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D I Sessler

Publications and source records attributed to D I Sessler.

At least 19 recordsLinked to original sources

Thermoregulatory thresholds for vasoconstriction in pediatric patients anesthetized with halothane or halothane and caudal bupivacaine.

The thermoregulatory threshold for vasoconstriction has been studied in infants and children given isoflurane, but not in those given halothane anesthesia. More importantly, the effect of vasoconstriction on central temperature in pediatric patients remains unknown. Also unknown is the effect of caudal analgesia on vasoconstriction thresholds. Accordingly, in the first portion of this study, we determined the central thermoregulatory threshold in 23 infants and children given approximately 0.6% halothane and caudal anesthesia for abdominal surgery. Patients were prospectively assigned to one of four weight groups: 5-10, 10-20, 20-30, and 30-50 kg. The threshold was considered the central temperature triggering peripheral vasoconstriction, and significant vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. Thresholds were similar (approximately 35.7 degrees C) in each study group, suggesting that thermoregulatory responses to halothane anesthesia are similar in infants and children of differing weights. However, they were higher than expected based on the previously reported thresholds in pediatric patients given isoflurane anesthesia. After peripheral vasoconstriction, central temperature continued to decrease in patients weighing more than 30 kg but remained constant or increased slightly in the others. These data suggest that thermoregulatory responses are more effective in infants and small children than in bigger children or adults. In the second part of this study we evaluated the effect of caudal analgesia on the thermoregulatory threshold for vasoconstriction. Children undergoing hypospadias repair were anesthetized with halothane (0.9%) and oxygen. Following induction, they were randomly assigned to caudal analgesia (n = 7) or penile nerve block (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Caudal

Thermoregulatory vasoconstriction during isoflurane anesthesia minimally decreases cutaneous heat loss.

The authors tested the extent to which thermoregulatory vasoconstriction decreases cutaneous heat loss during isoflurane anesthesia. Thermoregulatory vasoconstriction was provoked by central hypothermia in five nonsurgical volunteers given isoflurane anesthesia. Peripheral arteriovenous shunt flow was quantified using forearm-fingertip skin-surface temperature gradients and volume plethysmography. Capillary blood flow on the chest was evaluated using laser Doppler flowmetry. The central temperature triggering peripheral vasoconstriction (the thermoregulatory threshold) was 34.6 +/- 0.4 degrees C. Central body temperature decreased less than or equal to 0.2 degrees C in the period from 1 h preceding onset of significant vasoconstriction until 1.5 h afterward. Chest skin-surface blood flow decreased 21% during the period from 2 h before to 1 h after significant fingertip vasoconstriction. In contrast, fingertip blood flow decreased approximately 50-fold in the same period. The correlation between fingertip blood flow and skin-temperature gradient was excellent. Total heat loss decreased approximately 26% (25.3 +/- 3.9 W) in the period from 2 h before significant peripheral vasoconstriction to 1 h afterward. Loss from the arms and legs (upper arm, lower arm, thigh, and calf) decreased approximately 24% in the same period. Heat loss from the trunk and head decreased only 14%; in contrast, loss from the hands and feet decreased approximately 57%. There were no clinically important changes in blood pressure or heart rate during vasoconstriction, but oxyhemoglobin saturation (measured by pulse oximetry) increased slightly. These data suggest that thermoregulatory vasoconstriction only minimally decreases cutaneous heat loss.

Adult

Central temperature changes are poorly perceived during epidural anesthesia.

Hypothermia and shivering are common during epidural anesthesia for cesarean delivery but are not always accompanied by a sensation of coldness. To test the hypothesis that central temperature changes are not perceived during epidural anesthesia, we measured central and skin temperatures and thermal perception in 30 patients undergoing cesarean delivery with epidural anesthesia. Central temperature decreased 1.0 +/- 0.6 degrees C from control values during anesthesia and surgery, but thermal perception scores did not reflect central temperatures (P = 0.56) or changes in central temperature (P = 0.63). A feeling of warmth was significantly correlated with increased mean skin temperature (P = 0.02) and increased upper body skin temperature (P = 0.03). We conclude that central temperature is poorly perceived and is less important than skin temperature in determining thermal perception during high levels of epidural anesthesia.

Adult

Painful stimulation minimally increases the thermoregulatory threshold for vasoconstriction during enflurane anesthesia in humans.

