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Perioperative Hypothermia: A Hot Topic in Anesthesia Shea Aiken, MD PACU September 2009 A 67 year old female with a history

notable only for controlled hypertension and hypercholesterolemia presented to Stanford University Hospital where she was scheduled for laparoscopic removal of a hepatic cystic lesion, which was discovered during work-up for right upper quadrant pain. Her labs were unremarkable with a hematocrit of 40. She was on a statin and atenalol, with a resting heart rate of 58 bpm. She was brought back to the operating room in her usual state of health following standard premedication, and underwent an uneventful intravenous induction followed by inhalational maintenance general endotracheal anesthesia. The nursing staff placed a Foley catheter, orogastric decompression was performed by the anesthesiologist, and an esophageal temperature probe was positioned. The initial recorded temperature was 36.1C. A lower body Bair Hugger was placed on the patient, attached, and turned on. The circulating RN then asked the anesthesia resident to temporarily turn the Bair Hugger off while she prepped the patient for surgery, fearing that it would blow air into her sterile field. The resident did so, and the usual prep and drape proceeded without incident. The intraoperative course was complicated by unexpected large volume blood loss and significant oozing from the liver following resection of the hepatic cyst. Total blood loss totaled 1.2L for the case, and was reportedly discreet in that the patient never mounted a tachycardia (nor increased HR above 65), nor did she become hypotensive. The anesthesiologist reported that by the time he was notified about blood loss in the surgical field a VBG showed a pH of 7.18, base deficit of 12 and a Hct of 34. A 14g PIV was placed, and resuscitation was initiated. The patient had received 3.8L of crystalloid and 500ml of hetastarch when the first unit of blood arrived, at which point the anesthesiologist attached the IV tubing to a fluid warmer. The temperature was noted to have dropped nearly a full degree Celsius over the previous 30 minutes, and was recorded at 34.9C. It was at that point that the anesthesiologist noticed that the Bair Hugger had never been turned back on. The patient was resuscitated with a total of 4.8L of crystalloid, 500ml of hetastarch and 1 unit of PRBCs. The room temperature was turned all the way up, and following the end of the surgical procedure an additional upper body Bair Hugger was placed. The anesthesia team delayed awakening the patient for 45 minutes following closure to warm the patient, and upon reaching 35C the volatile agent was turned off, the patient awoke, was following commands, and was extubated. On arrival to the PACU she had a recorded oral temperature of 34.8C.

Discussion: The case above isnt entirely unusual and often times goes without significant concern, however as Medicare institutes its new quality control reimbursement guidelines for perioperative hypothermia cases like this will undoubtedly headline many discussions. As it currently stands, Medicare is prepared to reward those anesthesiologists who prioritize avoiding hypothermia by placing forced air warmers intraoperatively, or can document a temperature of 36C 30 minutes prior to the end of case, or within 15 minutes following arrival to the PACU. Those practitioners who fail to meet these criteria will not be reimbursed for the case. Medicares decision to implement such a policy isnt without substantiation, although it can be easily argued that outcome data is lacking in robustness. Nevertheless, it carries the potential to have significant negative impacts on reimbursement, and thus requires that each anesthesiologist understand the mechanisms, prevention, and treatment strategies of perioperative hypothermia. The human body maintains normal thermoregulation through a process of afferent thermal sensing, processing, and efferent responses. Heat and cold receptors are widely distributed in the body, with cold signals traveling along A delta fibers, and warm receptors being conveyed by C fibers. The messages conveyed from the skin surface, deep abdominal and thoracic tissue, and spinal cord are sent to the thermoregulatory control center of the body, the hypothalamus. Efferent responses then leave the hypothalamus and primarily result in both physiological and behavioral adaptations (such as changing to warmer clothes, or adjusting the ambient room temperature). The main autonomic changes against heat are sweating and active cutaneous vasodilatation, where as changes to cold involves thermoregulatory vasoconstriction in arteriovenous shunts located primarily in fingers and toes, and nonshivering thermogenesis (mostly in children) and shivering.1 The problem, when it comes to temperature regulation, with general anesthesia is that it removes a patients ability to regulate temperature through behavior. It also inhibits thermoregulation in a dose dependent manner by inhibiting vasoconstriction and shivering. The resulting redistribution of body heat from the core to the periphery decreases the core temperature from 1C to 1.5C during the first hour of general anesthesia.1 Complicating the matter is the use of muscle relaxants, which also inhibit shivering. Furthermore, volatile anesthetics, opioids and propofol all lower the thresholds for vasoconstriction and shivering.2,3 As a result, patients become poikilothermic (reptile like), with body temperatures that are determined by the environment. Approximately 90% of all heat is lost through the surface of the skin, with radiation and convection usually contributing far more to the process than evaporation or conduction.1 The core temperature begins to level off after the first hour, then generally stops dropping after 3 to 5 hours of anesthesia, at which point the body has reached an equilibrium between heat loss and heat production. The hypothermic conundrum encountered with general anesthetics cannot be avoided through use of neuraxial anesthesia. Because all thermoregulatory responses are neurally mediated, by their very nature neuraxial nerve blocks will inhibit these mechanisms. The

