T H E J O U R N A L OF
PEDIATRIC S MAY
1992
Volume 120
Number 5
MEDICAL PROGRESS Accidental hypothermia Howard M. Corneli, MD From the Department of Pediatrics, University of Utah College of Medicine, and the Emergency Department, Primary Children's Medical Center, Salt Lake City, Utah
A child recovers completely after more than an hour's submersion in an icy Utah stream1; another survives 40 minutes under the ice of a Norwegian river. 2 A third child returns to normal after 21/2 hours without a puise, 3 and a fourth is revived from a body temperature of 15 ~ C (59 ~ F). 4 Such dramatic survivals after accidental hypothermia are now well known.5 Children may be especially susceptible to the combination of rapid cooling and preserved circulation that appears to provide a protective effect. 6 Nevertheless, although hypothermia sometimes affords protection against anoxia that would otherwise prove fatal, 7 it is often an ominous sign.81~ Children are at extraordinary risk for death or disability from accidents that cause hypothermia, especially drowning. 11 This paradox has given rise to the realization that hypothermic protection is unusual, and that even optimal management may not produce a good outcome. Pediatricians should, however, be prepared to manage accidental hypothermia so as to increase each patient's chance of survival. Fortunately, the "shroud of mystery" that has surrounded the treatment of accidental hypothermia 12 has begun to lift in recent years. ETIOLOGY Hypothermia, defined as a core temperature below 3 5 o C, may result from any of a host of insults to homeostasis: Environmental exposure Immersion Reprint requests: Howard M. Corneli, MD, Emergency Department, Primary Children's Medical Center, 100 N. Medical Dr., Salt Lake City, UT 84113. 9/18/34715
Trauma Shock Sepsis Iatrogenic causes (medical transport and treatment) Alcohol and drugs (e.g., barbiturates) Anorexia nervosa Malnutrition (tropical hypothermia) Hypoglycemia Water intoxication Burns Dermatoses Hypothyroidism, hypoadrenalism Hypothalamic lesions Children lose heat more easily because of their large surface-to-mass ratio and their decreased insulation by fat. "Urban hypothermia" among adults often occurs with exposure involving inebriation, trauma, or mental aberration, CPR ECC VF
Cardiopulmonary resuscitation Extracorporealcirculation Ventricular fibrillation
or with inadequate heating in housing for the elderly) 2, 13 Children are subject to accidental hypothermia from exposure, but they are especially at risk for immersion hypothermia, which combines rapid cooling with hypoxic injury to multiple systems, especially the central nervous system. Children also have iatrogenic cooling during medical transport and treatment. Both adults and children are increasingly exposed to hypothermia associated with outdoor recreation. This article will not consider other forms of hypothermia, 671
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T a b l e I. Physiology and clinical signs in hypothermia
Core temperature
Physiology
Signs
31 ~176 C (88o-95 ~ F)
Increased BMR, "r Vasoconstriction Mild tachycardia ADH increase
Shivering Cyanosis Clumsiness, dysarthria Diuresis
29%31 ~ C (84-88 ~ F)
Decreasing BMR, Vo2 Decreased cerebral blood flow Acidosis or alkalosis Fluid shift
Shivering stops Confusion, delirium Muscle rigidity Decreased or absent BP
Hypovolemia 25%29 ~ C (77~
~ F)
<25 ~ C (<77 ~ F)
Loss of Erythema, edema thermoregulation Vasodilation Stupor, coma Decreased HR, SV, CO Pulselessness Slowed nerve conduction Absent reflexes Suspended CNS activity Fixed, dilated pupils Decreased cardiac Dysrthythmias conduction Increased cardiac Ventricular fibrillation irritability Apnea Asystole
Appearance of death
