TEMPERATURE 2017, VOL. 4, NO. 1, 9–12 http://dx.doi.org/10.1080/23328940.2016.1243509
FRONT MATTER: EDITORIAL
The importance of body temperature: An anesthesiologist’s perspective The anesthesiologist is entrusted with many important responsibilities during the perioperative experience beyond anesthetizing the patient, including securing the airway, attenuating the stress response, ensuring the patient has a sustainable hemodynamics, implementing a ventilation strategy, preserving euvolemia, and maintaining normothermia. From an outsider’s prospective, of all of these concerns one may think that maintaining normothermia would be the easiest of tasks, yet for a wide variety of reasons discussed below, intraoperative hypothermia (< 36 C) occurs frequently when the patients are under general anesthesia. Inadvertent hypothermia is one of the most common complications during the perioperative period and has been recognized to contribute to surgical site infections, increased blood loss, myocardial ischemia, increased duration of postanesthetic recovery and hospitalization, and patient discomfort.1 In fact, a collaboration between numerous healthcare organizations, including the Centers for Medicare and Medicaid Services, called the Surgical Care Improvement Project outlined the avoidance of hypothermia as one of its core measures of quality improvement.2 Non-compliance with SCIP can result in decreased reimbursements. In this editorial, instead of providing a complete review of the scientific underpinnings leading to hypothermia, we would rather present the issue of perioperative hypothermia through the eyes of the clinical anesthesiologist. A typical patient goes through 3 distinct phases when he/she comes for a surgery to the hospital: Preoperative, Intraoperative and postoperative. In each of these phases, unique situations affect core body temperature and various methods can be applied to mitigate the resulting hypothermia.
Preoperative period Although preemptive warming of the patient has been shown to reduce intraoperative hypothermia, it is not possible due to various reasons. For example, an awake patient may not like a warming blanket, it may interfere with physical examination or patient may have open wounds. Unfortunately, intraoperative hypothermia is more common in prolonged surgeries and consequences of hypothermia such as surgical site infection and coagulopathy are particularly problematic in these large surgeries. Furthermore, some patients (especially those hospitalized or recently evacuated from a trauma site) present preoperatively with varying levels of hypothermia due to decompensation of patient disease (e.g. sepsis).
Intraoperative period Causes of intraoperative hypothermia
Loss of heat during the intraoperative period is multifactorial with contributions from the anesthetic, surgical exposure and time, patient factors, and operating room environment. The induction and maintenance of general anesthesia will, in its own right, lead to a drop in the patient’s core temperature. This initial loss is likely secondary to redistribution of heat from the core to the periphery, not so much a loss of heat from the system. As time moves on, loss of heat from the patient to the environment becomes the primary mechanism leading to intraoperative hypothermia. General anesthetics alter how body responds to hypothermia. Firstly, general anesthetics vasodilate and reduce shivering and non-shivering thermogenesis. Moreover, behavioral modification such as wearing warmer clothes or seeking warmer temperature is not possible for a patient who is in coma, paralyzed and has an endotracheal tube in his/her mouth! Finally anesthetics change when the effector response to hypothermia is initiated. In unanesthetized humans, a change in core body
