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PubMed1987

Severe lactic acidosis as a presenting feature of pheochromocytoma.

High plasma concentrations of epinephrine and norepinephrine have the potential for generating substantial hyperlactatemia by virtue of their metabolic and vasoconstrictor effects; both these influences affect lactate metabolism in the direction of overproduction and underutilization. Nonetheless, lactic acidosis is not a recognized presenting feature of pheochromocytoma. In this report, we describe a patient with pheochromocytoma in whom the endogenous outpouring of epinephrine and norepinephrine resulted in severe lactic acidosis that featured prominently in the clinical presentation. Pheochromocytoma should be listed among the clinical entities associated with or predisposing to lactic acidosis.

Acidosis, Lactic↗
PubMed1989

Regulation of rat kidney mitochondrial metabolism in acute acidosis.

Proximal tubular ammoniagenesis is amplified under conditions of acute and chronic metabolic acidosis. Current hypotheses postulate that alterations in intracellular pH (pHi) or in the pH gradient across the inner mitochondrial membrane (delta pHm) influence mitochondrial glutamine metabolism. Enhanced glutamine transport across the inner mitochondrial membrane might constitute a key regulatory factor in acidosis. To examine changes in delta pHm, a technique was used to determine pHi and intramitochondrial pH (pHm) simultaneously. Regulation of the enzyme alpha ketoglutarate dehydrogenase (alpha KGDH) was assessed by evaluating enzyme activity at varied levels of medium pH, Ca++, and adenosine diphosphate (ADP). The results indicate that pHi decreased with an acid external pH. A fall in pHi correlated to increase activity of alpha KGDH associated with increased affinity for the substrate, alpha KG. Increments in either buffer Ca++ or ADP concentration increased enzyme affinity for alpha KG at pH 7.6 but not at pH 6.8. These results, compatible with previous reports, indicate that pH, Ca++, and ADP are effectors of the enzyme alpha KGDH. Alterations in pH across the inner mitochondrial membrane might augment flux through alpha KG by accelerating glutamine metabolism. Increased alpha KG oxidation over the range of 10 to 500 mumol/L Ca++ concentration is compatable with data for Ca++ regulation reported for the solubilized enzyme. These studies provide evidence that the above factors, through enhancing alpha KGDH activity, participate in regulation of ammoniagenesis during states of acidosis.

Acidosis↗
PubMed1996

Primary distal renal tubular acidosis as a result of a gradient defect.

It has been generally accepted that primary distal renal tubular acidosis (DRTA) is the result of a defect in proton secretion in the distal nephron (secretory defect). We report an infant with DRTA, evidenced by spontaneous hyperchloremic metabolic acidosis with low urinary ammonium excretion rate and inability to decrease urine pH during acidosis, who nevertheless exhibited an intact ability to increase urinary carbon dioxide partial pressure (pCO2) during maximal urine alkalinization and normal ability to acidify the urine after furosemide, suggestive of a gradient-type defect DRTA. This patient had never been exposed to amphotericin B. To our knowledge, this is the first fully documented report of primary DRTA that can be attributed to gradient defect.

Acetazolamide↗
PubMed1996

Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy.

Foscarnet is used as therapy of cytomegalovirus (CMV) infection in immunosuppressed subjects. We present a patient with human immunodeficiency virus infection under treatment with foscarnet for CMV retinitis who complained of thirst and polyuria. Laboratory data showed hypernatremia with increased plasma osmolality and metabolic hyperchloremic acidosis. A water deprivation test demonstrated a nephrogenic diabetes insipidus. Other laboratory studies, including urine pH, anion gap, titratable acidity, and bicarbonate, showed a distal tubular acidification defect. All abnormalities were transient, with recovery a few days after foscarnet withdrawal. No cases of renal acidosis, and only one case of nephrogenic diabetes insipidus, has been previously reported as a complication of foscarnet treatment. Our patient developed both nephrogenic diabetes insipidus and renal tubular acidosis with a temporal pattern that demonstrated a link between foscarnet therapy and these abnormalities.

AIDS-Related Opportunistic Infections↗
PubMed1997

The clinical spectrum of chronic metabolic acidosis: homeostatic mechanisms produce significant morbidity.

Chronic metabolic acidosis is a process whereby an excess nonvolatile acid load is chronically placed on the body due to excess acid generation or diminished acid removal by normal homeostatic mechanisms. Two common, often-overlooked clinical conditions associated with chronic metabolic acidosis are aging and excessive meat ingestion. Because the body's homeostatic response to these pathologic processes is very efficient, the serum HCO3- and blood pH are frequently maintained within the "normal" range. Nevertheless, these homeostatic responses engender pathologic consequences, such as nephrolithiasis, bone demineralization, muscle protein breakdown, and renal growth. Based on this, the concept of eubicarbonatemic metabolic acidosis is introduced. Even in patients with a normal serum HCO3- and blood pH, it is important to treat the acid load and prevent pathologic homeostatic responses. These homeostatic responses, as well as the mechanisms responsible for their initiation, are reviewed.

