Patients with diabetic neuropathy are at risk of a greater intraoperative reduction in core temperature.

BACKGROUND: Core hypothermia develops after the induction of general anesthesia, but intraoperative vasoconstriction usually prevents its progression. However, diabetes mellitus is often associated with autonomic neuropathy, which leads to abnormal peripheral neurovascular function. Accordingly, we tested the hypothesis that diabetic patients experience a greater reduction in core temperature during general anesthesia than nondiabetic patients.
METHODS: We studied 36 nondiabetic patients (control group) and 27 diabetic patients (diabetic group) undergoing elective abdominal surgery. Both groups were divided into young (< 60 yr) and older age (>/= 60 yr) groups. Standard noninvasive autonomic tests (heart rate variation at deep periodical breathing, Valsalva maneuver, and head-up tilt) were carried out for each patient. The relation between the results of these tests of autonomic function and the tympanic membrane temperature during general anesthesia was assessed in relation to peripheral vasoconstriction.
RESULTS: Thirteen patients in the diabetic group showed abnormal responses to two or more of the basal autonomic function tests (patients with autonomic dysfunction). Changes in core temperature among the groups were similar at 90 min after the induction of anesthesia. However, the core temperature of the diabetic patients with autonomic dysfunction was lower from 120 min (35.1 degrees C) onward compared with the young or older nondiabetic patients and the diabetic patients with normal autonomic function. Peripheral vasoconstriction, evaluated using the forearm-fingertip skin surface temperature gradient, was delayed in patients with autonomic dysfunction compared with the others.
CONCLUSIONS: The current results indicate that diabetic autonomic neuropathy is associated with more severe intraoperative hypothermia. We postulate that diabetic patients become more hypothermic because their peripheral neuropathy delays the onset of thermoregulatory vasoconstriction and reduces its efficacy once triggered. These patients may therefore fail to develop a normal core temperature plateau.