© 2017 Taylor & Francis
10
R. MATIKA ET AL.
temperature of as little as 0.4 C can trigger an effector response. However, under general anesthesia, the effectors are not engaged until the change is up to 4 C. The location and size of the surgical incision has a major impact on intraoperative heat loss. For example, in large abdominal surgeries, where the surgeons may have a sizable portion of the bowels strewn across the surgical field with enormous metal retractors exposing the abdominal cavity for optimal exposure, radiant heat and water (evaporative) loss can be significant. Moreover, the duration of surgery also directly correlated with incidence of hypothermia. Longer surgeries inherently mean prolonged exposure to general anesthetics, more blood loss and transfusion hence more incidence of hypothermia. Also, patient disease and underlying conditions can also affect heat loss. An example may be severe peripheral vascular disease where forced air warming blankets to the poorly perfused lower extremities has less benefit than if a person with normal perfusion. Finally operative room environment is also a major contributor to the heat loss. Conductive heat loss is typically less common in modern operating rooms as patient is primarily in contact with foam and gel paddings that have good insulation properties. However, conductive heat loss can play a greater role in pediatric, particularly neonatal patients owing to larger body surface are. Convective heat loss is also less common as the patient is covered by sterile draping and air speeds in the operating room is 20cm/sec or lesser. Evaporative heat loss occurs through the surgical wound, non-humidified respiratory gas exchange, and sweating. By far the largest contributor to heat loss intraoperatively is through heat radiation. Operating rooms are generally kept very cool and rarely above 23 C and often 18 C or cooler. The temperature gradient between surrounding surfaces and patient’s core body determines the speed and degree of radiant heat loss. Raising the temperature of the operating room should mitigate this problem; however it is not possible for various reasons including operating room staff’s comfort, possible contamination caused by sweating of the operating staff among others. On a lighter note, some anesthesiologists have pulled the esophageal temperature probe into oropharynx to falsely show the surgeon that the patient is hypothermic and then used the threat of raising room temperature to make surgeons operate faster! Some surgeons come back by questioning the anesthesiologist’s ‘skills’ to maintain the patient’s normothermia. It is not uncommon to have interdepartmental meetings to find ‘consensus’ on operative room temperature. Immediate consequences of intraoperative hypothermia
The hypothermic patient represents a real clinical issue for both surgeons and anesthesiologists. In many cases, mild hypothermia (34–36 C) is thought to be a temporary problem that will eventually be resolved with little clinical significance. This illusion is dispelled when the problem of bleeding occurs. Mild hypothermia affects the coagulation cascade and most noticeably in platelet function and can lead to more blood loss and higher transfusion requirements. Often we see fresh frozen plasma, cryoprecipitate, platelets, and recombinant clotting factors given to hypothermic patients and one wonders how much a reduction in the use of these products could be gained by avoiding hypothermia in the first place. Another effect of mild hypothermia that becomes apparent early in the case is drug metabolism. Many intravenously administered anesthetics and neuromuscular blockers can be significantly prolonged, whereas the effects of volatile anesthetics are only mildly prolonged. We have seen many instances of anesthesiology residents scratching their heads trying to figure out why their patients are taking longer to emerge from anesthesia. Even ventilation management can be affected by hypothermia due to misinterpretation of arterial blood gas values. This is because with hypothermia patients will appear hypocarbic and alkalotic on temperature-corrected arterial blood gas analysis. Treatment of intraoperative hypothermia
The treatment of hypothermia relies on external transfer of heat to the patient and more importantly to decrease further heat loss. Cutaneous warming is the most common and effective method of warming the patient intraoperatively. Forced air warming blankets can eliminate cutaneous heat loss and are placed directly on top of the patient in areas outside of the surgical field. Limitations on the use of these devices are primarily based on the location and size of the operation. More than once we have seen a completely exposed patient undergoing a large
TEMPERATURE
11
vascular surgery case with a forced air warming blanket on one leg, below the knee, with documented poor circulation and a history of claudication. In such cases, the use of the forced air warming blanket will have minimal effect. Moreover, forced air warming blankets have been associated with increased surgical site infection and burns in certain instances. Another appealing option to warm the patient is the use warmed IV fluids. Various medical devices will warm IV fluids before they are delivered to the patient. The fluid leaving the system is warmed to 38 C to 40 C and delivered directly to the patient’s venous system. In most routine cases in adults, use of these systems provides little benefit. This is partially because the volume administrated is relatively low and the speed in which the fluid flows is slow enough that the administered fluids are cooled before entering the patient’s body. However, with significant hemorrhage, large and rapid amounts of intravenous fluids and blood products are administered and using such devices can significantly help reduce hypothermia.