Allchangesshownmayvary in temperatureof onset.Not all signscorrespond to the physiologicchanges shownon the same line of the Table. ADH, Antidiuretichormone;BMR, basalmetabolicrate; BP,bloodpressure; CNS, centralnervoussystem;CO,cardiacoutput;HR, heart rate; SV, stroke volume; F-Oe,oxygenconsumption. including induced (therapeutic), inadvertent (perioperative), and neonatal hypothermia) 4-~7 Cold injuries such as frostbite and pernio (chilblains) are beyond the scope of this review but are discussed elsewhere. 18' 19 PATHOPHYSIOLOGY An understanding of hypothermia requires a discussion of how the human body loses heat. 2~ Radiation, heat energy leaving the skin at the speed of light, accounts for perhaps half of all heat loss even in a warm room, and even more as the temperature of the surroundings decreases. H u m a n skin is a nearly perfect radiator, especially when wrapped around a spheroid such as the human head; 75% of heat loss at - 1 5 ~ C (5 ~ F) can occur through the head. Conduction of heat is poor in air but 24 times faster in water. Hypothermia has occurred after several hours of immersion in water as warm as 16 ~ C (65 ~ F). Wet clothing loses most of its insulating ability because of conduction. Cold ground, snow, and metal (whether an airplane fuselage or metal stretcher) are also excellent heat sinks. Convection occurs as warm air next to the skin is replaced by cool air. Even in still conditions, convection carries off
roughly 25% of lost body heat; in a 63 k m / h r (35 mph) wind, this increases by 14 times. Evaporation from the skin accounts for only about 7% of heat loss at rest but can carry off up to six times the body's basal metabolic rate. Respiratory heat losses combine several of these mechanisms to account for approximately 14% of heat loss at rest. This loss increases with exertion or altitude, especially in cold or dry air. Almost all body systems react to cold. Table I presents some of the more important physiologic changes and associated findings. Much of our understanding of this pathophysiology comes from controlled hypothermia in cardiac surgery.14, 23 Reuler24 wrote a complete review of the physiology of hypothermia. The central features result from decreases in mental function, respiration, metabolism, cardiac output, cardiac stability, vasomotor regulation, and blood volume. At a body temperature greater than approximately 30 ~ to 32 ~ C, compensatory mechanisms work to restore homeostasis. At less than this temperature, thermoregulation begins to fail. Over the next few degrees of cooling, to approximately 28 ~ C (82 ~ F), a process of dangerous and often lethal decompensation begins. This process creates an inability to rewarm spontaneously. At less than 25 ~ to 28 ~ C, many patients will appear dead, and in this range many undergo asystole or ventricular fibrillation, the lethal dysrhythmias that form the final pathway of hypothermic death. It is only at this stage, however, that hypothermia affords significant protection; most survivors of prolonged immersion have core temperatures less than 28 ~ to 30 ~ C, 5 and patients may tolerate anoxia for up to 60 minutes or longer at 20 ~ C. Although the progression outlined in Table I is valid for most patients, individuals vary in their appearance at a given temperature. In general, neurologic signs such as pupillary reactivity and deep tendon reflexes tend to decrease with increasing hypothermiaY Some patients will have clouded mentation even with mild hypothermia; others may be responsive to voice or pain at 20 ~ to 27 ~ C. 13, 25 In part this difference may be due to slower cooling, providing time for adaptation. Changes in mentation may produce behavior that leads to further cooling. Confusion causes some victims to engage in paradoxical undressing, and others to press on with hikes or climbs when wiser and warmer companions see the need to turn back. Paradoxical, dangerous, clumsy, or confused activity should lead supervisors of youth sports and outings to suspect hypothermia. The changes in cardiac rhythm are also unpredictable. Case reports abound in which sinus rhythm was detected at least initially during severe or profound hypothermia; one patient had a heart rate of 50 beats/min and spontaneous respirations at 21.5 ~ C. 26 Although children are said to be
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more prone to asystole than are adults, 27 ventricular fibrillation often develops in children. On the electrocardiogram, the so-called J wave, or Osborn wave, forms a characteristic hump at the J point immediately after the QRS complex. Although almost pathognomonic of hypothermia, this wave does not occur in all cases; its incidence ranges from 11% in some series 13 to 80% in others. 28 Of the many other electrocardiographic changes that occur, relatively few affect treatment. 