Olga Plattner

The Threshold for Thermoregulatory Vasoconstriction during Nitrous Oxide/Isoflurane Anesthesia Is Lower in Elderly Than in Young Patients

Background:Thermoregulatory vasoconstriction minimizes further core hypothermia during anesthesia. Elderly patients become more hypothermic during surgery than do younger patients, and take longer to rewarm postoperatively. These data indicate that perianesthetic thermoregulatory responses may be especially impaired in the elderly. Accordingly, the authors tested the hypothesis that the thermoregulatory threshold for vasoconstriction during nitrous oxide/isoflurane anesthesia is reduced more in elderly than in young patients. Methods:The authors studied 12 young patients aged 30–50 yr and 12 elderly patients aged 60–80 yr. All were undergoing major orthopedic or open abdominal surgery. Anesthesia was induced with thiopental and fentanyl, and maintained only with nitrous oxide (70%) and isoflurane (0.6–0.8%). Core temperature was measured in the distal esophagus. Fingertip vasoconstriction was evaluated using forearm minus fingertip, skin-temperature gradients. A gradient of 4° C identified significant vasoconstriction, and the core temperature triggering vasoconstriction identified the thermoregulatory threshold. Results:The vasoconstriction threshold was significantly less in the elderly patients (33.9 ± 0.6° C) than in the younger ones (35.1 ± 0.3° C) (P < 0.01). The gender distribution, weight, and height of the elderly and young patients did not differ significantly. The end-tidal isoflurane concentration at the time of vasoconstriction did not differ significantly in the two groups. Conclusions:These data indicate that thermoregulatory responses in the elderly are initiated at temperatures ≈ 1.2° C less than that in younger patients. Thus, it is likely that elderly surgical patients become more hypothermic than do younger patients, at least in part, because they fail to trigger protective thermoregulatory responses.

Local radiant heating increases subcutaneous oxygen tension

BACKGROUND We evaluated a novel bandage that incorporates a thermostatically controlled radiant heater. We first determined optimal bandage temperature, based on increases in subcutaneous oxygen tension, a measure correlating well with resistance to infection and wound strength. We then tested the hypothesis that prolonged radiant heating would increase collagen deposition in experimental thigh wounds. METHODS The experimental bandages were positioned on the anterior thigh of 8 volunteers, and heated for 2 hours at 38 degrees C, 42 degrees C, or 46 degrees C, in a random order. Subcutaneous oxygen tension under the bandage was recorded from an electrode positioned within a subcutaneous tonometer. We studied 10 volunteers in the second protocol. For 1 week, the experimental bandage was continuously applied to one thigh, and heated to 38 degrees C using a 2-hour on/off cycle. On the alternate week, a standard gauze bandage was applied to the contralateral thigh. Treatment order was randomly assigned. Wound collagen deposition under each bandage was evaluated with subcutaneous polytetrafluoroethylene tubes, which were removed and assayed for hydroxyproline on the eighth day. Data are presented as means +/- SDs. RESULTS Skin temperature during heating ranged from 36 degrees C to 37.5 degrees C. Oxygen tension increased approximately 50% during heating, but the increase was comparable at the three tested temperatures. Even after heating was discontinued, subcutaneous oxygen tension remained elevated for the remaining 3 study hours. Collagen deposition after 1 week of active heating was 3.4 +/- 1.0 microg/ cm. After 1 week of control treatment, collagen deposition was 3.2 +/- 1.1 microg/cm (P = not significant). CONCLUSIONS Our data suggest that radiant heating at 38 degrees C significantly increases subcutaneous oxygen tension, and presumably resistance to infection. However, prolonged heating at this temperature does not increase wound collagen deposition.

Postanesthetic vasoconstriction slows peripheral-to-core transfer of cutaneous heat, thereby isolating the core thermal compartment

Forced-air warming during anesthesia increases core temperature comparably with and without thermoregulatory vasoconstriction. In contrast, postoperative forced-air warming may be no more effective than passive insulation. Nonthermoregulatory anesthesia-induced vasodilation may thus influence heat transfer. We compared postanesthetic core rewarming rates in volunteers given cotton blankets or forced air. Additionally, we compared increases in peripheral and core heat contents in the postanesthetic period with data previously acquired during anesthesia to determine how much vasomotion alters intercompartmental heat transfer. Six men were anesthetized and cooled passively until their core temperatures reached 34 [degree sign] C. Anesthesia was then discontinued, and shivering was prevented by giving meperidine. On one day, the volunteers were covered with warmed blankets for 2 h; on the other, volunteers were warmed with forced air. Peripheral tissue heat contents were determined from intramuscular and skin thermocouples. Predicted changes in core temperature were calculated assuming that increases in body heat content were evenly distributed. Predicted changes were thus those that would be expected if vasomotor activity did not impair peripheral-to-core transfer of applied heat. These results were compared with those obtained previously in a similar study of anesthetized volunteers. Body heat content increased 159 +/- 35 kcal (mean +/- SD) more during forced-air than during blanket warming (P < 0.001). Both peripheral and core temperatures increased significantly faster during active warming: 3.3 +/- 0.7[degree sign]C and 1.1 +/- 0.4[degree sign]C, respectively. Nonetheless, predicted core temperature increase during forced-air warming exceeded the actual temperature increase by 0.8 +/- 0.3[degree sign]C (P < 0.001). Vasoconstriction thus isolated core tissues from heat applied to the periphery, with the result that core heat content increased 32 +/- 12 kcal less than expected after 2 h of forced-air warming (P < 0.001). In contrast, predicted and actual core temperatures differed only slightly in the anesthetized volunteers previously studied. In contrast to four previous studies, our results indicate that forced-air warming increases core temperature faster than warm blankets. Postanesthetic vasoconstriction nonetheless impeded peripheral-to-core heat transfer, with the result that core temperatures in the two groups differed less than might be expected based on systemic heat balance estimates. Implications: Comparing intercompartmental heat flow in our previous and current studies suggests that anesthetic-induced vasodilation influences intercompartmental heat transfer and distribution of body heat more than thermoregulatory shunt vasomotion. (Anesth Analg 1997;85:899-906)

