Services on Demand
Print version ISSN 0034-7094
Rev. Bras. Anestesiol. vol.56 no.1 Campinas Jan./Feb. 2006
Hipotermia no período peri-operatório*
Hipotermia en el período perioperatorio
Camila B. BiazzottoI; Márcio BrudniewskiI,II; André P. SchmidtI,II; José Otávio Costa Auler Júnior, TSAIII
IMédico Especialista em Anestesiologia
pelo CET da Disciplina de Anestesiologia do Hospital das Clínicas da Faculdade
de Medicina da Universidade de São Paulo
IIMédico Preceptor do CET da Disciplina de Anestesiologia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
IIIProfessor Titular da Disciplina de Anestesiologia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo
BACKGROUND AND OBJECTIVES: Perioperative
hypothermia is a common event, however seldom diagnosed and treated. Hypothermia
may be beneficial or noxious for the patient depending on specific situations
and procedures. This paper is a literature review of hypothermia indications
and complications, as well as its diagnosis, prevention and treatment.
CONTENTS: Major perioperative causes and complications of hypothermia are presented, in addition to its benefits.
CONCLUSIONS: Perioperative hypothermia may be due to direct anesthetic inhibition of thermoregulation, decreased metabolism and loss of heat to the cold environment of operating rooms, even with active warming. When it is inadvertent, it may be associated to several complications, but when adequately indicated, it may protect vital organs such as central nervous system and heart. Normothermia decreases undesirable hypothermia effects, being warming the most effective preventive method. Active or passive warming approaches should be adopted and muscle shivering should be adequately treated to prevent discomfort and increased metabolic demand.
Key Words: COMPLICATIONS: hypothermia; HYPOTHERMIA: cardioprotecion, neuroprotection; PHYSIOLOGY, Temperature
JUSTIFICATIVA Y OBJETIVOS:
La hipotermia ocurre frecuentemente durante el período perioperatorio,
siendo, sin embargo, raramente diagnosticada y tratada. La hipotermia puede
ser benéfica o perjudicial al paciente dependiendo de la situación
y del procedimiento específico. Este artículo tiene como objetivo
hacer una revisión de la literatura sobre las indicaciones y complicaciones
de la hipotermia, así como su diagnóstico, prevención y tratamiento.
CONTENIDO: Son presentadas las principales causas y complicaciones de la hipotermia perioperatoria, bien como sus beneficios.
CONCLUSIONES: La hipotermia puede ocurrir durante el acto anestésico-quirúrgico debido a la inhibición directa de la termorregulación por los anestésicos, a la disminución del metabolismo y a la pérdida de calor para el ambiente frío de las salas quirúrgicas, mismo con la utilización de calentamiento activo. Cuando ocurre de forma inadvertida, puede estar asociada a numerosas complicaciones, pero cuando bien indicada puede proteger órganos vitales, como el sistema nervioso central y el corazón. La manutención de la normotermia reduce los efectos indeseables de la hipotermia, siendo la prevención a través del calentamiento el método más efectivo. Estrategias de calentamiento activo o pasivo deben ser empleadas y los temblores musculares deben ser adecuadamente tratados, previniendo el malestar y el aumento de la demanda metabólica.
Core body temperature is one of the most strictly controlled physiological parameters. Human thermoregulating system allows ranges from 0.2 to 0.4 ºC around 37 ºC to maintain metabolic functions1.
Unintentional perioperative hypothermia, defined as core blood temperature below 36 ºC, is a common event, due to direct thermoregulation inhibition of anesthetics, decreased metabolism and exposure to the cold environment of operating rooms2,3. When body cavities are exposed during surgical procedures, there might be further heat loss4. Didactically, hypothermia is classified in mild (34 to 36 ºC), moderate (30 to 34 ºC) and severe (below 30 ºC)5.
Perioperative temperature monitoring provides early detection of hypothermia and may help perioperative thermal control. Body temperature maintenance during surgery is important because hypothermia is associated to several complications. However, when adequately indicated, it may protect vital organs in which ischemia is expected, such as neuronal and myocardial cells. Deep global hypothermia is the primary technique to protect central nervous system (CNS) in procedures requiring circulatory stop, but its use is limited due to the need of cardiopulmonary bypass (CPB)6.
Decreasing concentration of anesthetic drugs in the CNS during anesthesia recovery allows the body to restart its thermoregulating responses. Body temperature tends to return to normal. Residual anesthesia and opioids employed to control postoperative pain decrease the efficacy of such responses. The time needed for such may vary from 2 to 5 hours, depending on the level of hypothermia and the age of the patient7.
Hypothalamus is the primary temperature regulation site, integrating thermal impulses from skin and deep tissues. When these impulses exceed the temperature thresholds in any direction, autonomic thermoregulating responses arise, which maintain temperature within adequate levels8,9.
Thermoregulating control precision is similar for males and females8,9, though decreased in elderly and severely ill patients. Major responses to hypothermia are skin vasoconstriction, nonshivering thermogenesis, shivering and behavioral changes. