Cerebral edema and depression of sensorium in nonketotic hyperosmolar coma.
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Biomedical subjects
Publications and source records attributed to H J Carroll.
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The effect of change in extracellular (interstitial) volume on vascular volume (VV) is mediated through interstitial pressure. Since the effect of swollen or shrunken cells on interstitial pressure should be identical to that of changes in interstitial volume on interstitial pressure, it would be appropriate to consider that intracellular volume (ICV) as well as extracellular volume (ECV) contributes to control of VV. Total body water rather than ECV, therefore, should be considered as the fluid volume which regulates VV. Support for these conclusions has been provided by theoretical analysis of the factors that regulate capillary fluid exchange. In further support of this hypothesis, clinical examples are described, in which renal salt retention was observed despite increases in ECV (ICV was markedly decreased), and in which renal salt loss occured despite decrease in ECV (in the presence of increased cell volume).
Potassium filtered at the glomerulus is almost completely reabsorbed before the distal tubule; it must therefore be secreted into the collecting duct. The rate of potassium secretion is determined by a number of factors, notably aldosterone, distal sodium delivery, and serum potassium. Normal serum potassium is maintained by the interplay of passive leak of potassium from the cells and its active return to the cells. Transmembrane potassium distribution is influenced largely by acid-base equilibrium and hormones including insulin and catecholamines. In the diabetic with ketoacidosis hyperkalemia, in the face of potassium depletion, is attributable to reduced renal function, acidosis, release of potassium from cells due to glycogenolysis, and lack of insulin. Chronic hyperkalemia in diabetics is most often attributable to hyporeninemic hypoaldosteronism but other conditions including urinary tract obstruction may also contribute. A variety of clinical situations (e.g., volume depletion) and drugs (e.g., nonsteroidal antiinflammatory agents, and heparin) may acutely provoke hyperkalemia in susceptible individuals.
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