29 Several factors promote circulatory collapse in hypothermia. Stroke volume, filling pressure, contractility, and heart rate all decline. Hypovolemia and sludging of blood follow extravasation of intravascular fluid and marked diuresis. Vasodilation completes the process, and muscle rigidity makes the measurement of blood pressure and pulse difficult even when some circulation persists. Metabolic processes slow by approximately 6% for each 1~ C decrease in body temperature; at 28 ~ C the basal metabolic rate falls by half. Breathing may be extremely slow and shallow. Hypoventilation and decreased dissociation of oxyhemoglobin further impair delivery of oxygen by a sluggish circulation; fortunately, oxygen demand also decreases. Protection against anoxia is a direct result of decreased cellular metabolism. Such protection has been attributed to a "diving reflex" akin to that seen in deep-diving mammals. 3~ Some evidence questions the presence of such a reflex in human beings.31 In any case, the apparent requirement for survival would be that metabolism decrease before hypoxia becomes critical; that is, that cooling take place before circulatory arrest leads to cellular ischemia. The renal effects of hypothermia include a brisk diuresis, resulting in part from decreased tubular reabsorption32 but also from decreased production of antidiuretic hormone. This in turn results from the early phase of vasoconstriction, which forces blood to the core and causes central volume receptors to sense increased blood volume. This perceived volume excess is augmented in cases of immersion by the hydrostatic squeeze of the surrounding water. 33 Other physiologic changes may be unpredictable; both hypoglycemia and hyperglycemia are common (hypoglycemia may cause hypothermia). Variable findings include, among others, hypokalemia or hyperkalemia and alkalosis or acidosis. Victims of severe hypothermia may meet their physiologic needs despite marked hypotension, bradycardia, and hypoventilation, whereas overly aggressive treatment of these findings has been linked, at least anecdotally, with cardiac arrest, usually caused by VF. Frequent case reports describe victims of hypothermia, found with signs of life, who undergo cardiac arrest during rescue or resuscitation.6, 8, 13, 27, 34, 35 By contrast, other reports describe victims in whom a perfusing cardiac rhythm persists despite marked hypotension and bradycardia; these victims tend to be easier to rewarm and are more likely to recover. 26, 36
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Several factors may cause death after rescue. Temperatures continue to decline for some time after a victim is removed from a cold environment. This "afterdrop" was long thought to be due to the return of cold blood from the periphery to the core; in part it may be. 37 Experimental evidence with physical models3s and with blood flow in volunteers 39 suggests, however, that some of the afterdrop may result from the ongoing conduction of heat from the warmer core into colder surface layers. The distinction becomes important in treatment, because the "circulatory" model argues against peripheral rewarming, whereas the "conduction" model indicates that afterdrop would persist regardless of rewarming strategies. In fact, clinical reports suggest that both models possess some validity; afterdrop occurs in most types of rewarming but may be decreased when peripheral warming is withheld. Perhaps a more critical cause of death after rescue is "rewarming shock," For reasons discussed above, victims of hypothermia have marked circulatory insufficiency. The additional metabolic burden of rewarming, the removal of a hydrostatic squeeze (in cases of immersion), and additional vasodilation all create a setting in which the diminished circulation can no longer meet physiologic demands. 33,4~ Finally, almost all experts agree that rough handling, overly aggressive manipulation, the sudden influx of cold fluids, and exertion by the patient all contribute to some cases of sudden death after rescue. DIAGNOSIS The diagnosis of hypothermia requires only two essentials: a low-recording thermometer and a high index of suspicion. Ordinary thermometers do not record less than 34 ~ C (94 ~ F). Low-recording thermometers should be stocked in any complete medical kit, from the physician's office to the search-and-rescue storeroom. Alternatives available in most hospitals include temperature probes (from the newborn nursery or anesthesiology department), laboratory or ordinary room