Plasma volume during surgery in unsupplemented glucocorticoid-treated patients.
نویسندگان
چکیده
SUMMARY Changes in plasma volume and plasma cortisol concentrations were investigated in seven unsupplemented and three supplemented glucocorticoid-treated patients and in eight control patients subjected to abdominal surgery. No differences in postoperative plasma volume deficit could be demonstrated between normal and glucocorticoid-treated patients, or between patients with a normal or an impaired adrenocortical response to surgery. These results may lend further support to observations indicating that arterial hypotension during operation in glucocorticoid-treated patients is not caused by adrenocortical insufficiency. Experimental studies in the adrenalectomized dog have all demonstrated major decreases in plasma volume during stress-induced adrenocortical insuffi-ciency (Swingle et al., 1938; Swingle et al, 1959; Marks et al., 1965), but there are no corresponding studies in humans. We have found previously a high incidence of arterial hypotension during operation in unsupplemented glucocorticoid-treated patients, which is not related to plasma cortisol concentrations (Kehlet and Binder, 1973b). However , it has been suggested (Cope, 1965) that during long-term glucocorticoid therapy the tissues become adapted to a higher glucocorticoid concentration, so that a decrease towards normal concentrations represents , relatively, a hypoadrenal state. The present study was undertaken to investigate whether changes in plasma volume take place during surgery in glucocorticoid-treated patients where no exogenous glucocorticoid was given, and to correlate these findings with the clinical course and the adrenocortical function. Eight normal and ten glucocorticoid-treated patients undergoing elective major abdominal surgery (cholecystectomy, hysterectomy) were studied. Age, sex, weight and the dose of glucocorticoid are shown in table I. In order to secure complete catabolism of exogenous glucocorticoid, glucocorticoid treatment was stopped 36 hours before operation. Supplementary glucocorticoids were administered to three of the glucocorticoid-treated patients (table I) as follows: 100 mg cortisol phosphate-ester* i.m. at the time of premedication and 100 mg cortisol phosphate -ester* i.v. at the time of skin incision. Operative blood loss was calculated by weighing the sponges and measuring suctioned blood. Neither plasma nor blood transfusions were given. After premedication with pethidine and atropine, anaesthesia was induced with thiopentone, endotracheal intubation being facilitated by suxamethonium, and anaesthesia was maintained with droperidol, fen-tanyl, nitrous oxide and oxygen. Arterial pressure and heart rate were recorded at 5-min intervals during each surgical procedure. Plasma volume was determined 24 hours before, and 2 hours after skin incision using the T1824 Evans Blue technique as described by Leth and Binder (1970). Plasma for spectrophotometric T1824 analysis was sampled from a contralateral cubital vein …
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عنوان ژورنال:
- British journal of anaesthesia
دوره 46 6 شماره
صفحات -
تاریخ انتشار 1974