Metabolic acidosis evaluation

All patients admitted to a hospital during 6 months who had taken at least one dose of metformin were retrospectively evaluated for susceptibility factors for metformin-associated lactic acidosis (8). There were 263 hospitalizations in 204 patients. In 71 admissions there was at least one contraindication, such as renal or liver disease, renal dysfunction, congestive cardiac failure, metabolic acidosis, or an intravenous iodinated contrast medium given within 48 hours of metformin. In 29 (41%) metformin was continued despite the contraindication. The most frequent contraindication was a raised serum creatinine, but in only eight of the 32 admissions was metformin withdrawn. Of nine patients using metformin who died (not necessarily directly related to metformin), six had an absolute contraindication. In two patients who died and in one who survived, blood lactate was increased and this was temporally related to the use of metformin. 

Since topiramate can be associated with metabolic acidosis in both children and adults the incidence and magnitude of the effect of topiramate on serum bicarbonate concentrations in an adult population have been evaluated in a retrospective cohort study in 54 patients (40 women), of whom 26 had low serum bicarbonate concentrations while taking topiramate (mean concentration 18.8 mmol/1, range 13-21) (1131). However, this was not associated with any clinically significant problems. 

Kraut JA, Kurtz I Metabolic acidosis of CKD diagnosis, clinical characteristics, and treatment. Am J Kidney Dis 2005 45 978-993. KDIGO clinical practice guidelines for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Kidney Int 2009 76(suppl 113) S1-S130. 

The disorders of isoleucine and valine metabolism are detected in a sequential process that begins with the evaluation of the symptoms and signs displayed by the patient. Clinical chemistry is helpful in the assessment of ketogenesis by urinary tests for ketones or quantification of 3-hydroxybuty-rate and acetoacetate in the blood. The electrolytes and pH may provide evidence of acidosis and it is important to assess the presence or absence of hyperammonemia. Amino acid analysis of the plasma and urine may be helpful. In virtually all instances the definitive diagnosis will come from organic acid analysis of the urine. 

Explain that the acid-base status can be deduced from the blood biochemistry in cases of uncompensated respiratory or metabolic disorder. Demonstrate examples of compensated disorders (e.g. compensated respiratory acidosis and compensated metabolic alkalosis) in which the same abnormality of blood biochemistry may be reached by different routes. Hence explain the need, in such cases, to seek each cause and evaluate its effect. 

Some months later, a statement by the Australian Drug Evaluation Committee reflected similar thinking and made closely similar recommendations (52). It was pointed out, inter alia, that the rapid metabolism of fructose and sorbitol can cause rapid accumulation of uric and lactic acids as well as phosphate depletion, especially in states of anoxia, and that acidosis and decreased tissue energy metabolism can occur. Glucose has, among other things, the advantage that it poses no risk to patients with familial laevulose intolerance. 

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