Acid-Base Equilibrium↗
PubMed1997

Marked dilutional acidosis complicating management of right ventricular myocardial infarction.

Dilutional acidosis is a poorly recognized cause of metabolic acidosis. Indeed, the prevailing view has been that even massive expansion of the extracellular fluid volume with non-bicarbonate-containing solutions would not lead to clinically significant hypobicarbonatemia. We describe the development of marked dilutional acidosis as a complication of management of right ventricular myocardial infarction. The pathogenesis, clinical significance, prevention, and treatment of the entity are discussed.

Acidosis↗
PubMed1999

Association of acidosis and nutritional parameters in hemodialysis patients.

There is extensive literature supporting an important role for acidosis in inducing net protein breakdown, both in experimental animals and humans. However, the clinical importance of the moderate intermittent metabolic acidosis frequently observed in hemodialysis patients has not been determined. We performed a cross-sectional analysis of the baseline laboratory data in the first 1,000 patients recruited to the Hemodialysis Study, looking for correlations between predialysis serum total carbon dioxide levels and parameters related to dietary intake and nutritional status. We found the mean predialysis serum total carbon dioxide level was moderately low (21.6 +/- 3.4 mmol/L; mean +/- SD) despite the use of bicarbonate dialysate and an average single-pool Kt/V of 1.54. Predialysis serum total carbon dioxide level correlated negatively with normalized protein catabolic rate (P < 0.001), suggesting patients with lower serum total carbon dioxide levels have a greater protein intake. The degree of acidosis observed in our patients does not seem to have a deleterious effect on the nutritional status of these patients because correlation of serum total carbon dioxide level with nutritional parameters, such as serum creatinine and serum albumin levels, was either negative or not statistically significant. Further investigation of the effect of modifying serum bicarbonate concentration on nutritional markers is needed to test these hypotheses.

Acidosis↗
PubMed1999

Distal renal tubular acidosis and high urine carbon dioxide tension in a patient with southeast Asian ovalocytosis.

Southeast Asian ovalocytosis (SAO) is the best-documented disease in which mutation in the anion exchanger-1 (AE1) causes decreased anion (chloride [Cl-]/bicarbonate [HCO3-]) transport. Because AE1 is also found in the basolateral membrane of type A intercalated cells of the kidney, distal renal tubular acidosis (dRTA) might develop if the function of AE1 is critical for the net excretion of acid. Studies were performed in a 33-year-old woman with SAO who presented with proximal muscle weakness, hypokalemia (potassium, 2.7 mmol/L), a normal anion gap type of metabolic acidosis (venous plasma pH, 7. 32; bicarbonate, 17 mmol/L; anion gap, 11 mEq/L), and a low rate of ammonium (NH4+) excretion in the face of metabolic acidosis (26 micromol/min). However, the capacity to produce NH4+ did not appear to be low because during a furosemide-induced diuresis, NH4+ excretion increased almost threefold to a near-normal value (75 micromol/L/min). Nevertheless, her minimum urine pH (6.3) did not decrease appreciably with this diuresis. The basis of the renal acidification defect was most likely a low distal H+ secretion rate, the result of an alkalinized type A intercalated cell in the distal nephron. Unexpectedly, when her urine pH increased to 7.7 after sodium bicarbonate administration, her urine minus blood carbon dioxide tension difference (U-B Pco2) was 27 mm Hg. We speculate that the increase in U-B Pco2 might arise from a misdirection of AE1 to the apical membrane of type A intercalated cells.

Acidosis, Renal Tubular↗
PubMed2000

Hepatic steatosis and lactic acidosis caused by stavudine in an HIV-infected patient.

Lactic acidosis and hepatic steatosis caused by mitochondrial toxicity of nucleoside reverse transcriptase inhibitors (NRTI) is a rare cause of liver disease with a high mortality rate. This report describes a male, HIV-positive patient with a 4-week history of nausea, vomiting and abdominal pain. His medication consisted of prednisone 5 mg od (because of auto-immune thrombocytopenia), didanosine (for 2 years) and stavudine (for 3 months). Laboratory studies showed cholestasis and elevation of aminotransferases. Lactic level was not measured. Liver biopsy revealed steatosis and cholestatic hepatitis. In the absence of other causes of liver disease a probable diagnosis of stavudine-induced hepatic toxicity was made. After discontinuation of NRTI, he recovered completely. Because lactic acidosis had not been confirmed, stavudine was restarted and within 1 week the lactate level increased significantly. Therefore stavudine was discontinued again. One year later the patient is doing well on a double protease inhibitor regimen. In conclusion, clinicians treating patients with NRTI should be aware of the risk of lactic acidosis and hepatic steatosis. When this is suspected, all NRTI must be stopped. The diagnosis can be made when elevated lactate levels and hepatic steatosis are present in the absence of other causes of liver disease.