Generalized autonomic stimulation enhances hemodynamic responses and may, in a similar fashion, facilitate thermoregulatory responses. We thus tested the hypothesis that painful stimulation increases the central temperature threshold for vasoconstriction during general anesthesia. Healthy volunteers were anesthetized with 1.3% end-tidal enflurane on 2 separate days. On 1 day (randomly assigned), painful stimulation was produced by tetanic electrical stimulation. On the other day, electrical stimulation was not given. Significant thermoregulatory vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. The distal esophageal temperature triggering significant vasoconstriction was considered the thermoregulatory threshold. The threshold was 35.5 +/- 0.8 degrees C during electrical stimulation and 35.1 +/- 0.6 degrees C without stimulation (P = 0.050, 95% confidence interval for the difference = 0-0.7 degree C). These data suggest that thresholds determined in nonsurgical volunteers will be slightly (but not clinically significantly) less than those in operative patients. Similarly, intraoperative vasoconstriction thresholds likely will be slightly less when surgical pain is prevented by simultaneous regional or local analgesia.

Adult

Limb tourniquets and central temperature in anesthetized children.

We have observed an association between the use of tourniquets for limb surgery and a progressive increase in body temperature in pediatric patients. Consequently, we evaluated the effect of leg tourniquet(s) on intraoperative nasopharyngeal temperature in pediatric patients. We measured central temperature in three groups of children anesthetized with halothane and nitrous oxide: those with unilateral tourniquets (n = 15), those with bilateral tourniquets (n = 8), and a control group not requiring tourniquets (n = 24). Intraoperative ambient temperatures were maintained near 23 degrees C, respiratory gases were actively heated and humidified, and skin was warmed using a circulating water blanket set at 38 degrees C. The control patients remained normothermic during anesthesia and surgery. In contrast, central temperature increased 1.0 +/- 0.6 degrees C in 90 min in those with one tourniquet and 1.7 +/- 0.6 degrees C in those with bilateral tourniquets. The tourniquet-induced hyperthermia appeared to result from decreased effective heat loss from distal skin and from constraint of metabolic heat to the central thermal compartment. These data suggest that pediatric patients requiring intraoperative tourniquets should not be aggressively warmed during surgery.

Anesthesia

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.

Adult

Improved preservation of skeletal muscle in amputated limbs using pulsatile hypothermic perfusion with University of Wisconsin solution. A preliminary study.

To determine whether pulsatile hypothermic perfusion with University of Wisconsin preservation solution is superior to topical cooling as a method for the preservation of amputated limbs, six pairs of amputated canine limbs were preserved for twelve to fifteen hours. One limb of each pair was subjected to topical cooling and the other, to pulsatile hypothermic perfusion with University of Wisconsin solution. The bioenergetic status of the limbs was monitored by 31phosphorus magnetic-resonance spectroscopy, and histological evaluation was performed to assess ischemic changes in the preserved tissue. The pH and tissue levels of adenosine triphosphate declined three times more slowly in the limbs that were preserved by pulsatile hypothermic perfusion than in the topically cooled limbs. Consistent with these findings, the perfused limbs also had less histological evidence of ischemic injury. The data from this in vitro study show that pulsatile hypothermic perfusion with University of Wisconsin solution, in combination with an optimum degree of topical cooling, is superior to topical cooling alone as a method of preserving the bioenergetic status of amputated limbs.

Adenosine

Limited heat transfer between thermal compartments during rewarming in vasoconstricted patients.

Thermoregulatory vasoconstriction may serve to separate and limit heat transfer between peripheral and central thermal compartments, in effect providing a thermal buffer for central temperature. We hypothesized that thermoregulatory vasoconstriction would limit heat transfer to the central compartment in patients warmed cutaneously. Hypothermic patients (central temperatures < 35 degrees C) recovering from surgery were randomly assigned to receive forced-air warming (n = 6) or warmed cotton blankets (n = 6). The forced-air warmer delivers approximately 50 W of heat, compared to a heat loss of approximately 50 W with warmed cotton blankets. Despite a significantly greater increase in mean skin-surface temperature with forced-air warming, central temperature in the two groups did not significantly differ. All patients vasoconstricted and there was no difference in oxygen consumption between groups. These data confirm that thermoregulatory vasoconstriction limits heat transfer from peripheral to central thermal compartments and impedes skin surface warming of the body core.

Blood Pressure

Comparison of four objective methods of monitoring digital venous congestion.

