Temperature monitoring is imperative during procedures.Photos courtesy Lloyd Hiebert Hypothermia is a challenge that can have dire physiologic and economic effects in every veterinarian’s practice. As a human anesthesiologist, I face similar challenges in maintaining patient normothermia, as do veterinarians in their operating rooms. Lessons learned in the human operating room can benefit those in the veterinary operating room. Hypothermia in dogs and cats can be defined as follows: Mild hypothermia: 98 to 99.9 F Moderate hypothermia: 96 to 98 F Severe hypothermia: 92 to 96 F Critical hypothermia: 92 F or less Mechanisms of heat loss The pathophysiology of hypothermia is best understood by considering the four mechanisms of heat loss in the operating room (OR). 1) Radiation. Radiation is the No. 1 cause of heat loss in the OR. Radiation is the transfer of body heat in the form of infra-red radiant energy to cold objects not in contact with the patient’s body. An example, heat loss to the walls of a cold OR. 2) Convection. Convection is the loss of body heat by the physical movement of ambient air around the patient’s body exemplified by heat loss to the cold circulating air of the OR. Radiation and convection account for 90 percent of heat loss in the OR. 3) Conduction. Conduction involves the direct flow of body heat to surrounding surfaces in direct contact with the body. An example here is heat loss to the cold OR table. 4) Evaporation. Evaporation of warmed moisture on the patient’s body carries with it body heat. When prep solutions, such as alcohol or betadine, dry after application, body heat is carried away, as well. Heat loss during anesthesia is best understood by dividing the patient body into the core and peripheral compartments. The core compartment, defined as the head and thorax, represents 50 to 60 percent of body mass. The temperature here remains relatively uniform. Meanwhile, the peripheral compartment, is comprised of the legs and tail. The temperature here is 3.6 to 7.2 F cooler than the core compartment, creating a temperature gradient between the core and peripheral compartments. The peripheral compartment temperature can fluctuate depending on the ambient temperature. The core to peripheral temperature gradient is normal. This gradient is controlled by the hypothalamus to mitigate heat loss to the environment. The hypothalamus redirects blood flow from the peripheral to the core compartment by peripheral vasoconstriction and increases metabolic heat production to maintain stable core compartment temperature. Neurogenic thermoregulation by the hypothalamus exists to maintain stable core compartment temperature. General anesthesia causes a loss of neurogenic thermoregulation by the hypothalamus thereby redistributing warm core blood to the periphery. Virtually all anesthetic drugs are vasodilators, which cause a loss of compensatory peripheral vasoconstriction. Consequently, warm core blood flows to the periphery, where it is cooled by the four mechanisms of heat loss. The patient essentially becomes a heat radiator. Additionally, there is a 20 to 40 percent decrease in metabolic rate and, consequently, a drastic drop in heat production. What are the three phases of hypothermia? When considering hypothermia during general anesthesia, it is instructive to think of hypothermia in three phases. Phase 1 is the initial rapid decrease in body temperature, which occurs during the first hour of anesthesia as seen in the accompanying graph, (Table 1). This is caused by the rapid redistribution of blood flow from the core to peripheral compartment due to peripheral vasodilation by anesthetic drugs. Body heat is then lost through the skin by the four mechanisms of heat loss. Redistribution of blood flow depends on the core to peripheral temperature gradient. A large temperature gradient causes a greater flow of warm core blood to the periphery. Phase 1 accounts for 81 percent of the heat loss that will potentially occur during the course of an anesthetic. Since Phase 1 is the time when interventions are most effective, active warming must start immediately upon anesthetic induction and sooner if possible. Phase 2 is a slow linear decline in body temperature that occurs over two to four hours. During this phase, heat loss exceeds metabolic heat production because the hypothalamus has been rendered inactive by general anesthesia. The decreased metabolic rate causes a loss of heat production by 20 to 40 percent. The rate of temperature decrease depends on the difference between heat lost and the heat produced and the mass of the patient. A Saint Bernard will have a slower rate of heat loss than a Chihuahua. Phase 3 is essentially a plateau in which there is core temperature stability. This occurs after three to four hours of anesthesia in which metabolic heat production equals heat loss. Table 1 Temperature monitoring Accurate temperature monitoring is imperative in providing appropriate hypothermia interventions. Although rectal temperature monitoring is frequently used, it does not represent core or peripheral temperature. Esophageal temperature most closely represents core body temperature. The esophagus is in direct contact with the posterior wall of the atrium and near the pulmonary vessels, thereby giving the esophageal temperature