Aims/hypothesis. To test the hypothesis that subnormal thirst sensation could contribute to the development of the hypernatraemia characteristic of hyperosmolar coma, we studied osmoregulation in survivors of hyperosmolar coma. Methods. Eight survivors of hyperosmolar coma, eight control subjects with Type II (non-insulin-dependent) diabetes mellitus and eight healthy control subjects underwent water deprivation during which measurements of thirst, plasma osmolality and vasopressin were taken. Results. Water deprivation caused greater peak plasma osmolality in the hyperosmolar coma group (301.7±2.7 mmol/kg) than in Type II diabetic (294.3 ± 3.2 mmol/kg, p < 0.01) or control group (296.9 ± 3.0 mmol/kg, p < 0.01) and a greater increase in plasma vasopressin concentration (hyperosmolar coma, 5.8 ± 1.3 pmol/l, Type II diabetes, 1.8 ± 1.3 pmol/l, p < 0.001, control subjects, 2.2 ± 1.8 pmol/l, p < 0.001). Thirst ratings were lower following water deprivation in the hyperosmolar coma group (3.5 ± 0.8 cm) than in Type II diabetes (7.7 ± 1.6 cm, p < 0.001) or control subjects (7.4 ± 1.3 cm, p < 0.001), and the hyperosmolar group patients drank less in 30 min following water deprivation (401 ± 105 ml) than Type II diabetic (856 ± 218 ml, p<0.001) or control subjects (789±213 ml, p < 0.001). Conclusion/interpretation. Survivors of hyperosmolar coma have subnormal osmoregulated thirst and fluid intake, which might contribute to the hypernatraemic dehydration typical of the condition.
- Hyperosmolar coma
- Type II (non-insulin-dependent) diabetes