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metabolic Derangements Imperiling the Perforated Ulcer PatientIII. Derangements and Shifts of Sodium and Chloride
ANNE WIGHT, M.D.;
SELWYN TAYLOR, M.Ch., F.R.C.S.;
CHARLES L. MINOR, M.D.;
WILLIAM LOHNES, M.D.;
JAMES F. HOPKIRK, M.D.;
OLIVER COPE, M.D.
AMA Arch Surg. 1956;72(1):166-178.
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INTRODUCTION
Cellular function is affected by the composition and concentration of electrolytes within the cells, and their concentrations, in turn, are governed by a complicated equilibrium with the electrolytes in the fluid bathing the cells. A disease state or a therapy influencing the extracellular phase to the extent of altering the intracellular electrolytes may be damaging to cell function. In the first paper of this series, concerned with the fluid shifts occurring after ulcer perforation, observations are described which might be explained by penetration of extracellular electrolytes across cell barriers.1 Substantiation or refutation of this possibility in the patient with a perforated peptic ulcer should alter our therapy.
Post-traumatic salt retention has received much attention in the literature,* and simultaneous drops in serum sodium and chloride concentrations have been described. In 1944, Coller and his associates described a fall of the chloride level associated with chloride retention.5 A
. . . [Full Text PDF of this Article]
Author Affiliations
Boston
From the Department of Surgery, Harvard Medical School, and the Surgical Services, Massachusetts General Hospital.
Footnotes
Submitted for publication April 20, 1955.
This work was supported by a Contract between the Office of Naval Research and Harvard University.
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