Hypermetabolism in the acute stage of hemorrhagic cerebrovascular disease.
Oxygen consumption (VO2), carbon dioxide production (VCO2), urinary nitrogen excretion, respiratory quotient, resting energy expenditure (REE), %REE, and the consumption rates of carbohydrate, fat, and protein (%CHO, %Fat, %Prot, respectively) were determined pre- and postoperatively by indirect calorimetry in 13 patients with ruptured intracranial aneurysms and 11 patients with hypertensive intracerebral hemorrhage in the acute stage. The preoperative VCO2, VO2, urinary nitrogen excretion, respiratory quotient, REE, and %REE were, respectively (mean +/- standard deviation): 171 +/- 46 ml/min, 203 +/- 56 ml/min, 10.3 +/- 1.7 gm/day, 0.84 +/- 0.01, 1397 +/- 389 Cal/day, and 129% +/- 8%. The values for VCO2, VO2, REE, and %REE were all increased above normal levels. The %Prot was increased to 26.1% +/- 9.1%. In the postoperative period, the VCO2, VO2, urinary nitrogen excretion, REE, and %REE significantly increased to: 186 +/- 44 ml/min, 229 +/- 56 ml/min, 14.8 +/- 2.9 gm/day, 1557 +/- 384 Cal/day, and 141% +/- 21%, respectively. The %Fat and %Prot also increased significantly, but the %CHO significantly decreased. Preoperatively, in the patients with ruptured intracranial aneurysms, there was a greater increase in %Prot in eight patients classified (according to Fischer) as having a Group 3 or 4 subarachnoid hemorrhage (SAH) on computerized tomography than in five patients classified as having a Group 1 or 2 SAH. In summary, increased metabolic expenditure, especially increased catabolism of protein and fat, is characteristic of accompanying hemorrhagic cerebrovascular disease, and there is an increase in consumption of fat and protein in the postoperative period. Lack of precise knowledge about the cause and consequences of these metabolic responses makes it impossible at present to judge the optimal extent of nutritional replacement. The hypermetabolic state should be taken into consideration when caring for these patients as it may cause weight loss, poor wound healing, and susceptibility to infection.[1]References
- Hypermetabolism in the acute stage of hemorrhagic cerebrovascular disease. Touho, H., Karasawa, J., Shishido, H., Morisako, T., Yamada, K., Shibamoto, K. J. Neurosurg. (1990) [Pubmed]
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