals were removed from the heating cabin as soon as they presented manifestations of shock.Dogs of HS group were put into an ordinary environment,while dogs of CHF group received CHF treatment.The core temperature(Tc,mean arterial pressure(MAP,blood gas analysis,serum electrolytes and survival rate of dogs in two groups were observed.Results The time from heat exposure to shock was 107.0±28.5min and 111.4±22.2min in HS group and CHF group respectively(t=-0.354,P=0.729.The Tc in CHF group declined to normal level 15 to 30 minitues after CHF treatment,while the Tc in HS group remained at a level higher than that before heat exposure at 90min after shock.The Tc of two groups showed significant difference at each time point after shock(P < 0.01.The MAP of both groups was obviously lowered than that before heatstroke.The MAP of CHF group raised gradually 30 min after treatment,while the MAP of HS group rose very slowly,and it was significantly lower than that of CHF group at each time point after 45min(P < 0.05,P < 0.01.All the dogs in both groups manifested hyperventilation and respiratory alkalosis when shock appeared.After shock,respiratory alkalosis in HS group gradually became metabolic acidosis,with some animals manifested combined metabolic and respiratory acidosis because of respiratory decompensation,while the blood gas levels in CHF group recovered to normal gradually.The blood gas levels of two groups showed significant difference at each time point after shock(P < 0.05,P < 0.01.Hypernatremia,hyperchloraemia and hyperpotassaemia were found in all animals of both

  10. Glucose concentration and blood acid-basis status in high-yielding dairy cows during heat stress

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    Vujanac Ivan

    2011-01-01

    Full Text Available The objective of this work was to examine the effect of heat stress on glucose and pH values in blood of high-yielding dairy cows in the early stage of lactation, as well as to determine whether the changes in these parameters are interdependent under such conditions. An experiment was performed on high-yielding dairy cows during the summer and the spring periods. Forty cows were selected, twenty each for the two periods under investigation. In the course of the experiment, the temperature humidity index (THI was determined for the entire period of investigations, and then also the average daily THI, nightmorning THI (average value of hourly THI measured from 22h on the previous day until 10h of the current day, as well as the day-night THI (average value of hourly THI measured during the period from 10h to 22h of the current day. The pH and glucose concentration were determined in blood samples taken in the morning and afternoon of days 30, 60, and 90 of lactation during the spring and summer periods of the investigations. Based on the results for the THI, it was established that the animals were not exposed to the effect of extreme heat stress during the spring period of investigations, while they were periodically exposed to moderate but also extreme heat stress during the summer, in particular in the afternoon hours. It can be concluded from the results obtained for the blood pH that the cows were in respiratory alkalosis during the summer in the morning and afternoon hours on day 30, in the afternoon hours of days 60 and 90 of lactation, as well as in the afternoon on day 90 of lactation during the spring period of investigations. During the summer period, there were no statistically significant differences between the pH value determined in the morning and afternoon hours on day 30 of lactation, while the pH value was significantly higher in the afternoon hours than in the morning hours on days 60 and 90 of lactation. There were no

  11. Etiologic and therapeutic analysis in patients with hypokalemic nonperiodic paralysis.

    Science.gov (United States)

    Sung, Chih-Chien; Cheng, Chih-Jen; Chiang, Wen-Fang; Chau, Tom; Hsu, Yu-Juei; Yang, Sung-Sen; Lin, Shih-Hua

    2015-03-01

    Hypokalemic nonperiodic paralysis represents a group of heterogeneous disorders with a large potassium (K(+)) deficit. Rapid diagnosis of curable causes with appropriate treatment is challenging to avoid the sequelae of hypokalemia. We prospectively analyzed the etiologies and therapeutic characteristics of hypokalemic nonperiodic paralysis. Over an 8-year period, patients with hypokalemic nonperiodic paralysis were enrolled by excluding those with hypokalemic periodic paralysis due to acute shift of K(+) into cells. Blood and spot urine samples were collected for the measurements of electrolytes, pH, and biochemistries. Intravenous potassium chloride (KCl) at a rate of 10-20 mmol/h was administered until muscle strength recovered. We had identified 58 patients with hypokalemic nonperiodic paralysis from 208 consecutive patients with hypokalemic paralysis, and their average K(+) concentration was 1.8 ± 0.2 mmol/L. Among patients with low urinary K(+) excretion (n = 17), chronic alcoholism, remote diuretic use, and anorexia/bulimia nervosa were the most common causes. Among patients with high urinary K(+) excretion (n = 41) and metabolic acidosis, renal tubular acidosis and chronic toluene abuse were the main causes, while primary aldosteronism, Gitelman syndrome, and diuretics were the leading diagnoses with metabolic alkalosis. The average KCl dose needed to restore muscle strength was 3.8 ± 0.8 mmol/kg. Initial lower plasma K(+), volume depletion, and high urinary K(+) excretion were associated with higher recovery KCl dosage. During therapy, patients with paradoxical hypokalemia (n = 32) who required more KCl supplementation than patients without (4.1 ± 0.7 vs 3.4 ± 0.7 mmol/kg, P paralysis may aid in early diagnosis. Patients with initial lower plasma K(+), renal K(+) wasting, and hypovolemia required higher recovery K(+) dosage. Paradoxical hypokalemia is prone to develop in hypovolemic patients even during K(+) supplementation with volume repletion

  12. The organic anion transport inhibitor probenecid increases brain concentrations of the NKCC1 inhibitor bumetanide.

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    Töllner, Kathrin; Brandt, Claudia; Römermann, Kerstin; Löscher, Wolfgang

    2015-01-05

    Bumetanide is increasingly being used for experimental treatment of brain disorders, including neonatal seizures, epilepsy, and autism, because the neuronal Na-K-Cl cotransporter NKCC1, which is inhibited by bumetanide, is implicated in the pathophysiology of such disorders. However, use of bumetanide for treatment of brain disorders is associated with problems, including poor brain penetration and systemic adverse effects such as diuresis, hypokalemic alkalosis, and hearing loss. The poor brain penetration is thought to be related to its high ionization rate and plasma protein binding, which restrict brain entry by passive diffusion, but more recently brain efflux transporters have been involved, too. Multidrug resistance protein 4 (MRP4), organic anion transporter 3 (OAT3) and organic anion transporting polypeptide 2 (OATP2) were suggested to mediate bumetanide brain efflux, but direct proof is lacking. Because MRP4, OAT3, and OATP2 can be inhibited by probenecid, we studied whether this drug alters brain levels of bumetanide in mice. Probenecid (50 mg/kg) significantly increased brain levels of bumetanide up to 3-fold; however, it also increased its plasma levels, so that the brain:plasma ratio (~0.015-0.02) was not altered. Probenecid markedly increased the plasma half-life of bumetanide, indicating reduced elimination of bumetanide most likely by inhibition of OAT-mediated transport of bumetanide in the kidney. However, the diuretic activity of bumetanide was not reduced by probenecid. In conclusion, our study demonstrates that the clinically available drug probenecid can be used to increase brain levels of bumetanide and decrease its elimination, which could have therapeutic potential in the treatment of brain disorders. Copyright © 2014 Elsevier B.V. All rights reserved.

  13. Additive hypocalciuric effects of amiloride and hydrochlorothiazide in patients treated with calcitriol.

    Science.gov (United States)

    Alon, U; Costanzo, L S; Chan, J C

    1984-01-01

    To compare the effects of hydrochlorothiazide (HCTZ) alone and in combination with amiloride on urinary calcium excretion we performed 14 acute studies on 7 patients with vitamin-D-induced calciuria. Each patient was studied first with HCTZ alone, and 1-32 weeks later with the same or lower dose of HCTZ combined with amiloride. Administration of HCTZ alone did not change UCaV during the 1st day of therapy, and caused a significant reduction from 44.4 +/- 28.8 to 26.0 +/- 14.4 mg/m2/24 h (p less than 0.02) on the 4th day. In contrast, combined diuretic regimen caused a significant reduction in UCaV from 36.0 +/- 16.7 to 23.6 +/- 14.4 mg/m2/24 h (p less than 0.02) on the 1st day and further reduction to 13.3 +/- 6.9 mg/m2/24 h (p less than 0.01) on the 4th day. UCaV on the 4th day was significantly lower with the HCTZ-amiloride combination (p less than 0.05). The combined therapy caused a greater reduction in FECa/FENa than HCTZ alone on the 1st day (p less than 0.02) and on the 4th day (p less than 0.01). HCTZ-induced hyperkaluria, hypokalemia and alkalosis were prevented by the addition of amiloride. In another patient, low-dose HCTZ-amiloride had a maximal dissociative effect on FECa/FENa and was more effective than HCTZ given alone in a double dose. 3 patients were treated with the low-dose HCTZ-amiloride regimen for a total of 23 months. UCaV was kept persistently low.(ABSTRACT TRUNCATED AT 250 WORDS)

  14. Role of tolvaptan in the management of hyponatremia in patients with lung and other cancers: current data and future perspectives

    International Nuclear Information System (INIS)

    Thajudeen, Bijin; Salahudeen, Abdulla K

    2016-01-01

    Hyponatremia is the most frequently observed electrolyte abnormality in clinical practice, and its frequency is almost double in hospitalized cancer patients. As a subset of cancer, hyponatremia is quite common in lung cancer patients, and it is often coupled with the diagnosis of syndrome of inappropriate antidiuretic hormone secretion. The presence of hyponatremia is consequential in that its presence adversely affects cancer patients’ prognosis and outcomes. Limited data suggest that correcting hyponatremia in lung cancer patients can increase response to anticancer treatment, may help reduce length of hospital stay and cost, and reduce morbidity and mortality. The type of treatment for hyponatremia depends on several factors; the key factors are the duration and severity of neurological symptoms of hyponatremia and the status of extracellular volume. When hyponatremia is caused by syndrome of inappropriate antidiuretic hormone, hypertonic saline is indicated for acute symptomatic cases, whereas fluid restriction is recommended in chronic asymptomatic hyponatremia. The latter allows a slower rate of correction, thus avoiding the dreaded complication of osmotic demyelination syndrome. Fluid restriction is, however, insufficient or impractical, and often the use of pharmacological therapy such as antidiuretic hormone receptor antagonists becomes necessary. Availability of these antagonists as an effective treatment in the management of hyponatremia has been a major breakthrough, and furthermore, its clinical or investigational use in cancer-related hyponatremia may offer a potential opportunity to gain further insights into the prognostic impact of hyponatremia correction on cancer patients’ outcomes. Tolvaptan is a prototype of ADH receptor antagonists that acts at renal tubular levels to increase free water excretion without inducing major systemic electrolyte abnormalities such as hypokalemia or alkalosis. The aim of this paper is to provide a brief review

  15. Capsiate supplementation reduces oxidative cost of contraction in exercising mouse skeletal muscle in vivo.

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    Kazuya Yashiro

    Full Text Available Chronic administration of capsiate is known to accelerate whole-body basal energy metabolism, but the consequences in exercising skeletal muscle remain very poorly documented. In order to clarify this issue, the effect of 2-week daily administration of either vehicle (control or purified capsiate (at 10- or 100-mg/kg body weight on skeletal muscle function and energetics were investigated throughout a multidisciplinary approach combining in vivo and in vitro measurements in mice. Mechanical performance and energy metabolism were assessed strictly non-invasively in contracting gastrocnemius muscle using magnetic resonance (MR imaging and 31-phosphorus MR spectroscopy (31P-MRS. Regardless of the dose, capsiate treatments markedly disturbed basal bioenergetics in vivo including intracellular pH alkalosis and decreased phosphocreatine content. Besides, capsiate administration did affect neither mitochondrial uncoupling protein-3 gene expression nor both basal and maximal oxygen consumption in isolated saponin-permeabilized fibers, but decreased by about twofold the Km of mitochondrial respiration for ADP. During a standardized in vivo fatiguing protocol (6-min of repeated maximal isometric contractions electrically induced at a frequency of 1.7 Hz, both capsiate treatments reduced oxidative cost of contraction by 30-40%, whereas force-generating capacity and fatigability were not changed. Moreover, the rate of phosphocreatine resynthesis during the post-electrostimulation recovery period remained unaffected by capsiate. Both capsiate treatments further promoted muscle mass gain, and the higher dose also reduced body weight gain and abdominal fat content. These findings demonstrate that, in addition to its anti-obesity effect, capsiate supplementation improves oxidative metabolism in exercising muscle, which strengthen this compound as a natural compound for improving health.

  16. Hyponatremic hypochloremic dehydration in children with cystic fibrosis in Slovenia; the incidence and recommendations for prevention and treatment

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    Marina Praprotnik

    2015-05-01

    Full Text Available Background: Young children and rarely adolescents with cystic fibrosis can develop hyponatremic hypochloremic dehydration with metabolic alkalosis. The purpose of this article was to review the incidence of this metabolic disorder in our CF patients.Methods: We investigated the medical records of all children diagnosed with cystic fibrosis who are under follow-up in the CF center at the University Childrenʹs Hospital Ljubljana, and were hospitalised or treated on an outpatient basis due to hyponatremic, hypochloremic dehydration in the period from 2007–2012. Data analysis included clinical and laboratory findings.Results: A total of 4 children (7.2 % from Ljubljana CF center (55 patients under the age of 19 years were enrolled in the study. We observed 5 episodes of hyponatremic hypochloremic dehydration in 4 patients (one boy had two episodes. All were homozigous for ΔF 508 mutation. Two had episodes in summer and two in autumn, so that no season prevalence of its occurence was found. Median age at admission to the hospital due to hyponatremic hypochloremic dehydration was 7 months (range 4–34. One boy had a hypovolemic shock at the time of admission to the hospital.Conclusions: The results of our study show that dehydration with hypoelectrolytaemia is a rare complication in children with CF in Slovenia, but due to the severity of clinical signs it is an important disorder. Vomiting and fatigue are the warning signs that should alert parents and physicians to consider the possibility of this complication which can be prevented by proper hydration and salt replacement. If left untreated, it can cause seizures, arrhythmias and even death.

  17. Hypercalcemia Associated with Calcium Supplement Use: Prevalence and Characteristics in Hospitalized Patients

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    Maria C. Machado

    2015-03-01

    Full Text Available Background: The ingestion of large amounts of milk and antacids to treat peptic ulcer disease was a common cause of hypercalcemia in the past (the “milk-alkali syndrome”. The current popularity of calcium and supplements has given rise to a similar problem. Objectives: To evaluate the prevalence and characteristics of hypercalcemia induced by calcium intake (“calcium supplement syndrome”; or CSS in hospitalized patients. Methods: We conducted a retrospective; electronic health record (EHR-based review of patients with hypercalcemia over a 3-year period. Diagnosis of CSS was based on the presence of hypercalcemia; a normal parathyroid hormone (PTH level; renal insufficiency; metabolic alkalosis; a history of calcium intake; and documented improvement with treatment. Results: Of the 72 patients with non-PTH mediated hypercalcemia; 15 (20.8% satisfied all the criteria for the diagnosis of CSS. Calcium; vitamin D; and multivitamin ingestion were significantly associated with the diagnosis (p values < 0.0001; 0.014; and 0.045 respectively; while the presence of hypertension; diabetes; and renal insufficiency showed a trend towards statistical significance. All patients received intravenous fluids; and six (40% received calcium-lowering drugs. The calcium level at discharge was normal 12 (80% of patients. The mean serum creatinine and bicarbonate levels decreased from 2.4 and 35 mg/dL on admission respectively; to 1.6 mg/dL and 25.6 mg/dL at discharge respectively. Conclusion: The widespread use of calcium and vitamin D supplementation can manifest as hypercalcemia and worsening of kidney function in susceptible individuals. Awareness among health care professionals can lead to proper patient education regarding these health risks.

  18. Clinical and diagnostic methods for evaluation of sharp foreign body syndrome in buffaloes

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    Nasr-Eldin M. Aref

    2013-06-01

    Full Text Available Aim: The present study was designed to evaluate clinically and under laboratory condition the sharp foreign body syndrome (SFBS in buffaloes with special emphasis on the diagnostic value of radiography, ultrasonography and blood gases and acidbase balance. Materials and Methods: 196 buffaloes with a history of anorexia, reduction of milk production and no response to previous medical treatment were included in the present study. These animals were subjected to clinical and radiographical examinations. Positive cases for SFBS were further evaluated by sonography, hemato-biochemical and blood gas and acid base balance analysis.Results: Out of 196 admitted cases, 49 (25% cases were confirmed as SFBS by clinical and radiographical examination. Positive cases were subsequently divided into two main categories (complicated and non complicated according to radiographical and sonographical findings. SFBS with no complication was diagnosed in 16 cases while 33 cases showed various degrees of complication including reticular adhesion (abdominal and diaphragmatic, n= 23, diaphragmatic hernia (n = 6 and traumatic pericarditis (n = 4. Leukocytosis, hyperprotenemia and increased activity of AST and ALT were of additional values in the diagnosis of SFBS. A consistent finding of primary metabolic alkalosis was recorded in all cases except one with advanced traumatic pericarditis that showed metabolic acidosis. Conclusion: While there is no substitution for clinical examination, using of ultrasonography and radiography simultaneously are essential for proper evaluation and differentiation between various sequelae of SFBS in buffaloes. Radiography is an efficient tool for visualization of metallic foreign body while ultrasonography is an excellent device in assessing fibrinous deposits. Hemato-biochemical and blood gases and acid base balance are of additional values in discriminating between various outcomes of SFBS.

