The role of bicarbonate pathophysiology and therapy in Asiatic cholera

Abstract

Metabolic acidosis in Asiatic cholera was due to fecal loss of bicarbonate, with stool clearances of bicarbonate ranging up to 41 ml. per minute. The carbon dioxide content of stool (up to 75.6 mEq. per L.) consistently exceeded that of arterial plasma. Such a carbon dioxide content was within the physiologic limits normally present in the lower parts of the small bowel and cecum, and could be explained by a deficient reabsorption of bicarbonate associated with the rapid intestinal transit time observed in cholera. Acidosis should be treated after the initial correction of shock and dehydration. An average of 0.43 mEq. per kg. of bicarbonate administered intravenously was required to raise the carbon dioxide content of plasma 1 mEq. per L. A similar amount was required in control patients with diarrhea from other causes. Although acute renal tubular necrosis may be a complication in Asiatic cholera, patients included in this report showed at least qualitatively appropriate renal tubular functions in concentrating the urine and adjusting hydrogen ion concentration to meet a changing systemic acid-base balance. Glomerular filtration was depressed early after correction of shock and acidosis in these subjects but improved later.