Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated wtih hyperkalemia

Carl Edward Orringer, J. C. Eustace, Chris Wunsch, L. B. Gardner

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Abstract

To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (± S.E.M.) venous lactate concentration was 12.7±1.0 meq per liter, the mean carbon dioxide content 17.1±1.1 nmol per liter, and the mean arterial pH 7.14±0.06. Sixty minutes later their values were 6.6±0.7 meq per liter (P<0.005), 23.6±1.1 mmol per liter (p<0.005) and 7.38±0.04 (P<0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.

Original languageEnglish
Pages (from-to)796-799
Number of pages4
JournalNew England Journal of Medicine
Volume297
Issue number15
StatePublished - Dec 1 1977

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Lactic Acidosis
Hyperkalemia
Acid-Base Equilibrium
Acidosis
Seizures
Lactic Acid
Carbon Dioxide
Protons
Potassium
Serum

ASJC Scopus subject areas

  • Medicine(all)

Cite this

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title = "Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated wtih hyperkalemia",
abstract = "To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (± S.E.M.) venous lactate concentration was 12.7±1.0 meq per liter, the mean carbon dioxide content 17.1±1.1 nmol per liter, and the mean arterial pH 7.14±0.06. Sixty minutes later their values were 6.6±0.7 meq per liter (P<0.005), 23.6±1.1 mmol per liter (p<0.005) and 7.38±0.04 (P<0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.",
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AU - Wunsch, Chris

AU - Gardner, L. B.

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N2 - To define the time course of the metabolic acidosis that follows a single grand-mal seizure, we obtained serial blood samples from eight consecutive patients. Immediately after a seizure, the mean (± S.E.M.) venous lactate concentration was 12.7±1.0 meq per liter, the mean carbon dioxide content 17.1±1.1 nmol per liter, and the mean arterial pH 7.14±0.06. Sixty minutes later their values were 6.6±0.7 meq per liter (P<0.005), 23.6±1.1 mmol per liter (p<0.005) and 7.38±0.04 (P<0.005) respectively. The spontaneous resolution of the acidosis was due, in large part, to the metabolism of lactate and to the concomitant removal of hydrogen ion. There was no change in the serum potassium concentration, despite the development of a severe systemic acidemia and the subsequent return to normal of the pH. We suggest that the patient with seizures may serve as a unique model of lactic acidosis.

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