  19. Renal intercalated cells and blood pressure regulation

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    Susan M. Wall

    2017-12-01

    Full Text Available Type B and non-A, non-B intercalated cells are found within the connecting tubule and the cortical collecting duct. Of these cell types, type B intercalated cells are known to mediate Cl⁻ absorption and HCO₃⁻ secretion largely through pendrin-dependent Cl⁻/HCO₃⁻ exchange. This exchange is stimulated by angiotensin II administration and is also stimulated in models of metabolic alkalosis, for instance after aldosterone or NaHCO₃ administration. In some rodent models, pendrin-mediated HCO₃⁻ secretion modulates acid-base balance. However, the role of pendrin in blood pressure regulation is likely of more physiological or clinical significance. Pendrin regulates blood pressure not only by mediating aldosterone-sensitive Cl⁻ absorption, but also by modulating the aldosterone response for epithelial Na⁺ channel (ENaC-mediated Na⁺ absorption. Pendrin regulates ENaC through changes in open channel of probability, channel surface density, and channels subunit total protein abundance. Thus, aldosterone stimulates ENaC activity through both direct and indirect effects, the latter occurring through its stimulation of pendrin expression and function. Therefore, pendrin contributes to the aldosterone pressor response. Pendrin may also modulate blood pressure in part through its action in the adrenal medulla, where it modulates the release of catecholamines, or through an indirect effect on vascular contractile force. This review describes how aldosterone and angiotensin II-induced signaling regulate pendrin and the contributory role of pendrin in distal nephron function and blood pressure.

  20. Mesenteric microcirculatory dysfunctions and translocation of indigenous bacteria in a rat model of strangulated small bowel obstruction

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    Fernando Luiz Zanoni

    2009-01-01

    Full Text Available PRUPOSE: Bacterial translocation has been shown to occur in critically ill patients after extensive trauma, shock, sepsis, or thermal injury. The present study investigates mesenteric microcirculatory dysfunctions, the bacterial translocation phenomenon, and hemodynamic/metabolic disturbances in a rat model of intestinal obstruction and ischemia. METHODS: Anesthetized (pentobarbital 50 mg/kg, i.p. male Wistar rats (250-350 g were submitted to intestinal obstruction or laparotomy without intestinal obstruction (Sham and were evaluated 24 hours later. Bacterial translocation was assessed by bacterial culture of the mesenteric lymph nodes (MLN, liver, spleen, and blood. Leukocyte-endothelial interactions in the mesenteric microcirculation were assessed by intravital microscopy, and P-selectin and intercellular adhesion molecule (ICAM-1 expressions were quantified by immunohistochemistry. Hematocrit, blood gases, lactate, glucose, white blood cells, serum urea, creatinine, bilirubin, and hepatic enzymes were measured. RESULTS: About 86% of intestinal obstruction rats presented positive cultures for E. coli in samples of the mesenteric lymph nodes, liver, and spleen, and 57% had positive hemocultures. In comparison to the Sham rats, intestinal obstruction induced neutrophilia and increased the number of rolling (~2-fold, adherent (~5-fold, and migrated leukocytes (~11-fold; this increase was accompanied by an increased expression of P-selectin (~2-fold and intercellular adhesion molecule-1 (~2-fold in the mesenteric microcirculation. Intestinal obstruction rats exhibited decreased PaCO2, alkalosis, hyperlactatemia, and hyperglycemia, and increased blood potassium, hepatic enzyme activity, serum urea, creatinine, and bilirubin. A high mortality rate was observed after intestinal obstruction (83% at 72 h vs. 0% in Sham rats. CONCLUSION: Intestinal obstruction and ischemia in rats is a relevant model for the in vivo study of mesenteric microcirculatory

  1. Potentiation of the effect of thiazide derivatives by carbonic anhydrase inhibitors: molecular mechanisms and potential clinical implications.

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    Kamyar Zahedi

    Full Text Available Carbonic anhydrase inhibitors (CAI are mild diuretics, hence not widely used in fluid overloaded states. They are however the treatment of choice for certain non-kidney conditions. Thiazides, specific inhibitors of Na-Cl cotransport (NCC, are mild agents and the most widely used diuretics in the world for control of mild hypertension.In addition to inhibiting the salt reabsorption in the proximal tubule, CAIs down-regulate pendrin, therefore leaving NCC as the major salt absorbing transporter in the distal nephron, and hence allowing for massive diuresis by the inhibitors of NCC in the setting of increased delivery of salt from the proximal tubule.Daily treatment of rats with acetazolamide (ACTZ, a known CAI, for 10 days caused mild diuresis whereas daily treatment with hydrochlorothiazide (HCTZ for 4 days caused hardly any diuresis. However, treatment of rats that were pretreated with ACTZ for 6 days with a combination of ACTZ plus HCTZ for 4 additional days increased the urine output by greater than 2 fold (p<0.001, n = 5 compared to ACTZ-treated animals. Sodium excretion increased by 80% in the ACTZ plus HCTZ group and animals developed significant volume depletion, metabolic alkalosis and pre-renal failure. Molecular studies demonstrated ∼75% reduction in pendrin expression by ACTZ. The increased urine output in ACTZ/HCTZ treated rats was associated with a significant reduction in urine osmolality and reduced membrane localization of AQP-2 (aquaporin2.These results indicate that ACTZ down-regulates pendrin expression and leaves NCC as the major salt absorbing transporter in the distal nephron in the setting of increased delivery of salt from the proximal tubule. Despite being considered mild agents individually, we propose that the combination of ACTZ and HCTZ is a powerful diuretic regimen.

  2. The nutritional limitations of plant-based beverages in infancy and childhood.

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    Vitoria, Isidro

    2017-10-24

    Breastfeeding, infant formula and cow's milk are basic foods in infant nutrition. However, they are being increasingly replaced either totally or partially by plant-based beverages.The composition of 164 plant-based beverages available in Spain was reviewed based on the nutritional labeling of the package and the manufacturers' webpages. This was compared to the composition of cow's milk and infant formula. In addition, the nutritional disease associated with consumption of plant-based beverages in infants and children was reviewed by means of a literature search in Medline and Embase since 1990 based on the key words "plant-based beverages" or "rice beverages" or "almond beverages" or "soy beverages" and "infant" or "child".The nutritional composition of 54 soy beverages, 24 rice beverages, 22 almond beverages, 31 oat beverages, 6 coconut beverages, 12 miscellaneous beverages and 15 mixed beverages was described. At least 30 cases of nutritional disease in children associated with nearly exclusive consumption of plant-based beverages have been published. A characteristic association has been observed between soy beverage and rickets, rice beverage and kwashiorkor, and almond-based beverage and metabolic alkalosis.The nutritional quality of plant-based beverages is lower than that of cow's milk and infant formula, therefore they are not a nutritional alternative. Predominant or exclusive use of these beverages in infant feeding can lead to serious nutritional risks. In the case of nonexclusive feeding with these beverages, the pediatrician should be aware of the nutritional risks and limitations of these beverages in order to complement their deficiencies with other foods.

  3. Hypercalcemia Associated with Calcium Supplement Use: Prevalence and Characteristics in Hospitalized Patients.

    Science.gov (United States)

    Machado, Maria C; Bruce-Mensah, Araba; Whitmire, Melanie; Rizvi, Ali A

    2015-03-09

    The ingestion of large amounts of milk and antacids to treat peptic ulcer disease was a common cause of hypercalcemia in the past (the "milk-alkali syndrome"). The current popularity of calcium and supplements has given rise to a similar problem. To evaluate the prevalence and characteristics of hypercalcemia induced by calcium intake ("calcium supplement syndrome"; or CSS) in hospitalized patients. We conducted a retrospective; electronic health record (EHR)-based review of patients with hypercalcemia over a 3-year period. Diagnosis of CSS was based on the presence of hypercalcemia; a normal parathyroid hormone (PTH) level; renal insufficiency; metabolic alkalosis; a history of calcium intake; and documented improvement with treatment. Of the 72 patients with non-PTH mediated hypercalcemia; 15 (20.8%) satisfied all the criteria for the diagnosis of CSS. Calcium; vitamin D; and multivitamin ingestion were significantly associated with the diagnosis (p values < 0.0001; 0.014; and 0.045 respectively); while the presence of hypertension; diabetes; and renal insufficiency showed a trend towards statistical significance. All patients received intravenous fluids; and six (40%) received calcium-lowering drugs. The calcium level at discharge was normal 12 (80%) of patients. The mean serum creatinine and bicarbonate levels decreased from 2.4 and 35 mg/dL on admission respectively; to 1.6 mg/dL and 25.6 mg/dL at discharge respectively. The widespread use of calcium and vitamin D supplementation can manifest as hypercalcemia and worsening of kidney function in susceptible individuals. Awareness among health care professionals can lead to proper patient education regarding these health risks.

  4. Interdependent feedback regulation of breathing by the carotid bodies and the retrotrapezoid nucleus.

    Science.gov (United States)

    Guyenet, Patrice G; Bayliss, Douglas A; Stornetta, Ruth L; Kanbar, Roy; Shi, Yingtang; Holloway, Benjamin B; Souza, George M P R; Basting, Tyler M; Abbott, Stephen B G; Wenker, Ian C

    2017-11-22

    The retrotrapezoid nucleus (RTN) regulates breathing in a CO 2 - and state-dependent manner. RTN neurons are glutamatergic and innervate principally the respiratory pattern generator; they regulate multiple aspects of breathing, including active expiration, and maintain breathing automaticity during non-REM sleep. RTN neurons encode arterial PCO2/pH via cell-autonomous and paracrine mechanisms, and via input from other CO 2 -responsive neurons. In short, RTN neurons are a pivotal structure for breathing automaticity and arterial PCO2 homeostasis. The carotid bodies stimulate the respiratory pattern generator directly and indirectly by activating RTN via a neuronal projection originating within the solitary tract nucleus. The indirect pathway operates under normo- or hypercapnic conditions; under respiratory alkalosis (e.g. hypoxia) RTN neurons are silent and the excitatory input from the carotid bodies is suppressed. Also, silencing RTN neurons optogenetically quickly triggers a compensatory increase in carotid body activity. Thus, in conscious mammals, breathing is subject to a dual and interdependent feedback regulation by chemoreceptors. Depending on the circumstance, the activity of the carotid bodies and that of RTN vary in the same or the opposite directions, producing additive or countervailing effects on breathing. These interactions are mediated either via changes in blood gases or by brainstem neuronal connections, but their ultimate effect is invariably to minimize arterial PCO2 fluctuations. We discuss the potential relevance of this dual chemoreceptor feedback to cardiorespiratory abnormalities present in diseases in which the carotid bodies are hyperactive at rest, e.g. essential hypertension, obstructive sleep apnoea and heart failure. © 2017 The Authors. The Journal of Physiology © 2017 The Physiological Society.

  5. Predicting the safety and efficacy of buffer therapy to raise tumour pHe: an integrative modelling study

    Science.gov (United States)

    Martin, N K; Robey, I F; Gaffney, E A; Gillies, R J; Gatenby, R A; Maini, P K

    2012-01-01

    Background: Clinical positron emission tomography imaging has demonstrated the vast majority of human cancers exhibit significantly increased glucose metabolism when compared with adjacent normal tissue, resulting in an acidic tumour microenvironment. Recent studies demonstrated reducing this acidity through systemic buffers significantly inhibits development and growth of metastases in mouse xenografts. Methods: We apply and extend a previously developed mathematical model of blood and tumour buffering to examine the impact of oral administration of bicarbonate buffer in mice, and the potential impact in humans. We recapitulate the experimentally observed tumour pHe effect of buffer therapy, testing a model prediction in vivo in mice. We parameterise the model to humans to determine the translational safety and efficacy, and predict patient subgroups who could have enhanced treatment response, and the most promising combination or alternative buffer therapies. Results: The model predicts a previously unseen potentially dangerous elevation in blood pHe resulting from bicarbonate therapy in mice, which is confirmed by our in vivo experiments. Simulations predict limited efficacy of bicarbonate, especially in humans with more aggressive cancers. We predict buffer therapy would be most effectual: in elderly patients or individuals with renal impairments; in combination with proton production inhibitors (such as dichloroacetate), renal glomular filtration rate inhibitors (such as non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors), or with an alternative buffer reagent possessing an optimal pK of 7.1–7.2. Conclusion: Our mathematical model confirms bicarbonate acts as an effective agent to raise tumour pHe, but potentially induces metabolic alkalosis at the high doses necessary for tumour pHe normalisation. We predict use in elderly patients or in combination with proton production inhibitors or buffers with a pK of 7.1–7.2 is most

  6. Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

    Directory of Open Access Journals (Sweden)

    Martin Natasha K

    2011-06-01

    Full Text Available Abstract Background The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations. Methods We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA, a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231, we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB therapies chronically. Results Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment. Conclusions DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment.

  7. Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

    Science.gov (United States)

    2011-01-01

    Background The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations. Methods We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA), a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231), we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB) therapies chronically. Results Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment. Conclusions DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment. PMID:21663677

  8. Roles of renal ammonia metabolism other than in acid-base homeostasis.

    Science.gov (United States)

    Weiner, I David

    2017-06-01

    The importance of renal ammonia metabolism in acid-base homeostasis is well known. However, the effects of renal ammonia metabolism other than in acid-base homeostasis are not as widely recognized. First, ammonia differs from almost all other solutes in the urine in that it does not result from arterial delivery. Instead, ammonia is produced by the kidney, and only a portion of the ammonia produced is excreted in the urine, with the remainder returned to the systemic circulation through the renal veins. In normal individuals, systemic ammonia addition is metabolized efficiently by the liver, but in patients with either acute or chronic liver disease, conditions that increase the addition of ammonia of renal origin to the systemic circulation can result in precipitation and/or worsening of hyperammonemia. Second, ammonia appears to serve as an intrarenal paracrine signaling molecule. Hypokalemia increases proximal tubule ammonia production and secretion as well as reabsorption in the thick ascending limb of the loop of Henle, thereby increasing delivery to the renal interstitium and the collecting duct. In the collecting duct, ammonia decreases potassium secretion and stimulates potassium reabsorption, thereby decreasing urinary potassium excretion and enabling feedback correction of the initiating hypokalemia. Finally, the stimulation of renal ammonia metabolism by hypokalemia may contribute to the development of metabolic alkalosis, which in turn can stimulate NaCl reabsorption and contribute to the intravascular volume expansion, increased blood pressure and diuretic resistance that can develop with hypokalemia. The evidence supporting these novel non-acid-base roles of renal ammonia metabolism is discussed in this review.

