Postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia.

STUDY OBJECTIVE: To evaluate the postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia. DESIGN: Prospective, randomized clinical trial. SETTING: Operating room and postanesthesia care unit of a university hospital. PATIENTS: 74 healthy, ASA status I, II, and III patients (average age 58 yrs) undergoing elective colon surgery. INTERVENTIONS: Patients were randomly assigned to be kept normothermic or approximately 2.5 degrees C hypothermic during surgery. Anesthesia was maintained with isoflurane, nitrous oxide, and fentanyl. Postoperatively, surgical pain was treated with patient-controlled analgesia (PCA) opioid. MEASUREMENTS AND MAIN RESULTS: An observer blinded to group assignment and core temperatures evaluated shivering, thermal comfort, surgical pain, heart rates (HRs), and blood pressures (BPs) during the first six postoperative hours. Morphometric characteristics, oxygen saturation, fluid balance, PCA-administered opioid, and visual analog pain scores were comparable in the two groups. Hypothermic patients felt uncomfortably cold during recovery, and their postoperative core temperatures remained significantly less than in the normothermic patients for more than four hours. Peripheral vasoconstriction and shivering were common in the hypothermic patients but rare in those kept normothermic. HRs and BPs were comparable in the two groups. CONCLUSIONS: These data confirm that the effects of intraoperative hypothermia on postoperative HR and BP are modest in relatively young, generally healthy patients. In contrast, intraoperative hypothermia caused substantial postoperative thermal discomfort, and full recovery from hypothermia required many hours. Delayed return to care normothermia apparently resulted largely from postoperative thermoregulatory impairment.

Serum laminin in Graves' disease.

We determined serum levels of laminin in 23 patients with Graves' disease (GD) and in 24 patients with toxic nodular goiter (TNG). Elevated levels of soluble laminin were observed in patients with GD prior to treatment (median concentration 1376 ng mL-1 [range 712-2402]), compared to patients with TNG (median 442 ng mL-1 [284-891]), and normal controls (median 492 ng mL-1 [range 235-675], n = 26), respectively. In GD patients serum laminin levels decreased during thiamazole treatment and normalized within 8 weeks of therapy. There was no correlation between serum laminin levels and serum levels of thyroid hormones and/or auto-antibodies, respectively. Whether serum laminin is a marker for alterations of extracellular matrix during GD and release of basement membrane components in the circulation and/or reflects an impaired clearance remains to be elucidated.

Elevated serum levels of IL-10 and IFN-gamma in patients with acute Plasmodium falciparum malaria.

Serum levels of interleukin-10 (IL-10) and interferon-gamma (IFN-gamma) were determined in 37 patients with acute Plasmodium falciparum malaria in Bangkok, Thailand. Serum levels of IL-10 and IFN-gamma were markedly elevated in patients with malaria prior to treatment (717 +/- 260 pg/ml versus 2.2 +/- 1.3 pg/ml in healthy controls; 123 +/- 71 pg/ml versus 29 +/- 9 pg/ml, respectively; mean +/- SD). Serum levels of IFN-gamma and IL-10 dropped significantly during treatment and were normal 14 and 21 days, respectively, after treatment was started. Prior to therapy a correlation between serum levels of IFN-gamma and IL-10 existed (r = 0.563). These results suggest that stimulatory and inhibitory cytokines for macrophage activation and/or antibody production (i.e., TH1- and TH2-type immunoreaction, respectively) are coexpressed during acute P. falciparum infection and stress the multifactorial network between host and parasite in malaria immunology.

Morphometric influences on intraoperative core temperature changes.

Intraoperative core hypothermia develops in three characteristic phases: 1) core-to-peripheral redistribution of body heat that is most prominent during the first hour after induction of anesthesia; 2) subsequent slow linear decrease in core temperature resulting largely from heat loss exceeding metabolic heat production; and 3) core temperature plateau resulting when thermoregulatory vasoconstriction decreases cutaneous heat loss and constrains metabolic heat to the core thermal compartment. Accordingly, we tested the hypotheses that: 1) core cooling does not depend on body fat (BF) or the ratio of weight-to-surface area (Wt/SA) during the initial redistribution phase; 2) the core cooling phase; 2) the core cooling rate is a function of the Wt/SA ratio during the second phase; and 3) the rate of core cooling during the plateau phase (after vasoconstriction) will be determined by the percentage of BF. In 40 patients undergoing elective colon surgery, the amount of redistribution hypothermia was inversely proportional to the percentage of BF (delta TC = 0.034.BF-2.2, r2 = 0.63) and the Wt/SA ratio (delta TC = 0.052.Wt/SA-3.35, r2 = 0.66). The core cooled linearly during the second phase, and the cooling rate was inversely proportional to the Wt/SA ratio (rate = 0.035.(Wt/SA)-2.2, r2 = 0.29). Thermoregulatory vasoconstriction was effective in virtually all patients independent of their morphology, and produced a four-fold reduction in the core cooling rate. These results indicate that patient morphometric characteristics substantially influence intraoperative core temperature changes, and that the effect depends on the hypothermia phase.

