Acute renal failure after radiofrequency liver ablation of metastatic carcinoid tumor.

IMPLICATIONS: We report a case of prolonged radiofrequency liver ablation for metastatic carcinoid tumor complicated by hemolysis, rhabdomyolysis, and transient acute renal failure. Brief radiofrequency liver ablation procedures or those for a small number of tumor sites are not associated with these complications.

Sympathetic blockade does not enhance tissue warming during isolated heated limb perfusion.

UNLABELLED: Isolated, heated limb perfusion is used for the treatment of locally recurrent melanoma, intransit metastases, and acral lentiginous melanomas. Tissue warming during this procedure requires adequate perfusion within the isolated extremity. At our institution, spinal or epidural anesthesia was used to produce sympathetic blockade and vasodilation for lower extremity procedures. More recently, we began using mild systemic hyperthermia to produce active thermoregulatory vasodilation. In the presence of heat stress, sympathetic blockade may actually decrease skin blood flow because active cutaneous vasodilation, which is associated with sweating, is dependent on intact sympathetic innervation. We therefore investigated whether the continued use of neuraxial blockade was justified. Twenty patients undergoing lower extremity perfusions were alternately assigned to receive either combined general and spinal anesthesia or general anesthesia alone. All were aggressively warmed using forced air and circulating water. There were no significant differences in tissue temperatures (measured at four sites in the isolated limb) between groups at any time before or after the start of perfusion. Similarly, pump flow (715 +/- 211 mL/min versus 965 +/- 514 mL/min) and the time required to achieve an average tissue temperature of 39 degrees C (43 +/- 16 vs 34 +/- 13 min) were not different between groups (spinal versus no spinal). Sweating was observed in all but three patients at esophageal temperatures of 37.9 +/- 0.6 degrees C. We conclude that sympathetic blockade confers no added benefit for tissue warming during isolated limb perfusions in the presence of induced mild systemic hyperthermia. IMPLICATIONS: Sympathetic blockade prevents adrenergic vasoconstriction, but also inhibits active, neurally mediated cutaneous vasodilation (a normal thermoregulatory response to heat). In slightly hyperthermic patients, we demonstrated that spinal anesthesia does not improve convective tissue warming during isolated, heated limb perfusion. Mild systemic hyperthermia may promote greater vasodilation than sympathetic blockade.

Nausea and vomiting following thyroid and parathyroid surgery.

STUDY OBJECTIVES: To determine the incidence of postoperative nausea and vomiting (PONV) following thyroid and parathyroid surgery. To determine whether PONV is reduced when propofol is used for maintenance of anesthesia as compared to isoflurane and to evaluate the costs and resource consumption associated with these two anesthetic regimens. DESIGN: Randomized, prospective study. SETTING: University-affiliated hospital--a referral center for endocrinologic surgery. PATIENTS: 118 ASA physical status I and II patients, aged 18 years and older, undergoing elective thyroid or parathyroid surgery. INTERVENTIONS: Patients received either isoflurane (0.5 to 1.3% end-tidal) or propofol (50 to 200 micrograms/kg/min) for maintenance of anesthesia. All patients received propofol for induction of anesthesia, succinylcholine or vecuronium, nitrous oxide, and fentanyl. Prophylactic antiemetics were not administered. Postoperative pain was treated with ketorolac, fentanyl, or acetaminophen. MEASUREMENTS AND MAIN RESULTS: Signs and symptoms of nausea and vomiting were graded on a four point scale as 1 = no nausea; 2 = mild nausea; 3 = severe nausea; 4 = retching and/or vomiting. Grades 3 and 4 were grouped together as PONV. The combined incidence of PONV was 54% over the 24-hour postoperative evaluation period. PONV was significantly more common in patients receiving isoflurane than propofol for maintenance of anesthesia (64% vs. 44%). In women (n = 87), the incidence of PONV was significantly greater in those patients who received isoflurane than those who received propofol for maintenance (71% vs. 42%). However, in men (n = 31), there was no significant difference in PONV between anesthetic regimens (47% with isoflurane vs. 50% with propofol). There were no differences in the duration of stay in the postanesthesia care unit, time to discharge from the hospital, or local wound complications (hematomas) between groups. The use of propofol for maintenance of anesthesia was associated with an additional cost, relative to the isoflurane group, of $54.26 per patient. CONCLUSION: Patients undergoing thyroid or parathyroid surgery are at high risk for the development of PONV. Propofol for maintenance of anesthesia, although more expensive than isoflurane, reduces the rate of PONV in women.

Thermoregulatory and anesthetic-induced alterations in the differences among femoral, radial, and oscillometric blood pressures.

