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Urea and alcohol are two substances that readily cross cell membranes and can produce hyperosmolality. Because of its permeant nature, urea has little effect on the shift of water across the cell membrane. Urea may be administered acutely in large doses to "draw" water from cells, but the effect is transient, as is the diuresis, and urea soon equilibrates throughout body water. Alcohol quickly equilibrates between intracellular and extracellular water, adding 22 mosm/L for every 1000 mg/L. This measured hyperosmolality does not produce symptoms by itself because of the equilibrium described, but in any case of stupor or coma in which measured osmolality exceeds that calculated from values of serum Na+ and glucose and BUN, ethanol intoxication should be considered as a possible explanation of the discrepancy (osmolar gap).
The combination of anion gap metabolic acidosis and an osmolar gap exceeding 10 mosm/kg is not specific for toxic alcohol ingestion. Nearly half of patients with alcoholic ketoacidosis or lactic acidosis have similar findings, caused in part by elevations of endogenous glycerol, acetone, and acetone metabolites.
Increased concentrations of solutes that do not readily enter cells produce a shift of water from the intracellular space to effect a true intracellular dehydration. Sodium and glucose are the solutes commonly involved. In these instances, the hyperosmolality does produce symptoms.
Clinical symptoms are mainly referred to the central nervous system. The severity of symptoms depends on the degree of hyperosmolality and rapidity of development. In acute hyperosmolality, symptoms of somnolence and confusion can appear when the osmolality exceeds 320–330 mosm/L, and coma, respiratory arrest, and death occur when it exceeds 340–350 mosm/L.
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