Abstract
Hypothermia has profound effects on every system in the body, causing an overall slowing of enzymatic reactions and reduced metabolic requirements. Hypothermic, acutely injured patients with multisystem trauma have adverse outcomes when compared with normothermic control patients. Trauma patients are inherently predisposed to hypothermia from a variety of intrinsic and iatrogenic causes. Coagulation and cardiac sequelae are the most pertinent physiological concerns. Hypothermia and coagulopathy often mandate a simplified approach to complex surgical problems. A modification of traditional classification systems of hypothermia, applicable to trauma patients is suggested. There are few controlled investigations, but clinical opinion strongly supports the active prevention of hypothermia in the acutely traumatized patient. Preventive measures are simple and inexpensive, but the active reversal of hypothermia is much more complicated, often invasive and controversial. The ideal method of rewarming is unclear but must be individualized to the patient and is institution specific. An algorithm reflecting newer approaches to traumatic injury and technical advances in equipment and techniques is suggested.
Conversely, hypothermia has selected clinical benefits when appropriately used in cases of trauma. Severe hypothermia has allowed remarkable survivals in the course of accidental circulatory arrest. The selective application of mild hypothermia in severe traumatic brain injury is an area with promise. Deliberate circulatory arrest with hypothermic cerebral protection has also been used for seemingly unrepairable injuries and is the focus of ongoing research.
Hypothermia is simply defined as a body temperature significantly below 37 °C.1 It has a profound effect on every system of the body, akin to that of a double-edged sword, causing both reduced oxygen and metabolic demands as well as disruptions in temperature-dependent enzymatic processes.2
Hypothermia and trauma outcomes
In trauma, several retrospective studies have found an association between higher death rate and an increasing degree of hypothermia, even accounting for differences in the severity of injury.3,4 Jurkovich and associates3 found that no trauma patient whose core temperature fell below 32 °C survived, and they regarded this as the critical temperature for survival. Hypothermia is recognized as one pillar of a “lethal triad” (hypothermia, acidosis and coagulopathy) of homeostatic failure that is believed to mark the limits of ongoing intervention, and necessitates an “abbreviated” laparotomy. 5–9 The “damage control” approach evolved after surgeons noted a subset of trauma patients who no matter how aggressively they were resuscitated and supported became physiologically exhausted and intolerant of further surgical intervention. Procedures must be accomplished quickly without exhausting the patients’ physiologic reserve through continued blood and heat loss.
Classification of hypothermia
In general, hypothermia is classified as mild (32° to 35 °C), moderate (28° to 32 °C) and severe (less than 28 °C).10–16 The Committee on Trauma of the American College of Surgeons has focused on the immediate harmful effects of hypothermia in the post-injury period. The Committee recommended considering any temperature below 36 °C as hypothermic and 32 °C and below as severely hypothermic. 17 Further definitions of hypothermia arise from research exploring the potential benefits of hypothermia on human viability. Researchers have defined further levels of hypothermia: deep, between 10° and 20 °C; profound, less than 10 °C; and ultraprofound, from 0 to 5 °C.18–21
Current recommendations for an abbreviated operation and accepting a damage control approach recognize 34 °C as a critical decision-making temperature.22,23 We believe that a modification to standard classifications of hypothermia is appropriate, to recognize the importance of temperature in trauma: a temperature of less than 34 °C should not be labelled “mild” in any multiply injured patient; a body temperature warmer than 34 °C (class I) should be distinguished from more worrisome hypothermia of 34° to 32 °C (class II). This distinction is not recognized by the usual systems. Classes III and IV should refer to the generally accepted criteria for moderate and severe hypothermia (Table I).
