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PubMed2005

Topiramate and metabolic acidosis: a case series and review of the literature.

Topiramate is a new anticonvulsant drug recommended for treatment of partial and generalized seizures in children and adults. It has been found to cause a nonanion gap metabolic acidosis in some patients, which is related to carbonic anhydrase inhibition. This adverse reaction is more common in children than adults and is rarely symptomatic. Clinicians need to be aware of this potential side effect especially in children undergoing major surgery. Children who are treated with topiramate should have a careful history taken preoperatively looking for signs of a metabolic acidosis and baseline blood chemistries should be measured prior to surgery to detect an asymptomatic metabolic acidosis.

Acidosis↗
PubMed2005

Fulminant lactic acidosis in two patients with Type 2 diabetes treated with metformin.

Lactic acidosis is a known adverse risk of metformin treatment. We report two cases in whom fulminant lactic acidosis developed during treatment. There were no contraindications to metformin treatment and both were admitted with abdominal discomfort for some days, causing dehydration. Both patients had renal failure on admission, developed multiple organ failure and both suffered a massive stroke. One patient died and the other survived but is severely disabled. We suggest, in both cases, that acute renal failure developed as a result of dehydration, causing metformin accumulation and lactic acidosis. We recommend that all patients on metformin should consider discontinuation of metformin treatment in the event of a severe medical condition causing dehydration.

Acidosis, Lactic↗
PubMed1995

The prediction of fetal acidosis at birth by computerised analysis of intrapartum cardiotocography.

OBJECTIVE: To assess the capability of a computer software interpretation program, using intrapartum fetal heart rate and intrauterine pressure as recorded in a cardiotocogram to predict fetal acidosis at birth. DESIGN AND SUBJECTS: A retrospective analysis of digitised fetal heart rate and uterine activity values obtained from 73 high risk women in labour. SETTING: Two university teaching hospitals. METHODS: A computer software program was constructed to analyse the digitised data and predict acidosis. The results of the analysis were compared with actual umbilical arterial blood pH and base excess at delivery. RESULTS: The software cardiotocogram interpreter was able to predict a pH of less than 7.15 with an accuracy of 77%, a sensitivity of 88% and specificity of 75% in this set of data. It was able to predict a base excess of less than -8 mmol/l with an accuracy of 81%, a sensitivity of 76% and specificity of 82%. CONCLUSIONS: A computerised method of analysing fetal heart rate and uterine activity using a simple algorithm has demonstrated a capability to predict fetal acidosis at the time of delivery. Further research in this area is warranted.

Acidosis↗
PubMed1993

Evolving concepts about the role of acidosis in ischemic neuropathology.

Cerebral ischemia is one of the most common neurological insults. Many pathological events are undoubtedly triggered by ischemia, but only recently has it become accepted that ischemic cell injury arises from a complex interaction between multiple biochemical cascades. Tissue acidosis is a well established feature of ischemic brain tissue, but its role in ischemic neuropathology is still not fully understood. Within the last few years, new evidence has challenged the historically negative view of acidosis and suggests that it may play more of a beneficial role than previously thought. This review reintroduces the concept of acidosis to ischemic brain injury and presents some new perspectives on its neuroprotective potential.

Acidosis↗
PubMed1982

Pathophysiology of metabolic acidosis: effect of low pH on the hepatic uptake of lactate, pyruvate and alanine.

The uptake of lactate, pyruvate and alanine in perfused rat liver was investigated under normal perfusion conditions (pH 7.4, PCO2 40 mmHg) and under conditions mimicking partially compensated metabolic acidosis (pH 6.9, PCO2 20 mmHg). At 1 mM lactate as well as 10 mM lactate in the medium a lowering of pH from 7.4 to 6.9 did not affect the lactate plus pyruvate uptake. A significant effect of the low pH was seen on pyruvate uptake which at 1 mM lactate was increased from 0.027 +/- 0.008(4) mumol/min per g liver at normal pH to 0.084 +/- 0.013(4) at low pH. At 10 mM lactate the liver produced pyruvate, but the production was significantly reduced by a lowering of the pH, being 0.45 +/- 0.13(8) mumol/min per g liver at pH 7.4 and 0.22 +/- 0.06(4) at pH 6.9. THe counterbalancing changes in lactate metabolism were too small to attain statistical significance. The stimulation of gluconeogenesis by an increase in FFA from 0 to 1 mM in the medium was unaffected by pH. Alanine uptake was decreased from 0.48 +/- 0.05(6) to 0.39 +/- 0.07(3) by lowering the pH from 7.4 to 6.9. We conclude that metabolic acidosis does not in itself inhibit the capacity of the perfused rat liver to remove lactate and pyruvate from the blood. If the same is true in man, no beneficial effect of bicarbonate treatment on lactate clearance in patients with lactic acidosis should be expected.

