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June 1963

Metabolic Change in Purulent and Tuberculous Meningitis: Further Observations

Author Affiliations

Donald B. Cheek, MD, DSc, Division of Growth, Harriet Lane Home, The Johns Hopkins Hospital, Baltimore 5, Md.; Director of Department of Metabolic and Electrolyte Research (Dr. Cheek); present address: Division of Growth, Harriet Lane Home, The Johns Hopkins Hospital.; From the Research Foundation, Royal Children's Hospital.

Am J Dis Child. 1963;105(6):542-548. doi:10.1001/archpedi.1963.02080040544003

Hyponatremia in patients with meningitis has been the subject of previous investigations.1-5 The hyponatremia of generalized tuberculous infection 6-8 and of tuberculous meningitis was thought by Sims et al 6 to be secondary to an initial hypotonicity of the tissue cells. A salt-losing condition was considered to exist during the course of severe tuberculous infection. Rapoport, West, and Brodsky 1 suggested that this salt-losing state in tuberculous meningitis might be related to an abnormal effect of the central nervous system on renal function. At the same time these workers showed an inability of such patients to clear a large NaCl load. Harrison, Finberg, and Fleishman 2 demonstrated normal body fluid compartments but an increase in red cell Na content—without loss of K, or, in other words, the presence of an excess of cell cation. There was, however, loss of K in muscle cells with reciprocal increase in cell Na

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