  9. Small cell carcinoma of the prostate presenting with Cushing Syndrome. A narrative review of an uncommon condition.

    Science.gov (United States)

    Rueda-Camino, José Antonio; Losada-Vila, Beatriz; De Ancos-Aracil, Cristina Lucía; Rodríguez-Lajusticia, Laura; Tardío, Juan Carlos; Zapatero-Gaviria, Antonio

    2016-01-01

    Small cell carcinoma (SCC) of the prostate is an uncommon condition; there are very few cases in which presenting symptoms are consistent with Cushing Syndrome (CS). We report a new case in which CS triggers the suspicion of an SCC of the prostate and a review of the published cases of SCC of the prostate presenting with CS. The origin of these neoplasms is still unclear. It may be suspected when laboratory features appear in patients diagnosed with prostatic adenocarcinoma which becomes resistant to specific therapy. SCC usually occurs after the 6th decade. Patients suffering SCC of the prostate presenting with CS usually present symptoms such as hypertension, hyperglycemia, alkalosis or hypokalemia; cushingoid phenotype is less frequent. Cortisol and ACTH levels are often high. Prostatic-specific antigen levels are usually normal. CT scan is the preferred imaging test to localize the lesion, but its performance may be improved by adding other tests, such as FDG-PET scan. All patients have metastatic disease at the time of diagnosis. Lymph nodes, liver and bone are the most frequent metastases sites. Surgery and Ketokonazole are the preferred treatments for CS. The prognosis is very poor: 2- and 5-year survival rates are 27.5 and 14.3%, respectively. Key messages When a patient presents with ectopic Cushing Syndrome but lungs are normal, an atypical localization should be suspected. We should suspect a prostatic origin if Cushing Syndrome is accompanied by obstructive inferior urinary tract symptoms or in the setting of a prostatic adenocarcinoma with rapid clinical and radiological progression with relatively low PSA levels. Although no imaging test is preferred to localize these tumors, FDG-PET-TC can be very useful. Hormone marker scintigraphy (e.g. somatostatin) could be used too. As Cushing Syndrome is a paraneoplastic phenomenon, treatment of the underlying disease may help control hypercortisolism manifestations. These tumors are usually metastatic by the

  10. Poor phenotype-genotype association in a large series of patients with Type III Bartter syndrome.

    Directory of Open Access Journals (Sweden)

    Alejandro García Castaño

    Full Text Available Type III Bartter syndrome (BS is an autosomal recessive renal tubule disorder caused by loss-of-function mutations in the CLCNKB gene, which encodes the chloride channel protein ClC-Kb. In this study, we carried out a complete clinical and genetic characterization in a cohort of 30 patients, one of the largest series described. By comparing with other published populations, and considering that 80% of our patients presented the p.Ala204Thr Spanish founder mutation presumably associated with a common phenotype, we aimed to test the hypothesis that allelic differences could explain the wide phenotypic variability observed in patients with type III BS.Clinical data were retrieved from the referral centers. The exon regions and flanking intronic sequences of the CLCNKB gene were screened for mutations by polymerase chain reaction (PCR followed by direct Sanger sequencing. Presence of gross deletions or duplications in the region was checked for by MLPA and QMPSF analyses.Polyuria, polydipsia and dehydration were the main common symptoms. Metabolic alkalosis and hypokalemia of renal origin were detected in all patients at diagnosis. Calciuria levels were variable: hypercalciuria was detected in 31% of patients, while 23% had hypocalciuria. Nephrocalcinosis was diagnosed in 20% of the cohort. Two novel CLCNKB mutations were identified: a small homozygous deletion (c.753delG in one patient and a small deletion (c.1026delC in another. The latter was present in compound heterozygosis with the already previously described p.Glu442Gly mutation. No phenotypic association was obtained regarding the genotype.A poor correlation was found between a specific type of mutation in the CLCNKB gene and type III BS phenotype. Importantly, two CLCNKB mutations not previously described were found in our cohort.

  11. Erythrocytosis in a Patient with Type 1 Diabetes Mellitus and Concomitant Gitelman’s Syndrome

    Directory of Open Access Journals (Sweden)

    Müge Keskin

    2016-06-01

    Full Text Available Gitelman’s syndrome (GS is characterized by hypokalemia, hypomagnesaemia, hypocalciuria, metabolic alkalosis, and neurological symptoms. The association of GS with type 1 diabetes is rare, described only in a few case reports. We report a patient with an unusual combination of GS and type 1 diabetes mellitus with erythrocytosis. A 26-year-old male with GS and type 1 diabetes, who was on intensive insulin therapy with poor compliance, presented with the complaint of headache. On physical examination, his blood pressure was 120/70 mmHg and there was no neurological deficit or proximal muscle weakness. He had no previous medical history of obstructive sleep apnea, heart or lung disease. He had negative smoking history. His laboratory tests revealed erythrocytosis with a hemoglobin level of 18.9 g/dL (13.6-17.2 g/dL and a hematocrit level of 54.8% (39.5-50.3%. Cranial magnetic resonance imaging was normal. He had no evidence of hypovolemia. Hematological workout excluded polycythemia vera and chronic myeloid neoplasm. A bone marrow aspiration revealed a hypercellular marrow with increased erythroid precursors, megakaryocytes and granulocytes. The reticulin stain grade was zero. There was no iron accumulation with iron stain. There was no radiologic evidence of any kind of erythropoietin-producing tumors. His echocardiography was normal. Serum insulin-like growth factor-1 levels and endogenous androgens were within normal limits. After 2 therapeutic phlebotomies, his symptoms improved and his hemoglobin was 16.1 mg/dL. Our patient, besides having GS and type 1 diabetes, was complicated with idiopathic erythrocytosis, all having deleterious effects on hemodynamic status of the patient.

  12. High Antifouling Property of Ion-Selective Membrane: toward In Vivo Monitoring of pH Change in Live Brain of Rats with Membrane-Coated Carbon Fiber Electrodes.

    Science.gov (United States)

    Hao, Jie; Xiao, Tongfang; Wu, Fei; Yu, Ping; Mao, Lanqun

    2016-11-15

    In vivo monitoring of pH in live brain remains very essential to understanding acid-base chemistry in various physiological processes. This study demonstrates a potentiometric method for in vivo monitoring of pH in the central nervous system with carbon fiber-based proton-selective electrodes (CF-H + ISEs) with high antifouling property. The CF-H + ISEs are prepared by formation of a H + -selective membrane (H + ISM) with polyvinyl chloride polymeric matrixes containing plasticizer bis(2-ethylhexyl)sebacate, H + ionophore tridodecylamine, and ion exchanger potassium tetrakis(4-chlorophenyl)borate onto carbon fiber electrodes (CFEs). Both in vitro and in vivo studies demonstrate that the H + ISM exhibits strong antifouling property against proteins, which enables the CF-H + ISEs to well maintain the sensitivity and reversibility for pH sensing after in vivo measurements. Moreover, the CF-H + ISEs exhibit a good response to pH changes within a narrow physiological pH range from 6.0 to 8.0 in quick response time with high reversibility and selectivity against species endogenously existing in the central nervous system. The applicability of the CF-H + ISEs is illustrated by real-time monitoring of pH changes during acid-base disturbances, in which the brain acidosis is induced by CO 2 inhalation and brain alkalosis is induced by bicarbonate injections. The results demonstrate that brain pH value rapidly decreases in the amygdaloid nucleus by ca. 0.14 ± 0.01 (n = 5) when the rats breath in pure CO 2 gas, while increases in the cortex by about 0.77 ± 0.12 (n = 3) following intraperitoneal injection of 5 mmol/kg NaHCO 3 . This study demonstrates a new potentiometric method for in vivo measurement of pH change in the live brain of rats with high reliability.

  13. Effect of oral alkali supplementation on progression of chronic kidney disease.

    Science.gov (United States)

    Gaggl, Martina; Sliber, Christopher; Sunder-Plassmann, Gere

    2014-01-01

    Metabolic acidosis is a frequent but asymptomatic complication in chronic kidney disease (CKD). In early stages of CKD acidosis is limited to the renal tissue and progresses to reduced serum bicarbonate levels. Reduced renal tissue pH and increased ammoniagenesis are the key mechanisms of the kidney to enhance acid excretion to the urine. The expressed protein patterns in the proximal tubular epithelial cells change remarkably, the proximal convoluted tubule develops hypertrophy, and an intra-renal enhanced renin-angiotensin-system leads to interstitial fibrosis. Since nephrons are numerically reduced in CKD each remaining functional unit has to progressively increase these mechanisms to keep up the equilibrium. The adverse effects of chronic metabolic acidosis include aside from acceleration of progression of kidney disease, the development or exacerbation of bone disease, increased degradation of muscle with muscle wasting, enhanced protein degradation and inflammation. Genome wide association studies demonstrated that tubular acid-base transporters are involved in the development of arterial hypertension. Several retrospective analyses have indicated that low serum bicarbonate predicts death in cohorts with CKD and cardiovascular disease. All studies confirmed a U-shaped association of mortality and serum bicarbonate, indicating that both, acidosis and alkalosis are associated with increased mortality. Randomized controlled trials showed that base substitution, either by modification of the diet or by simply adding alkalizing agents, might halt the decline of kidney function in subjects with CKD. In 2012 a meta-analysis concluded that alkali therapy might provide a long-term favorable effect on renal function in patients with CKD.

  14. Role and mechanisms of regulation of the basolateral Kir4.1/Kir5.1K+channels in the distal tubules.

    Science.gov (United States)

    Palygin, O; Pochynyuk, O; Staruschenko, A

    2017-01-01

    Epithelial K + channels are essential for maintaining electrolyte and fluid homeostasis in the kidney. It is recognized that basolateral inward-rectifying K + (K ir ) channels play an important role in the control of resting membrane potential and transepithelial voltage, thereby modulating water and electrolyte transport in the distal part of nephron and collecting duct. Monomeric K ir 4.1 (encoded by Kcnj10 gene) and heteromeric K ir 4.1/K ir 5.1 (K ir 4.1 together with K ir 5.1 (Kcnj16)) channels are abundantly expressed at the basolateral membranes of the distal convoluted tubule and the cortical collecting duct cells. Loss-of-function mutations in KCNJ10 cause EAST/SeSAME tubulopathy in humans associated with salt wasting, hypomagnesaemia, metabolic alkalosis and hypokalaemia. In contrast, mice lacking K ir 5.1 have severe renal phenotype that, apart from hypokalaemia, is the opposite of the phenotype seen in EAST/SeSAME syndrome. Experimental advances using genetic animal models provided critical insights into the physiological role of these channels in electrolyte homeostasis and the control of kidney function. Here, we discuss current knowledge about K + channels at the basolateral membrane of the distal tubules with specific focus on the homomeric K ir 4.1 and heteromeric K ir 4.1/K ir 5.1 channels. Recently identified molecular mechanisms regulating expression and activity of these channels, such as cell acidification, dopamine, insulin and insulin-like growth factor-1, Src family protein tyrosine kinases, as well as the role of these channels in NCC-mediated transport in the distal convoluted tubules, are also described. © 2016 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

  15. Baking soda misuse as a home remedy: case experience of the California Poison Control System.

    Science.gov (United States)

    Al-Abri, S A; Kearney, T

    2014-02-01

    Baking soda is a common household product promoted by the manufacturer as an antacid. It contains sodium bicarbonate and has the potential for significant toxicity when ingested in excessive amounts. Characterizing the patterns and outcomes from the misuse of baking soda as a home remedy can guide the clinical assessment and preventative counselling of patients at risk for use of this product. We conducted a retrospective review of all symptomatic cases involving ingestion and misuse of a baking soda powder product that were reported to the California Poison Control System between the years 2000 and 2012. Of the 192 cases we identified, 55·8% were female, ages ranged 2 months to 79 years, and the most common reasons for misuse included antacid (60·4%), 'beat a urine drug test' (11·5%) and treat a UTI (4·7%). Most cases (55·2%) had significant symptoms warranting a medical evaluation, whereas 12 patients required hospital admission developed either electrolyte imbalances, metabolic alkalosis or respiratory depression. Misuse of baking soda can result in serious electrolyte and acid/base imbalances. Patients at highest risk of toxicity may include those who chronically use an antacid, those who use the method to 'beat' urine drug screens, pregnant women and young children. Self-treatment with baking soda as a home remedy may also mask or delay medical care thereby complicating or exacerbating an existing medical problem. We suggest that healthcare providers counsel high-risk patients about the potential complications of misuse of baking soda as a home remedy. © 2013 John Wiley & Sons Ltd.

  16. A comparison of traditional and quantitative analysis of acid-base imbalances in hypoalbuminemic dogs.

    Science.gov (United States)

    Torrente, Carlos; Manzanilla, Edgar G; de Gopegui, Rafael Ruiz

    2014-01-01

    To compare the traditional (HH) and quantitative approaches used for the evaluation of the acid-base balance in hypoalbuminemic dogs. Prospective observational study. ICU of a veterinary teaching hospital. One hundred and five client-owned dogs. Jugular venous blood samples were collected from each patient on admission to determine: total plasma protein (TP), albumin (Alb), blood urea nitrogen (BUN), glucose (Glu), hematocrit (HCT), Na(+) , Cl(-) , K(+) , phosphate (Pi ), pH, PvCO2, bicarbonate (HCO3 (-) ), anion gap (AG), adjusted anion gap for albumin (AGalb ) or phosphate (AGalb-phos ), standardized base excess (SBE), strong ion difference (SID), concentration of nonvolatile weak buffers (Atot ), and strong ion gap (SIG). Patients were divided in 2 groups according to the severity of the hypoalbuminemia: mild (Alb = 21-25 g/L) and severe (Alb ≤20 g/L). All parameters were compared among groups. Patients with severe hypoalbuminemia showed significant decrease in TP (P = 0.011), Atot (P = 0.050), and a significant increase in adjusted AG (P = 0.048) and the magnitude of SIG (P = 0.011) compared to animals with mild hypoalbuminemia. According to the HH approach, the most frequent imbalances were simple disorders (51.4%), primarily metabolic acidosis (84.7%) associated with a high AG acidosis. However, when using the quantitative method, 58.1% of patients had complex disorders, with SIG acidosis (74.3%) and Atot alkalosis (33.3%) as the most frequent acid-base imbalances. Agreement between methods only matched in 32 cases (kappa acid-base balance was poor and many imbalances detected using the quantitative approach were missed using the HH approach. Further studies are necessary to confirm the clinical utility of using the quantitative approach in the decision-making process of the severely ill hypoalbuminemic patients. © Veterinary Emergency and Critical Care Society 2014.

  17. Effects of intravenous solutions on acid-base equilibrium: from crystalloids to colloids and blood components.

    Science.gov (United States)

    Langer, Thomas; Ferrari, Michele; Zazzeron, Luca; Gattinoni, Luciano; Caironi, Pietro

    2014-01-01

    Intravenous fluid administration is a medical intervention performed worldwide on a daily basis. Nevertheless, only a few physicians are aware of the characteristics of intravenous fluids and their possible effects on plasma acid-base equilibrium. According to Stewart's theory, pH is independently regulated by three variables: partial pressure of carbon dioxide, strong ion difference (SID), and total amount of weak acids (ATOT). When fluids are infused, plasma SID and ATOT tend toward the SID and ATOT of the administered fluid. Depending on their composition, fluids can therefore lower, increase, or leave pH unchanged. As a general rule, crystalloids having a SID greater than plasma bicarbonate concentration (HCO₃-) cause an increase in plasma pH (alkalosis), those having a SID lower than HCO₃- cause a decrease in plasma pH (acidosis), while crystalloids with a SID equal to HCO₃- leave pH unchanged, regardless of the extent of the dilution. Colloids and blood components are composed of a crystalloid solution as solvent, and the abovementioned rules partially hold true also for these fluids. The scenario is however complicated by the possible presence of weak anions (albumin, phosphates and gelatins) and their effect on plasma pH. The present manuscript summarises the characteristics of crystalloids, colloids, buffer solutions and blood components and reviews their effect on acid-base equilibrium. Understanding the composition of intravenous fluids, along with the application of simple physicochemical rules best described by Stewart's approach, are pivotal steps to fully elucidate and predict alterations of plasma acid-base equilibrium induced by fluid therapy.

  18. Predicting the safety and efficacy of buffer therapy to raise tumour pHe: an integrative modelling study.

    Science.gov (United States)

    Martin, N K; Robey, I F; Gaffney, E A; Gillies, R J; Gatenby, R A; Maini, P K

    2012-03-27

    Clinical positron emission tomography imaging has demonstrated the vast majority of human cancers exhibit significantly increased glucose metabolism when compared with adjacent normal tissue, resulting in an acidic tumour microenvironment. Recent studies demonstrated reducing this acidity through systemic buffers significantly inhibits development and growth of metastases in mouse xenografts. We apply and extend a previously developed mathematical model of blood and tumour buffering to examine the impact of oral administration of bicarbonate buffer in mice, and the potential impact in humans. We recapitulate the experimentally observed tumour pHe effect of buffer therapy, testing a model prediction in vivo in mice. We parameterise the model to humans to determine the translational safety and efficacy, and predict patient subgroups who could have enhanced treatment response, and the most promising combination or alternative buffer therapies. The model predicts a previously unseen potentially dangerous elevation in blood pHe resulting from bicarbonate therapy in mice, which is confirmed by our in vivo experiments. Simulations predict limited efficacy of bicarbonate, especially in humans with more aggressive cancers. We predict buffer therapy would be most effectual: in elderly patients or individuals with renal impairments; in combination with proton production inhibitors (such as dichloroacetate), renal glomular filtration rate inhibitors (such as non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors), or with an alternative buffer reagent possessing an optimal pK of 7.1-7.2. Our mathematical model confirms bicarbonate acts as an effective agent to raise tumour pHe, but potentially induces metabolic alkalosis at the high doses necessary for tumour pHe normalisation. We predict use in elderly patients or in combination with proton production inhibitors or buffers with a pK of 7.1-7.2 is most promising.

  19. Exogenous sphingosine-1-phosphate boosts acclimatization in rats exposed to acute hypobaric hypoxia: assessment of haematological and metabolic effects.

    Directory of Open Access Journals (Sweden)

    Sonam Chawla

    Full Text Available The physiological challenges posed by hypobaric hypoxia warrant exploration of pharmacological entities to improve acclimatization to hypoxia. The present study investigates the preclinical efficacy of sphingosine-1-phosphate (S1P to improve acclimatization to simulated hypobaric hypoxia.Efficacy of intravenously administered S1P in improving haematological and metabolic acclimatization was evaluated in rats exposed to simulated acute hypobaric hypoxia (7620 m for 6 hours following S1P pre-treatment for three days.Altitude exposure of the control rats caused systemic hypoxia, hypocapnia (plausible sign of hyperventilation and respiratory alkalosis due to suboptimal renal compensation indicated by an overt alkaline pH of the mixed venous blood. This was associated with pronounced energy deficit in the hepatic tissue along with systemic oxidative stress and inflammation. S1P pre-treatment improved blood oxygen-carrying-capacity by increasing haemoglobin, haematocrit, and RBC count, probably as an outcome of hypoxia inducible factor-1α mediated erythropoiesis and renal S1P receptor 1 mediated haemoconcentation. The improved partial pressure of oxygen in the blood could further restore aerobic respiration and increase ATP content in the hepatic tissue of S1P treated animals. S1P could also protect the animals from hypoxia mediated oxidative stress and inflammation.The study findings highlight S1P's merits as a preconditioning agent for improving acclimatization to acute hypobaric hypoxia exposure. The results may have long term clinical application for improving physiological acclimatization of subjects venturing into high altitude for occupational or recreational purposes.

  20. Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

    International Nuclear Information System (INIS)

    Robey, Ian F; Martin, Natasha K

    2011-01-01

    The glycolytic nature of malignant tumors contributes to high levels of extracellular acidity in the tumor microenvironment. Tumor acidity is a driving force in invasion and metastases. Recently, it has been shown that buffering of extracellular acidity through systemic administration of oral bicarbonate can inhibit the spread of metastases in a mouse model for metastatic breast cancer. While these findings are compelling, recent assessments into the use of oral bicarbonate as a cancer intervention reveal limitations. We posited that safety and efficacy of bicarbonate could be enhanced by dichloroacetate (DCA), a drug that selectively targets tumor cells and reduces extracellular acidity through inhibition of glycolysis. Using our mouse model for metastatic breast cancer (MDA-MB-231), we designed an interventional survival study where tumor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB) therapies chronically. Dichloroacetate alone or in combination with bicarbonate did not increase systemic alkalosis in mice. Survival was longest in mice administered bicarbonate-based therapies. Primary tumor re-occurrence after surgeries is associated with survival rates. Although DB therapy did not significantly enhance oral bicarbonate, we did observe reduced pulmonary lesion diameters in this cohort. The DCA monotherapy was not effective in reducing tumor size or metastases or improving survival time. We provide in vitro evidence to suggest this outcome may be a function of hypoxia in the tumor microenvironment. DB combination therapy did not appear to enhance the effect of chronic oral bicarbonate. The anti-tumor effect of DCA may be dependent on the cancer model. Our studies suggest DCA efficacy is unpredictable as a cancer therapy and further studies are necessary to determine the role of this agent in the tumor microenvironment

  1. Pseudo-Bartter syndrome in an infant with congenital chloride diarrhoea

    Directory of Open Access Journals (Sweden)

    Igrutinović Zoran

    2011-01-01

    Full Text Available Introduction. Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. We are presenting an infant with pseudo-Bartter syndrome caused by congenital chloride diarrhoea. Case Outline. A male newborn born in the 37th gestational week (GW to young healthy and non-consanguineous parents. In the 35th GW a polyhydramnios with bowel dilatation was verified by ultrasonography. After birth he manifested several episodes of hyponatremic dehydration with hypochloraemia, hypokalaemia and metabolic alkalosis, so as Bartter syndrome was suspected treatment with indomethacin, spironolactone and additional intake of NaCl was initiated. However, this therapy gave no results, so that at age six months he was rehospitalized under the features of persistent watery diarrhoea, vomiting, dehydration and acute renal failure (serum creatinine 123 μmol/L. The laboratory results showed hyponatraemia (123 mmol/L, hypokalaemia (3.1 mmol/L, severe hypochloraemia (43 mmol/L, alcalosis (blood pH 7.64, bicarbonate 50.6 mmol/L, high plasma renin (20.6 ng/ml and aldosterone (232.9 ng/ml, but a low urinary chloride concentration (2.1 mmol/L. Based on these findings, as well as the stool chloride concentration of 110 mmol/L, the patient was diagnosed congenital chloride diarrhoea. In further course, the patient was treated by intensive fluid, sodium and potassium supplementation which resulted in the normalization of serum electrolytes, renal function, as well as his mental and physical development during 10 months of follow-up. Conclusion. Persistent watery diarrhoea with a high concentration of chloride in stool is the key finding in the differentiation of congenital chloride diarrhoea from Bartter syndrome. The treatment of congenital chloride diarrhoea consists primarily of adequate water and electrolytes replacement.

  2. Effect of sodium bicarbonate on [HCO3-], pH, and gastrointestinal symptoms.

    Science.gov (United States)

    Carr, Amelia J; Slater, Gary J; Gore, Christopher J; Dawson, Brian; Burke, Louise M

    2011-06-01

    Sodium bicarbonate (NaHCO₃) is often ingested at a dose of 0.3 g/kg body mass (BM), but ingestion protocols are inconsistent in terms of using solution or capsules, ingestion period, combining NaHCO₃ with sodium citrate (Na₃C₆H₅O₇), and coingested food and fluid. To quantify the effect of ingesting 0.3 g/kg NaHCO₃ on blood pH, [HCO₃-], and gastrointestinal (GI) symptoms over the subsequent 3 hr using a range of ingestion protocols and, thus, to determine an optimal protocol. In a crossover design, 13 physically active subjects undertook 8 NaHCO₃ experimental ingestion protocols and 1 placebo protocol. Capillary blood was taken every 30 min and analyzed for pH and [HCO₃-]. GI symptoms were quantified every 30 min via questionnaire. Statistics used were pairwise comparisons between protocols; differences were interpreted in relation to smallest worthwhile changes for each variable. A likelihood of >75% was a substantial change. [HCO₃-] and pH were substantially greater than in placebo for all other ingestion protocols at almost all time points. When NaHCO3 was coingested with food, the greatest [HCO₃-] (30.9 mmol/kg) and pH (7.49) and lowest incidence of GI symptoms were observed. The greatest incidence of GI side effects was observed 90 min after ingestion of 0.3 g/kg NaHCO₃ solution. The changes in pH and [HCO₃-] for the 8 NaHCO₃-ingestion protocols were similar, so an optimal protocol cannot be recommended. However, the results suggest that NaHCO₃ coingested with a high-carbohydrate meal should be taken 120-150 min before exercise to induce substantial blood alkalosis and reduce GI symptoms.

  3. Hibernation and gas exchange.

    Science.gov (United States)

    Milsom, William K; Jackson, Donald C

    2011-01-01

    Hibernation in endotherms and ectotherms is characterized by an energy-conserving metabolic depression due to low body temperatures and poorly understood temperature-independent mechanisms. Rates of gas exchange are correspondly reduced. In hibernating mammals, ventilation falls even more than metabolic rate leading to a relative respiratory acidosis that may contribute to metabolic depression. Breathing in some mammals becomes episodic and in some small mammals significant apneic gas exchange may occur by passive diffusion via airways or skin. In ectothermic vertebrates, extrapulmonary gas exchange predominates and in reptiles and amphibians hibernating underwater accounts for all gas exchange. In aerated water diffusive exchange permits amphibians and many species of turtles to remain fully aerobic, but hypoxic conditions can challenge many of these animals. Oxygen uptake into blood in both endotherms and ectotherms is enhanced by increased affinity of hemoglobin for O₂ at low temperature. Regulation of gas exchange in hibernating mammals is predominately linked to CO₂/pH, and in episodic breathers, control is principally directed at the duration of the apneic period. Control in submerged hibernating ectotherms is poorly understood, although skin-diffusing capacity may increase under hypoxic conditions. In aerated water blood pH of frogs and turtles either adheres to alphastat regulation (pH ∼8.0) or may even exhibit respiratory alkalosis. Arousal in hibernating mammals leads to restoration of euthermic temperature, metabolic rate, and gas exchange and occurs periodically even as ambient temperatures remain low, whereas body temperature, metabolic rate, and gas exchange of hibernating ectotherms are tightly linked to ambient temperature. © 2011 American Physiological Society.

  4. Multum in Parvo: Explorations with a Small Bag of Carbon Dioxide

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    EJM Campbell

    2001-01-01

    Full Text Available A collection of 12 papers published between 1957 and 1972 are revisited. The papers had a common theme of the use of rebreathing carbon dioxide and explored a variety of topics in respiratory physiology. The first study established a method for the noninvasive and indirect estimation of arterial carbon dioxide pressure that was suitable for the routine clinical monitoring of respiratory failure and whose clinical utility remains to this day, but which also provided observations that were the stimulus for the studies that followed. The rate of rise in the partial pressure of carbon dioxide (PCO2 during rebreathing led to an analysis of body carbon dioxide storage capacity. Knowledge of carbon dioxide storage led to a method for quantifying lactate production in exercise without the need for blood sampling. The changes in ventilation that accompanied the increase in PCO2 provided the basis for a rapid method for measuring aspects of breathing control (Read's method, which was later modified to measure the ventilatory response to hypoxia. The physiology of breath-holding was explored through observations of the fall in breath-holding time as PCO2 climbed. Rebreathing also allowed increases in voluntary ventilation to be achieved without the development of alkalosis, leading to studies of maximal voluntary ventilation and respiratory muscle fatigue. Equilibration of PCO2 during rebreathing was used to measure mixed venous PCO2 during exercise and develop an integrated approach to the physiology of exercise in health and disease; alveolar-arterial disequilibrium in PCO2 during exercise was uncovered. Equilibration of PCO2, as well as PO2, during rebreathing of carbon dioxide and nitrogen gas mixtures showed different time courses of venous gases at the onset of exercise. Starting with the rebreathing of carbon dioxide in oxygen mixtures in a small rubber bag, an astonishing range of topics in respiratory physiology was explored, with observations

  5. Mode of action associated with development of hemangiosarcoma in mice given pregabalin and assessment of human relevance.

    Science.gov (United States)

    Criswell, Kay A; Cook, Jon C; Wojcinski, Zbigniew; Pegg, David; Herman, James; Wesche, David; Giddings, John; Brady, Joseph T; Anderson, Timothy

    2012-07-01

    Pregabalin increased the incidence of hemangiosarcomas in carcinogenicity studies of 2-year mice but was not tumorigenic in rats. Serum bicarbonate increased within 24 h of pregabalin administration in mice and rats. Rats compensated appropriately, but mice developed metabolic alkalosis and increased blood pH. Local tissue hypoxia and increased endothelial cell proliferation were also confirmed in mice alone. The combination of hypoxia and sustained increases in endothelial cell proliferation, angiogenic growth factors, dysregulated erythropoiesis, and macrophage activation is proposed as the key event in the mode of action (MOA) for hemangiosarcoma formation. Hemangiosarcomas occur spontaneously in untreated control mice but occur only rarely in humans. The International Programme on Chemical Safety and International Life Sciences Institute developed a Human Relevance Framework (HRF) analysis whereby presence or absence of key events can be used to assess human relevance. The HRF combines the MOA with an assessment of biologic plausibility in humans to assess human relevance. This manuscript compares the proposed MOA with Hill criteria, a component of the HRF, for strength, consistency, specificity, temporality, and dose response, with an assessment of key biomarkers in humans, species differences in response to disease conditions, and spontaneous incidence of hemangiosarcoma to evaluate human relevance. Lack of key biomarker events in the MOA in rats, monkeys, and humans supports a species-specific process and demonstrates that the tumor findings in mice are not relevant to humans at the clinical dose of pregabalin. Based on this collective dataset, clinical use of pregabalin would not pose an increased risk for hemangiosarcoma to humans.

  6. Nitrogen metabolism, acid-base regulation, and molecular responses to ammonia and acid infusions in the spiny dogfish shark (Squalus acanthias).

    Science.gov (United States)

    Nawata, C Michele; Walsh, Patrick J; Wood, Chris M

    2015-07-01

    Although they are ureotelic, marine elasmobranchs express Rh glycoproteins, putative ammonia channels. To address questions raised by a recent study on high environmental ammonia (HEA) exposure, dogfish were intravascularly infused for 24 h at 3 ml kg(-1) h(-1) with isosmotic NaCl (500 mmol l(-1), control), NH4HCO3 (500 mmol l(-1)), NH4Cl (500 mmol l(-1)), or HCl (as 125 mmol l(-1) HCl + 375 mmol l(-1) NaCl). While NaCl had no effect on arterial acid-base status, NH4HCO3 caused mild alkalosis, NH4Cl caused strong acidosis, and HCl caused lesser acidosis, all predominantly metabolic in nature. Total plasma ammonia (T(Amm)) and excretion rates of ammonia (J(Amm)) and urea-N (J(Urea-N)) were unaffected by NaCl or HCl. However, despite equal loading rates, plasma T(Amm) increased to a greater extent with NH4Cl, while J(Amm) increased to a greater extent with NH4HCO3 due to much greater increases in blood-to-water PNH3 gradients. As with HEA, both treatments caused large (90%) elevations of J(Urea-N), indicating that urea-N synthesis by the ornithine-urea cycle (OUC) is driven primarily by ammonia rather than HCO3(-). Branchial mRNA expressions of Rhbg and Rhp2 were unaffected by NH4HCO3 or NH4Cl, but v-type H(+)-ATPase was down-regulated by both treatments, and Rhbg and Na(+)/H(+) exchanger NHE2 were up-regulated by HCl. In the kidney, Rhbg was unresponsive to all treatments, but Rhp2 was up-regulated by HCl, and the urea transporter UT was up-regulated by HCl and NH4Cl. These responses are discussed in the context of current ideas about branchial, renal, and OUC function in this nitrogen-limited predator.

  7. Acid-base and ionic fluxes in rainbow trout (Oncorhynchus mykiss) during exposure to chloramine-T

    Energy Technology Data Exchange (ETDEWEB)

    Powell, M.D.; Perry, S.F. [Department of Biology, University of Ottawa, 30 Marie Curie Ottawa, Ontario, K1N 6N5 (Canada)

    1998-09-01

    The effects of chloramine-T and its degradation products, sodium hypochlorite (NaOCl) and para-toluenesulphonamide (pTSA), on whole body acid-base and branchial and renal ion (Na{sup +}and Cl{sup -}) fluxes were examined in rainbow trout (Oncorhynchus mykiss). Exposure to chloramine-T (3.5 h, 18 mg l{sup -1}) resulted in increases in plasma total CO{sub 2} but no coincident rise in P{sub a}CO{sub 2} or reduction in blood pH. Exposure of fish to 2, 9 or 18 mg l{sup -1} chloramine-T (3.5 h duration) resulted in a reduction in net acid uptake suggesting the development of a metabolic alkalosis. Exposure to the chloramine-T breakdown product pTSA (dissolved in DMSO) resulted in increased net acid uptake (decreased acid excretion) suggesting a metabolic acidosis. Whole body ion fluxes demonstrated increases in the losses of both Na{sup +}and Cl{sup -} with chloramine-T, NaOCl and pTSA. However, the effect of DMSO alone could not be isolated. Confirmatory studies using fish in which the urinary bladder (to allow collection of urine) and dorsal aorta (to allow injection of [{sup 14}C]polyethylene glycol 4000 ([{sup 14}C]PEG), an extracellular fluid marker) were catheterised, revealed that changes in whole body ion fluxes during chloramine-T exposure could not be explained by increased renal efflux through urine flow, glomerular filtration or renal clearance. Branchial effluxes of [{sup 14}C]PEG were not significantly affected by chloramine-T exposure suggesting that the changes in whole body ionic fluxes were caused by transcellular rather than paracellular processes. (Copyright (c) 1998 Elsevier Science B.V., Amsterdam. All rights reserved.)

  8. Swimming Three Ice Miles within Fifteen Hours.

    Science.gov (United States)

    Stjepanovic, Mirko; Nikolaidis, Pantelis T.; Knechtle, Beat

    2017-08-31

    Ice Mile swimming (1608 m in water of below 5 °Celsius) is becoming increasingly popular. This case study aimed to identify body core temperature and selected haematological and biochemical parameters before and after repeated Ice Miles. An experienced ice swimmer completed three consecutive Ice Miles within 15 h. Swim times, body core temperatures, and selected urinary and haematological parameters were recorded. Body core temperature reached its maximum between 5, 8 and 15 min after immersion (37.7°C, 38.1°C, and 38.0°C, respectively). The swimmer suffered hypothermia during the first Ice Mile (35.4°C) and body core temperature dropped furthermore to 34.5°C during recovery after the first Ice Mile. He developed a metabolic acidosis in both the first and the last Ice Mile (pH 7.31 and pH 7.34, respectively). We observed hyperkalaemia ([K⁺] > 5.5 mM) after the second Ice Mile (6.9 mM). This was followed by a drop in [K⁺] to3.7 mM after the third Ice Mile. Anticipatory thermogenesis (i.e. an initial increase of body core temperature after immersion in ice cold water) seems to be a physiological response in a trained athlete. The results suggest that swimming in ice-cold water leads to a metabolic acidosis, which the swimmer compensates with hyperventilation (i.e. leading to respiratory alkalosis). The shift of serum [K⁺] could increase the risk of a cardiac arrhythmia. Further studies addressing the physiology and potential risks of Ice Mile swimming are required to substantiate this finding.

