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Biomedical subjects

M Bernardin

Publications and source records attributed to M Bernardin.

6 recordsLinked to original sources
PubMed1994

Hyperchloremic acidosis during grand mal seizure lactic acidosis.

OBJECTIVE: To evaluate the prevalence and the mechanism of hyperchloremic acidosis component (HClA) during lactic acidosis secondary to grand mal seizures. DESIGN: Retrospective study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: 35 patients admitted for grand mal seizures with lactic acidosis (pH < 7.35, TCO2 < 20 mmol/l and PaCO2 < 8 kPa). MEASUREMENTS: HClA was defined by the ratio: excess anion gap/HCO3 deficit (delta AG/delta TCO2) < 0.8. A difference in the distribution space of protons and their accompanying anion, i.e., a displacement of chloride from cells by the entering lactate, was evaluated by the ratio natremia/chloremia (Na+/Cl-). RESULTS: Immediately after seizures, a profound lactic acidosis was observed (pH = 7.22 +/- 0.17 (mean +/- SD), AG: 23.8 +/- 7.1 mmol/l, TCO2 = 14.5 +/- 5.3 mmol/l, lactate: 14.6 +/- 6.9 mmol/. HClA was present on admission in 11 patients (31.5%). Its prevalence increased to 73% after recovery. delta AG/delta TCO2 ratios were unrelated to creatinine, level and PaCO2, but dependent on the ratio Na+/Cl- (r = 0.803; p < 0.001, delta AG/delta TCO2 = 6.4 x (Na+/Cl-)-7.9). These data demonstrate that HClA is not a respiratory or renal phenomenon and suggest differences in the distribution spaces of hydrogen ions and their accompanying anions. CONCLUSION: HClA component may be associated with lactic acidosis in grand mal seizures and appears to be secondary to a lactate antiport. This phenomenon could be an immediate physiological response to a sudden metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1991

[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↗
PubMed1989

[Primary hyperaldosteronism caused by unilateral macronodular hyperplasia].

A case or primary hyperaldosteronism due to unilateral macronodular adrenal hyperplasia is presented. This entity is exceptional: a review of the literature has yielded only three similar cases. The significance of these adrenal nodules is discussed; in particular, they are compared with the nodules found in hypertensive subjects. Their course after surgery is similar to that of Conn's adenoma.

Adrenal Gland Diseases↗