thermometers, and indirect tympanic thermometers. Core temperatures may best be measured at the tympanic membrane; esophageal and bladder temperature probes are also useful.41 Deep rectal temperatures require that a thermometer be inserted at least 10 cm into the rectum; such measurements are adequate, although subject to artifact and time lags. Measurement of oral temperature during hypothermia is unreliable. The risk of missing the presence of hypothermia is very real. Persons treating children need to recall that any severe injury or illness can be associated with hypothermia. Unexpected hypothermia often occurs in victims of trauma, 42 as well as in those exposed to any degree of cold, wet, or wind. Hypotbermia can be stratified both by severity (Table I) and by acuity. Acute hypothermia refers in generaI to cases
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following immersion in icy water. Subacute hypothermia usually develops after environmental exposure to cold air for a period of hours. Chronic hypothermia develops after a period of days of milder exposure; this form is less common in children. Submersion hypothermia should he seen as acute hypothermia with the added injuries of a neardrowning accident. COMPLICATIONS Hypothermia gives rise to a number of complications: Pneumonia Pulmonary edema Adult respiratory distress syndrome Sepsis Immune complex suppression Rhabdomyolysis Acute tubular necrosis Disseminated intravascular coagulation Thrombocytopenia Decreased platelet function Cerebral edema Pancreatitis Hypoglycemia or hyperglycemia Prolonged coma Slow neurologic recovery (up to 6 months or more) Fitzgerald and Jessop 43 provided a more complete discussion. Coagulopathy, pulmonary disease, central nervous system dysfunction, sepsis, immune complex suppression, and renal failure are especially common and likely to require intensive care even after rewarming is complete. When a near-drowning accident occurs, it is now generally accepted that aggressive control of intracranial pressure by means of barbiturate coma and induced hypothermia does not add to survival rates. 7 All other efforts at supportive care are probably indicated for near-drowningvictims with hypothermia who respond to initial resuscitation and rewarming. One complication, prolonged coma and gradual recovery, may be especially important to pediatricians. In children Who have recovered normal neurologic function after a hypothermic near-drowning accident, a protracted course appears more the rule than the exception. 1,5 TREATMENT If the first step in treatment is to recognize hypothermia, the second is to understand the protection afforded by hypothermia. On one hand, victims warmer than 30 ~ to 32 ~ C will not enjoy hypothermic protection, but they usually rewarm with removal from cold and simple warming measures. On the other hand, victims of severe or profound hypothermia often appear beyond resuscitation but may make
The Journal of Pediatrics May 1992
striking recoveries. A Swiss climber returned to work 2 weeks after being rewarmed from 19 ~ C and an hour of asystole without cardiopulmonary resuscitation, plus 2 more hours with CPR. 44 The appearance of death is common in patients cooler than 25 ~ to 28 ~ C, and ordinary rules of thumb for prognosis fail: in a series of adults with hypothermia, the Glasgow Coma Scale score, trauma score, and CRAMS score (circulation, respiration, abdomen, motor, speech) all failed to predict outcome. 45 Patients have survived more than 3 hours of asystole46 or 4 hours of CPR. 47 Rescuers need to recognize hypothermia and prevent further heat loss; the need for shelter, dry insulation, and some form of warmth will be obvious. Rewarming during transport has been criticized, the conventional wisdom being that it is harmful to warm the patient before supportive measures can be instituted--that rewarming be withheld to maintain hypothermic protection. As previously noted, external rewarming may be ineffective or even dangerous in severe hypothermia. In fact, however, many patients arrive colder at the hospital than when they left the scene. General rewarming measures include heating transport vehicles, removing wet or cold clothing, covering with dry blankets, administering warmed fluids intravenously, administering heated and humidified oxygen, and handling gently. The concept of leaving patients in a "metabolic icebox," whether in transport or at the hospital, is falling out of favor. Despite the theoretic advantages of hypothermic protection,48 it is becoming clearer that continued hypothermia is dangerous and deleterious. Another contentious topic has been the how and when of advanced life support in hypothermia. Most authors believe that if a patient has severe hypothermia, any breathing and any perfusing rhythm are probably sufficient, regardless of rate and regardless of the depth of respiration or the blood pressure. 