  9. Acid-Base and Plasma Biochemical Changes Using Crystalloid Fluids in Stranded Juvenile Loggerhead Sea Turtles (Caretta caretta).

    Science.gov (United States)

    Camacho, María; Quintana, María Del Pino; Calabuig, Pascual; Luzardo, Octavio P; Boada, Luis D; Zumbado, Manuel; Orós, Jorge

    2015-01-01

    The aim of this study was to compare the efficacy and effects on acid-base and electrolyte status of several crystalloid fluids in 57 stranded juvenile loggerhead turtles. Within a rehabilitation program four different crystalloid fluids were administered (0.9% Na Cl solution; 5% dextrose + 0.9% Na Cl solutions 1:1; 0.9% Na Cl + lactated Ringer's solutions 1:1; lactated Ringer's solution). Crystalloid fluids were intracoelomically administered during three days (20 ml/kg/day). Animals were sampled at three different moments: Upon admission for evaluating the type of acid-base or biochemical disorder, post-fluid therapy treatment for controlling the evolution of the disorder, and post-recovery period for obtaining the baseline values for rehabilitated loggerhead turtles. Each sample was analyzed with a portable electronic blood analyzer for pH, pO2, pCO2, lactate, sodium, potassium, chloride, glucose, and BUN concentration. Admission and post-fluid therapy treatment values were compared with those obtained for each turtle immediately before release. The highest percentage of acid-base recovery and electrolyte balance was observed in turtles treated with mixed saline-lactated Ringer's solution (63.6%), followed by turtles treated with physiological saline solution (55%), lactated Ringer's solution (33.3%), and dextrose-saline solutions (10%). Most turtles treated with lactated Ringer's solution had lower lactate concentrations compared with their initial values; however, 66.6% of turtles treated with lactated Ringer's solution had metabolic alkalosis after therapy. Significant higher concentrations of glucose were detected after saline-dextrose administration compared with all the remaining fluids. This is the first study evaluating the effects of several crystalloid fluids on the acid-base status and plasma biochemical values in stranded loggerhead sea turtles. Reference convalescent venous blood gas, acid-base, and plasma biochemical values, useful for veterinary

  10. Laxative-induced rhabdomyolysis

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    Alfonso Merante

    2010-03-01

    Full Text Available Alfonso Merante1, Pietro Gareri2,3, Norma Maria Marigliano2, Salvatore De Fazio2, Elvira Bonacci1, Carlo Torchia1, Gaetano Russo1, Pasquale Lacroce1, Roberto Lacava3, Alberto Castagna3, Giovambattista De Sarro2, Giovanni Ruotolo11Geriatrist, Geriatric Unit “Pugliese-Ciaccio” Hospital, Catanzaro, Italy; 2Department of Experimental and Clinical Medicine, Faculty of Medicine and Surgery, University Magna Graecia of Catanzaro, Clinical Pharmacology and Pharmacovigilance Unit, Mater Domini University Hospital, Catanzaro, Italy; 3Geriatrist, Operative Unit Elderly Health Care, Catanzaro, ItalyAbstract: The present study describes a case of laxative-induced rhabdomyolysis in an elderly patient. An 87-year-old woman was hospitalized for the onset of confusion, tremors, an inability to walk, and a fever that she had been experiencing for 36 hours. She often took high dosages of lactulose and sorbitol syrup as a laxative (about 70 g/day. During her physical examination, the patient was confused, drowsy, and she presented hyposthenia in her upper and lower limbs, symmetric and diffuse moderate hyporeflexia, and her temperature was 37.8°C. Laboratory tests revealed severe hyponatremia with hypokalemia, hypocalcemia, hypochloremia, and metabolic alkalosis. Moreover, rhabdomyolysis markers were found. The correction of hydroelectrolytic imbalances with saline, potassium and sodium chlorure, calcium gluconate was the first treatment. During her hospitalization the patient presented acute delirium, treated with haloperidol and prometazine chloridrate intramuscularly. She was discharged 12 days later, after resolution of symptoms, and normalized laboratory tests. Over-the-counter drugs such as laxatives are usually not considered dangerous; on the other hand, they may cause serum electrolytic imbalance and rhabdomyolysis. A careful monitoring of all the drugs taken by the elderly is one of the most important duties of a physician since drug interactions and

  11. Acid-base and ionic fluxes in rainbow trout (Oncorhynchus mykiss) during exposure to chloramine-T

    International Nuclear Information System (INIS)

    Powell, M.D.; Perry, S.F.

    1998-01-01

    The effects of chloramine-T and its degradation products, sodium hypochlorite (NaOCl) and para-toluenesulphonamide (pTSA), on whole body acid-base and branchial and renal ion (Na + and Cl - ) fluxes were examined in rainbow trout (Oncorhynchus mykiss). Exposure to chloramine-T (3.5 h, 18 mg l -1 ) resulted in increases in plasma total CO 2 but no coincident rise in P a CO 2 or reduction in blood pH. Exposure of fish to 2, 9 or 18 mg l -1 chloramine-T (3.5 h duration) resulted in a reduction in net acid uptake suggesting the development of a metabolic alkalosis. Exposure to the chloramine-T breakdown product pTSA (dissolved in DMSO) resulted in increased net acid uptake (decreased acid excretion) suggesting a metabolic acidosis. Whole body ion fluxes demonstrated increases in the losses of both Na + and Cl - with chloramine-T, NaOCl and pTSA. However, the effect of DMSO alone could not be isolated. Confirmatory studies using fish in which the urinary bladder (to allow collection of urine) and dorsal aorta (to allow injection of [ 14 C]polyethylene glycol 4000 ([ 14 C]PEG), an extracellular fluid marker) were catheterised, revealed that changes in whole body ion fluxes during chloramine-T exposure could not be explained by increased renal efflux through urine flow, glomerular filtration or renal clearance. Branchial effluxes of [ 14 C]PEG were not significantly affected by chloramine-T exposure suggesting that the changes in whole body ionic fluxes were caused by transcellular rather than paracellular processes. (Copyright (c) 1998 Elsevier Science B.V., Amsterdam. All rights reserved.)

  12. [Clinical evaluation of acid-base status: Henderson-Hasselbalch, or Stewart-Fencl approach?

    Science.gov (United States)

    Matoušovic, Karel; Havlín, Jan; Schück, Otto

    Two approaches have been used in clinical evaluation the acid-base status: traditional (bicarbonate-centered) is based on the Henderson-Hasselbalch equation complemented by calculation of the anion gap, and more recent quantitative approach proposed by Stewart and Fencl. The latter method defines the three independent variables, which regulate pH. These include: the difference between the sum of charges carried by strong plasma cations and anions termed the strong ion difference - SID (decrease causes acidosis, and vice versa); the total concentration of the weak non-volatile acids [Atot] (inorganic phosphate and albumin, decrease causes alkalosis and vice versa), and pCO2. According to this approach, pH and bicarbonate are dependent variables. Their concentrations change if and only if one or more independent variables are altered.The main advantage of the Stewart-Fencl approach is the calculation of the concentration of plasma acids, which are not routinely measured. In the traditional approach, their presence is inferred from the anion gap. The correction of the value of anion gap according to the serum albumin level increases the specificity. This correction brings traditional approach closer to the Stewart-Fencl method that precisely calculates unmeasured strong anions by further adjustment of the corrected anion gap according to the serum phosphate, calcium and magnesium levels. The precise calculation of unmeasured anions is important in critically ill patients with the metabolic breakdown, where the traditional approach may overlook the presence of unmeasured anions. Consideration of the sodium-chloride difference draws the attention to acid-base disturbance caused by change of the strong ion difference.

  13. The Effect of Supplemental Oxygen in Obesity Hypoventilation Syndrome

    Science.gov (United States)

    Masa, Juan F.; Corral, Jaime; Romero, Auxiliadora; Caballero, Candela; Terán-Santos, Joaquin; Alonso-Álvarez, Maria L.; Gomez-Garcia, Teresa; González, Mónica; López-Martínez, Soledad; De Lucas, Pilar; Marin, José M.; Marti, Sergi; Díaz-Cambriles, Trinidad; Chiner, Eusebi; Merchan, Miguel; Egea, Carlos; Obeso, Ana; Mokhlesi, Babak

    2016-01-01

    Study Objectives: Low flow supplemental oxygen is commonly prescribed to patients with obesity hypoventilation syndrome (OHS). However, there is a paucity of data regarding its efficacy and safety. The objective of this study was to assess the medium-term treatment efficacy of adding supplemental oxygen therapy to commonly prescribed treatment modalities in OHS. Methods: In this post hoc analysis of a previous randomized controlled trial, we studied 302 sequentially screened OHS patients who were randomly assigned to noninvasive ventilation, continuous positive airway pressure, or lifestyle modification. Outcomes at 2 mo included arterial blood gases, symptoms, quality of life, blood pressure, polysomnography, spirometry, 6-min walk distance, and hospital resource utilization. Statistical analysis comparing patients with and without oxygen therapy in the three treatment groups was performed using an intention-to-treat analysis. Results: In the noninvasive ventilation group, supplemental oxygen reduced systolic blood pressure although this could be also explained by a reduction in body weight experienced in this group. In the continuous positive airway pressure group, supplemental oxygen increased the frequency of morning confusion. In the lifestyle modification group, supplemental oxygen increased compensatory metabolic alkalosis and decreased the apnea-hypopnea index during sleep. Oxygen therapy was not associated with an increase in hospital resource utilization in any of the groups. Conclusions: After 2 mo of follow-up, chronic oxygen therapy produced marginal changes that were insufficient to consider it, globally, as beneficial or deleterious. Because supplemental oxygen therapy did not increase hospital resource utilization, we recommend prescribing oxygen therapy to patients with OHS who meet criteria with close monitoring. Long-term studies examining outcomes such as incident cardiovascular morbidity and mortality are necessary. Clinical Trials Registration

  14. Do anesthetics and sampling strategies affect transcription analysis of fish tissues?

    Directory of Open Access Journals (Sweden)

    Hevrøy Ernst M

    2007-06-01

    Full Text Available Abstract Background The aim of the current examination was to evaluate if sedation and anesthetic treatment techniques affect the quality of RNA extracted from liver, gill, head kidney and brain tissues in Atlantic salmon Salmo salar L. Blood parameters were measured and tissue specimens sampled in six groups of fish; one control group (0 minutes, two groups kept in pure seawater in 90 liter tanks for 30 and 120 minutes, two groups treated with the anesthetic isoeugenol for 30 and 120 minutes, and one group kept in pure seawater for 105 minutes and then anaesthetized with metacaine for 15 minutes. RNA quality was assessed with the NanoDrop ND-1000 spectrophotometer (260/280 and 260/230 nm ratios and with the Agilent Bioanalyzer (28S/18S ratio and RIN data in samples either preserved in liquefied nitrogen (N2 or in RNAlater. In addition, the transcriptional levels of two fast-responding genes were quantified in gill and brain tissues. Results The results show that physiological stress during sampling does not affect the quality of RNA extracted from fish specimens. However, prolonged sedation (2 hours resulted in a metabolic alkalosis that again affected the transcriptional levels of genes involved in ionoregulation and respiration. In gills, Na+-K+-ATPase α1b was significantly downregulated and hypoxia inducible factor 1 (HIF1 significantly upregulated after two hours of treatment with isoeugenol, suggesting that this commonly used sedative affects osmo-regulation and respiration in the fish. The results also suggest that for tissue preservation in general it is better to flash-freeze fish specimens in liquefied N2 than to use RNAlater. Conclusion Prolonged sedation may affect the transcription of fast-responding genes in tissues of fish. Two hours of sedation with isoeugenol resulted in downregulation of the Na+-K+-ATPase α1b gene and upregulation of the HIF1 gene in gills of Atlantic salmon. The quality of RNA extracted from tissue specimens

  15. Co-Regulated Pendrin and Aquaporin 5 Expression and Trafficking in Type-B Intercalated Cells under Potassium Depletion

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    Giuseppe Procino

    2013-12-01

    Full Text Available Background: We recently reported that aquaporin 5 (AQP5, a water channel never identified in the kidney before, co-localizes with pendrin at the apical membrane of type-B intercalated cells in the kidney cortex. Since co-expression of AQP5 and pendrin in the apical membrane domain is a common feature of several other epithelia such as cochlear and bronchial epithelial cells, we evaluated here whether this strict membrane association may reflect a co-regulation of the two proteins. To investigate this possibility, we analyzed AQP5 and pendrin expression and trafficking in mice under chronic K+ depletion, a condition that results in an increased ability of renal tubule to reabsorb bicarbonate, often leads to metabolic alkalosis and is known to strongly reduce pendrin expression. Methods: Mice were housed in metabolic cages and pair-fed with either a standard laboratory chow or a K+-deficient diet. AQP5 abundance was assessed by western blot in whole kidney homogenates and AQP5 and pendrin were localized by confocal microscopy in kidney sections from those mice. In addition, the short-term effect of changes in external pH on pendrin trafficking was evaluated by fluorescence resonance energy transfer (FRET in MDCK cells, and the functional activity of pendrin was tested in the presence and absence of AQP5 in HEK 293 Phoenix cells. Results: Chronic K+ depletion caused a strong reduction in pendrin and AQP5 expression. Moreover, both proteins shifted from the apical cell membrane to an intracellular compartment. An acute pH shift from 7.4 to 7.0 caused pendrin internalization from the plasma membrane. Conversely, a pH shift from 7.4 to 7.8 caused a significant increase in the cell surface expression of pendrin. Finally, pendrin ion transport activity was not affected by co-expression with AQP5. Conclusions: The co-regulation of pendrin and AQP5 membrane expression under chronic K+-deficiency indicates that these two molecules could cooperate as an

  16. Metabolic disorders in acute infectious diarrhea in children

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    S. V. Khaliullina

    2017-01-01

    Full Text Available The purpose of the study: estimate the frequency of registration of different types of acid-base state disorders in children with acute infectious diarrhea; to determine the clinical features of acute intestinal infections that occur with metabolic acidosis (MA and without it to choose the tactics of effective correction.Мaterials and methods: retrospective cohort study was conducted of 246 patients hospitalized in a hospital with clinic of acute infectious diarrhea.Results of the study: laboratory-confirmed acidosis, were recorded in 40.7% (95% CI 34.6–46.8, 100/246 children, incl. With a pH below 7.25 in 9.3% (95% CI 5–7–12.9, 23/246. The condition of alkalosis revealed in 4.9% (95% CI 2.2–7.6 of 12/246 examined. Hyperchloremic acidosis had a place in 81% (95% CI 73.3–88.7, 81/100 patients, with a high anionic deficiency in 19% (95% CI 11.3–26.7, 19/100, P <0.001. Decompensated MA with pH <7.25 was recorded in 6.2% (95% CI 0.9–11.5, 5/81 examined with hyperchloremic acidosis and in 94.7% (95% CI 84.6–104, 8, 18/19 – with keto- and lactate-acidosis. Subcompensated MA was more often detected with rotavirus infection, RVI (50.6% (95% CI (39.4–61.8, 39/77, p <0.001. Metabolic disorders with RVI were more likely to correspond to acidosis with a high anion gap (52, 6% (95% CI 30.1–75.1 10/19, p=0.02. Bacterial diarrheas were more often observed in children without disturbances of the KHS (22.4% (95% CI 15.3–29, 5, 30/134, p=0.014. In assessing the characteristics of different types of MA we identified that the presence of tachypnea increases the probability of detecting acidosis with a high anion gap of 3.5 times (OR 3.5 CI 1.3–9.3.Conclusion: Our studies didn’t reveal pathognomonic clinical symptoms of various variants of metabolic acidosis.

  17. Effects of chronic waterborne nickel exposure on growth, ion homeostasis, acid-base balance, and nickel uptake in the freshwater pulmonate snail, Lymnaea stagnalis.