BACKGROUND: A decrease in radial artery blood pressure relative to central arterial blood pressure is commonly associated with the rewarming phase of cardiopulmonary bypass. Decreased hand vascular resistance has been suggested as a possible mechanism. Although decreased blood viscosity due to hemodilution may contribute to decreased hand vascular resistance, thermoregulatory vascular responses to core hyperthermia also may be important. METHODS: Seven healthy volunteers were studied. Volunteers first were cooled until thermoregulatory vasoconstriction was evident. Next, each was warmed until intense sweating developed. After a cool-down period, general anesthesia was induced with propofol and N2O. Femoral artery pressure (a surrogate for central arterial pressure) and radial artery and oscillometric (brachial artery) pressures were compared during each of six defined thermoregulatory and anesthetic study conditions. To determine the effect of hand vascular resistance on blood pressure differences, measurements were compared before and after occlusion of hand blood flow. Upper-extremity blood flow was evaluated by forearm and fingertip plethysmography and laser Doppler flowmetry. RESULTS: Forearm, fingertip, and cutaneous blood flow increased significantly during warming and were maximal during intense sweating. During thermoregulatory vasoconstriction, femoral, radial, and oscillometric mean blood pressures were similar. In contrast, radial artery mean pressure was 5 +/- 1 mmHg less than femoral artery mean pressure and 12 +/- 8 mmHg less than oscillometric mean pressure during intense sweating. Hand compression reduced these differences. The contour of the radial artery pressure waveform was dramatically altered by thermoregulatory and anesthetic conditions. Radial artery systolic pressure exceeded both femoral artery and oscillometric systolic pressures during vasoconstriction but was less than these during intense sweating. Hand compression reestablished the exaggerated radial artery systolic pressure during all study conditions. CONCLUSIONS: Thermoregulatory and anesthetic-induced alterations in upper-extremity blood flow substantially influence the relations among femoral artery, radial artery, and oscillometric blood pressure measurements.

Absence of nonshivering thermogenesis in anesthetized adult humans.

BACKGROUND: Typically, core temperature rapidly decreases after induction of anesthesia, but reaches a stable plateau after several hours. This plateau typically occurs in conjunction with the onset of thermoregulatory vasoconstriction. Decreased heat loss, caused by vasoconstriction, may not be sufficient to establish thermal steady state without a concomitant increase in heat production. Accordingly, the authors tested the hypothesis that nonshivering thermogenesis contributes to thermal steady state during anesthesia. Rewarming from hypothermia is often associated with an afterdrop (a further reduction in core temperature, despite cutaneous warming). Because total body heat content increases during cutaneous warming, heat storage during afterdrop must reflect increased temperature and heat content of the peripheral tissue mass. Thermal balance was measured during rewarming to estimate the thermal capacity of the peripheral tissues. METHODS: Five volunteers were anesthetized with isoflurane and paralyzed with vecuronium. Oxygen consumption was measured during cooling to a core temperature at least 1 degree C less than that which triggered vasoconstriction. Volunteers were subsequently rewarmed using a circulating-water blanket and forced-air warmer. Oxygen consumption and cutaneous heat flux were measured to assess thermal balance and peripheral tissue heat storage during rewarming. RESULTS: The core temperature threshold for vasoconstriction was 35.2 +/- 0.8 degrees C. Oxygen consumption decreased 9 +/- 5%/degrees C during active cooling before vasoconstriction and 9 +/- 3%/degrees C after vasoconstriction. After the start of rewarming, core temperature continued to decrease for an additional 32 +/- 8 min. The magnitude of this afterdrop was 0.6 +/- 0.1 degree C. Peripheral tissue heat storage measured from the start of rewarming until the first net increase in core temperature was 144 +/- 60 kcal, which approximately equals 2 h of resting metabolic heat production. CONCLUSIONS: The authors concluded that nonshivering thermogenesis is not an important thermoregulatory response in adults anesthetized with isoflurane. Afterdrop and delayed core temperature recovery during rewarming reflect the large heat storage capacity of peripheral tissues.

The effects of preinduction warming on temperature and blood pressure during propofol/nitrous oxide anesthesia.

