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  Vol. 115 No. 2, February 1968 TABLE OF CONTENTS
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Pathogenesis and Pathophysiology of Hypertonic Dehydration With Diarrhea

A Clinical Study of 59 Infants With Observations of Respiratory and Renal Water Metabolism

Erika Bruck, MD; Güner Abal, MD; Thomas Aceto, Jr., MD

Am J Dis Child. 1968;115(2):122-144.

Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

HYPERTONIC DEHYDRATION with infantile diarrhea has long attracted interest in Buffalo because here the incidence seems to be higher than that reported in the literature from other areas in the USA and it occurs predominantly in winter. The sodium concentration in the serum of infants hospitalized with severe diarrhea is above 150 mEq/liter in more than one third of the cases. The high incidence of hypertonic dehydration in Buffalo and controversial therapeutic recommendations, some of which are based on theoretical considerations, aroused interest in planning a controlled study which would help to evaluate causes and therapy of this disturbance. Factors contributing to pathogenesis and pathophysiology of hypertonic dehydration were studied in individual patients.

Plan of Study

Patients admitted to the Children's Hospital of Buffalo with dehydration and a concentration of sodium in the serum above 150 mEq/liter were admitted to the study. The patients were referred to the investigators by . . . [Full Text PDF of this Article]


Author Affiliations

Buffalo

From the Department of Pediatrics, State University of New York at Buffalo School of Medicine and the Children's Hospital of Buffalo, Buffalo. Dr. Abal is now at Ankara University Medical School and Children's Hospital, Ankara, Turkey.


Footnotes

Received for publication Sept 18, 1967.

Submitted by the authors for the Mitchell I. Rubin Festschrift issue of the Journal.

Reprint requests to 219 Bryant St, Buffalo 14222 (Dr. Bruck).

Methods for urinalysis:—pH, phenaphthazine (Nitrazine) paper; specific gravity, gradient tube,1 standardized daily; protein, sulfosalicylic acid; sugar, Benedict's qualitative reagent; acetone, Acetest tablets. Osmolarity was determined with Hill-Baldes osmometer in the first series of cases, later with the Fiske osmometer.

Methods for blood and serum analyses:—blood was allowed to clot and was centrifuged under mineral oil; pH, cases 1 to 44, Cambridge Research model pH meter, at room temperature, using Rosenthal's2 correction for temperature; cases 45 to 59, Radiometer (Model PHM 4), pH meter with capillary glass electrode at 38 C; carbon dioxide content, Van Slyke manometric apparatus, using 0.2 ml serum; chloride, Van Slyke's modification of Sendroy's method;3 sodium and potassium, by flame photometer with internal standard of lithium nitrate; calcium, micromodification, using 0.5 ml of serum, of Roe and Kahn's method;4 phosphorus: Gomori's method;5 serum urea nitrogen, modified Conway method;6 total protein, gradient tube;1 sugar, Somogyi-Nelson.7



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