    Science.gov (United States)

    Niyogi, Som; Brix, Kevin V; Grosell, Martin

    2014-05-01

    The freshwater pulmonate snail, Lymnaea stagnalis, is the most sensitive aquatic organism tested to date for Ni. We undertook a series of experiments to investigate the underlying mechanism(s) for this observed hypersensitivity. Consistent with previous experiments, juvenile snail growth in a 21-day exposure was reduced by 48% relative to the control when exposed to 1.3 μg l(-1) Ni (EC20 less than the lowest concentration tested). Ca(2+) homeostasis was significantly disrupted by Ni exposure as demonstrated by reductions in net Ca(2+) uptake, and reductions in Ca(2+) concentrations in the hemolymph and soft tissues. We also observed reduced soft tissue [Mg(2+)]. Snails underwent a significant alkalosis with hemolymph pH increasing from 8.1 to 8.3 and hemolymph TCO2 increasing from 19 to 22 mM in control versus Ni-exposed snails, respectively. Unlike in previous studies with Co and Pb, snail feeding rates were found to be unaffected by Ni at the end of the exposure. Snails accumulated Ni in the soft tissue in a concentration-dependent manner, and Ni uptake experiments with (63)Ni revealed a biphasic uptake profile - a saturable high affinity component at low exposure concentrations (36-189 nM) and a linear component at the high exposure concentrations (189-1,897 nM). The high affinity transport system had an apparent Km of 89 nM Ni(2+) and Vmax of 2.4 nmol g(-1)h(-1). This equates to a logK of 7.1, significantly higher than logK's (2.6-5.2) for any other aquatic organisms evaluated to date, which will have implications for Biotic Ligand Model development. Finally, pharmacological inhibitors that block Ca(2+) uptake pathways in snails did not inhibit Ni uptake, suggesting that the uptake of Ni does not occur via Ca(2+) uptake pathways. As with Cu and Pb, the exact mechanism for the significant disruption in Ca(2+) homeostasis and reduction in juvenile snail growth remains unknown. Copyright © 2014 Elsevier B.V. All rights reserved.

  18. Clorhidrorrea congénita:: primer reporte en Cuba Congenital chlorhydria:: first report in Cuba

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    Carlos Ramírez Pérez

    2009-12-01

    Full Text Available En el presente trabajo se exponen los antecedentes prenatales, perinatales y posnatales de un lactante de 6 meses de edad, del sexo masculino, con clorhidrorrea congénita, así como el cuadro clínico, diagnóstico y tratamiento utilizado. Un elemento significativo lo constituyó la expulsión anal de abundante líquido no meconial desde las primeras horas de nacido, así como alcalosis metabólica grave y la presencia de desnutrición rápidamente progresiva. En los exámenes complementarios se constató hipocloremia de un 50 % con respecto a las cifras de referencia y un pH sanguíneo mayor de 7,50. El diagnóstico confirmatorio se obtuvo al comprobar concentraciones de cloro en heces fecales superiores a las de la suma de sodio y potasio. Se proponen indicadores diagnósticos prenatales entre los que tienen gran valor la consanguinidad, el polihidramnios y los resultados del ultrasonido en el tercer trimestre del embarazo. El diagnóstico precoz permitió establecer el tratamiento y evitó el frecuente desenlace fatal. Es el primer caso de esta enfermedad que se informa en el país.In present paper are showed the prenatal, perinatal and postnatal backgrounds from a male breast-fed baby aged 6 months presenting with congenital chlorhydria, as well as the clinical picture, diagnosis and treatment applied. A significant element was the anal expulsion of non-meconium abundant fluid from the first hours of born, as well as a severe metabolic alkalosis and the presence of a quickly progressive malnutrition. In complementary examinations was confirmed a 50% hypochloremia regarding the reference figures and a blood pH over 7,50. Confirmatory diagnosis was achieved verifying the chlorine concentrations in feces higher to that of the sum of sodium and potassium. Prenatal diagnostic indicators are proposed those with higher value including the consanguinity, polyhydramnios and the US results during the third trimester of pregnancy. Early diagnosis

  19. Hemogasometria em cães com desidratação experimental tratados com soluções eletrolíticas comerciais administradas por via intravenosa Blood gas analysis in dogs with experimental dehidration treated with commercial electrolytes solutions by intravenous route

    Directory of Open Access Journals (Sweden)

    José Dantas Ribeiro Filho

    2008-10-01

    make them an option to treat dogs with metabolic alkalosis.

  20. Response properties of the genetically encoded optical H2O2 sensor HyPer.

    Science.gov (United States)

    Weller, Jonathan; Kizina, Kathrin M; Can, Karolina; Bao, Guobin; Müller, Michael

    2014-11-01

    Reactive oxygen species mediate cellular signaling and neuropathologies. Hence, there is tremendous interest in monitoring (sub)cellular redox conditions. We evaluated the genetically engineered redox sensor HyPer in mouse hippocampal cell cultures. Two days after lipofection, neurons and glia showed sufficient expression levels, and H2O2 reversibly and dose-dependently increased the fluorescence ratio of cytosolic HyPer. Yet, repeated H2O2 treatment caused progressively declining responses, and with millimolar doses an apparent recovery started while H2O2 was still present. Although HyPer should be H2O2 specific, it seemingly responded also to other oxidants and altered cell-endogenous superoxide production. Control experiments with the SypHer pH sensor confirmed that the HyPer ratio responds to pH changes, decreasing with acidosis and increasing during alkalosis. Anoxia/reoxygenation evoked biphasic HyPer responses reporting apparent reduction/oxidation; replacing Cl(-) exerted only negligible effects. Mitochondria-targeted HyPer readily responded to H2O2-albeit less intensely than cytosolic HyPer. With ratiometric two-photon excitation, H2O2 increased the cytosolic HyPer ratio. Time-correlated fluorescence-lifetime imaging microscopy (FLIM) revealed a monoexponential decay of HyPer fluorescence, and H2O2 decreased fluorescence lifetimes. Dithiothreitol failed to further reduce HyPer or to induce reasonable FLIM and two-photon responses. By enabling dynamic recordings, HyPer is superior to synthetic redox-sensitive dyes. Its feasibility for two-photon excitation also enables studies in more complex preparations. Based on FLIM, quantitative analyses might be possible independent of switching excitation wavelengths. Yet, because of its pronounced pH sensitivity, adaptation to repeated oxidation, and insensitivity to reducing stimuli, HyPer responses have to be interpreted carefully. For reliable data, side-by-side pH monitoring with SypHer is essential. Copyright

  1. Patterns of unexpected in-hospital deaths: a root cause analysis

    Science.gov (United States)

    2011-01-01

    Background Respiratory alarm monitoring and rapid response team alerts on hospital general floors are based on detection of simple numeric threshold breaches. Although some uncontrolled observation trials in select patient populations have been encouraging, randomized controlled trials suggest that this simplistic approach may not reduce the unexpected death rate in this complex environment. The purpose of this review is to examine the history and scientific basis for threshold alarms and to compare thresholds with the actual pathophysiologic patterns of evolving death which must be timely detected. Methods The Pubmed database was searched for articles relating to methods for triggering rapid response teams and respiratory alarms and these were contrasted with the fundamental timed pathophysiologic patterns of death which evolve due to sepsis, congestive heart failure, pulmonary embolism, hypoventilation, narcotic overdose, and sleep apnea. Results In contrast to the simplicity of the numeric threshold breach method of generating alerts, the actual patterns of evolving death are complex and do not share common features until near death. On hospital general floors, unexpected clinical instability leading to death often progresses along three distinct patterns which can be designated as Types I, II and III. Type I is a pattern comprised of hyperventilation compensated respiratory failure typical of congestive heart failure and sepsis. Here, early hyperventilation and respiratory alkalosis can conceal the onset of instability. Type II is the pattern of classic CO2 narcosis. Type III occurs only during sleep and is a pattern of ventilation and SPO2 cycling caused by instability of ventilation and/or upper airway control followed by precipitous and fatal oxygen desaturation if arousal failure is induced by narcotics and/or sedation. Conclusion The traditional threshold breach method of detecting instability on hospital wards was not scientifically derived; explaining

  2. Patterns of unexpected in-hospital deaths: a root cause analysis

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    Curry J Paul

    2011-02-01

    Full Text Available Abstract Background Respiratory alarm monitoring and rapid response team alerts on hospital general floors are based on detection of simple numeric threshold breaches. Although some uncontrolled observation trials in select patient populations have been encouraging, randomized controlled trials suggest that this simplistic approach may not reduce the unexpected death rate in this complex environment. The purpose of this review is to examine the history and scientific basis for threshold alarms and to compare thresholds with the actual pathophysiologic patterns of evolving death which must be timely detected. Methods The Pubmed database was searched for articles relating to methods for triggering rapid response teams and respiratory alarms and these were contrasted with the fundamental timed pathophysiologic patterns of death which evolve due to sepsis, congestive heart failure, pulmonary embolism, hypoventilation, narcotic overdose, and sleep apnea. Results In contrast to the simplicity of the numeric threshold breach method of generating alerts, the actual patterns of evolving death are complex and do not share common features until near death. On hospital general floors, unexpected clinical instability leading to death often progresses along three distinct patterns which can be designated as Types I, II and III. Type I is a pattern comprised of hyperventilation compensated respiratory failure typical of congestive heart failure and sepsis. Here, early hyperventilation and respiratory alkalosis can conceal the onset of instability. Type II is the pattern of classic CO2 narcosis. Type III occurs only during sleep and is a pattern of ventilation and SPO2 cycling caused by instability of ventilation and/or upper airway control followed by precipitous and fatal oxygen desaturation if arousal failure is induced by narcotics and/or sedation. Conclusion The traditional threshold breach method of detecting instability on hospital wards was not

  3. Prostaglandin-E2 Mediated Increase in Calcium and Phosphate Excretion in a Mouse Model of Distal Nephron Salt Wasting.

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    Manoocher Soleimani

    Full Text Available Contribution of salt wasting and volume depletion to the pathogenesis of hypercalciuria and hyperphosphaturia is poorly understood. Pendrin/NCC double KO (pendrin/NCC-dKO mice display severe salt wasting under basal conditions and develop profound volume depletion, prerenal renal failure, and metabolic alkalosis and are growth retarded. Microscopic examination of the kidneys of pendrin/NCC-dKO mice revealed the presence of calcium phosphate deposits in the medullary collecting ducts, along with increased urinary calcium and phosphate excretion. Confirmatory studies revealed decreases in the expression levels of sodium phosphate transporter-2 isoforms a and c, increases in the expression of cytochrome p450 family 4a isotypes 12 a and b, as well as prostaglandin E synthase 1, and cyclooxygenases 1 and 2. Pendrin/NCC-dKO animals also had a significant increase in urinary prostaglandin E2 (PGE-2 and renal content of 20-hydroxyeicosatetraenoic acid (20-HETE levels. Pendrin/NCC-dKO animals exhibit reduced expression levels of the sodium/potassium/2chloride co-transporter 2 (NKCC2 in their medullary thick ascending limb. Further assessment of the renal expression of NKCC2 isoforms by quantitative real time PCR (qRT-PCR reveled that compared to WT mice, the expression of NKCC2 isotype F was significantly reduced in pendrin/NCC-dKO mice. Provision of a high salt diet to rectify volume depletion or inhibition of PGE-2 synthesis by indomethacin, but not inhibition of 20-HETE generation by HET0016, significantly improved hypercalciuria and salt wasting in pendrin/NCC dKO mice. Both high salt diet and indomethacin treatment also corrected the alterations in NKCC2 isotype expression in pendrin/NCC-dKO mice. We propose that severe salt wasting and volume depletion, irrespective of the primary originating nephron segment, can secondarily impair the reabsorption of salt and calcium in the thick ascending limb of Henle and/or proximal tubule, and reabsorption of

  4. Effect of an isoflavones-containing red clover preparation and alkaline supplementation on bone metabolism in ovariectomized rats

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    S Kawakita

    2009-02-01

    /body weight ratio observed in untreated post-ovariectomy group. Untreated ovariectomy caused about 48% decrease of cancellous bone mass in the femoral neck while this abnormality was prevented at similar extent by both RCE and RCE + BP treatments. Ovariectomy determined an over 80% increase of bone alkaline phosphatase (BALP level but both RCE and RCE + BP treatments significantly mitigated such variable. The BALP decrease yielded by the combined RCE + BP treatment was statistically lower than RCE alone. Taken together these data show that red clover preparation in dosages amenable to clinical practice do improve OVX-induced osteoporosis while a mild metabolic alkalosis might further synergize some therapeutic aspects. Keywords: red clover, alkaline supplementation, osteoporosis, ovariectomy

  5. Hyperosmotic perfusion of the beating rat heart and the role of the Na+/K+/2Cl- co-transporter and the Na+/H+ exchanger.

    Science.gov (United States)

    Falck, G; Schjøtt, J; Bruvold, M; Krane, J; Skarra, S; Jynge, P

    2000-02-01

    The aim of the present study was to investigate the role of the Na+/K+/2Cl- co-transporter and the Na+/H+ exchanger on contractile function and electrolyte regulation during hyperosmotic perfusion of the heart. Langendorff perfused rat hearts were subjected to hyperosmolal perfusion in 10-min intervals. Perfusates were made hyperosmotic by adding mannitol to the buffer (370, 450 and 600 mOsmol/kg H2O). Cardiac contractile function was monitored with a balloon in the left ventricle (LV) coupled to a pressure transducer. Cardiac effluent was sampled repeatedly throughout and after hyperosmotic perfusion and analysed for content of Na+, K+, and Cl-. All three hyperosmotic perfusates initially reduced LV developed pressure (LVDP), but for 370 and 450 mOsmol/kg H2O, LVDP recovered to baseline within 4 min of perfusion. With 600 mOsmol/kg H2O, LVDP recovered slowly and was 50% below baseline after 10 min of hyperosmotic perfusion. Inhibition of the Na+/H+ exchanger with 5-(N-ethyl-N-isopropyl) amiloride (EIPA) and 3-methylsulfonyl-4-piperidinobenzoyl-guanidine methanesulfonate (HOE 694) abolished the recovery of LVDP to the 600 mOsmol/kg H2O perfusate, whereas inhibition of the Na+/K+/2Cl- co-transporter had no impact on LVDP. Potassium was taken up by the heart during hyperosmotic perfusion and this uptake was significantly reduced with inhibition of the Na+/H+ exchanger. Intracellular pH was assessed with 31p magnetic resonance spectroscopy and hyperosmolality induced a significant alkalosis that was dependent upon the Na+/H+ exchanger. The rat heart responds to moderate elevations in osmolality with a transient reduction in contractile function, whereas an elevation of 300 mOsmol/kg H2O persistently reduces contractile function. The Na+/H+ exchanger, but not the Na+/K+/2Cl- co-transporter, is of importance in contractile recovery and electrolyte regulation during hyperosmotic perfusion in the rat heart.

  6. Branched-chain aminoacids and retraining of patients with chronic obstructive lung disease.

    Science.gov (United States)

    Menier, R; Talmud, J; Laplaud, D; Bernard, M P

    2001-12-01

    The aim of this work was to improve the efficacy of rehabilitation by retraining, by oral supply in branched-chain aminoacids (BCAA). Patients with chronic respiratory insufficiency mainly suffer from obstructive bronchitis due to tobacco or asthma. Nutritional assessment is one of the components of respiratory rehabilitation, with retraining. Intense physical training for several days negativates the nitrogen balance, the beginning of a training programme for sedentary patients increases their need in proteins. An additional supply in branched-chain aminoacids increases proteic anabolism, by synthesis increase and catabolism slackening of proteins. Moreover it is known that exposure to high altitude reduces lean mass by inducing a muscular atrophy, which can be avoided by the BCAA provided. This leads to wonder if extra supply of BCAA could play similar role in muscular mass loss induced by pathological chronic hypoxia. The prospective and comparative survey carried out in Toki-Eder (private hospital in Cambo) consisted in supplying (during five weeks or more) 30 retrained patients suffering from chronic obstructive bronchitis, and in matching them with 30 witnesses (obstructive patients retrained without additional supply in BCAA). Their mean hypoxemia amounted to 7 torr for age. Each of them improved their reached maximal power, and their VO2 SL, very highly significantly. Each of them developed a moderate metabolic acidosis (whose possible mechanisms are discussed) and slightly increased their ventilation at rest. On the other hand only the supplied patients improved their PaO2 at rest highly significantly, a result which poses the question of the responsible mechanism, most likely a decrease of pulmonary shunt effect. The hypotheses concerning the acid load due to BCAA ingestion are discussed. Only the supplied patients developed hypocapnia expressing a gaseous alkalosis which might be due to a direct effect of BCAA on the respiratory centers. This observation

  7. Post-prandial alkaline tide in freshwater rainbow trout: effects of meal anticipation on recovery from acid-base and ion regulatory disturbances.