Postoperative period The postoperative period is where many clinicians first see the sequelae of intraoperative hypothermia. The most common manifestation of this is shivering. Postoperative shivering following general anesthesia has multiple and complex etiologies, and is not entirely due to thermoregulation. Hypothermic patients can shiver not only from a drop in core temperature but also from mechanisms not full elucidated, but likely related to disinhibition of descending control over spinal reflexes as a result of the anesthetic. That being said, most patients who shiver post-operatively are also hypothermic. Post-operative shivering is potentially dangerous for the patient. The most feared complications of prolonged shivering are significantly increased oxygen consumption, increased intracranial pressure, increased intraocular pressure, and worsened wound pain, damage to the surgical repair or even myocardia ischemia. The best treatment for the shivering patient would be to time-travel back a couple hours and warm the patient properly and avoid the problem in the first place. But until that technology is created, the focus is on rewarming the patient and administering medications which likely act on the central regulatory system. Rewarming is best accomplished using forced air warming blankets. Medications available to treat shivering are numerous, but the most commonly used is meperidine, an opioid that also binds multiple other proteins including dopamine transporter and certain sodium channels. Second line of therapy typically involves other opioids, clonidine and antiserotinergic drugs. The precise mechanism by which these medications stop shivering is not well known. Long after patients leave the post anesthesia care unit, one of the most dreaded complications of hypothermia manifests, which is the surgical site infection. Hypothermia impairs immune function, decreases wound oxygen delivery, delays wound healing, and has been shown to even triplicate the rate of surgical site infections in certain surgeries. Surgical site infection places a tremendous burden both on the patient and on the healthcare delivery system by delayed recovery, multiple re-admissions and some times reoperations. It should be noted that despite all the shortcomings, induced hypothermia has been used as therapeutic strategy in certain conditions such as post cardiovascular arrest to improve brain recovery.3 A separate editorial will be required to discuss this in detail!
Conclusions and future directions Perioperative hypothermia represents a significant challenge and unfortunately is associated with some serious complications. Although perioperative hypothermia is partly a pharmacological problem (effect of general anesthetics on thermoregulatory pathways and effectors), current modalities to treat it exclusively rely on physical methods such as forced air warming. A pharmacological tool to treat intraoperative hypothermia will be novel way to address this problem. Over the last 15 years, we have learned a lot about various temperature-sensitive ion channels in our body that affect thermoregulation. While transient receptor potential channels such as TRPV1, V3 and V4 respond to warm to noxious heat stimuli, TRPM8 and A1 are proposed to respond to cool to noxious cold stimuli.4 The drugs that either activate or block these channels impact body temperature. For example, TRPV1 antagonists can cause hyperthermia and TRPM8 antagonist produce hypothermia. Although most of current research on these drugs is targeted toward analgesic development, it is intuitive to think we may be able to use these drugs to treat thermal dysregulation.
12
R. MATIKA ET AL.
References [1] Sessler DI. Mild perioperative hypothermia. N Engl J Med 1997; 336:1730-7; PMID:9180091; http://dx.doi.org/10.1056/ NEJM199706123362407 [2] Fry DE. Surgical site infections and the surgical care improvement project (SCIP): evolution of national quality measures. Surg Infect (Larchmt) 2008; 9:579-84; PMID:19216670; http://dx.doi.org/10.1089/sur.2008.9951 [3] Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346:549-56; PMID:11856793; http://dx.doi.org/10.1056/NEJMoa012689 [4] Julius D. TRP channels and pain. Annu Rev Cell Dev Biol 2013; 29:355-84; PMID:24099085; http://dx.doi.org/10.1146/ annurev-cellbio-101011-155833