Proposed Classification of Hypothermia in the Trauma Patient
Controversies
The currently accepted standard of care is to actively prevent and treat hypothermia. The current advanced trauma life support (ATLS) guidelines from the Committee on Trauma of the American College of Surgeons stress temperature control with aggressive efforts to avoid and to treat hypothermia.17 Whether the increased death rate in trauma patients is causally related to hypothermia or merely an associated factor marking progressive metabolic failure is unclear. Ronco and colleagues24 have documented that the process of dying is marked by a progressive failure of oxygen consumption and metabolic activity. Steinmann and colleagues11 found no difference in outcome in hypothermic trauma patients when they were stratified by injury severity. A small, randomized, prospective trial that actively warmed patients showed a significantly lower early death rate and decreased overall fluid requirements to meet standardized hemodynamic goals, although there was no overall difference in the survival rate to discharge.25 This was the first and only randomized, prospective, controlled trial to assess the effect of hypothermia as an independent variable in traumatic injury.
Physicians have often been intrigued by the potential benefits of hypothermia in critical illness. Dramatic survivals have been recorded with prolonged immersion in cold water.26 Concerning head trauma, Hippocrates himself stated that “a man will survive longer in winter than in summer, whatever be the part of the head in which the wound is situated.”27 In both the Second World War and war in Indochina, physicians believed that cooled patients would survive longer.25 French military physicians in Indochina even actively cooled combat casualties.28 Without large well-performed clinical trials to guide us, an appreciation of the effects of hypothermia in the trauma patient warrants further background study.
General physiologic consequences of hypothermia
Hypothermia exhibits an array of deleterious physiologic consequences if maximal physiologic performance in health is the comparative standard. The main consequences are summarized in Table II.4,10,12,14,16,29–34 In general, the effect is of a continuous overall slowing and depression of the functions of life. The patient may be in a state of agonal pulselessness without brain stem and deep tendon reflexes, yet remain viable. This state may not be distinguishable from death by any means other than rewarming.
Deleterious General Physiologic Consequences of Hypothermia
Changes in the cardiac and coagulation systems are particularly pertinent to a discussion of wounding and injury. The ventricle becomes irritable below 30 °C, with 25° to 28 °C quoted as the threshold temperature for ventricular fibrillation.14,29,35 Ventricular fibrillation in the setting of hypothermia below 28 °C is often refractory to defibrillation and pharmacologic intervention until the core temperature is raised.12,29 Tracheal and gastric intubation, cardiopulmonary resuscitation or even injudicious movement can induce ventricular fibrillation.10 This hazard, along with the ever-present risk of exacerbating spinal cord injuries, warrants careful handling and instrumentation of the hypothermic trauma patient. Perioperatively, maintenance of normothermia decreased the rate of hemodynamically important arrhythmias compared with patients who were allowed to cool to a mean of 34.5 °C in a nontrauma setting.36
Many of the early deaths in hypothermic trauma patients are believed to be due to exacerbation of acquired coagulopathies.15,37 Hypothermia, especially that associated with transfusion of large volumes of blood and fluids produces an acquired coagulopathy and exacerbates bleeding.38,39 Retrospective studies have suggested that hypothermia exacerbates intraoperative blood loss independent of the degree of injury40 and that significant bleeding develops despite adequate blood, plasma and platelet replacement.5 Factors thought to contribute to impaired coagulation in the trauma patient include the consumption and dilution of platelets and clotting factors, activation of the fibrinolytic cascade, alterations in electrolytes such as calcium, endothelial injury, endotoxin and other vasoactive mediator re lease, acidosis and hypothermia. 30,38,40–42 Clearly, a true appreciation of the isolated effects of hypothermia itself is difficult. With hypothermia, both the extrinsic and intrinsic pathways become dysfunctional with a prolongation of the prothrombin time (or international normalized ratio) and partial thromboplastin time when measured at the in-vivo temperature.41,42 The fact that these laboratory determinations are made after warming the sample to 37 °C may lead to falsely reassuring values. 41,42 Normal laboratory indices in an obviously coagulopathic patient, obtained from such an ex-vivo measurement suggest that the best therapy is active rewarming.15,42 Animal studies have demonstrated that platelet dysfunction is reversible solely by rewarming.43