Acidosis↗
PubMed2000

Haematopoietic indicators of fetal metabolic acidosis.

We aimed to study the haematopoietic response in normal and acidotic deliveries following vaginal and abdominal delivery and to compare this to the surrogate markers of perinatal acidosis. Blood gas analyses, complete blood pictures and erythropoietin assays were performed on umbilical or early neonatal blood samples. Placental sections were examined for the presence of nucleated red blood cells. Perinatal clinical risk factors and major neonatal outcomes were collected. The control population was 78 deliveries where the cord arterial pH was > 7.10. Controls born after labour were compared to those born prior to the onset of labour and to 14 acidotic infants born after labour. Nucleated red blood cells did not increase with labour in the control groups but were significantly higher (p < 0.05) in the acidotic group. Erythropoietin did not significantly change with either labour or acidosis. The predictive values from nucleated red blood cell counts were higher than those from low Apgar scores, atypical cardiotocograph traces, meconium-stained amniotic fluid, erythropoietin and the presence of nucleated red blood cells in placental sections. Nucleated red blood cell counts may be a useful surrogate marker of acidosis where blood gas analysis is unavailable. Further studies are required to examine the timing of the increase of erythropoiesis to help define the onset of the stimulus.

Acidosis↗
PubMed2005

Metabolic acidosis: an unrecognized cause of morbidity in the patient with chronic kidney disease.

In patients with chronic kidney disease, metabolic acidosis can occur as a result of insufficient ammoniagenesis within the damaged kidney. This, in turn, can bring about a variety of sequella that have their basis in hormonal and cellular abnormalities that effect stunted growth, loss of muscle and bone mass, and negative nitrogen balance. Cellular mechanisms accounting for these findings are reviewed. In bone, metabolic acidosis causes direct dissolution of bone; ostoeclastic activity is increased while osteoblastic activity is suppressed. In muscle, branched-chain amino acid oxidation is increased and the ubiquitin-proteasome pathway is activated: muscle wasting results. Even a modest degree of metabolic acidosis can be harmful and can initiate a series of maladaptive responses that are not easily reversed, although there is evidence that alkali therapy can be beneficial in reversing these responses.

Acidosis↗
PubMed1994

Accidental metabolic acidosis during hemodialysis.

Three incidents of metabolic acidosis during hemodialysis in 3 different patients are presented. Two patients became severely ill but recovered completely after treatment. In the third patient, the event was recognized before the acidosis became symptomatic. In all cases the acidosis was caused by an unbalanced supply of acidic dialysis concentrate. Two events were caused by mistaking acidic dialysis concentrate for acetate. In the third patient, the supply line from the bicarbonate concentrate jug was broken. The conductivity cell alarm was not activated during any of the incidents and in only 1 case during reconstruction of the accidents. The efficacy and safety of the conductivity cell alarm system regarding prevention of acid/base disturbances during hemodialysis are discussed.

Acidosis↗
PubMed1999

Metabolic acidosis in restraint-associated cardiac arrest: a case series.

The mechanism of death in patients struggling against restraints remains a topic of debate. This article presents a series of five patients with restraint-associated cardiac arrest and profound metabolic acidosis. The lowest recorded pH was 6.25; this patient and three others died despite aggressive resuscitation. The survivor's pH was 6.46; this patient subsequently made a good recovery. Struggling against restraints may produce a lactic acidosis. Stimulant drugs such as cocaine may promote further metabolic acidosis and impair normal behavioral regulatory responses. Restrictive positioning of combative patients may impede appropriate respiratory compensation for this acidemia. Public safety personnel and emergency providers must be aware of the life threat to combative patients and be careful with restraint techniques. Further investigation of sedative agents and buffering therapy for this select patient group is suggested.

Acidosis↗
PubMed1975

Proximal renal tubular acidosis in the tetralogy of fallot.