BACKGROUND: Core temperature decreases rapidly after induction of anesthesia, largely because heat is redistributed to peripheral tissues. The hypothesis that warming peripheral tissues before induction of general anesthesia (prewarming) minimizes hypothermia was tested. Because circulating blood volume may be greater during exposure to heat compared to cold, the hypothesis that prewarming decreases the amount of hypotension associated with induction of anesthesia was tested also. Finally, the hypothesis that the difference between direct radial arterial blood pressure and blood pressure measured oscillometrically at the brachial artery depends on thermoregulatory and anesthetic conditions was tested. METHODS: Each of six volunteers underwent general anesthesia (propofol and nitrous oxide) twice on the same day. Each anesthetic lasted 1 h and was preceded by either 2 h of active warming with forced air or 2 h of passive cooling by exposure to a typical operating room environment. After induction of each anesthetic, volunteers were fully exposed to the ambient environment. Volunteers recovered for 2 h before starting the second preinduction treatment. RESULTS: Initial tympanic membrane temperatures were similar before each preinduction treatment: 36.7 +/- 0.4 degrees C when volunteers were not warmed and 36.7 +/- 0.6 degrees C when volunteers were warmed. Tympanic membrane temperature did not change during the preinduction period without warming but increased slightly (delta T = 0.4 +/- 0.2 degree C) during warming. After induction of anesthesia, core temperatures decreased to 36.1 +/- 0.4 degree C over 1 h when volunteers were prewarmed but decreased to 34.9 +/- 0.4 degrees C when they were not. Radial arterial systolic, diastolic, and mean blood pressures were lower before induction of anesthesia when volunteers were warmed compared to when no warming was given. Oscillometric diastolic and mean pressures also were lower during prewarming; however, oscillometric systolic pressure did not differ significantly. Prewarming did not result in less hypotension after induction. Without warming, the difference (radial arterial minus oscillometric) in systolic blood pressure measurements was approximately 17 mmHg. Warming was associated with a reversal of the systolic pressure difference to approximately -6 mmHg. After induction of anesthesia, the differences in systolic and mean pressure measurements became more negative with respect to the preinduction values regardless of preinduction warming treatment. CONCLUSIONS: These data confirm our hypothesis that redistribution hypothermia can be minimized by preinduction warming of peripheral tissues. Prewarming decreases blood pressure but does not prevent subsequent hypotension after induction. The difference between radical arterial blood pressure and oscillometric blood pressure depends on thermoregulatory vasomotor changes but also may be influenced by vasodilation associated with administration of propofol and nitrous oxide.

Thermoregulatory vasoconstriction during propofol/nitrous oxide anesthesia in humans: threshold and oxyhemoglobin saturation.

To determine the thermoregulatory effects of propofol and nitrous oxide, we measured the threshold for peripheral vasoconstriction in seven volunteers over a total of 13 study days. We also evaluated the effect of vasoconstriction on oxyhemoglobin saturation (SpO2). Anesthesia was induced with an intravenous bolus dose of propofol (2 mg/kg), followed by an infusion of 180 micrograms.kg-1 x min-1 for 15 min, and maintained with 60% nitrous oxide and propofol (80-160 micrograms.kg-1 x min-1). Central and skin surface temperatures and SpO2 (using two different pulse oximeters) were measured continuously; plasma propofol concentrations and arterial PO2 were measured at 15-min intervals. Volunteers were cooled with a circulating water blanket until definitive peripheral vasoconstriction was detected. The tympanic membrane temperature triggering vasoconstriction was considered the thermoregulatory threshold. Vasoconstriction developed on seven study days during propofol/nitrous oxide anesthesia at a central temperature of 33.3 +/- 1.0 degrees C (mean +/- SD) and plasma propofol concentration of 3.9 +/- 1.1 micrograms/mL. The thresholds during anesthesia were significantly lower than those during the control period (36.7 +/- 0.3 degrees C), but the correlation between plasma propofol concentrations and vasoconstriction thresholds was poor. On the remaining six study days, vasoconstriction did not develop despite central temperatures ranging from 32.1 to 32.7 degrees C. Corresponding propofol concentrations were 4.1-10.9 micrograms/mL. These data suggest that anesthesia with propofol, in typical clinical concentrations, and 60% nitrous oxide substantially inhibits thermoregulatory vasoconstriction. Vasoconstriction increased SpO2 by approximately 2% without a significant concomitant change in PO2. The observed increase in SpO2 probably reflects decreased transmission of arterial pulsations to venous blood in the finger.

Intraoperative warming therapies: a comparison of three devices.

