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PubMed2004

[Lactic acidosis in diabetic patient treated with metformin].

We present a case of metabolic acidosis in a man, recently diagnosed with type 2 diabetes mellitus under treatment with metformin. Metformin (along with Fenformin and Butformin) is an oral antihyperglycemic agent belonging to the biguanide group employed in the treatment of non insulin dependent diabetes (NIDDM). Its main use is in association with other oral agents in obese diabetic patients with difficult metabolic control. In some of these patients, clearly beneficial developed lactic acidosis, specially in those who have predisposing factors (respiratory failure, liver disease or cardiovascular disease) and/or those who require high doses. For this reason we describe its pharmacokinetics, therapeutic indications and its correct use in this type of diabetic patient.

Acidosis, Lactic↗
PubMed1978

Treatment of fetal distress during diabetic keto-acidosis.

A case of diabetic acidosis during pregnancy is presented in which the fetal heart rate tracing demonstrated late decelerations. Sodium bicarbonate, intravenous fluids and insulin treatment resulted in correction of both the maternal acidosis and the abnormal fetal heart rate tracings. The rationale for bicarbonate therapy for treatment of the presumed fetal distress is discussed.

Adult↗
PubMed2004

Hyperglycaemic crises and lactic acidosis in diabetes mellitus.

Diabetic ketoacidosis, hyperglycaemic hyperosmolar state, and lactic acidosis represent three of the most serious acute complications of diabetes. There have been some advances in our understanding of the pathogenesis of these conditions over the last three decades, together with more uniform agreement on their treatment and innovations in technology. Accordingly their incidence, morbidity, and mortality are decreasing, but at rates that fall short of our aspirations. Hyperglycaemic crises in particular remain an important cause of morbidity and mortality in diabetic populations around the world. In this article, understanding of these conditions and advances in their management, and the available guidelines for their treatment, are reviewed. As far as is possible, the recommendations are based on clear published evidence; failing that, what is considered to be a common sense synthesis of consensus guidelines and recommendations is provided.

Acidosis, Lactic↗
PubMed1987

Extensive glomerular immaturity associated with renal tubular acidosis, nephrogenic diabetes insipidus and nephrocalcinosis.

Neonatal renal failure and glomerular immaturity have been described in 1983. The present paper describes 3 cases with the same histological features. However, follow-up of the patients during 14, 18 and 4 years, respectively, showed the following: The histologic immaturity may be followed by maturation. Thus, late maturation may be a term more suitable to designate this constellation. Renal failure may not necessarily ensue, at least not during early infancy. In the 3 cases presented in this report, the histological finding is associated with renal tubular acidosis, renal diabetes insipidus and nephrocalcinosis. The association of transient glomerular immaturity (or late glomerular maturation) and renal tubular acidosis may enhance the development of nephrocalcinosis.

Acidosis, Renal Tubular↗
PubMed1978

Hyperchloremic metabolic acidosis in diabetes mellitus: a case report and discussion of pathophysiologic mechanisms.

A 21-year old woman with poorly controlled diabetes mellitus was examined for persistent hyperchloremic metabolic acidosis. There was no evidence of ingestion of hydrochloric acid or its equivalent. Gastrointestinal loss of bicarbonate was absent. Proximal tubular bicarbonate reabsorption and distal nephron hydrogen-ion secretion were normal. Ammonia and net acid excretions were high, and thus there was no obvious cause for this acidosis. Further study revealed a very large loss of beta-hydroxybutyrate in the urine that closely approximated net acid excretion. This loss of potential bicarbonate was the principal cause for the hyperchloremic metabolic acidosis. Phosphate, urate, and beta-hydroxybutyrate fractional excretions were all abnormally high. Generalized aminoaciduria was also present, but the renal handling of glucose and bicarbonate was normal. With improved control of her diabetes, the generalized aminoaciduria disappeared, the urine beta-hydroxybutyrate loss ceased, the fractional excretions of phosphate and urate approached normal, and the acidosis was rapidly corrected.

Adult↗
PubMed1976

[The value of alkalizing treatments in severe diabetic keto-acidosis].

In 37 diabetic patients with severe acidosis (pH less than 7.0; [HCO3-] less than 5.0 mMol/l), administration of insulin was preceded by a rapid infusion of molar sodium bicarbonate in order to obtain partial correction of acidosis (pH approximately 7.20). 31 patients survived (83,8%); 6 patients died in cardio-circulatory failure associated in two cases with acute pulmonary edema. Initial administration of bicarbonate appears to be beneficial in preventing the deleterious effects of prolonged severe acidosis, such as cardiac arrhythmias, shock or acute pulmonary edema. Furthermore, partial correction of acidosis decreases the total dose of insulin necessary to compensate hyperglycemia and thereby reduces the danger of late hypoglycemia. This treatment calls for frequent checks on acid-base status and serum potassium. In most cases hypokalemia develops, but can be easily corrected by administration of potassium chloride. Normalization of arterial pH by bicarbonate infusion is not recommended in view of the development of late hypernatremia and metabolic alkalosis.

Acid-Base Equilibrium↗