A 9-year-old girl presented with tetralogy of Fallot and moderate metabolic acidosis. Despite a Blalock's fistula there was evidence of chronic hypoxia with cyanosis, clubbing of fingers and toes and very elevated blood hematocrit values. Renal acidification and bicarbonate titration demonstrated the existence of proximal renal tubular acidosis: renal bicarbonate threshold was low (18 mmoles/1) and normal urinary acidificaiton was present at subthreshold serum bicarbonate levels. Following corrective heart surgery, blood acid-base values and renal reabsorption of bicarbonate became normal. A causal relationship between extracellular fluid volume expansion dependent on the high hematocrit and proximal renal tubular acidosis is suggested.

Acidosis, Renal Tubular↗
PubMed1979

Increase in bilirubin binding to albumin with correction of neonatal acidosis.

Twenty-six serial measurements of free bilirubin concentration and apparent association constant of bilirubin for albumin (Ka) at a bilirubin: albumin molar ratio of 0.8 were performed and compared with baseline values in 11 newborn infants with acidosis before treatment and during recovery from acidosis. When arterial pH was corrected from 7.12 +/- 0.02 (Mean +/- S.EM.) to 7.34 +/- 0.02, there was a significant decrease in serum free bilirubin concentration and a significant increase in the Ka at molar ratio 0.8. The data offer in vivo evidence that correction of acidosis in the neonate results in an improvement of the apparent bilirubin binding affinity of albumin.

Acid-Base Equilibrium↗
PubMed1986

Hyperkalemic distal renal tubular acidosis in salt-losing congenital adrenal hyperplasia.

Functional indices of distal urinary acidification were assessed in two male infants, aged 1 and 3 months, with salt-losing congenital adrenal hyperplasia. In both cases the diagnosis was sustained by the presence of elevated plasma levels of 17-hydroxyprogesterone, hyponatremia, hyperkalemia, metabolic acidosis and increased plasma renin activity. Both patients were unable to lower urinary pH below 5.9 either during acute ammonium chloride-induced acidosis or after i.v. administration of furosemide. One patient also failed to decrease urine pH below 5.5 and to increase urinary potassium excretion during sodium sulfate infusion. Oral sodium bicarbonate loading was given to both patients but failed to induce a significant increase in the urine minus blood PCO2 gradient. This gradient remained low also after neutral phosphate administration. Repeated studies after acute administration of fludrocortisone in one case or after prolonged administration of hydrocortisone in the other resulted in complete normalization of all functional studies. We conclude that salt-losing congenital adrenal hyperplasia can lead to hyperkalemic distal renal tubular acidosis in early infancy. The defective renal secretion of hydrogen ion and potassium is probably related to the abolishment of the negative potential difference in the cortical collecting tubule induced by the impaired reabsorption of sodium.

Acidosis, Renal Tubular↗
PubMed1993

D-lactic acidosis: a treatable encephalopathy in pediatric patients.

A 20-month old infant, who had short bowel syndrome following extensive surgery for a mid gut volvulus, developed hyperchloremic acidosis, with a large anion gap after enteral feeding was instituted. The organic acidosis was at least partly due to an increased concentration of D-lactic acid. This patient, as did five other pediatric patients, presented with a typical encephalopathy syndrome. Early recognition of this syndrome and treatment with an intestinal antibiotic and discontinuation of enteral feeding enabled prompt correction of the hyperchloremic acidosis and a rapid clinical recovery.

Acidosis, Lactic↗
PubMed1975

Brain carbonic acid acidosis after acetazolamide.

In cats in barbiturate anesthesia extracellular pH and potassium were continously recorded from brian cortex by implanted microelectrodes. Implantation of the electrodes preserved the low permeability of the blood-brain-barrier to HCO3-minus and H+ions as indicated by the development of brain acidosis by I.V. injection of HCO3-minus. Acetazolamide (25 mg/kg) i.v. was followed by a marked brain acidosis which after 10 min had progressed to a drop in pH of 0.203 plus or minus 0.046 (x bar plus or minus S.D., n equals 8). The slowness ofthe development of acidosis points to a direct effect of the carbonic anhydrase inhibition on the brain tissue. As a further support for this conclusion was considered the finding of a prolonged response time of brain pH to HCO3-minus i.v. to CO2-minus inhalation, and to hyperventilation after the acetazolamide inhibtion. No changes in brain extracelllular potassium were found.

Acetazolamide↗
PubMed1976

Effects of respiratory alkalosis and acidosis on myocardial excitation.