49-53Most would withhold artifical respiration and chest compressions to avoid the risk of precipitating VF. If no breathing is present, an airway should be provided as gently as possible, first by positioning but, if unsuccessful, then by inserting an oral airway or by endotracheal intubation. Despite concern that intubation has precipitated VF in isolated cases, 47 experiments in dogs 54 and experience with large series of human subjects 12 suggest that intubation in patients with hypothermia is safe. Overventilation should be avoided. Knowing when to provide CPR is more difficult, and current recommendations represent a consensus of expert opinion. If core temperature is unknown, CPR should be started for apparent cardiac arrest, sl If a patient is known to be severely cold (<28 ~ C) and an electrocardiographic monitor shows a perfusing rhythm, regardless of rate, many authors would withhold CPR even in the absence of a palpable pulse) ~ Some would go so far as to withhold CPR in
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a pulseless, severely hypothermic patient even in the absence of a monitor49; most would not. 51, 52 The logic for these opinions (with the recognition that a controlled study would be difficult) follows from observations that effective perfusion is often restored with rewarming, that rewarming is more effective when any circulation is present, that VF (or asystole) slows most rewarming efforts, that CPR may precipitate VF, and that CPR is even less effective during hypothermia. 55 On the other hand, the evidence that CPR precipitates VF is circumstantial. Certainly no one should hesitate to provide CPR if the core temperature is unknown or is warmer than 28 ~ C, if the patient is pulseless after a thorough check for a pulse (many authors recommend checking for up to 1 minute to be certain) and no monitor is available, or if a monitor shows absence of narrow-QRS activity. Furthermore, prolonged CPR may be tolerated without sequelae. Work in animals suggests that CPR may not lose its effectiveness with time in hypothermia, as is the case at normal temperatures. 55 In the past it was suggested that CPR in hypothermia be performed at half the usual rate, but, at least until more is known about the mechanisms of CPR during hypothermia, normal rates should be employed. As follows from our discussion of hypovolemia and rewarming shock, volume expansion becomes an essential component of resuscitation.56 Various reports indicate that from 14% to 35% of blood volume can be lost at temperatures in the range of 20 ~ to 25 ~ C. 57 Most health care providers view "room temperature" fluids as thermally neutral, but at 21 ~ C "room temperature" is in fact colder than all but the coldest patients. Rapid influx of room-temperature fluids leads to further cooling and can cause VF. Isotonic crystalloid solutions (0.9% sodium chloride or lactated Ringer solution) should be warmed to approximately 40 ~ C (see discussion of rewarming, below) and infused rapidly in doses of 20 ml/kg as needed. Monitoring of central venous pressure provides a rough guide to volume resuscitation. If intravenous access proves difficult, intraosseous infusion may be useful. Military antishock trousers (MAST) appear ineffective in hypothermia 58 and could theoretically be harmful. 59 Experts agree that relatively few drugs are indicated in severe hypothermia, because most will have prolonged half-lives, with undesirable consequences after rewarming.23, 43, s2 Some drugs show diminished effectiveness; others (e.g., morphine) may have increased or altered effects. 6~ Drugs generally not recommended" include sodium bicarbonate, 61 insulin (hyperglycemia, though often present, resolves with rewarming), corticosteroids, antibiotics (except to treat known infections), and, contrary to folk wisdom, ethanol.