Abdominal Pain↗
PubMed1983

Lactic acidosis: current concepts.

Lactic acidosis is now a widely recognized disorder in clinical medicine. Experimental studies during the past decade demonstrate an important role of lactate disposal mechanisms in the pathogenesis of lactic acidosis. Such factors as decreased cardiovascular reserve, inadequate liver perfusion and alterations in liver intracellular pH appear to limit the normally large capacity of the liver to dispose of lactic acid. The continued high mortality of this disorder has led to a re-examination of the conventional, empirical treatment of lactic acidosis with sodium bicarbonate. Available data suggest that alkali may cause or exacerbate the conditions of excessive lactate production, decreased cardiac reserve and inadequate hepatic lactate disposal which exist in this disorder. In contrast, dichloroacetate therapy shows strikingly beneficial results, at least in early experimental studies.

Acidosis↗
PubMed2002

Buffer administration during CPR promotes cerebral reperfusion after return of spontaneous circulation and mitigates post-resuscitation cerebral acidosis.

To explore the effects of alkaline buffers on cerebral perfusion and cerebral acidosis during and after cardiopulmonary resuscitation (CPR), 45 anaesthetized piglets were studied. The animals were subjected to 5 min non-interventional circulatory arrest followed by 7 min closed chest CPR and received either 1 mmol/kg of sodium bicarbonate, 1 mmol/kg of tris buffer mixture, or the same volume of saline (n=15 in all groups), adrenaline (epinephrine) boluses and finally external defibrillatory shocks. Systemic haemodynamic variables, cerebral cortical blood flow, arterial, mixed venous, and internal jugular bulb blood acid-base status and blood gases as well as cerebral tissue pH and PCO(2) were monitored. Cerebral tissue acidosis was recorded much earlier than arterial acidaemia. After restoration of spontaneous circulation, during and after temporary arterial hypotension, pH in internal jugular bulb blood and in cerebral tissue as well as cerebral cortical blood flow was lower after saline than in animals receiving alkaline buffer. Buffer administration during CPR promoted cerebral cortical reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during lower blood pressure and flow in the reperfusion phase. The arterial alkalosis often noticed during CPR after the administration of alkaline buffers was caused by low systemic blood flow, which also results in poor outcome.

Acidosis↗
PubMed1998

Alkaline buffers for correction of metabolic acidosis during cardiopulmonary resuscitation with focus on Tribonat--a review.

A combined hypercarbic and metabolic acidosis develops during the low flow state of cardiac arrest treated with cardiopulmonary resuscitation. Several negative consequences of the acidosis have been demonstrated, two of the most important being reduced contractility of the ischaemic but still beating myocardium and impaired resuscitability of the arrested heart. Even though interventions to re-establish a spontaneous circulation should be the number one priority during cardiopulmonary resuscitation, attempts to treat the acidosis are often carried out in order to avoid the reported negative inotropic effect. Different alkaline buffers have been used, but it has been demonstrated over the years that such treatment may aggravate the situation due to a variety of deleterious side-effects of the buffers. A mixture of THAM, acetate, sodium bicarbonate and phosphate registered as Tribonat has been suggested as a suitable alternative to conventional buffer substances. The problems preceding the designation of Tribonat as well as studies evaluating its effects are reviewed in this article. Tribonat seems to offer a more well-balanced buffering without any major disadvantages compared with previously used alkaline buffers, even though improved survival has not been reported.

Acidosis↗
PubMedDate not supplied

Survival from profound alcohol-related lactic acidosis.

We present the case of a patient with profound alcohol-related lactic acidosis (lactate = 16.1 mmol/L; pH = 6.67) associated with a multitude of metabolic derangements who made a remarkable recovery following aggressive management. The patient was in extremis upon arrival in the emergency department (ED), and resuscitation was begun immediately. While in the ED, the problem list generated included: acute alcohol intoxication, severe lactic acidosis, dehydration, hypothermia, hypoglycemia, acute renal insufficiency, and hepatic failure. Resuscitation continued in the intensive care unit with remarkable improvement and satisfactory outcome. In this patient, the severe lactic acidosis and associated abnormalities were all attributed to acute and chronic effects of ethanol. A brief summary of the proposed mechanism by which these metabolic derangements developed and an outline of her management follows.

