Abstract
Objective
To evaluate the prevalence and the mechanism of hyperchloremic acidosis component (HC1A) 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
HC1A was defined by the ratio: excess anion gap/HCO3 deficit (ΔAG/ΔTCO2) <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/. HC1A was present on admission in 11 patients (31.5%). Its prevalance increased to 73% after recovery. ΔAG/ΔTCO2 ratios were unrelated to creatinine, level and PaCO2, but dependent on the ratio Na+/Cl− (r=0.803;p<0.001, ΔAG/ΔTCO2=6.4 X (Na+/Cl−)−7.9). These data demonstrate that HC1A is not a respiratory or renal phenomenon and suggest differences in the distribution spaces of hydrogen ions and their accompanying anions.
Conclusion
HC1A 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.
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Brivet, F., Bernardin, M., Cherin, P. et al. Hyperchloremic acidosis during grand mal seizure lactic acidosis. Intensive Care Med 20, 27–31 (1994). https://doi.org/10.1007/BF02425050
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DOI: https://doi.org/10.1007/BF02425050