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.