Particular susceptibility of the trauma patient
In general, extremes of age, environmental stresses, chronic illnesses (especially those with hypometabolic features), alcoholism and drug abuse, impaired neurologic state, sepsis, dermal compromise, impaired mobility, socioeconomic disadvantages and previous exposures all contribute to the likelihood of injury with cold exposure. 14,31,44–46 The elderly and infirm are particularly susceptible because they cannot increase heat production and decrease heat loss by vasoconstriction, and children are susceptible because of their increased body surface area-to-mass ratios and limited energy resources. 17 Urban hypothermia describes a subset of hypothermic victims who are commonly alcoholic, homeless, elderly or disabled.12 Submersion imparts marked cooling stresses with the thermal conductivity of water being 32 times greater than that of air.12,45
Of all the critically ill patients that the surgical intensivist is required to treat, the severely traumatized patient may be the most prone to hypothermic complications. The patient may be admitted after prolonged exposure, especially if discovery or extrication is delayed or difficult.10,45 Hypothermic stresses continue in the prehospital care phase and are often propagated throughout the early hospital phase. Standard ATLS guidelines warrant the infusion of 3 volumes of crystalloid fluids for every 1 volume of shed blood, often administered many degrees below that of body temperature. Banked blood being stored at 4 °C will act as a heat sink, actually absorbing heat from the patient at a time when the patient can least afford it.32 Standard care also stresses complete exposure of the patient to avoid missing injuries. Coincident head injuries (typically present in 60% of severe blunt trauma in a Canadian setting),47 well-meaning spinal precautions (restraints), and analgesia and sedation will prevent activity-induced thermogenesis. The frequent presence of alcohol and drugs can prevent appropriate conscious behavioural responses, cause hypothalamic dysfunction and blunt protective vasoconstrictive and shivering responses.4,10,45 If a laparotomy is required, further heat losses may be extensive and impossible to reverse until the abdominal cavity is closed.48 Anesthetic agents can promote further heat loss and impair thermoregulatory mechanisms.37–39,49 Hypotension itself may reset the hypothalamic set-point for shivering, which can further compound these problems.50,51
Prevention and treatment of hypothermia
The prevention and treatment of hypothermia in the traumatized patient are effectively different points on the continuum of good patient care. It is crucial to accurately measure the body temperature. Special thermometers capable of reading low temperatures must be used, as standard thermometers may not have low enough values to accurately reflect the degree of hypothermia.17 Rectal temperatures may lag behind actual core changes, especially if the rectum is loaded with cold stool.10
Prevention
Effective prevention is facilitated by attention to the etiologic factors that promote hypothermia in trauma patients. The victim should be initially removed or protected from environmental extremes. Passive warming should be applied at the scene, extrication and transportation times minimized, and resuscitative measures that create a negative heat flux such as the administration of cold fluids, should be either avoided or minimized. Once the patient is transported, one of the cornerstones of prevention and treatment of hypothermia has been the use of devices or practices to allow the use of heated resuscitation fluids.37 Fluids may be successfully rewarmed by microwave techniques. Fluid warmers are usually more convenient and are generally of 2 types: dry-wall fluid warmers and water-bath fluid exchangers. Both types of devices will allow the infusion of large volumes (more than 3L/h) of heated intravenous fluids. The water-bath type heating systems have a wider range of effective flow rates.52