This study sought to determine which of the four most commonly used objective monitoring modalities--pulse oximetry, laser Doppler flowmetry, skin surface temperature measurement, and skin surface fluorescence--is best able to detect early digital venous congestion. Digital venous congestion was induced in 12 hands by inflating a digital cuff to 5 mm Hg above the resting diastolic pressure. The cuff remained inflated for 1 hour while monitoring was done at 10-minute intervals. The baseline and experimental laser Doppler indices differed by at least 30% in each subject, and the laser Doppler index was always less than 40% during venous congestion. Skin surface fluorescence gave falsely normal results in three of eight hands, while pulse oximetry failed to detect venous congestion in any hand. The difference in temperature between the control and experimental fingers almost always exceeded the threshold of 2.5 degrees C. The results indicate that both laser Doppler flowmetry and skin surface temperature measurement are highly accurate methods of monitoring early digital venous congestion that are noninvasive and easy to use. Skin surface temperature measurement has further advantages in that thermometers are less expensive and easier to transport than laser Doppler devices. In contrast, skin surface fluorescence is invasive and cumbersome in addition to being less sensitive to experimentally induced early digital venous congestion than either laser Doppler flowmetry or skin surface temperature measurement. Pulse oximetry is unreliable in detecting early digital venous congestion.

Adult

The Allen's test: analysis of four methods.

Forty nonrandomly selected hands were studied with use of four types of Allen's test: (1) the digital systolic blood pressure method, (2) the subjective method, (3) the pulse oximeter method, and (4) the laser Doppler flowmetry method. The digital systolic blood pressure method, regarded as the standard, indicated abnormal pressure in three hands. Laser Doppler flowmetry gave the same results as those obtained by the digital systolic pressure method and, in addition, was easier to perform. Pulse oximetry falsely indicated adequacy of the collateral circulation in two of the three hands with abnormal digital systolic pressure. Eleven hands, including the three with abnormal digital systolic pressure, were abnormal according to the subjective method. The results of the present study indicate the following: (1) the laser Doppler Allen's test is accurate, quick, and easy to perform; (2) the pulse oximeter Allen's test should not be used because of potentially dangerous consequences to the patient in the event of a falsely normal result; and (3) the subjective Allen's test can be used as a quick screening test.

Adult

Isoflurane-induced vasodilation minimally increases cutaneous heat loss.

Central body temperature, which usually is well controlled, typically decreases more than 1 degree C during the 1st h of general anesthesia. This hypothermia has been attributed partially to an anesthetic-induced peripheral vasodilation, which increases cutaneous heat loss to the environment. Based on the specific heat of humans, heat loss would have to increase more than 70 W for 1 h (in a 70-kg person) to explain hypothermia after induction of general anesthesia. However, during epidural anesthesia, sympathetic blockade increases heat loss only slightly. Furthermore, thermoregulatory vasoconstriction in unanesthetized humans decreases heat loss to the environment only 15 W. Therefore, we tested the hypothesis that the hypothermia that follows induction of general anesthesia does not result from increased cutaneous heat loss. Heat loss and skin-surface and tympanic membrane temperatures, before and after induction of isoflurane anesthesia, were measured in five minimally clothed volunteers. Peripheral skin blood flow was evaluated with venous-occlusion volume plethysmography and skin-surface temperature gradients. Cutaneous heat losses in watts were summed from ten area-weighted thermal flux transducers. Tympanic membrane temperature, which was stable during the 30-min control period preceding induction, decreased 1.2 +/- 0.2 degrees C in the 50 min after induction. Isoflurane anesthesia decreased mean arterial blood pressure approximately 20%. Average skin-surface temperature increased over 15 min to 0.5 degree C above control. Heat loss from the trunk, head, arms, and legs decreased slightly, whereas loss from the hands and feet (10.5% of the body surface area) doubled (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

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.

Adult

Mild intraoperative hypothermia increases duration of action and spontaneous recovery of vecuronium blockade during nitrous oxide-isoflurane anesthesia in humans.

We compared the duration of action and recovery times for vecuronium in normothermic and mildly hypothermic patients. Ten patients were actively cooled to a central body temperature near 34.5 degrees C, and ten were maintained at a normothermic central temperature (greater than 36.5 degrees C); temperature was measured in the distal esophagus. Vecuronium 0.1 mg/kg was administered as an intravenous (iv) bolus to all patients, and the evoked mechanical response to train-of-four stimulation was recorded. Five hypothermic and five normothermic patients were allowed to recover spontaneously. In the remaining five in each group, neostigmine (40 micrograms/kg) and atropine (20 micrograms/kg) was administered when the first twitch (T1) height spontaneously recovered to 10% of control (T1 = 10% of the pre-vecuronium twitch tension). Vecuronium's duration of action (from injection of drug until T1 = 10%) was 28 +/- 4 and 62 +/- 8 min during normothermia and hypothermia, respectively (P less than 0.05). The corresponding values for spontaneous recovery from T1 = 10% to TOF ratio greater than 75% were 37 +/- 15 and 80 +/- 24 min (P less than 0.05), and for neostigmine-induced recovery were 10 +/- 3 and 16 +/- 11 min (difference not significant). We conclude that mild hypothermia increases the duration of action of and time for spontaneous recovery from vecuronium-induced neuromuscular blockade.