STUDY OBJECTIVE: To compare the effectiveness of three commonly used intraoperative warming devices. DESIGN: A randomized, prospective clinical trial. SETTING: The surgical suite of a university medical center. PATIENTS: Twenty adult patients undergoing kidney transplantation for end-stage renal disease. INTERVENTIONS: Patients were assigned to one of four warming therapy groups: circulating-water blanket (40 degrees C), heated humidifier (40 degrees C), forced-air warmer (43 degrees C, blanket covering legs), or control (no extra warming). Intravenous fluids were warmed (37 degrees C), and fresh gas flow was 5 L/min for all groups. No passive heat and moisture exchangers were used. MEASUREMENTS AND MAIN RESULTS: The central temperature (tympanic membrane thermocouple) decreased approximately 1 degree C during the first hour of anesthesia in all groups. After three hours of anesthesia, the decrease in the tympanic membrane temperature from baseline (preinduction) was least in the forced-air warmer group (-0.5 degrees C +/- 0.4 degrees C), intermediate in the circulating-water blanket group (-1.2 degrees C +/- 0.4 degrees C), and greatest in the heated humidifier and control groups (-2.0 degrees C +/- 0.5 degrees C and -2.0 degrees C +/- 0.7 degrees C, respectively). Total cutaneous heat loss measured with distributed thermal flux transducers was approximately 35W (watts = joules/sec) less in the forced-air warmer group than in the others. Heat gain across the back from the circulating-water blanket was approximately 7W versus a loss of approximately 3W in patients lying on a standard foam mattress. CONCLUSION: The forced-air warmer applied to only a limited skin surface area transferred more heat and was clinically more effective (at maintaining central body temperature) than were the other devices. The characteristic early decrease in central temperature observed in all groups regardless of warming therapy is consistent with the theory of anesthetic-induced heat redistribution within the body.

Isoflurane, but not mild hypothermia, depresses the human pupillary light reflex.

The pupillary light reflex is often evaluated in the perioperative period as a measure of cranial nerve and midbrain integrity. Although surgical concentrations of some anesthetic agents and severe hypothermia qualitatively alter the light reflex, confounding factors frequently present during postanesthetic recovery have not been specifically quantified. We therefore studied 12 volunteers to determine the effects of residual isoflurane concentrations and typical (mild) hypothermia on the human pupillary light reflex. Young, healthy volunteers were assigned to one of three treatments: 1) normothermic isoflurane-oxygen anesthesia; 2) isoflurane-oxygen anesthesia with 2.2 +/- 0.5 degree C central hypothermia; and 3) central hypothermia (1.6 +/- 0.3 degree C) without anesthesia, induced by internal jugular infusion of iced lactated Ringer's solution. In normothermic anesthetized volunteers, the amplitude of the light reflex was depressed 80-90% at end-tidal concentrations greater than 0.5% isoflurane: reflex (percent of control) = 14 - 67.log (percent isoflurane); r = -0.92. In the mildly hypothermic anesthetized volunteers, pupillary responses were not statistically different from those in anesthetized normothermic volunteers: reflex (percent of control) = 16 - 62.log (percent isoflurane); r = -0.97. Hypothermia alone did not alter the magnitude of the light reflex. Our data suggest that mild hypothermia does not depress the light reflex but that isoflurane reversibly depresses the light reflex in a dose-related manner.

Thermal balance and tremor patterns during epidural anesthesia.

Five healthy, nonpregnant volunteers were studied before and after induction of lumbar epidural anesthesia to determine the cause of central hypothermia during epidural anesthesia. Cutaneous heat loss was measured from 10 area-weighted sites using thermal flux transducers. Oxygen consumption was measured and converted to heat production in watts (W). After a 2-h control period at approximately 20 degrees C, epidural anesthesia was induced by injection of 30-50 ml 3% chloroprocaine. Additional boluses were given to extend the sensory blockade to at least the T5 dermatome. Tremor during epidural anesthesia was compared with normal shivering induced by rapid central venous infusion of approximately 4 l iced saline in six unanesthetized volunteers. Average skin temperature and cutaneous heat loss decreased during the control period, while tympanic membrane temperature remained stable. During the 1st h of epidural blockade, tympanic membrane temperature decreased 1.1 +/- 0.3 degrees C, and average skin temperature increased 0.9 +/- 0.5 degrees C. Cutaneous heat loss increased 16 +/- 6% (15 +/- 5 W), but metabolic heat production increased even more (and was associated with a shivering-like tremor). Tremor during epidural anesthesia and shivering induced by iced saline infusion had similar synchronous waxing-and-waning patterns. No abnormal EMG patterns were detected during epidural anesthesia. We conclude that central hypothermia during the 1st h of epidural anesthesia does not result from heat loss to the environment in excess of metabolic heat production, but results primarily from redistribution of body heat from central to peripheral tissues. Analysis of the tremor patterns suggests that oscillations recorded during epidural anesthesia in nonpregnant individuals is normal thermoregulatory shivering. Shivering occurred sooner and was more intense during iced saline infusion than during epidural anesthesia, despite comparable central hypothermia. The low intensity of shivering during epidural anesthesia, and in some individuals the delay in onset, may result from blockade of afferent cutaneous cold signals.