The lungs are a normal area of heat exchange and can simply and effectively be used to heat the victim with warm inspired gases. Humidification also increases the heat flux, besides being generally beneficial in liquidizing secretions and decreasing insensible fluid losses.53 Inspired gas temperatures up to 44° to 46 °C have been used safely.53–56 Ambient room temperature may need to be elevated even if this is uncomfortable for the medical staff.57
Treatment
To reverse hypothermia and its deleterious effects, a rewarming method should be implemented, guided by the degree of hypothermia and hemodynamic stability. Potential methods can be classified as passive external, active external or surface, and active internal or core rewarming (Table III2,13,25,29,46,58). Physiologically, categories of hypothermia severity reflect the degree of protective reflexes remaining. Mild cases reflect preserved heat production and compensatory reflexes. There is loss of heat production but preservation of vasoconstriction in moderate cases. In severe hypothermia both vasoconstrictive and endocrinologic reflexes are lost and the human responds to hypothermia essentially as a poikilothermic being. 10 Hemodynamically stable, mildly hypothermic patients generate a positive heat flux and are suitable for passive rewarming techniques.12,16,31,38 Essentially all trauma patients should be treated with measures that provide passive external rewarming (e.g., warm environment, covering). Patients who are moderately or severely hypothermic must be actively rewarmed.10,31,59
Methods of Warming Hypothermic Patients
The optimal rewarming method for the trauma patient is not clear. The method used will be partly guided by the specific injuries, physiological features of the patient, the phase of care and the institutional resources available. For example, pleural lavage in the setting of severe chest injuries, or peritoneal lavage in severe abdominal trauma would not be appropriate in the initial resuscitation phases. During operative intervention though, warm mediastinal lavage during a thoracotomy or warm peritoneal irrigation during a laparotomy would be intuitive. Postoperatively, introduction of fluids into any thoracoabdominal compartment would be detrimental in patients at risk of an abdominal compartment syndrome. Many, if not most, polytraumatized patients are not candidates for systemic heparinization and therefore are not suitable for standard cardiopulmonary bypass.
Active external rewarming
Active external rewarming may increase peripheral cellular metabolic activity, especially if shivering occurs, diverting blood flow to the periphery and exacerbating hypoperfusion of the core.31 The use of active external rewarming may also induce “rewarming shock” caused by peripheral vasodilatation when the periphery is rewarmed in the setting of an overall reduced intravascular volume.38,53,54 Volume and circulatory status must therefore be closely monitored.31,44,45 A further theoretical concern is premature inhibition of shivering by preferential warming of the skin and muscles since cold stress responses can be evoked by both central and peripheral thermoreceptors. 49,53,60 This may contribute to further cooling of the thermal core despite the initiation of peripheral warming, an effect known as “after-drop.”54
Active internal (core) rewarming
Core rewarming takes advantage of the introduction of heat to large surface areas such as the lungs, peritoneum, pleural cavities or endothelium (vasculature). Invasive core re warming has the potential advantage of rewarming the brain, heart, lungs and other core organs simultaneously so that, theoretically, perfusion should increase in concert with the increasing metabolic demands of the vital organs.31 Besides the vascular and respiratory routes, heat can be transmitted through the peritoneal, pleural or pericardial cavities with dialysate warmed up to 45 °C.53,61 Other potential routes of organ irrigation such as the bladder and colon may not be particularly effective owing to the limited surface area warmed.53
Extracorporeal blood rewarming
In accidental hypothermia, cardiopulmonary bypass has been recommended as the resuscitative method of choice for any severely hypothermic patient or any moderately hypothermic patient with hemodynamic instability.16,29,61 Standard renal hemodialysis circuits with heated dialysate may also be used.13 The requirement for systemic heparinization generally limits these strategies in multiply injured patients. Recent technical advances have brought a new generation of extracorporeal warming devices that may obviate the need for systemic heparinization.