Mild intraoperative hypothermia prolongs postanesthetic recovery.

BACKGROUND: Intraoperative hypothermia is common and persists for several hours after surgery. Hypothermia may prolong immediate recovery by augmenting anesthetic potency, delaying drug metabolism, producing hemodynamic instability, or depressing cognitive function. Accordingly, the authors tested the hypothesis that intraoperative hypothermia prolongs postoperative recovery. METHODS: Patients undergoing elective major abdominal surgery (n = 150) were anesthetized with isoflurane, nitrous oxide, and fentanyl. They were randomly assigned to routine thermal management (hypothermia) or extra warming (normothermia). Postoperative surgical pain was treated with patient-controlled analgesia. Fitness for discharge from the postanesthesia care unit was evaluated at 20-min intervals by investigators blinded to group assignment and postoperative core temperatures. Scoring was based on a modification of a previously published system that included activity, ventilation, consciousness, and hemodynamic responses. Patients were considered fit for discharge when they sustained a score of 80% (13 points) for at least two consecutive measurement periods. RESULTS: Morphometric characteristics and anesthetic management were similar in each group. Final intraoperative core temperatures differed by approximately 2 degrees C: 34.8 +/- 0.6 versus 36.7 +/- 0.6 degrees C (mean +/- SD, P < 0.001). Postoperative pain scores and postoperative use of patient-controlled opioid were similar. Hypothermic patients required approximately 40 min longer (94 +/- 65 vs. 53 +/- 36 min) to reach fitness for discharge, even when return to normothermia was not a criterion (P < 0.001). Duration of recovery in the two groups differed by approximately 90 min when a core temperature >36 degrees C was also required (P < 0.001). CONCLUSION: Maintaining core normothermia decreases the duration of postanesthetic recovery and may, therefore, reduce costs of care.

Mild intraoperative hypothermia reduces production of reactive oxygen intermediates by polymorphonuclear leukocytes.

Mild hypothermia directly impairs numerous immune functions in vitro. However, the in vivo effects of mild hypothermia on neutrophil phagocytosis and oxidative killing remain unknown. We tested the hypothesis that mild intraoperative hypothermia decreases neutrophil phagocytic capacity and generation of reactive oxygen intermediates (a measure of oxidative killing). Additionally, we evaluated the effects of in vitro temperature manipulations on each function. Thermal management was randomly assigned in 10 surgical patients, causing intraoperative core temperatures to range from 33 to 37 degrees C. Production of reactive oxygen intermediates and neutrophil phagocytosis were evaluated using flow cytometry at ambient temperature. Phagocytic capacity was assessed by uptake of fluorescein isothiocyanate-labeled Escherichia coli. Reactive oxygen production was estimated by the intracellular conversion of dihydrorhodamine 123 to rhodamine 123. Blood samples were obtained preoperatively, 1 h after surgery started, and 2 h postoperatively. Blood was also obtained from 10 matched control subjects and tested at 32, 37, and 40 degrees C. Neutrophil oxidative and phagocytic capacities were significantly reduced intraoperatively, compared with preoperative and postoperative values. Intraoperative production of reactive oxygen species was linearly related to core temperature. In contrast, there was no correlation between core temperature and phagocytic activity. In vitro production of reactive oxygen intermediates increased sixfold from 32 to 40 degrees C. In vitro phagocytic capacity increased fourfold in this temperature range. Production of oxidative intermediates was most closely related to intraoperative core temperature, decreasing nearly fourfold over a 4 degree C range. This in vitro temperature dependence was matched in vitro. Impaired neutrophil oxidative killing may contribute to the observed hypothermia-induced reduction in resistance to infection.