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T a b l e II. Rewarming methods Passive
Active external
Core
Warm room Warmed blankets Warm IV fluids (21~ ~ C) (36~ ~ C) Dry blankets Chemical Heated, humidified hot packs oxygen (40o-44~ C) Plumbed blankets, Warmed lavage Monitor pads Radiant warmers, Gastric, colonic lights Hot baths, Bladder immersion Partial (trunk) Pleural, pericardial immersion Peritoneal dialysis Hemodialysis Extracorporeal circulation
Glucose should be administered initially; despite the frequent presence of hyperglycemia, hypoglycemia can also accompany hypothermia and is a more immediate threat to the patient. Adrenergic medications, especially dopamine, have been shown to support blood pressure during hypothermia.62, 63 Lidocaine appears safe (although its efficacy is uncertain). Bretylium, in some case reports, has been associated with spontaneous defibrillation of hypothermic patients.64,65 In animal studies, however, bretylium did not appear to provide chemical defibrillation,66 and protection against the onset of fibrillation did not reach statistically significant levels. 6v The fact that some dogs underwent VF during infusion of bretylium makes its prophylactic use somewhat dubious; in the patient who has VF, attempts at chemical defibrillation may be warranted. Electrical defibrillation may be attempted at any temperature, but most efforts do not succeed until the temperature reaches 28 ~ to 30 ~ C. Rather than increasing the energy delivered at low temperatures, it may be wise to suspend unsuccessful attempts until warmer temperatures are reached. It is important to monitor the following: core temperatures (repeatedly or on a continuous basis), electrocardiographic tracings, vital signs including blood pressure, serum glucose and electrolyte levels, arterial blood gas levels (see next paragraph), urine output, and results of urinalysis. Diagnostic tests in cases of unknown cause should include thyroid function tests, toxin screening, ethanol levels, serum amylase, and tests for infection. One of the longest-lasting controversies in hypothermia revolves around whether or not to correct blood gas values for temperature. Because blood gas machines test samples at 37 ~ C, tables have been constructed to show the "actual" gas tensions and pH at the patient's temperature. (Uncorrected pH is lower than corrected values; uncorrected
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oxygen and carbon dioxide pressures are higher.) This logic possesses intuitive appeal, and rational arguments can be offered for temperature correction. 68 A more recent school of thought, however, draws on clinical,24 physiochemical,61 and even comparative physiologic69, 7o arguments to suggest that, at least for pH and carbon dioxide pressure, uncorrected values better reflect physiologic states, make analysis and diagnosis easier, and provide better outcomes. The details of these arguments would take too long to explicate here. Delaney et al. 71 recently reviewed arguments on both sides and explained the implications of either choice, deciding finally against correction of pH and carbon dioxide pressure. Children with hypothermia should probably receive 100% oxygen; correction (decreasing) of oxygen pressure is acceptable but may not change initial therapy. Pulse oximetry and transcutaneous measurement of gas tensions in severe hypothermia may be rendered inaccurate by decreased perfusion. REWARMING
The single topic that has provided the greatest debate in hypothermia is rewarming. Most authors divide rewarming into three broad classes: passive rewarming, active external rewarming, and core rewarming. Table II lists the modalities used in each. A rewarming method that proves safe for elderly patients with a mild degree of chronic hypothermia cannot be presumed to be safe for an inebriated adolescent who has slept in a snowbank, or effective for a child who has fallen into an icy river. Rewarming methods differ in availability, in ease of use, and in their potential disadvantages. Different patients will respond to the same methods with different rewarming rates. 72 One of the most critical factors hastening rewarming will be a preserved circulation. As Myers et al. 6s note, "Mortality rates, rather than warming rates, should dictate choice of therapy." Passive rewarming, initially designed for elderly persons with chronic hypothermia, requires that patients produce heat spontaneously (i.e., have mild hypothermia) and be stable. Passive rewarming is associated with a high mortality rate in adults with severe hypothermia. 73 In neonatal hypothermia, which might be held to be a pediatric analog of chronic hypothermia in adults, rapid rewarming produces better results. 15 Early theory, based in part on inhuman Nazi experiments now thoroughly stripped of credibility,74 favored active external rewarming. Other reports have suggested that active rewarming can be dangerous, 75 but it is now believed that much of the adverse outcome in those cases involved inadequate volume resuscitation and supportive care. 4~ Active external rewarming (also called surface rewarming) can provide more rapid return of normothermia. Other advantages may include availability and technical simplicity. On