In anesthetized dogs electrocardiogram and monophasic action potentials (MAPs) were recorded from the right atrium and the right ventricle by intracardiac suction electrode technique. The animals were subjected, by means of ventilation with CO2 and hyperventilation, to periods of respiratory acidosis and respiratory alkalosis, respectively. Pronounced respiratory acidosis induced an increased sympathetic activity followed by a decrease in heart rate and prolongation of the A-V conduction time whereas the shape and duration of the atrial and ventricular MAPs remained unaltered. Arterial hypoxia in combination with pronounced respiratory acidosis did not influence the MAP durations. Respiratory alkalosis resulted in an increased sympathetic influence on the heart activity whereas the shape and duration of the atrial and the ventricular MAPs remained unaffected. During pronounced hyperventilation with increasing central venous pressure an increased parasympathetic influence on the heart activity with decrease in the heart rate, prolongation of the A-V conduction time and shortening of the atrial MAP duration was recorded.

Acidosis, Respiratory↗
PubMed1977

Direct antilipolytic effect of acidosis in isolated rat adipocytes.

The possibility that acidosis inhibits lipolysis indirectly by causing ionic shifts or by favouring the accumulation of an inhibitor has been tested in isolated fat cells. Lipolysis induced by 3 muM noradrenaline (NA) was inhibited by 40-60% and that induced by 1 mM theophylline (THEO) by about 75% when the pH was reduced to 6.6. Lipolysis induced by NA + THEO was inhibited by 20-30%. Changing the concentration of Ca++ or Mg++ did not alter the degree of inhibition. Reducing the K+-ion concentration enhanced the inhibitory effect of low pH on lipolysis induced by NA or NA + THEO, whereas cyclic AMP accumulation was uninfluenced. Omitting glucose from the incubation medium caused a slight enhancement of pH-induced inhibition of lipolysis (from 60 to 70%, p less than 0.01). Reducing the concentration of albumin, which binds inhibitory substances such as FFA, reduced lipolysis more at normal than at reduced pH. At high FFA/albumin ratios (5 or above) lipolysis was similar at normal and reduced pH. The antilipolytic effect of decreased pH was equally pronounced in perifused fat cells, where inhibitory substances are not allowed to accumulate. Our results suggest that the antilipolytic effect of acidosis is mainly a direct effect of the increase in H+ ion concentration. The inhibitory effect of acidosis on various responses to beta-adrenoceptor stimulation may be caused by a decreased formation of cyclic AMP in turn caused directly by the decrease in pH.

Acidosis↗
PubMedDate not supplied

Accidental acute metabolic acidosis due to inappropriate selection of bicarbonate concentrate.

Haemodialysis using a bicarbonate concentrate (bicarbonate dialysis) is the treatment modality of choice for correction of metabolic acidosis in chronic renal failure. However, improper ratios of acid and bicarbonate concentrates in dialysis fluid can result in an iatrogenically induced metabolic acidosis. The following report presents a case of acute metabolic acidosis, which resulted from the accidental use of an inappropriate bicarbonate concentrate for haemodialysis treatment. Awareness of the problem and a rapid examination of the dialysis fluid in patients who unexpectedly deteriorate rather than improve with haemodialysis may help in averting potentially severe complications due to errors in the concentrate selection. Conductivity cell devises are not suitable for the control of the acid-base composition of the dialysis fluid (dialysate), therefore, monitoring of the dialysate pH in addition to conductivity should become part of the equipment in haemodialysis machines.

Acidosis↗
PubMed1999

[Fatal lactic acidosis in a patient with acquired immunodeficiency syndrome treated with stavudine, lamivudine and indinavir].

Recently, several class-related adverse events have been recognized with antiretroviral drugs. For nucleoside analogue reverse transcriptase inhibitors. (NRTI), lactic acidosis with hepatomegaly and hepatic steatosis have been reported. These appear to occur at a low frequency, but with a high fatality rate. We report a case of fatal lactic acidosis in a patient with acquired immunodeficiency syndrome (AIDS) treated with stavudine (d4T), lamivudine (3TC) and indinavir (IDV). A 48-year-old male AIDS patient was admitted with complaints of general fatigue and dyspnea. His medications at presentation included d4T, 3TC and IDV. Physical examination demonstrated icteric sclerae and abdominal tenderness with hepatomegaly. Laboratory data demonstrated a severe metabolic acidosis with an anion gap due to lactate accumulation. Despite intensive treatment, cardiorespiratory arrest occurred and this could not be resuscitated.

Acidosis, Lactic↗