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 language | English |
|---|---|
| Pages (from-to) | 796-799 |
| Number of pages | 4 |
| Journal | New England Journal of Medicine |
| Volume | 297 |
| Issue number | 15 |
| State | Published - Dec 1 1977 |
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Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated wtih hyperkalemia. / Orringer, Carl Edward; Eustace, J. C.; Wunsch, Chris; Gardner, L. B.
In: New England Journal of Medicine, Vol. 297, No. 15, 01.12.1977, p. 796-799.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Natural history of lactic acidosis after grand-mal seizures. A model for the study of an anion-gap acidosis not associated wtih hyperkalemia
AU - Orringer, Carl Edward
AU - Eustace, J. C.
AU - Wunsch, Chris
AU - Gardner, L. B.
PY - 1977/12/1
Y1 - 1977/12/1
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.
AB - 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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UR - http://www.scopus.com/inward/citedby.url?scp=0017694171&partnerID=8YFLogxK
M3 - Article
C2 - 19702
AN - SCOPUS:0017694171
VL - 297
SP - 796
EP - 799
JO - New England Journal of Medicine
JF - New England Journal of Medicine
SN - 0028-4793
IS - 15
ER -