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the negative side, excessively warm beat packs have burned cold patients with decreased cutaneous circulation. 76 Decreased circulation also renders surface warming less effective. Some methods limit access to the patient. Most important, peripheral vasodilation and the dumping of cold, acid blood into the core circulation may potentiate afterdrop, rewarming shock, and VF. Although modern practice has increasingly turned, therefore, to core rewarming, it would be unwise to abandon external rewarming altogether. Warm blankets and pads, lamps, and chemical heat packs (those which do not exceed 45 ~ C) are excellent devices for rewarming the patients with mild hypothermia who are frequently seen in emergency departments. In some settings (small hospitals, for instance) a hot bath may be the only practical means of providing large amounts of heat rapidly. This method has been effective in patients with preserved circulation, even in the face of severe hypothermia. Core methods seem more difficult than external rewarmins, but the simplicity of warming intravenously administered solutions and humidified oxygen places core rewarmins within reach of almost any provider. These methods are limited in the amount of heat they can transfer to the patient, 68 but they prevent further heat loss and provide essential support. They can be sufficient to provide slow rewarming in patients with intact circulation. 36 Parenteral solutions in plastic bags can be heated in a microwave oven, 77 and heated, humidified oxygen can be delivered both by the familiar heated humidifier and by various portable devices. 78 Providers utilizing warm fluids should make sure that they are actually delivering the warmth to the patient; even shortened intravenous tubing results in cooling of the fluids. 79 Many commercial blood warmers both limit flow rates and provide ineffective heating of fluids,s~ Warmed gastric lavage or enemas are also within the purview of most emergency centers and provide considerable heat transfer. Peritoneal dialysis can be achieved at many secondary centers, sl as can closed pleural lavage, which has the potential to provide even larger amounts of heat.S2, 83 Pleural lavage has supplanted open pericardial lavage; the cold, stiff myocardium is not susceptible to direct cardiac massage, and thoracotomy forfeits the closedchest mechanics of standard CPR. Hemodialysis employing a blood warmer may prove useful in dealing with overdose of certain drugs (e.g., barbiturates) when accompanied by hypothermia. Finally, anyone who has ever struggled for hours to rewarm a patient with circulatory arrest can appreciate the potential advantages of rewarming by extracorporeal circulation with a heart-lung machine. This technique has been used in patients with extreme hypothermia. The advantages include extremely rapid rewarming from the
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core outward, the support of circulation, the provision of volume replacement and oxygenation, the reversal of hemoconcentration, and decreased stress to the myocardium. 84 Such advantages are especially clear in the patient with asystole or VF, although excellent results have been reported in patients with intact circulation as well. Beyond its contraindication in major trauma (because anticoagulation is employed), the limitations of ECC center around availability. Many medical centers provide ECC for adults and adolescents. The application of pediatric techniques will be readily available only in tertiary centers providing pediatric cardiac surgery.I, 4 Pediatricians without local access to such a center should bear in mind that rapid rewarming by ECC has revived patients from profound hypothermia even after 3 hours of transport. 