Effective pain relief with continuous intrapleural bupivacaine after thoracotomy in infants and children

The effect of continuous intrapleural bupivacaine on pain relief after lateral thoracotomy was studied in nine infants (≤ 15 kg body weight) and 11 children (> 15 kg body weight). An intrapleural catheter was inserted under direct vision during surgery. After extubation, the patients were transferred to the ICU where vital signs and pain scores were monitored. An intrapleural infusion of bupivacaine 0.25% with adrenaline was given at a loading dose of 0.625 mg˙kg−1 body weight followed by a continuous infusion with a starting rate of 1.25 mg˙kg−1˙h−1. Haemodynamic and respiratory parameters did not differ significantly from control values throughout the study period in either group. The mean infusion rate could be reduced stepwise in both groups to 0.75 ± 0.32 mg˙kg−1˙h−1 and 0.73 ± 0.38 mg˙kg−1˙h−1 respectively. The pain score indicated a rapid onset of analgesia in both groups and remained low during the study period. The degree of analgesia amongst other factors was position dependent. The lack of any recognizable side effects or complications related to this method has been most encouraging. Only one child required a supplementary dose of an opioid. We conclude that continuous intrapleural access has proved to be a safe and suitable route for pain relief in infants and children following thoracotomy.

Pharyngeal Oxygen Insufflation During Airtraq Laryngoscopy Slows Arterial Desaturation in Infants and Small Children

BACKGROUND:The extent to which insufflation of oxygen into the posterior pharynx during laryngoscopy prolongs adequate saturation in infants and small children remains unknown. Therefore, we compared oxygen saturation over time in preoxygenated small children with and without posterior pharynx oxygen insufflation. METHODS:After induction of anesthesia with sevoflurane and propofol, infants and small children were preoxygenated with 100% oxygen for 3 minutes. An AirTraq laryngoscope size 0 or 1 with an appropriately sized cuffed endotracheal tube positioned in the side channel was prepared. Oxygen tubing was connected to the endotracheal U-shaped tube. However, oxygen at a flow of 4 L/min was provided only to half of the randomly selected participating patients. The trachea was intubated, the tube cuff was inflated, and the laryngoscope was removed from the mouth. The oxygen tubing was disconnected from the endotracheal tube and left exposed to ambient air until oxygen saturation decreased to 95%. Thereafter, patients’ lungs were manually ventilated with 100% oxygen until SpO2 returned to 100%. Subsequent anesthetic management was at the discretion of the attending anesthesiologist. RESULTS:Laryngoscopy took a median of 60 (Q1–Q3, 40–90) seconds. The mean time to 95% oxygen saturation was (mean ± SD) 166 ± 47 seconds in the oxygen insufflation group and 131 ± 39 seconds in small children without insufflation. Oxygen insufflation prolonged the mean time for saturation to decrease from 100% to 95% by an estimated 35 (95% confidence interval, 10–60) seconds, P = 0.01. CONCLUSIONS:Adding posterior pharyngeal oxygen insufflation to conventional preoxygenation prolonged the period of adequate oxygen saturation in infants and small children by an amount that is potentially clinically important.

Thermoregulatory vasoconstriction does not impede core warming during cutaneous heating.

Recent studies evaluating perioperative cutaneous-to-core heat transfer indicate that: Thermoregulatory vasoconstriction prevents further core cooling in anesthetized subjects during mild cooling. Thermoregulatory vasoconstriction only slightly decreases core cooling rates in anesthetized subjects during vigorous cooling. Thermoregulatory vasoconstriction does not impair vigorous core rewarming during anesthesia. Vigorous postanesthetic cutaneous warming increases core temperature much faster than passive insulation. Under conditions of mild thermal stress, thermoregulatory vasoconstriction is thus able to protect core temperature by reducing cutaneous heat transfer and functionally isolating the peripheral and core thermal compartment. Consequently, anesthetic-induced alterations in vasomotor tone is one of the major factors influencing core temperature in patients who are not actively cooled or warmed. In contrast, thermoregulatory tone is insufficient to prevent core temperature perturbations in patients undergoing vigorous cutaneous cooling or warming.