    Science.gov (United States)

    Cooper, C A; Wilson, R W

    2008-08-01

    The post-feeding alkaline tide (elevated blood pH and HCO3-) has been well characterised in air-breathing animals, but to date this phenomenon has only been demonstrated in one piscine species, a marine elasmobranch. We have investigated the acid-base and ion regulatory responses of a freshwater teleost to voluntary feeding as well as to involuntary filling of the stomach via an indwelling gastric intubation tube. One group of rainbow trout (Oncorhynchus mykiss) were fed a 1% body mass ration of homogenised food via the gastric intubation tube. Another group fed voluntarily on a 1% body mass ration. Blood samples were taken via dorsal aortic catheters from fish in both groups before feeding and over the subsequent 72 h. Trout fed via the gastric intubation tube exhibited post-prandial metabolic alkalosis of the blood (pH and plasma HCO3- increases of up to approximately 0.2 pH units and 3 mmol l(-1), respectively), that was more than twofold greater than the voluntary feeding fish, and took three times as long to recover (72 versus 24 h). Arterial PCO2 was unchanged in both groups indicating that freshwater trout do not retain CO2 to compensate for a post-prandial alkaline tide. Although excretion of HCO3- to the water increased post-prandially, NH4+ excretion followed a similar pattern, such that net acid equivalent fluxes were unaffected. Thus, sites other than the gills or kidney must be responsible for recovery of blood acid-base status, with intestinal HCO3- secretion being a likely candidate. In addition, fish fed via the gastric intubation tube experienced a large (17 mmol l(-1)) but acute (6 h) drop in plasma chloride and a very large (53%) and long lasting decline in plasma magnesium concentration, that were absent in voluntarily feeding fish. These results further indicate a potentially important role for neuro-endocrine mediated mechanisms when fish feed voluntarily, in promoting the earlier initiation of compensatory responses that regulate blood ion

  8. An Unusual Case of Licorice-Induced Hypertensive Crisis.

    Science.gov (United States)

    Ottenbacher, Ronovan; Blehm, Julie

    2015-08-01

    mineralocorticoid receptors resulting in excess mineralocorticoid activity or pseudohyperaldosteronism. The patient may present with findings similar to primary aldosteronism: hypertension with sodium retention, edema, hypokalemia, metabolic alkalosis and low plasma renin activity. Plasma aldosterone levels would be low (in primary aldosteronism it is elevated). Specific testing can be performed, but resolution of symptoms after the patient stops eating licorice strongly suggests the diagnosis.

  9. Acid-Base and Plasma Biochemical Changes Using Crystalloid Fluids in Stranded Juvenile Loggerhead Sea Turtles (Caretta caretta)

    Science.gov (United States)

    Camacho, María; Quintana, María del Pino; Calabuig, Pascual; Luzardo, Octavio P.; Boada, Luis D.; Zumbado, Manuel; Orós, Jorge

    2015-01-01

    Aim The aim of this study was to compare the efficacy and effects on acid-base and electrolyte status of several crystalloid fluids in 57 stranded juvenile loggerhead turtles. Methods Within a rehabilitation program four different crystalloid fluids were administered (0.9% Na Cl solution; 5% dextrose + 0.9% Na Cl solutions 1:1; 0.9% Na Cl + lactated Ringer's solutions 1:1; lactated Ringer's solution). Crystalloid fluids were intracoelomically administered during three days (20 ml/kg/day). Animals were sampled at three different moments: Upon admission for evaluating the type of acid-base or biochemical disorder, post-fluid therapy treatment for controlling the evolution of the disorder, and post-recovery period for obtaining the baseline values for rehabilitated loggerhead turtles. Each sample was analyzed with a portable electronic blood analyzer for pH, pO2, pCO2, lactate, sodium, potassium, chloride, glucose, and BUN concentration. Admission and post-fluid therapy treatment values were compared with those obtained for each turtle immediately before release. Results The highest percentage of acid-base recovery and electrolyte balance was observed in turtles treated with mixed saline-lactated Ringer’s solution (63.6%), followed by turtles treated with physiological saline solution (55%), lactated Ringer’s solution (33.3%), and dextrose-saline solutions (10%). Most turtles treated with lactated Ringer’s solution had lower lactate concentrations compared with their initial values; however, 66.6% of turtles treated with lactated Ringer’s solution had metabolic alkalosis after therapy. Significant higher concentrations of glucose were detected after saline-dextrose administration compared with all the remaining fluids. Conclusions This is the first study evaluating the effects of several crystalloid fluids on the acid-base status and plasma biochemical values in stranded loggerhead sea turtles. Reference convalescent venous blood gas, acid-base, and plasma

  10. Analysis and physiological implications of renal 2-oxoglutaramate metabolism.

    Science.gov (United States)

    Nissim, I; Wehrli, S; States, B; Nissim, I; Yudkoff, M

    1991-07-01

    The relative significance of the flux through the glutamine aminotransferase (glutaminase II) pathway to renal ammoniagenesis is poorly understood. A basic and unresolved question is whether 2-oxoglutaramate (2-OGM), a product of the glutaminase II reaction, is deamidated to yield 2-oxoglutarate and NH3, or whether 2-OGM accumulates as an unreactive lactam, depending on the environmental pH. In the current studies we utilized 13C n.m.r. as well as 15N n.m.r. as well as 15N n.m.r. to demonstrate that 2-OGM occurs as a lactam, i.e. 5-hydroxypyroglutamate, regardless of the environmental pH. Our additional aims were to determine whether human kidney cells (HK cells) in culture can produce 2-OGM and to ascertain a pH-dependent relationship between NH3 and 2-OGM production from glutamine. We therefore developed an isotope dilution assay for 2-OGM utilizing 5-hydroxy[4-13C,1-15N]pyroglutamate as the labelled species. Incubations of HK cells in minimal essential medium supplemented with 1 mM-[2-15N]glutamine demonstrated significantly higher production of 2-OGM at pH 6.8 and lower production at pH 7.6 compared with pH 7.4. Similarly both 15NH3 and [15N]alanine formation were significantly higher in acute acidosis (pH 6.8) and lower in acute alkalosis (pH 7.6) compared with that at physiological pH. Addition of 1 mM-amino-oxyacetate to the incubation medium at pH 7.4 significantly diminished [15N]alanine and 2-OGM production, but the production of 15NH3 via the glutamate dehydrogenase pathway was significantly stimulated. The current observations indicate that the glutaminase II pathway plays a minor role and that flux through glutamate dehydrogenase is the predominant site for regulation of ammoniagenesis in human kidney.

  11. Role of tolvaptan in the management of hyponatremia in patients with lung and other cancers: current data and future perspectives

    Directory of Open Access Journals (Sweden)

    Thajudeen B

    2016-08-01

    ADH receptor antagonists that acts at renal tubular levels to increase free water excretion without inducing major systemic electrolyte abnormalities such as hypokalemia or alkalosis. The aim of this paper is to provide a brief review while focusing on cancer hyponatremia; (1 of the epidemiology of hyponatremia and its pathophysiology and diagnostic approaches and (2 of the pharmacokinetics of tolvaptan and its clinical efficacy, safety, and compliance. Keywords: treatment, pharmacology, safety, tolerability, efficacy, adherence

  12. Blood oxygen transport in common map turtles during simulated hibernation.

    Science.gov (United States)

    Maginniss, Leigh A; Ekelund, Summer A; Ultsch, Gordon R

    2004-01-01

    We assessed the effects of cold and submergence on blood oxygen transport in common map turtles (Graptemys geographica). Winter animals were acclimated for 6-7 wk to one of three conditions at 3 degrees C: air breathing (AB-3 degrees C), normoxic submergence (NS-3 degrees C), and hypoxic (PO2=49 Torr) submergence (HS-3 degrees C). NS-3 degrees C turtles exhibited a respiratory alkalosis (pH 8.07; PCO2=7.9 Torr; [lactate]=2.2 mM) relative to AB-3 degrees C animals (pH 7.89; PCO2=13.4 Torr; [lactate]=1.1 mM). HS-3 degrees C animals experienced a profound metabolic acidosis (pH 7.30; PCO2=7.9 Torr; [lactate]=81 mM). NS-3 degrees C turtles exhibited an increased blood O2 capacity; however, isoelectric focusing revealed no seasonal changes in the isohemoglobin (isoHb) profile. Blood O2 affinity was significantly increased by cold acclimation; half-saturation pressures (P50's) for air-breathing turtles at 3 degrees and 22 degrees C were 6.5 and 18.8 Torr, respectively. P50's for winter animals submerged in normoxic and hypoxic water were 5.2 and 6.5 Torr, respectively. CO2 Bohr slopes (Delta logP50/Delta pH) were -0.15, -0.16, and -0.07 for AB-3 degrees C, NS-3 degrees C, and HS-3 degrees C turtles, respectively; the corresponding value for AB-22 degrees C was -0.37. The O2 equilibrium curve (O2EC) shape was similar for AB-3 degrees C and NS-3 degrees C turtles; Hill plot n coefficients ranged from 1.8 to 2.0. The O2EC shape for HS-3 degrees C turtles was anomalous, exhibiting high O2 affinity below P50 and a right-shifted segment above half-saturation. We suggest that increases in Hb-O2 affinity and O2 capacity enhance extrapulmonary O2 uptake by turtles overwintering in normoxic water. The anomalous O2EC shape and reduced CO2 Bohr effect of HS-3 degrees C turtles may also promote some aerobic metabolism in hypoxic water.

  13. Sodium bicarbonate ingestion improves Yo-Yo intermittent recovery test 1 performance: a randomized crossover trial

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    Dixon H

    2017-04-01

    through an increased lactate efflux, demonstrated by increased [BLa]. Keywords: alkalosis, anaerobic, blood lactate, ergogenic aid, performance, repeated sprints

  14. The role of oral sodium bicarbonate supplementation in maintaining acid-base balance and its influence on the cardiovascular system in chronic hemodialysis patients - results of a prospective study.

    Science.gov (United States)

    Voiculeț, C; Zară, O; Bogeanu, C; Văcăroiu, I; Aron, G

    2016-01-01

    Background: Major acid-base variations during dialysis and the imbalances in serum calcium levels intensified by them play a role in cardiovascular damage of hemodialysis patients. Early vascular walls modifications can be objectified by determining the pulse wave velocity (PWV) - a marker of vascular stiffness that is associated with increased risk of cardiovascular events. Material and methods: This was a prospective study conducted on 63 chronic hemodialysis patients with diuresis above 500 mL/ 24 hours and predialysis blood pressure below 160 mmHg (treatment controlled) randomized in two groups for 12 months - the study group receiving interdialitic oral sodium bicarbonate doses and control group, without oral sodium bicarbonate supplementation, but receiving higher bicarbonate prescriptions in dialysis. All the patients were monthly evaluated by biochemical tests (serum calcium, phosphate, iPTH, bicarbonate), the assessment of prescribed doses of phosphate binders being undergone. Two PWV determinations and chest X-ray exams for coronary calcifications were done - at the beginning and end of the study for every patient. Results: In the study group (n = 29), the mean age was 56.48 ± 12.78 years and the average duration of dialysis was 55.51 ± 34.53 months, the mean dialysis bicarbonate was 29.81 ± 1.41 mEq/ L and 27 of them (subgroup 0) had alkaline reserve (AR) 20-22 mEq/ L. The control group (n = 34) had a mean age of 57.35 ± 15.32 years and the mean dialysis duration 59.67 ± 34.79 months, with an average level of dialysis bicarbonate of 33 ± 2.2 mEq/ L necessary to maintain AR within guidelines. Depending on the mean AR obtained, this group was divided into three subgroups (subgroup 1, subgroup 2, and subgroup 3). There were statistically significant differences regarding the necessary of dialysis bicarbonate (p bicarbonate levels is an important step in hemodialysis patients' management because wide acidosis-alkalosis variation can increase

  15. [End stage of chronic kidney disease and metabolic acidosis].

    Science.gov (United States)

    Klaboch, J; Opatrná, S; Matoušovic, K; Schück, O

    2012-01-01

    Renal function disorder is inevitably associated with metabolic acidosis. An adult produces approximately 1 mmol of acids/kg of body weight every day (3 mmol/kg in children), derived from metabolization of proteins from food. Development of metabolic acidosis in patients with kidney disease is based on accumulation of acids and insufficient production of bicarbonates; alkaline loss represents a marginal issue here limited to patients with type II renal tubular acidosis only. The prevalence of this disorder increases with declining glomerular filtration (GFR) from 2% in patients with GFR 1.0-1.5 ml/s/1.73 m2 to 39% in patients with GFR ammoniac production in residual nephrons. This is an adaptive mechanism aimed at maintaining sufficient elimination of acids despite reduced volume of functional tissue. However, an increased ammoniac production simultaneously becomes a stimulus for activation of the complement via an alternative route and is thus one of the factors contributing, through this induced inflammation, to progression of tubular interstitial fibrosis that subsequently leads to further GFR reduction. Metabolic acidosis has a number of severe adverse effects on the organism, e.g. deterioration of kidney bone disease through stimulation of bone resorption and inhibition of bone formation, inhibition of vitamin D formation, increased muscle catabolism, reduced albumin production, glucose metabolism disorder, increased insulin resistance, reduced production of thyroid hormones, increased accumulation of β2-microglobulin etc. Non-interventional studies suggest that alkali supplementation may slow down progression of chronic nephropathies. However, this approach, safe and inexpensive, has not been widely implemented in clinical practice yet. With respect to dialyzed patients, abnormal levels of bicarbonates are associated with increased mortality. Both metabolic acidosis and alkalosis, rather regularly seen in a considerable number of patients, have a negative

  16. A Dairy Herd Case Investigation with Very Low Dietary Cation–Anion Difference in Prepartum Dairy Cows

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    Pedro Melendez

    2017-06-01

    Full Text Available During the periparturient period, subclinical hypocalcemia (total plasma Ca concentration <2.0 mmol/l is a potential problem for the dairy cow; consequently, its prevention is essential for success of fertility and productive performance. Dietary cation–anion difference (DCAD has been defined as the difference in milliequivalents of cations (Na, K and anions (Cl, S per kilogram of dry matter (DM and has a direct impact on blood acid–base metabolism. Diets rich in K and Na induce metabolic alkalosis, interfering with tissue sensitivity to parathyroid hormone, and diets rich in Cl and S (anionic salts cause metabolic acidosis, reducing the risk of hypocalcemia. Consequently, the use of anionic salts has become a popular method to prevent hypocalcemia in dairy cattle. Monitoring diets with anionic salts can be done by measuring urine pH, with optimal values between 6.2 and 6.8 for Holstein cows. The objective of this report is to present a herd case investigation involving a dairy farm feeding a very low DCAD (−143 mEq/kg DM, expecting improved Ca homeostasis. The diet of −143 mEq/kg (urine pH 5.2–5.8 was changed to a diet with −53 mEq/kg DM (urine pH 6.2–6.8. Blood samples were taken at the time of calving for 10 cows that calved before and then for 10 cows that calved after changing the diet. Cows with extremely low DCAD had Ca concentrations of 2.11 ± 0.22 mmol/l and cows with a more moderated DCAD, 2.11 ± 0.16 mmol/l (P > 0.05. Several other blood metabolites (P, Mg, Na, K, Cl, albumin, globulins, blood urea nitrogen, creatinine, and GGT were also similar between groups. This very low DCAD during the prepartum period may severely compromise animal physiology unnecessarily, with little advantage over normal calcium concentrations at parturition, when compared with a less negative DCAD (−53 mEq/kg DM. Feeding a less negative DCAD ration (−53 mEq/kg DM did not decrease plasma Ca levels right after

  17. Manifestações renais na síndrome de Joubert Renal symptoms in the Joubert syndrome

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    Ana Paula Weiss

    2009-06-01

    DESCRIPTION: A 2 month-old patient was admitted with hypotonia and hyperpneia. At the physical exam, besides irregular breathing pattern, abnormal eye movements and arterial hypertension without abnormalities in cardiac or pulmonary sounds were observed. At the initial clinical and laboratorial investigations, cardiac and pulmonary causes were excluded. The diagnostic hypothesis was: neurological illness associated with renal disease. Laboratorial analysis showed respiratory alkalosis, metabolic acidosis and hyperkalemia, with normal renal function. In the magnetic resonance, images of neurological alterations were compatible with the "molar tooth sign", frequently associated with Joubert syndrome. Renal investigation was performed and cystic images in renal parenchyma were found. COMMENTS: Cardiac and pulmonary illness are frequently associated with clinical manifestations such as tachypnea and metabolic alterations. Nevertheless, neurological investigation may be necessary, since some diseases that affect the central nervous system may manifest these signs and symptoms. Association between renal alterations and central nervous system malformations are frequent in several diseases and should be investigated. Joubert syndrome and its associated disorders are characterized by aplasia of the cerebellar vermis, ataxia, abnormal eye movements and irregular breathing pattern with psychomotor and mental delay. The most frequent renal problems associated with the disease are renal cysts and nephronophtisis that can progress to end-stage renal failure.