monitor the best approximation of core body temperature. Hypothermia prevention The prevention of hypothermia requires aggressive intervention preoperatively, intraoperatively, and postoperatively with thermal retention blankets and active warming devices. Preoperative warming Vasodilation by anesthetic drugs creates a massive flow of warm blood from the core to the cooler periphery. The potential 81 percent of temperature decline begins immediately upon anesthetic induction. This rapid redistribution of body heat can be prevented by equalization of the core to peripheral temperature gradient so that warm core blood is not being cooled in the periphery. This is accomplished by starting active warming immediately upon induction and continuing active warming during the preoperative prep as much as is practically possible. Ultimately, it is desirable to warm the patient preoperatively for at least 30 minutes, which prevents the rapid Phase 1 decline in body temperature. Heat stored in the peripheral compartment is transient making it imperative to minimize the delay between preoperative and intraoperative warming. For every minute of delay between preoperative and intraoperative warming, the likelihood of a drop in core temperature is increased by five percent. Indeed, effective preoperative warming with minimal delay to intraoperative warming are the two most important steps you can take in preventing hypothermia. Intraoperative warming Heat stored in the peripheral compartment is transient, requiring minimal delay between preoperative and intraoperative warming. Expose as much body surface area to your active warming device as possible and prevent as much heat loss as possible by using a thermal retention blanket. Frequently, over-body warming in nonsterile areas is inadequate, especially in cases of performing abdominal procedures. The under-body surface area is the largest area available for patient warming. Take advantage of this large area by utilizing an appropriate warming device that can be monitored and will not burn the under surface of the patient. Warmed IV fluids are essential on long cases with the IV line insulated along its length from the warmer to the patient. During abdominal procedures, irrigate the abdomen three times with warmed surgical irrigation since this will transfer heat to the mesenteric and intra-abdominal blood vessels. Convective heat loss can be curtailed by having the operating room temperature as high as the surgeon can tolerate. Surgeon heat stroke is not an acceptable payoff. Postoperative warming The end of the procedure does not mean active warming can be discontinued. Maintain active warming until the patient emerges from anesthesia. Postoperative return to normothermia occurs when hypothalamic anesthetic concentration decreases sufficiently to again trigger normal thermoregulatory defenses. These defenses include compensatory peripheral vasoconstriction and the return to normal metabolic heat production, which enable a return to normal core body temperature. The complications of hypothermia Leaving pets out in cold or freezing weather is one way they get hypothermia. Warn clients of the dangers and remind them to bring pets inside. Hypothermia has highly relevant physiologic and economic consequences. Without going into the physiologic mechanisms of each, the deleterious effects include, but are not limited to, the following: Cardiac arrhythmias Decreased platelet aggregation Deceased blood oxygen Postoperative protein breakdown Impaired kidney function Decreased drug metabolism Impaired liver function Decreased cardiac output Peripheral vasoconstriction Surgical site infections Poor wound healing Altered mental status Increased recovery time Death Preventing hypothermia enables hepatic enzyme and renal excretion efficiency in metabolizing anesthetic medications. Normothermia promotes rapid emergence from anesthesia. Prevention of hypothermia decreases anesthesia recovery time, increases clinical efficiency and promotes excellence in patient care. Clinical efficiency has a direct impact on clinic revenue. The recovery time costs in the “average” veterinary facility are $100 to $150 per hour. Imagine the impact on a facility’s bottom line if a patient emerges from an anesthetic immediately rather than two hours. It can make the difference between making a profit or losing money on a procedure. The vital importance of effective preoperative warming and minimizing delay between preoperative and intraoperative warming cannot be overstated. With the advanced warming products now available to maintain normothermia, allowing a patient to spiral into hypothermia is no longer an acceptable mode of patient care. Indeed, prevention of hypothermia preoperatively, intraoperatively, and postoperatively exemplifies excellence in patient care and practice management. Current advances in passive and active patient warming technology will change the standard of care for veterinary patients and make patient hypothermia a distant memory. Lloyd Hiebert, MD, is an anesthesiologist with more than 30 years of experience in the human operating room. He has developed patient positioning and warming products for both the human and veterinary OR and is president of VetORSolutions. He can be reached at contact@VetORSolutions.com.
