How Useful are Hypothermia Blankets?
ABSTRACT & COMMENTARY
Synopsis: Hypothermia blankets are no more effective in lowering body temperature than other cooling measures in ICU patients with temperatures less than 104°F. Patients in whom hypothermia blankets were used had greater temperature swings and more episodes of rebound hypothermia. Use of hypothermia blankets is primarily initiated by the nursing staff.
Source: O’Donnell J, et al. Clin Infect Dis 1997;24: 1208-1213.
This prospective, observational study of patients with temperatures of 102.5°F or higher was carried out in five adult ICUs at a 540-bed tertiary care university hospital. Over a four-month period, there were 94 episodes of fever 102.5°F or higher (median maximal temperature, 103.1°F; range 102.5-106.5°F), and these patients were prospectively followed with collection of clinical outcomes data, patient temperatures, and the pharmacological and physical cooling measures employed.
Hypothermia blankets were employed during 39 (41%) febrile episodes. Factors identified by multivariate logistic regression as the strongest independent predictors of hypothermia blanket use included a maximum temperature of 103.5°F or higher, mechanical ventilation, and acute disease involving the central nervous system. Acetaminophen use, both rate and number of doses, did not vary between those patients treated with hypothermia blankets and temperature-matched controls. However, 36% of hypothermia blanket-treated patients received other cooling measures, such as ice packs, cool baths, or alcohol rubs, compared to only 6% of those not treated with blankets. Hypothermia blankets were ordered primarily by the nursing staff (85% of patients); positioning of blankets and machine settings varied widely.
Patients were stratified by 0.5°F temperature increments for comparisons between hypothermia blanket-treated patients and controls. Fifteen patients were excluded from this analysis due to early death, inadequate temperature collections, or defervescence of fever prior to blanket placement. For temperatures of 102.5-102.9°F, there were four patients in the blanket-treated group and 31 controls. For temperatures between 103°F and 103.4°F, there were 10 and 15 patients, respectively. For temperatures of 103.5-103.9°F, there were four and two patients, respectively. For temperatures higher than 103.9°F, there were 12 blanket-treated patients but only one control. The rates of temperature reduction for these groups was compared by Cox regression and analysis of variance.
The mean cooling rate was the same for both groups (0.028°F/hr), with a significant reduction in temperature occurring over the first 72 hours in all groups; there was no statistically significant difference between the two groups in the probability of becoming afebrile. However, hypotheria blanket-treated patients had more temperature "zigzags" (defined as temperature increase and decrease of ³ 3°F in a 24-hour period). Perhaps more importantly, rebound hypothermia (defined as a decrease in temperature to < 97°F after initiation of cooling intervention) occurred in eight of the study patients for a total of 16 episodes and did not occur in the controls. Two patients required active rewarming. O’Donnell and colleagues conclude that for patients with temperatures less than 104°F, hypothermia blankets do not cool patients any faster than other measures and result in more temperature fluctuations and rebound hypothermia.
COMMENT BY MARK T. GLADWIN, MD
This prospective, observational study of hypothermia blanket use is broadly applicable to critical care practice. Fever is a common occurrence in the ICU, and its causes are diverse. In this study, the primary etiologies of fever were identified as infection in 64%, central fever in 7%, drug fever in 3%, tumor fever in 1%, other causes in 3%, and undetermined in 21% of patients. The five-patient units studied included a coronary ICU, medical ICU, cardiothoracic surgery ICU, trauma/general surgery ICU, and a neurosurgical ICU. Not unexpectedly, hypothermia blankets were frequently employed for temperatures higher than 102.5°F (41% of febrile episodes). Interestingly, physicians were directly involved in the decision to place cooling blankets for only 15% of patients.
Control of fever with antipyretic medications and physical cooling measures is a common practice in ICUs and raises two important questions: Does this practice improve outcome, and are physical cooling measures more effective than acetaminophen, treatment of underlying disorders, and simple observation ("tincture of time")? O’Donnell et al attempt to answer this second question.
Although prospective, this study was not a randomized, controlled trial. As a result, unequal numbers of patients were treated with blankets vs. other measures (designated as controls). A temperature of 103.5°F or higher was one of the strongest independent predictors of use of hypothermia blankets, and every patient except one who developed a temperature higher than 103.9°F was treated with a cooling blanket. Thus, the data derived are only useful for temperatures between 102.5°F (study entry criterion) and 103.9°F. Within this range, there were only 18 blanket treated patients and 48 controls. However, the majority of ICU patients with fever fall within this range, and the study’s results suggest that hypothermia blanket use is no more effective than other cooling interventions.