44 The alternative in such cases may be hours of unrewarding effort, with CPR performed throughout the ordeal. Such logic should prompt referral of severely hypothermic children with asystole or VF (who have some hope of resuscitation) to regional tertiary care centers that can also provide critical care. Extracorporeal circulation is not a panacea; most published successes involve isolated case reports. This therapy will not revive patients who are dead, and should be avoided where safer methods suffice. It would be wrong to assume that one is powerless without access to such techniques; successful resuscitations using simpler methods, even in profound hypothermia, continue to be reported. Rather than aiming for a certain rewarming rate, providers should select the methods from among those available that best suit the individual patient. Patients with severe to profound hypothermia require core rewarming. Those with moderate hypothermia and intact circulation may be rewarmed successfully with a combination of heated intravenously administered fluids and heated, humidified oxygen plus gentle external rewarming. Mild hypothermia will usually respond to external measures alone. If the selected methods fail to rewarm the patient, a more aggressive method is required. Failure to rewarm with the most aggressive available methods after an extended effort will probably result in death. The answer to the question of which patients to rewarm continues to evolve. 85 Any patient with even a chance of hypothermic protection deserves an attempt at rewarming. The longest reported period of submersion with intact survival is now 66 minutes. Should we withhold resuscitation efforts in patients submerged in ice-cold water for 70 minutes, or for 90 minutes? For patients without submersion, extreme duration of exposure is not incompatible with life. Few of the reported survivals would have occurred without the courage of clinicians who challenged conventional wisdom about who could be saved. Limits to resuscitation do exist, however. Hypothermia does not alter the presence of obvious fatal injuries. Failure
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to restore a circulating cardiac rhythm within about 30 minutes after rewarming to 32 ~ to 35 ~ C makes further efforts unlikely to be successful. Efforts to develop laboratory markers of actual death (e.g, severe hyperkalemia >10 mmol/L or serum ammonia >250/zmol/L) 34, 86 have thus far been based on limited experience or disparate cases and should be viewed as preliminary.85 Cool-water drowning does not offer the protection offered by ice-cold water. In Seattle, where icy water temperatures are uncommon, Q u a n e t al. 1~ found no protective effect of hypothermia. Orlowski 53 noted that water colder than 10 ~ C (50 ~ F) accounts for all reported cases of survival after prolonged (>_15 minutes) submersion, and 16 of 17 cases probably involved water colder than 5 o C (41 ~ F). Even in ice-water drowning, hypothermia by no means guarantees survival; patients may still die of anoxia as well as lung injury, multisystem failure, or trauma. Rapid cooling with brief immersion suggests preserved circulation and a better chance for survival; contrariwise, little cooling after long submersion suggests a grave prognosis. PREVENTION If hypothermia is bad for patients, if only near-drowning in the coldest water can offer protection, and if hypothermic protection is the exception rather than the rule, it will be obvious that prevention of hypothermia is far more useful than treatment. Efforts to decrease drowning accidents have been discussed extensively in the pediatric literature. 11 Pediatricians must help to bring these issues before legislative councils, parents' groups, and the media. Traditional drown-proofing techniques, with the head held in the water, place children at increased risk of chilling in icy water. Even strong swimming skills become useless in icy water, where gasping and incoordination rapidly develop. Instead, children in parts of the country with icy water temperatures should be taught the heat-escape-lessening position (HELP), in which the arms are held tightly to the anterior axillary line and the knees are flexed to the chest. 87 As a quick trial in a pool will demonstrate, such a position requires some sort of flotation device; a life vest is doubly important in cold water, because it will further decrease heat loss from the trunk. Beyond drowning, persons involved in sports and outdoor recreation must work to increase awareness of hypothermia. Children can enjoy mountaineering, hiking, white-water boating, and other sports, but they cannot be expected to employ the abstract reasoning involved in preparing against cold and wet in the outdoors. Finally, just as iatrogenic hypothermia is now seen as a preventable complication of newborn resuscitation, the same mentality should come into play throughout pediatrics and the emergency medical services to prevent chilling of ill
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a n d injured children during rescue, transport, and treatment. REFERENCES
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