  18. Estudo da capacidade alcalinizante de tampões metabolizáveis em bovinos sadios The alkalinizing effects of different metabolizable buffers in healthy steers

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    M.L.R. Leal

    2007-08-01

    generate a discrete metabolic alkalosis compensated organically by a small retention of CO2. Best alkalinizing effects are obtained by bicarbonate and L-lactato infusions. Bicarbonate infusions causes a high urinary pH.

  19. Experimental antegrade enema: effects on water, electrolyte and acid-base balances with different solutions Enema anterógrado experimental: equilíbrio hídrico eletrolítico e ácido-base em coelhos submetidos a enema com diferentes soluções

    Directory of Open Access Journals (Sweden)

    Laura Helman

    2007-10-01

    Full Text Available PURPOSE: To study the effects on the water, electrolyte, and acid-base balances in rabbits submitted to antegrade enema with different solutions through appendicostomy. METHODS: Forty male New Zealand rabbits were submitted to appendicostomy, and distributed in 4 groups, according to the antegrade enema solution: PEG group, polyethylene glycol electrolyte solution (n=10; ISS group, isotonic saline solution (n=10; GS group, glycerin solution (n=10; SPS group, sodium phosphate solution (n=10. After being weighed, arterial blood gas analysis, red blood count, creatinine and electrolytes were measured at 4 times: preoperatively (T1; day 6 postop, before enema (T2; 4h after enema (T3; and 24h after T3 (T4. RESULTS: In PEG group occurred Na retention after 4h, causing alkalemia, sustained for 24h with HCO3 retention. In ISS group occurred isotonic water retention and hyperchloremic acidosis after 4h, which was partially compensated in 24h. GS group showed metabolic acidosis after 4h, compensated in 24h. In SPS group occurred hypernatremic dehydration, metabolic acidosis in 4h, and hypokalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis with partially compensated dehydration in 24h. CONCLUSIONS: All solutions used in this study caused minor alterations on water, electrolyte or acid-base balances. The most intense ones were caused by hypertonic sodium phosphate solution (SPS and isotonic saline solution (ISS and the least by polyethyleneglycol electrolyte solution (PEG and glycerin solution 12% (GS.OBJETIVO: Estudar os efeitos no equilíbrio hídrico, eletrolítico e ácido-base, do enema anterógrado com diferentes soluções em coelhos através de apendicostomia. MÉTODOS: 40 coelhos Nova Zelândia, machos, submetidos a apendicostomia, distribuídos em quatro grupos segundo a solução de enema: grupo PEG (n = 10 solução de polietilenoglicol com eletrólitos; grupo SF (n = 10 solução fisiológica; grupo SG (n = 10 solução glicerinada

  20. Estresse térmico durante o pré-abate em frangos de corte Heat stress during the pre-slaughter on broiler chicken

    Directory of Open Access Journals (Sweden)

    Camila Brossi

    2009-07-01

    to become very susceptible to heat stress. When the environment temperature rises above the thermoneutrality zone, the bird is submitted to a stress condition, which can generate acute hyperthermia, respiratory alkalosis, electrolyte imbalance, reduction in food consumption, lower growth rate, increased mortality rate and even negative effects on meat quality due to the incidence of pale meat and dark in other cases, interfering in properties such as industrial yield, water holding capacity, color and tenderness. The results of the evaluation of quality parameters observed in literature showed that the heat stress, chronic or acute, suffered by broiler chickens, generates negative consequences on the functional properties of meat. Further studies with this research line should be conducted, mainly in Brazil, for being a tropical country with high temperatures in the summer in order to understand, prevent and overcome the extent or intensity of this stress, avoiding problems and damages to the meat chain.

  1. Clinical characteristics of chronic kidney disease of nontraditional causes in Salvadoran farming communities.

    Science.gov (United States)

    Herrera, Raúl; Orantes, Carlos M; Almaguer, Miguel; Alfonso, Pedro; Bayarre, Héctor D; Leiva, Irma M; Smith, Magaly J; Cubias, Ricardo A; Torres, Carlos G; Almendárez, Walter O; Cubias, Francisco R; Morales, Fabrizio E; Magaña, Salvador; Amaya, Juan C; Perdomo, Edgard; Ventura, Mercedes C; Villatoro, Juan F; Vela, Xavier F; Zelaya, Susana M; Granados, Delmy V; Vela, Eduardo; Orellana, Patricia; Hevia, Reynaldo; Fuentes, E Jackeline; Mañalich, Reinaldo; Bacallao, Raymed; Ugarte, Mario; Arias, María I; Chávez, Jackelin; Flores, Nelson E; Aparicio, Claudia E

    2014-04-01

    : hypermagnesuria (100%), hyperphosphaturia (50%), hypernatriuria (45.7%), hyperkaluria (23.9%), hypercalciuria (17.4%), electrolyte polyuria (43.5%), metabolic alkalosis (45.7%), hyponatremia (47.8%), hypocalcemia (39.1%), hypokalemia (30.4%), hypomagnesemia (19.6%). Imaging: Ultrasound showed fatty liver (93.5%) and vascular Doppler showed tibial artery damage (66.7%). Neurological symptoms: abnormal tendon reflexes (45.6%), Babinski sign and myoclonus (6.5%), sensorineural hearing loss (56.5%). This chronic kidney disease studied behaves clinically like chronic tubulointerstitial nephropathy, but with systemic manifestations not attributable to kidney disease. While male agricultural workers predominated, women and adolescents were also affected. Findings support a hypothesis of multifactorial etiology with a key role played by nephrotoxic environmental agents.

  2. Sodium bicarbonate intake improves high-intensity intermittent exercise performance in trained young men.

    Science.gov (United States)

    Krustrup, Peter; Ermidis, Georgios; Mohr, Magni

    2015-01-01

    intake of sodium bicarbonate in trained young men, with concomitant elevations in blood alkalosis and peak blood lactate levels, as well as lowered rating of perceived exertion.

  3. Urea cycle disorders in Thai infants: a report of 5 cases.

    Science.gov (United States)

    Wasant, Pornswan; Srisomsap, Chantragan; Liammongkolkul, Somporn; Svasti, Jisnuson

    2002-08-01

    Urea Cycle Disorders (UCD) is an inborn error of urea synthesis in which ammonium and other nitrogenous precursors of urea accumulate leading to episodic coma and a high mortality rate. Therapy with peritoneal dialysis, essential amino acids or their nitrogen-free analogues has increased survival. The authors report 5 cases of urea cycle disorders, all of whom developed and were rescued from hyperammonemic coma. However, the eventual outcome was quite variable. Argininosuccinate lyase deficiency (ALD) Case 1. A 2 month old male infant, a product of a consanguineous marriage (Suphanburi province); developed poor feeding on day 7, lethargy, convulsion, hepatomegaly and respiratory alkalosis leading to respiratory failure and coma. Hyperammonemia, elevation of glutamic acid and argininosuccinic acid and its anhydrides confirmed the diagnosis of ALD. He is now 9 years old and severely retarded. Case 2. A male infant with history of lethargy, poor feeding on day 3, treated as sepsis and required respiratory support for 6 days; subsequently readmitted at age 2 weeks with vomitting, lethargy, seizure activity and hyperammonemia, and was treated by a local pediatrician in Songkhla province. There was a history of parental consanguinity and he was referred to Siriraj Hospital on day 64 with severe essential amino acid deficiency and acrodermatitis enteropathica with markedly elevated plasma citrulline level. In spite of aggressive treatment; the patient developed sepsis and he expired on day 78. Ornithine transcarbamylase deficiency (OTC) Case 3. An eleven-month-old male infant, the product of a non-consanguineous marriage, developed neonatal onset of hyperammonemia on day 5 after poor feeding, lethargy, hypothermia, seizure, apnea and coma. He was rescued from neonatal hyperammonemic coma on day 9 after aggressive treatment, but expired at eleven months of age after overwhelming sepsis. Case 4. A male infant, sibling of case 3 was referred to Siriraj Hospital on day 8 with

  4. Developing a systems approach to prevent meconium aspiration syndrome: lessons learned from multinational studies.

    Science.gov (United States)

    Bhutani, V K

    2008-12-01

    Passage of fetal bowel movement (meconium) is common (in about one out of six births), and in some the staining of the amniotic fluid is a sign of fetal distress. Inhalation of meconium (aspiration syndrome, in upto one out of five to eight such births) just before or at birth may be preventable by a coordinated approach by well-trained and informed birth attendants. Respiratory failure secondary to meconium aspiration syndrome (MAS) remains a major cause of morbidity and mortality in the neonatal population. Infants with hypoxemic respiratory failure because of MAS, persistent pulmonary hypertension of the newborn and pneumonia/sepsis have an increased survival with extracorporeal membrane oxygenation (ECMO). Other treatment options earlier limited to inotropic support, continuous airway pressure (CPAP), conventional ventilatory management, respiratory alkalosis, paralysis and intravenous vasodilators have been replaced by synchronized intermittent mandatory ventilation (SIMV), high-frequency oscillatory ventilation (HFOV), surfactant and inhaled nitric oxide (iNO). HFOV has been advocated for use to improve lung inflation while potentially decreasing lung injury through volutrauma. Other reports describe the enhanced efficacy of HFOV when combined with iNO. Subsequent to studies reporting that surfactant deficiency or inactivation may contribute to neonatal respiratory failure, exogenous surfactant therapy has been implemented with apparent success. Recent studies have shown that iNO therapy in the neonate with hypoxemic respiratory failure can result in improved oxygenation and decreased need for ECMO. However, these innovative interventions are costly, require a sophisticated infrastructure and are not universally accessible. In this paper, a context of systems-approach for prenatal, natal and postnatal management of babies delivered through meconium stained amniotic fluid (MSAF) so that adverse outcomes are minimized and the least number of babies require

  5. Blood gas profile of copper-poisoned in sheep treated with ammonium tetrathiomolybdatePerfil de gases sanguíneos de ovinos intoxicados por cobre e tratados com tetratiomolibidato de amônio

    Directory of Open Access Journals (Sweden)

    Maria Claudia Araripe Sucupira

    2012-05-01

    Full Text Available The aim of this study was to evaluate the blood gas profile of experimentally copper-poisoned sheep (in the pre-hemolytic, hemolytic and post-hemolytic phases that have been treated or not treated with ammonium tetrathiomolybdate. Ten lambs of the Santa Ines breed were divided into two groups: control and ATTM (treated (ammonium tetrathiomolibydate. The animals were submitted to increasing doses of copper sulfate until macroscopic hemoglobinuria was detected.All of the control animals from died within four days of hemolytic crisis, and one sheep from ATTM died during the treatment. There was no difference in blood gas parameters between experimental groups. Higher values of pCO2 were observed during the hemolytic crisis (HC in both groups. The control group had higher mean values of hCO3 in the times HC and 2 days after hemolytic crisis (dA when compared with the time 15 before hemolytic crises (dB. The sheep that were treated with ATTM presented lower values of hCO3 at 7dB and higher levels at the HC. The control and ATTM groups exhibited higher values of BE during the HC. Poisoning resulted in disorder in the acid-base equilibrium, characterized by metabolic alkalosis and respiratory acidosis. Treatment with ATTM was able to reverse the changes in acid-base balance in copper poisoning sheep. O objetivo desse estudo foi avaliar o perfil de gases sanguineos em ovinos experimentalmente intoxicados com cobre (fases: pré-hemoltica, hemolitica e pós-hemolitica tratados ou não com tetratiomolibidato de amônio (ATTM. Dez cordeiros da raça Santa Inês foram divididos em dois grupos:controle (tratados com solução fisiologica a 0,9% e ATTM (tratados com 3,4 mg/kg de tetratiomolibidato de amonio. Os animais foram submetidos a doses crescentes de sulfato de cobre até a observação de hemoglobinúria macroscópica. Todos os animais do grupo controle morreram dentro de quatro dias após observação da hemoglobinúria, e um cordeiro do grupo ATTM

  6. Diet, evolution and aging--the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet.

    Science.gov (United States)

    Frassetto, L; Morris, R C; Sellmeyer, D E; Todd, K; Sebastian, A

    2001-10-01

    difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.

  7. Clinical and laboratory features of hepatocellular carcinoma

    Directory of Open Access Journals (Sweden)

    Andrés Cárdenas

    2007-02-01

    have electrolyte disturbances like hyponatremia, hypokalemia, and metabolic alkalosis, associated with defective water handling or with diuretic use. Serum aminotransferases, alkaline phosphatase and gammaglutamyl transpeptidase are often abnormal in a nonspecific pattern. Some serum markers are useful in diagnosis of HCC. The most commonly used is alpha-fetoprotein (AFP. AFP is a glycoprotein that is normally produced during gestation by the fetal liver and the yolk sac.

    In adults, normal values are less than 20 ng/ml and AFP is often elevated in patients with HCC. Serum concentrations of AFP do not correlate with clinical features of HCC, such as size, stage and prognosis but is generally accepted that serum levels greater than 500 ng/ml in a high risk patient is diagnosis of HCC.

    Other serum markers - Because of the limitations of serum AFP measurements, other serum markers of HCC used alone or in combination with the serum AFP have been evaluated for diagnosis or determining prognosis in patients with HCC. These include lens culinaris agglutinin-reactive AFP and des-gamma carboxyprothrombin, glypican-3, human hepatocyte growth factor, and insulin-like growth factor.

     

  8. Selected Abstracts of the 1st Congress of joint European Neonatal Societies (jENS 2015; Budapest (Hungary; September 16-20, 2015; Session “Brain & Development”

    Directory of Open Access Journals (Sweden)

    Various Authors

    2015-09-01

    PERINATAL ASPHYXIA REVEALS LASTING BEHAVIORAL DEFICITS • A. Kerenyi, E. Sipos, P. Bakos, K. Demeter, P. Pottyondi, J. Haller, M. Szabo, K. Kaila, E. Mikics, A. Denes, A. FeketeABS 28. EFFECT OF EARLY NUTRITION ON PRETERM CEREBRAL MATURATION AND BRAIN INJURY REFLECTED BY MR-IMAGING AT TERM • L. Beauport, J. Schneider, P. Hagmann, M. Faouzi, C.J. Fischer Fumeaux, A.C. TruttmannABS 29. NEURITE OUTGROWTH IN RESPONSE TO CEREBROSPINAL FLUID DERIVED FROM NEC-SENSITIVE PRETERM PIGS • J. Sun, S. Pankratova, D.E.W. Chatterton, P.T. SangildABS 30. URINARY NEUTROPHIL GELATINASE-ASSOCIATED LIPOCALIN (NGAL AFTER GLOBAL HYPOXIA-ISCHEMIA IN NEWBORN PIGLETS • H.T. Garberg, M.U. Huun, G. Dyrhaug, R. Solberg, O.D. SaugstadABS 31. CEREBRAL DEEP GREY MATTER ALKALOSIS IN BABIES WITH NEONATAL ENCEPHALOPATHY IS ASSOCIATED WITH AN INCREASED SEIZURE BURDEN • C. Uria-Avellanal, D. Price, M. Sokolska, S. Mitra, A. Bainbridge, X. Golay, N. RobertsonABS 32. THE PROGNOSTIC VALUE OF NIRS DURING THERAPEUTIC HYPOTHERMIA IN TERM ASPHYXIATED NEWBORNS • P. Costa, A. Graça, I. Sampaio, C. MonizABS 33. EEG DISCONTINUITY PREDICTS CEREBRAL TISSUE INJURY AND ADVERSE NEURODEVELOPMENT IN COOLED NEWBORNS • J. Dunne, D. Wertheim, P. Clarke, O. Kapellou, P. Chisholm, J. Boardman, D. ShahABS 34. A RANDOMIZED CONTROLLED TRIAL OF COOLING COMBINED WITH INHALED XENON FOR PERINATAL ASPHYXIAL ENCEPHALOPATHY WITH CEREBRAL MAGNETIC RESONANCE ENDPOINTS – THE TOBY-Xe TRIAL • D. Azzopardi, N. Robertson, A. Bainbridge, E. Cady, A. Deierl, G. Fagiolo, N. Franks, J. Griffiths, J. Hajnal, E. Juszczak, B. Kapetanakis, L. Linsell, M. Maze, O. Omar, B. Strohm, N. Tusor, A.D. EdwardsABS 35. MULTIORGAN DYSFUNCTION IN NEWBORNS WITH HYPOXIC-ISCHEMIC ENCEPHALOPATHY IN THE HYPOTERMIA ERA • M. Alsina, A. Martin-Ancel, P. Alamillo, M. Leon, A Garcia-AlixABS 36. HYPOXIC-ISCHAEMIC BRAIN INJURY: DELIVERY BEFORE INTRAPARTUM EVENTS • D. Odd, A. Heep, K. Luyt, T. DraycottABS 37. IS NEONATAL ESTABLISHED HEARING LOSS PERMANENT IN