Acidosis, Lactic↗
PubMed1990

Metabolic acidosis in diarrheic calves: the importance of alkalinizing agents in therapy.

Metabolic acidosis is one of the prime factors responsible for the death of many diarrheic calves. This article begins with a general discussion about the recognition of metabolic acidosis. The remaining sections detail the utilization of certain subjective and objective methods to assess the severity of acidosis as well as the approach to treatment of this metabolic condition.

Acetates↗
PubMed2003

[Metformin-associated lactic acidosis remains a serious complication of metformin therapy].

We report 4 cases of lactic acidosis in diabetic patients usually treated with metformin. For the first 3 patients, the clinical history was similar because lactic acidosis was precipitated by gastro-intestinal disorders whereas all of them were simultaneously treated with several nephrotoxic drugs. These 3 patients presented with acute renal failure on arrival at hospital. Their issue was fatal whereas any obvious cause of overproduction of lactate was found. The fourth case, which was due to a voluntary intoxication, was the only one presenting with a favourable evolution. The metformin plasma and red blood cell levels were performed for 2 of 4 patients and confirmed the overdose. These observations remind that metformin-associated lactic acidosis remains a serious complication, and that medical doctors must respect strictly contra-indications and guidelines for withdrawing metformin.

Acidosis, Lactic↗
PubMed1989

[Hypokalemic quadriplegia and coma in renal tubular acidosis].

A case is reported of an acute episode of severe hypokalaemia (K+ = 1.1 mmol.l-1) associated with hyperchloraemic acidosis and simultaneous high urine pH (pH = 7) in a 24 year old woman with type I distal tubular acidosis and nephrocalcinosis. The flaccid paralysis involved the trunk, neck, facial and pharyngeal muscles. She was in areflexic quadriplegia, coma and respiratory failure requiring endotracheal intubation and positive pressure ventilation. There were no cardiac disturbances, presumably because of the chronic potassium depletion, the patient's youth and healthy myocardium. Despite the usually recommended maximal potassium infusion rate (0.25 mmol.kg-1.h-1), there was a transient worsening of her neuromuscular status. Only 12 h later, the first movements were noticed. In order to prevent such a deterioration, a more rapid potassium infusion could have been used. However, in our case, the occurrence of hypokalaemic extrasystoles was reduced and the patient was still intubated and ventilated. It was therefore decided not to run the risk of myocardial inexcitability carried out with supramaximal infusion rates and to keep the usual protocol. Besides, several pitfalls have to be avoided during the treatment of the numerous metabolic disorders coexisting with severe hypokalaemia, such as metabolic acidosis and hyperglycaemia.

Acidosis, Renal Tubular↗
PubMed1999

[Severe lactic acidosis disease disclosing milk-protein intolerance to cows' milk].

UNLABELLED: The age of discovery and initial symptoms of cow milk allergy can vary. Lactic acidosis is exceptionally associated to this allergy. CASE REPORT: A 32-day-old girl was admitted for a severe malaise with metabolic acidosis and hyperlactacidemia. There were no neonatal or family problems; breastfeeding was stopped on the 25th day. Fever was noted on the 29th day and her mother reported behavior anomalies followed by a severe malaise with unconsciousness between the 29th and 32nd day. At admission, the infant showed a severe neurological distress, hypotonia and lethargy. Infection and neurological imaging were normal. A compensated metabolic acidosis with hyperlactacidemia (5.96 mmol/L) was noted. There was no argument for esophageal reflux nor vagal hypertony; mitochondrial cytopathy was also excluded. After a 24 hours fast, the clinical state gradually improved and normalized at h48. The infant was discharged with a milk protein hydrolysate formula. Her mother attempted to reintroduce cow milk on the 59th and 64th day, but this was immediately followed by allergic manifestations which supported the diagnosis of cow milk allergy. CONCLUSION: Neurological distress and hyperlactacidemia exceptionally reveal this type of intolerance. The mechanism of hyperlactacidemia remains unclear; it is possibly the consequence of severe changes of the intestinal mucosa, an exclusive glycolytic tissue.

Acidosis, Lactic↗
PubMedDate not supplied

Lactic acidosis associated with nucleoside reverse transcriptase inhibitors.

Limitations on antiretroviral therapies as a result of resistance and adverse events have been described in the literature. Lactic acidosis has been reported in patients on nucleoside reverse transcriptase inhibitors on rare occasions. Successful assessment and treatment of lactic acidosis is dependent on the nurse's role in the recognition of this condition. This article provides an overview of the clinical presentation, diagnosis, treatment strategies and nursing management of lactic acidosis in patients with HIV/AIDS.

Acidosis, Lactic↗