O’Donnell et al theorize that this relative lack of efficacy may be due to a shivering response, and they cite three studies demonstrating that heat loss by conduction (such as hypothermia blankets, cold water immersion, and application of ice packs) is less effective and produces more shivering then heat loss by convection (via fans) or evaporation (using ice water or alcohol sponge baths) (Morgan SP. J Neurosci Nurs 1990;22:19-24; Tek D, et al. Emerg Med Clin North Am 1992;10:299-310; Wyndham CH, et al. J Appl Physiol 1959;14:771-776). However, since data on shivering were not sought prospectively in this study, the authors were unable to test this hypothesis.
Whether fever should be controlled at all is a more contentious issue, one not addressed in the present study. In attempting to answer this question, it is important to clearly distinguish fever from hyperthermia. Fever represents an increased temperature caused by the action of circulating pyrogenic cytokines on the hypothalamic set-point. Efferent autonomic nervous system output leads to cutaneous vasoconstriction, reduced sweating, and increased muscle tone or overt shivering. This must be differentiated from hyperthermia, a state of pyrexia characterized by a normal hypothalamic set point but a failure of the body to maintain the desired set point (Simon GB. N Engl J Med 1993;329:483-487). Hyperthermia can not be differentiated from fever based on temperature characteristics such as peak temperature, and the clinician must rely on historical clues.
Patients develop hyperthermia secondary to disorders of increased heat production such as exertional hyperthermia and heat stroke, malignant hyperthermia, thyrotoxicosis, pheochromocytoma, delirium tremens, drug abuse (cocaine and amphetamines), and status epilepticus, as well an in disorders of diminished heat dissipation such as classic heat stroke, extensive use of occlusive dressings, dehydration, autonomic dysfunction, and use of anticholinergic medications. Heat stroke is commonly seen in elderly patients taking diuretics or anticholinergic medications. These medications impair diaphoresis, making the patient susceptible to even mild ambient temperature elevation. Patients with heat stroke present acutely with temperatures often higher than 40°C, delirious, hypotensive, and tachycardic. Disseminated intravascular coagulation, elevation of serum muscle enzymes, rhabdomyolysis, and electrolyte and acid-base disturbances often follow.
Malignant hyperthermia is a rare autosomal dominant condition triggered by inhalational anesthetic agents and depolarizing muscle relaxants (succinylcholine) and is thought to be mediated by excessive calcium release into skeletal muscle, resulting in muscle hypermetabolism. Severe hyperthermia up to 45°C, with muscle rigidity, hypotension, and lactic acidosis manifests immediately to as late as 11 hours after anesthetic delivery.
Neuroleptic malignant syndrome has mixed pathogenesis with skeletal muscle spasticity leading to heat generation, impaired hypothalamic thermoregulation, and autonomic dysfunction preventing heat loss. Many neuroleptics can trigger this disorder, including phenothiazines (chlorpromazine-Thorazine), anti-emetics (reglan-Metoclopramide, compazine-Prochlorperazine), and the commonly used medication, haloperidol. Hypothalamic injury is the final and least common cause of hyperthermia and includes various disorders such as cerebrovascular accident, encephalitis, sarcoidosis, and trauma.
While severe hyperthermia is clearly associated with a poor outcome if untreated, the outcome of fever, an adaptive response to infection and tissue injury, is likely benign (Kluger MJ, et al. Infect Dis Clin North Am 1996;10:1-20). There are three lines of evidence that support an adaptive value of fever. The first is evolutionary and derives from the observation that both warm blooded (endothermic) and cold blooded (ectothermic) vertebrates will mount a fever in response to injected bacteria and endotoxin. The argument follows that fever is energetically expensive, and if it were not adaptive, it would not be conserved over millions of years. The second line of evidence stems from correlational studies. Studies in humans and animals have correlated degree of body temperature elevation with survival rate. Toms and colleagues (Br J Exp Pathol 1977;58:444-458) studied ferrets infected with influenza virus and found an inverse relationship between the presence of live virions in nasal washings and the rectal temperature. The third line of evidence comes from studies of antipyretic medications and environmental induction of hypothermia or hyperthermia in animals. Medications that lower temperature have been demonstrated to worsen mortality in rabbits, goats, and lizards subjected to a variety of infectious insults. For more information, the reader is referred to recent reviews: Klein NC, et al. Infect Dis Clin North Am 1996;10:211-216; Mackowiak PA. Ann Intern Med 1994;120:1037-1040.
It appears that fever may have evolved as a host defense mechanism that enhances host immunologic responses and weakens some pathogenic microorganisms. On the other hand, fever increases metabolic rate and oxygen consumption and may be detrimental to the ICU patient with inadequate nutrient and cardiopulmonary reserve. Until we understand more about the outcome of fever in the critically ill patient, a course of moderation is advised. Aggressive efforts to control fever may do more harm than good, as evidenced by the observed 16 episodes of blanket-induced rebound hypothermia in this study.
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