problem is magnified by the fact that not only are afferent and efferent signals disrupted, the central processing center (the hypothalamus) interprets input from blocked regions as being abnormally high. Furthermore, because core temperature is rarely monitored by anesthesiologists during neuraxial anesthesia, and because the patient is unable to sense that they are cold (neural inputs disrupted and misinterpreted), undetected hypothermia during regional anesthesia is also common. The ensuing hypothermia that results from the above described mechanisms is not without consequences. There are of course times when mild hypothermia may be desired by the anesthesia and surgical teams, such as during certain neurosurgical procedures. However, one must be conscious of the fact, amongst other things, that perioperative hypothermia can be associated with protein wasting4 and decreased synthesis of collagen. One study was able to show that these factors triple the incidence of wound infection and increase the length of hospital stay by 20% in patients who were hypothermic during colon resection.5 Blood studies have shown that hypothermia inhibits platelet function, and interferes with the coagulation cascade. Drug metabolism is slowed (particularly of importance is the neuromuscular blockers), patients are slow to emerge, and the postoperative recovery period is prolonged.6 If severe enough, cardiac arrhythmias may occur, and the incidence of morbid cardiac events is tripled. There are many ways the anesthesiologist may prevent intraoperative hypothermia, and avoid not only the physiologic disturbances, but also the economic consequences that result from delayed emergence, residual neuromuscular blockade, delayed PACU discharge times, and increased length of hospital stays. Respiration is a source of 10% of heat loss, and although the routine use of semi-closed circle systems and humidifiers can help with this, they contribute little to perioperative thermal management. Sessler (1997) states that each liter of intravenous fluid infused into adult patients at ambient temperature, or each unit of blood infused at 4C decreases the mean body temperature approximately .25C. Warming of the fluids can prevent this marked decrease in body temperature. Lastly, the skin is the predominant source of heat loss during surgery, and although increasing the ambient temperature can be sufficient to prevent this loss, this measure is often uncomfortable for the surgical team. When ambient temperatures are not kept high (as is often the case), a single layer of insulation (blankets, drapes) can reduce the heat loss by 30%. The use of forced air warmers has been shown to be an effective measure, if not the most effective measure that we, as anesthesiologists, can employ. Its use can be extended into the recovery unit, where warming of a hypothermic patient becomes the last close-observation time period where intervention can avoid or minimize the complications associated with hypothermia. In this particular case, although a forced air warmer was placed over the patient in recovery, she did experience a prolonged recovery period. Time will tell if any future inintended consequences arise. In review of the case and literature, it is not surprising that in the cold operating room environment, the lack of forced air warming, and the judicious use of fluids at room temperature, the patient became hypothermic. There are many steps along the way that could have easily been prevented. And as we learn more about the detrimental effects of hypothermia, and as reimbursements are linked to avoiding

hypothermia, it is likely that we, as anesthesiologists, will begin to recognize and pay closer attention to the temperature of our patients. References
1. Sessler, DI. Mild Perioperative Hypothermia. NEJM 1997; 336 (24): 1730-1737 2. Xiong J., Kurz A., Sessler DI., et al. Isoflurane produces marked and nonlinear decreases in the vasoconstriction and shivering thresholds. Anesthesiology 1996; 85:240-245 3. Kurz A., Go JC., Sessler DI., Kaer K., Larson MD., Bjorksten AR. Alfentanyl slightly increases the sweating threshold and markedly reduces the vasoconstriction thresholds. Anesthesiology 1995; 83: 293-299 4. Carli F., Emery PW. Freemantle CJ. Effect of perioperative normothermia on postoperative protein metabolism in elderly patients undergoing hip arthroplaty. Br J Anaesth 1989; 63: 276-282 5. Kurz A., Sessler DI., Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. NEJM 1996; 334: 1209-1215 6. Lenhardt R., Kurz A., Sessler DI, Marker E., Narzt E., Lackner F. Intraoperative hypothermia prolongs duration of postoperative recovery. Anesthesiology 1991; 74: 815-819