Ryan Matika Department of Anesthesiology, University of Arizona, Tucson, AZ, USA
Mohab Ibrahim Department of Anesthesiology, University of Arizona, Tucson, AZ, USA Department of Pharmacology, University of Arizona, Tucson, AZ, USA
Amol Patwardhan Department of Anesthesiology, University of Arizona, Tucson, AZ, USA Department of Pharmacology, University of Arizona 1501 N. Campbell Ave., P.O. Box 245114. 85724 Tucson, AZ, USA [email protected]
FRONT MATTER: EDITORIAL
The importance of body temperature: An anesthesiologist’s perspective The anesthesiologist is entrusted with many important responsibilities during the perioperative experience beyond anesthetizing the patient, including securing the airway, attenuating the stress response, ensuring the patient has a sustainable hemodynamics, implementing a ventilation strategy, preserving euvolemia, and maintaining normothermia. From an outsider’s prospective, of all of these concerns one may think that maintaining normothermia would be the easiest of tasks, yet for a wide variety of reasons discussed below, intraoperative hypothermia (< 36 C) occurs frequently when the patients are under general anesthesia. Inadvertent hypothermia is one of the most common complications during the perioperative period and has been recognized to contribute to surgical site infections, increased blood loss, myocardial ischemia, increased duration of postanesthetic recovery and hospitalization, and patient discomfort.1 In fact, a collaboration between numerous healthcare organizations, including the Centers for Medicare and Medicaid Services, called the Surgical Care Improvement Project outlined the avoidance of hypothermia as one of its core measures of quality improvement.2 Non-compliance with SCIP can result in decreased reimbursements. In this editorial, instead of providing a complete review of the scientific underpinnings leading to hypothermia, we would rather present the issue of perioperative hypothermia through the eyes of the clinical anesthesiologist. A typical patient goes through 3 distinct phases when he/she comes for a surgery to the hospital: Preoperative, Intraoperative and postoperative. In each of these phases, unique situations affect core body temperature and various methods can be applied to mitigate the resulting hypothermia.
Preoperative period Although preemptive warming of the patient has been shown to reduce intraoperative hypothermia, it is not possible due to various reasons. For example, an awake patient may not like a warming blanket, it may interfere with physical examination or patient may have open wounds. Unfortunately, intraoperative hypothermia is more common in prolonged surgeries and consequences of hypothermia such as surgical site infection and coagulopathy are particularly problematic in these large surgeries. Furthermore, some patients (especially those hospitalized or recently evacuated from a trauma site) present preoperatively with varying levels of hypothermia due to decompensation of patient disease (e.g. sepsis).
Intraoperative period Causes of intraoperative hypothermia
Loss of heat during the intraoperative period is multifactorial with contributions from the anesthetic, surgical exposure and time, patient factors, and operating room environment. The induction and maintenance of general anesthesia will, in its own right, lead to a drop in the patient’s core temperature. This initial loss is likely secondary to redistribution of heat from the core to the periphery, not so much a loss of heat from the system. As time moves on, loss of heat from the patient to the environment becomes the primary mechanism leading to intraoperative hypothermia. General anesthetics alter how body responds to hypothermia. Firstly, general anesthetics vasodilate and reduce shivering and non-shivering thermogenesis. Moreover, behavioral modification such as wearing warmer clothes or seeking warmer temperature is not possible for a patient who is in coma, paralyzed and has an endotracheal tube in his/her mouth! Finally anesthetics change when the effector response to hypothermia is initiated. In unanesthetized humans, a change in core body