Gentilello and associates25 adopted a simple technique to provide extracorporeal blood warming using percutaneous femoral access, known as continuous arteriovenous rewarming. No pump is needed with this system as perfusion of the heparin-bonded heat exchanger is dependent on the patient’s blood pressure. If the patient’s hemodynamic status is suspect, extracorporeal pumps with heat exchangers may avoid the need for formal cardiopulmonary bypass. Gregory and colleagues58 described the clinical use of an effective venovenous circulatory system that did not require heparinization, presumably due to coincident coagulopathies in their hypothermic trauma population. Animal studies have documented deaths due to in-situ thrombosis of the extracorporeal circulation; therefore, standard monitors such as foam, clot and low-pressure detectors should be used with this technique.61 The development of centrifugal vortex bio-pumps that permit either partial cardiac bypass62 or venovenous bypass63 without heparinization will allow extracorporeal blood warming and cardiovascular support without systemic heparinization. If only warming not hemodynamic support is required, vascular access for the centrifugal vortex pump can be obtained percutaneously or through an open approach in both venous and arterial vessels. Further study will be required before widespread application can be recommended, but these techniques may bring extracorporeal strategies into the hands of a greater number of physicians.
Recommendations for treatment
Despite varying opinions, no differences in survival with the various treatment methods have been reported for hypothermic patients in general31,55,64 or for hypothermic trauma patients.25 As with so many other critical care situations, prevention of hypothermia is simpler and more effective than the treatment. Most of the preventive measures can be simply and cheaply instituted as part of a standard resuscitation. If faced with an unstable, moderately or severely hypothermic trauma patient, we would individualize the rewarming, based on the injuries present and body cavities involved. We would also critically evaluate what surgical interventions are urgently required and limit the duration of any operative procedure with a ready acceptance of an abbreviated, damage control approach. We would strongly advocate the avoidance of initiating or prolonging any surgical intervention in a class III or class IV hypothermic trauma patient. A suggested algorithm for our approach to the hypothermic trauma patient is given in Table IV.
Suggested Management of Hypothermia
Pronouncement of death
In general, no hypothermic patient should be pronounced dead without rewarming.17 The axiom is that hypothermic patients should not be considered dead until they are “warm and dead.” This has resulted in logistic strains beyond reason in many critical care settings. Exceptions to this axiom obviously include catastrophic injuries such as decapitations, significant anoxic events in normothermic patients who are subsequently without pulse or respiratory effort, and a serum potassium level greater than 10 mmol/L.17,33,65
Specific therapeutic applications of hypothermia in trauma
For select clinical settings, hypothermia may benefit the trauma patient and may be deliberately induced by caregivers. Resuscitative hypothermia constitutes post-insult therapeutic hypothermia and is distinguished from protective (pre-treatment) or preservation (intra-insult) hypothermia. 66 A promising area of current clinical application is the use of moderate hypothermia in traumatic brain injury. Some deeply hypothermic trauma patients have survived remarkably long periods of pulselessness when purposely not rewarmed before definitive control of the cardiorespiratory system with extracorporeal resuscitation. Large animal studies of novel methods of resuscitation suggest potential means of extending a patient’s viability until emergency surgical interventions can be undertaken. It must be remembered that these are controversial or experimental uses of hypothermia used in select patients.
