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[Hyperchloremic acidosis in metabolic acidosis with anion gap excess. Comparison with diabetic ketoacidosis].

The occurrence of hyperchloremia during diabetic ketoacidosis (DKA) recovery and the lack of correlation between anion gap excess (delta AG) and bicarbonate deficit (delta TCO2) on admission suggest an hyperchloremic acidosis (HCLA) component. The hypothesis that this phenomenon is not specific of DKA and can occur in other metabolic acidoses with increased anion gap was tested. HCLA component, defined by the ratio delta AG/delta TCO2 less than or equal to 0.80, was evaluated on admission and during therapy in 31 patients with DKA and 53 patients with non diabetic metabolic acidosis (ND-MA). HCLA component prevalence was similar on admission (32 p. 100 for DKA versus 41 p. 100 for ND-MA), but it increased during therapy only in DKA patients (86 p. 100 at 9 h - P less than 0.001). In view of the significant correlation (r = 0.636; P less than 0.001) observed between delta AG/delta TCO2 and creatinine, kidney acid base defense appears clearly in DKA patients: the more severe the volume depletion, the greater the ketone retention and the less prominent the HCLA. This phenomenon seems to be secondary to a large tubular excretion of ketones. In the 53 ND-MA patients no correlation between delta AG/delta TCO2 and creatinine could be found. A transfer of chloride from cells to the extracellular space secondary to intracellular diffusion of lactate ions could explain the HCLA component.

Acid-Base Equilibrium↗

[Clinical picture of lactate acidosis. 4: Clinical significance of lactate acidosis].

The diagnosis of lactate acidosis is complicated by the fact that lactate determination is not a routine method in clinical chemistry. In fact, lactate analysis is performed only in special laboratories. Even in greater clinics this method is not routinely performed in differential diagnosis of acidotic states. Various diseases are accompanied by a lactate emia or even by lactate acidosis. Anaerobic synthesis of lactate is an emergency reaction to supply minimum energy to tissues with insufficient oxygen supply. The main diseases complicated by increased blood lactate concentrations are shock, circulatory collapse, cardiac failure and peripheral circularoty disturbance. Additionally diabetes mellitus, septical infections, and-the most prominent situation-biguanide intoxications are complicated by an increase in blood lactate concentration.

Acidosis↗

[The clinical picture of lactate acidosis. 5. Lactatemia without acidosis. Conclusions].

Several inherited metabolic diseases are accompanied by a greater or lesser increase in blood lactate concentration under certain metabolic conditions. These diseases are glycogenosis type I (glocuse-6-phosphate deficiency), fructose-1,6-diphosphatase deficiency, glucose-induced hyperlactate emia, idiopathic lactate acidosis. The conditions are discussed when hyperlactate emia develops. Very large increases in blood lactate concentration are found during muscular activity, lactate concentrations can be as much as 20 mmol/l under these conditions. Regarding these values, the increase in blood lactate concentration during intravenous carbohydrate infusion is minimum, even in the case of fructose infusions (1-4 mmol/l). Therapeutical measures for treatment of increased lactate concentration are discussed. A causal therapy is optimum; however, the precondition is a definite diagnosis. Besides bicarbonate infusions (or infusions of other alkalizing substances) dialysis seems to be a favourable therapy in certain cases. In future, prognosis of lactate emia should be better if the diagnostic measures and differential diagnosis are improved.

Acidosis↗