© 2017 Taylor & Francis
10
R. MATIKA ET AL.
temperature of as little as 0.4 C can trigger an effector response. However, under general anesthesia, the effectors are not engaged until the change is up to 4 C. The location and size of the surgical incision has a major impact on intraoperative heat loss. For example, in large abdominal surgeries, where the surgeons may have a sizable portion of the bowels strewn across the surgical field with enormous metal retractors exposing the abdominal cavity for optimal exposure, radiant heat and water (evaporative) loss can be significant. Moreover, the duration of surgery also directly correlated with incidence of hypothermia. Longer surgeries inherently mean prolonged exposure to general anesthetics, more blood loss and transfusion hence more incidence of hypothermia. Also, patient disease and underlying conditions can also affect heat loss. An example may be severe peripheral vascular disease where forced air warming blankets to the poorly perfused lower extremities has less benefit than if a person with normal perfusion. Finally operative room environment is also a major contributor to the heat loss. Conductive heat loss is typically less common in modern operating rooms as patient is primarily in contact with foam and gel paddings that have good insulation properties. However, conductive heat loss can play a greater role in pediatric, particularly neonatal patients owing to larger body surface are. Convective heat loss is also less common as the patient is covered by sterile draping and air speeds in the operating room is 20cm/sec or lesser. Evaporative heat loss occurs through the surgical wound, non-humidified respiratory gas exchange, and sweating. By far the largest contributor to heat loss intraoperatively is through heat radiation. Operating rooms are generally kept very cool and rarely above 23 C and often 18 C or cooler. The temperature gradient between surrounding surfaces and patient’s core body determines the speed and degree of radiant heat loss. Raising the temperature of the operating room should mitigate this problem; however it is not possible for various reasons including operating room staff’s comfort, possible contamination caused by sweating of the operating staff among others. On a lighter note, some anesthesiologists have pulled the esophageal temperature probe into oropharynx to falsely show the surgeon that the patient is hypothermic and then used the threat of raising room temperature to make surgeons operate faster! Some surgeons come back by questioning the anesthesiologist’s ‘skills’ to maintain the patient’s normothermia. It is not uncommon to have interdepartmental meetings to find ‘consensus’ on operative room temperature. Immediate consequences of intraoperative hypothermia
The hypothermic patient represents a real clinical issue for both surgeons and anesthesiologists. In many cases, mild hypothermia (34–36 C) is thought to be a temporary problem that will eventually be resolved with little clinical significance. This illusion is dispelled when the problem of bleeding occurs. Mild hypothermia affects the coagulation cascade and most noticeably in platelet function and can lead to more blood loss and higher transfusion requirements. Often we see fresh frozen plasma, cryoprecipitate, platelets, and recombinant clotting factors given to hypothermic patients and one wonders how much a reduction in the use of these products could be gained by avoiding hypothermia in the first place. Another effect of mild hypothermia that becomes apparent early in the case is drug metabolism. Many intravenously administered anesthetics and neuromuscular blockers can be significantly prolonged, whereas the effects of volatile anesthetics are only mildly prolonged. We have seen many instances of anesthesiology residents scratching their heads trying to figure out why their patients are taking longer to emerge from anesthesia. Even ventilation management can be affected by hypothermia due to misinterpretation of arterial blood gas values. This is because with hypothermia patients will appear hypocarbic and alkalotic on temperature-corrected arterial blood gas analysis. Treatment of intraoperative hypothermia
The treatment of hypothermia relies on external transfer of heat to the patient and more importantly to decrease further heat loss. Cutaneous warming is the most common and effective method of warming the patient intraoperatively. Forced air warming blankets can eliminate cutaneous heat loss and are placed directly on top of the patient in areas outside of the surgical field. Limitations on the use of these devices are primarily based on the location and size of the operation. More than once we have seen a completely exposed patient undergoing a large
TEMPERATURE
11
vascular surgery case with a forced air warming blanket on one leg, below the knee, with documented poor circulation and a history of claudication. In such cases, the use of the forced air warming blanket will have minimal effect. Moreover, forced air warming blankets have been associated with increased surgical site infection and burns in certain instances. Another appealing option to warm the patient is the use warmed IV fluids. Various medical devices will warm IV fluids before they are delivered to the patient. The fluid leaving the system is warmed to 38 C to 40 C and delivered directly to the patient’s venous system. In most routine cases in adults, use of these systems provides little benefit. This is partially because the volume administrated is relatively low and the speed in which the fluid flows is slow enough that the administered fluids are cooled before entering the patient’s body. However, with significant hemorrhage, large and rapid amounts of intravenous fluids and blood products are administered and using such devices can significantly help reduce hypothermia.