Hypothermia in traumatic brain injury
In 1993, 3 small preliminary studies documented decreased intracranial pressures (ICPs) and cerebral metabolic requirements, and found trends toward an improved neurologic outcome with cooling in severe traumatic brain injury.67–69 These studies targeted patients with nonpenetrating brain injury and excluded those with major systemic trauma associated with hypotension or hypoxia. 67,68 They were followed by a larger study by Marion and colleagues from Pittsburgh.70 This study showed improved outcomes in a group of severely brain injured patients with Glasgow Coma Scale (GCS) scores of 5 to 7 on admission, who were cooled to 33 °C within a mean of 10 hours after injury and were maintained at this temperature for 24 hours.70 This treatment provided little benefit in patients with initial GCS scores of 3 or 4.70 Seventy-three out of 155 patients with severe head injuries were excluded, including those with prolonged hypotension or hypoxia, who would presumably be those with the most severe extracranial systemic injuries. Although one of the early studies67 suggested a nonsignificant trend toward increased sepsis in the hypothermia group, this trend was not replicated in the study of Marion and colleagues.70
Hypothermia has long been known to decrease cerebral blood flow by 6% to 7% per degree Celsius as well as to decrease brain volume, cerebral venous pressure and cerebrospinal fluid volume.10,14,35,71 Although hypothermia is known to reduce the cerebral requirements for oxygen, the true benefits of hypothermia are likely more complicated.66 Hypothermia may reduce the actual basal cerebral metabolic rate rather than just electrophysiologic activity.70 The attenuation of brain injury is believed to be from reducing cerebral ischemia, edema and tissue injury, and in helping to preserve the blood–brain barrier, reducing extracellular excitatory neurotransmitters, or by suppressing the post-traumatic inflammatory response. 66,68,70 Significantly lower concentrations of the excitatory neurotransmitter glutamate and the cytokine interleukin-1β have been detected in the cerebrospinal fluid of cooled versus non-cooled patients having severe head injury.68,70
We currently use therapeutic hypothermia in the treatment of severe head injuries. This technique is not applied to patients until other systemic injuries are identified and managed, and hemodynamic stability is assured. Our severely head injured patients are treated in accordance with standard therapies, including the prompt surgical evacuation of intracranial hemorrhage, maintenance of cerebral perfusion as reflected by jugular bulb venous extractions (CvO2ER), and following and treating increased ICPs with sedation, neuromuscular blocking agents, osmotic diuretics and cerebrospinal fluid drainage as appropriate. 72 All severely head-injured patients are considered potential candidates for resuscitative (post-insult) cooling in the early post-injury period when the patient’s neurologic course is uncertain. If the patient’s ICP and CvO2ER are stable at 24 hours, hypothermia will be cautiously withdrawn. Cooling is instituted as long as there is difficulty in controlling ICP and maintaining an adequate CvO2 ER. Mild infections are not considered a contraindication to cooling, although the patient is warmed if there are concerns regarding systemic effects of infection. There is no arbitrary time to which the application of hypothermia is limited.
Utilizing resuscitative hypothermia in patients with traumatic brain injuries is an admittedly controversial clinical area. Animal models that have specifically included the secondary injury that frequently occurs clinically have failed to show a benefit of postinjury hypothermia.73 Animal work also raises the possibility that post-insult hypothermia only delays rather than prevents the loss of selectively vulnerable neurons.66,74 Some authors caution against the routine use of hypothermia for head injuries and are particularly concerned about core after-drop, cardiovascular instability, shivering and increased ICPs that may be seen upon rewarming.34 Future clarification of the role of hypothermia from a randomized multicentre trial is anticipated.
Accidental deep hypothermia with circulatory arrest
Trauma patients who are deeply hypothermic and have no vital signs are a rare but fascinating subset for whom attempts at early prehospital rewarming may be counterproductive. If these same patients were normothermic or mildly hypothermic, no resuscitative efforts would be justified, recognizing the universally dismal results of out-of-hospital arrest in blunt trauma.
Walpoth and colleagues75 have recently reported a remarkable series documenting 15 of 32 long-term survivors of accidental deep hypothermia who suffered prolonged circulatory arrest before rewarming. Nine of these 15 patients were environmentally exposed after traumatic injuries. Nine were without vital signs on discovery, and 6 suffered arrest a mean of 14 minutes into transport. The initiation of a perfusing circulation on cardiac bypass required an average time of 141 minutes. The patients were intubated and cardiopulmonary resuscitation was instituted, but no attempt at rewarming was made before the initiation of bypass. At long-term follow-up (mean 6.7 years), there were no hypothermia-related sequelae that impaired the quality of life of these patients, and all had resumed their former lifestyles. Based on these findings, the authors recommended against attempts at rewarming outside the hospital, 76 a departure from the standard recommendations.29,31,77 The data are limited and patients in this subset are few. The high survival in a usually dismal situation is intriguing and deserves further evaluation.