Adult

Perioperative thermal insulation.

To determine the efficacy of passive insulators advocated for prevention of cutaneous heat loss, we determined heat loss in unanesthetized volunteers covered by one of the following: a cloth "split sheet" surgical drape; a Convertors disposable-paper split sheet; a Thermadrape disposable laparotomy sheet; an unheated Bair Hugger patient-warming blanket; 1.5-mil-thick plastic hamper bags; and a prewarmed, cotton hospital blanket. Cutaneous heat loss was measured using 10 area-weighted thermal flux transducers while volunteers were exposed to a 20.6 degrees C environment for 1 h. Heat loss decreased significantly from 100 +/- 3 W during the control periods to 69 +/- 6 W (average of all covers) after 1 h of treatment. Heat losses from volunteers insulated by the Thermadrape (61 +/- 6 W) and Bair Hugger covers (64 +/- 5 W) were significantly less than losses from those insulated by plastic bags (77 +/- 11 W). The paper drape (67 +/- 7 W) provided slightly, but not significantly, better insulation than the cloth drape (70 +/- 4 W). Coverage by prewarmed cotton blankets initially resulted in the least heat loss (58 +/- 8 W), but after 40 min, resulted in heat loss significantly greater than that for the Thermadrape (71 +/- 7 W). Regional heat loss was roughly proportional to surface area, and the distribution of regional heat loss remained similar with all covers. These data suggest that cost and convenience should be major factors when choosing among passive perioperative insulating covers. It is likely that the amount of skin surface covered is more important than the choice of skin region covered or the choice of insulating material.

Adult

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.

Adult

Physiologic responses to mild perianesthetic hypothermia in humans.

To evaluate physiologic responses to mild perianesthetic hypothermia, we measured tympanic membrane and skin-surface temperatures, peripheral vasoconstriction, thermal comfort, and muscular activity in nine healthy male volunteers. Each volunteer participated on three separate days: 1) normothermic isoflurane anesthesia; 2) hypothermic isoflurane anesthesia (1.5 degrees C decrease in central temperature); and 3) hypothermia alone (1.5 degrees C decrease in central temperature) induced by iced saline infusion. Involuntary postanesthetic muscular activity was considered thermoregulatory when preceded by central hypothermia and peripheral cutaneous vasoconstriction. Tremor was considered normal shivering when electromyographic patterns matched those produced by cold exposure in unanesthetized individuals. During postanesthetic recovery, central temperatures in hypothermic volunteers increased rapidly when residual end-tidal isoflurane concentrations were less than or equal to 0.3% but remained 0.5 degree C less than control values throughout 2 h of recovery. All volunteers were vasodilated during isoflurane administration. Peripheral vasoconstriction occurred only during recovery from hypothermic anesthesia, at end-tidal isoflurane concentrations of less than approximately 0.4%. Spontaneous tremor was always preceded by central hypothermia and peripheral vasoconstriction, indicating that muscular activity was thermoregulatory. Maximum tremor intensity during recovery from hypothermic anesthesia occurred when residual end-tidal isoflurane concentrations were less than or equal to 0.4%. Three patterns of postanesthetic muscular activity were identified. The first was a tonic stiffening that occurred in some normothermic and hypothermic volunteers when end-tidal isoflurane concentrations were approximately 0.4-0.2%. This activity appeared to be largely a direct, non-temperature-dependent effect of isoflurane anesthesia. In conjunction with lower residual anesthetic concentrations, stiffening was followed by a synchronous, tonic waxing-and-waning pattern and spontaneous electromyographic clonus, both of which were thermoregulatory. Tonic waxing-and-waning was by far the most common pattern and resembled that produced by cold-induced shivering in unanesthetized volunteers; it appears to be thermoregulatory shivering triggered by hypothermia. Spontaneous clonus resembled flexion-induced clonus and pathologic clonus and did not occur during hypothermia alone; it may represent abnormal shivering or an anesthetic-induced modification of normal shivering. We conclude that among the three patterns of muscular activity, only the synchronous, tonic waxing-and-waning pattern can be attributed to normal thermoregulatory shivering.

Adult