Postoperative period The postoperative period is where many clinicians first see the sequelae of intraoperative hypothermia. The most common manifestation of this is shivering. Postoperative shivering following general anesthesia has multiple and complex etiologies, and is not entirely due to thermoregulation. Hypothermic patients can shiver not only from a drop in core temperature but also from mechanisms not full elucidated, but likely related to disinhibition of descending control over spinal reflexes as a result of the anesthetic. That being said, most patients who shiver post-operatively are also hypothermic. Post-operative shivering is potentially dangerous for the patient. The most feared complications of prolonged shivering are significantly increased oxygen consumption, increased intracranial pressure, increased intraocular pressure, and worsened wound pain, damage to the surgical repair or even myocardia ischemia. The best treatment for the shivering patient would be to time-travel back a couple hours and warm the patient properly and avoid the problem in the first place. But until that technology is created, the focus is on rewarming the patient and administering medications which likely act on the central regulatory system. Rewarming is best accomplished using forced air warming blankets. Medications available to treat shivering are numerous, but the most commonly used is meperidine, an opioid that also binds multiple other proteins including dopamine transporter and certain sodium channels. Second line of therapy typically involves other opioids, clonidine and antiserotinergic drugs. The precise mechanism by which these medications stop shivering is not well known. Long after patients leave the post anesthesia care unit, one of the most dreaded complications of hypothermia manifests, which is the surgical site infection. Hypothermia impairs immune function, decreases wound oxygen delivery, delays wound healing, and has been shown to even triplicate the rate of surgical site infections in certain surgeries. Surgical site infection places a tremendous burden both on the patient and on the healthcare delivery system by delayed recovery, multiple re-admissions and some times reoperations. It should be noted that despite all the shortcomings, induced hypothermia has been used as therapeutic strategy in certain conditions such as post cardiovascular arrest to improve brain recovery.3 A separate editorial will be required to discuss this in detail!
Conclusions and future directions Perioperative hypothermia represents a significant challenge and unfortunately is associated with some serious complications. Although perioperative hypothermia is partly a pharmacological problem (effect of general anesthetics on thermoregulatory pathways and effectors), current modalities to treat it exclusively rely on physical methods such as forced air warming. A pharmacological tool to treat intraoperative hypothermia will be novel way to address this problem. Over the last 15 years, we have learned a lot about various temperature-sensitive ion channels in our body that affect thermoregulation. While transient receptor potential channels such as TRPV1, V3 and V4 respond to warm to noxious heat stimuli, TRPM8 and A1 are proposed to respond to cool to noxious cold stimuli.4 The drugs that either activate or block these channels impact body temperature. For example, TRPV1 antagonists can cause hyperthermia and TRPM8 antagonist produce hypothermia. Although most of current research on these drugs is targeted toward analgesic development, it is intuitive to think we may be able to use these drugs to treat thermal dysregulation.
12
R. MATIKA ET AL.
References [1] Sessler DI. Mild perioperative hypothermia. N Engl J Med 1997; 336:1730-7; PMID:9180091; http://dx.doi.org/10.1056/ NEJM199706123362407 [2] Fry DE. Surgical site infections and the surgical care improvement project (SCIP): evolution of national quality measures. Surg Infect (Larchmt) 2008; 9:579-84; PMID:19216670; http://dx.doi.org/10.1089/sur.2008.9951 [3] Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346:549-56; PMID:11856793; http://dx.doi.org/10.1056/NEJMoa012689 [4] Julius D. TRP channels and pain. Annu Rev Cell Dev Biol 2013; 29:355-84; PMID:24099085; http://dx.doi.org/10.1146/ annurev-cellbio-101011-155833
Ryan Matika Department of Anesthesiology, University of Arizona, Tucson, AZ, USA
Mohab Ibrahim Department of Anesthesiology, University of Arizona, Tucson, AZ, USA Department of Pharmacology, University of Arizona, Tucson, AZ, USA
Amol Patwardhan Department of Anesthesiology, University of Arizona, Tucson, AZ, USA Department of Pharmacology, University of Arizona 1501 N. Campbell Ave., P.O. Box 245114. 85724 Tucson, AZ, USA [email protected]