Deep hypothermic circulatory arrest
Case reports are beginning to report the successful salvage of patients whose injuries were repaired in bloodless fields, with the patient protected by profound hypothermia. This technique may permit repair of what are considered to be technically irreparable injuries (in a perfused operative field), such as retrohepatic caval injuries due to either blunt or penetrating causes.78,79 The patient’s blood volume is effectively drained into the venous reservoir of the heart–lung machine to be reinfused once vascular integrity is re-established. At present, these techniques are only appropriate when there are no other extensive injuries (especially head injuries) that preclude systemic heparinization, and the appropriate personnel and cardiac bypass equipment are available and rapidly accessible.
Suspended animation
Controlled profound hypothermia as an adjunct to a state of suspended animation has recently been entertained as a realistic goal by reputable investigators.18–21 Suspended animation has been defined as the protection and preservation of the whole organism during prolonged clinical death, for transport and repair (resuscitative surgery) without a pulse, followed by delayed resuscitation to complete recovery.19 Dogs have survived normothermic hemorrhagic shock followed by up to 60 minutes of suspended animation with ultraprofound hypothermic circulatory arrest at 5 °C and have recovered completely with histologically “clean” brains.80 This has required the use of extra-corporeal circulation to induce and reverse the state of suspended animation, utilizing heparin-bonded circuitry, obviating the need for systemic heparinization.21,81 It is certain that induction of suspended animation independent of cardiopulmonary bypass and extension of the tolerance of total circulatory arrest beyond 1 hour after normothermic shock will require further developments in basic and clinical science. With a committed and active scientific community currently exploring these issues, this approach may one day provide the ultimate damage control approach to allow evacuation and delayed surgical repair of otherwise lethal injuries.
At present, the technical limitations of quickly accessing the central circulation and instituting extracorporeal circulatory support with which to cool an injured patient are logistically limiting. Japanese investigators have developed a portable manual extracorporeal circulatory system, but this is in its technical infancy.82 A more practical strategy may be that of emergency hypothermic aortic arch flushing.65 This simpler approach has provided a remarkably normal neurologic outcome despite 15 minutes of exsanguinated cardiac arrest in large animal studies. The technique involves the early institution of mild cerebral hypothermia (35.8 °C) by a single flush of cooled saline administered through a catheter directed into the aortic arch through a femoral artery.83 Such a technique might facilitate evacuation to a definitive care centre with a pulseless but potentially viable victim.
Conclusions
Much remains to be learned about hypothermia in the trauma patient. Currently accepted surgical principles mandate the avoidance of hypothermia, which is seen as a predictor of a poor prognosis. We believe that the acutely traumatized patient must be evacuated promptly and resuscitated aggressively. Simple measures of avoiding prolonged exposure, warming blood, administering warm fluids, applying warmed gases, and using convective air blankets should be standard protocol through all phases of care (prehospital, Emergency Department, operative and critical care phases). Hypothermia must be suspected, prevented and treated early if it occurs in the polytraumatized patient. A modification to the classification of hypothermia in trauma patients and a management approach to these patients is suggested. Treatment must be individualized, based on the patient’s physiology and anatomy, the phase of care and the institution’s resources. Ongoing developments may one day radically alter our perspectives allowing modifications to our approaches to the most severely injured patients.
Acknowledgments
We thank John C. Fenwick, Director of Critical Care, Vancouver General Hospital, University of British Columbia, Vancouver, BC, for his editorial assistance.
Footnotes
Section editor: Dr. Donna I. McRitchie
Section Editor’s comments: Hypothermia in trauma patients continues to be a significant ongoing problem with most cases being iatrogenic. In the acute situation, there always seem to be more pressing, and sometimes overwhelming, issues to deal with than remembering to keep the patient warm and covered. By repeatedly bringing up this issue, we will remind ourselves to give it the priority it deserves.
- Accepted June 10, 1999.
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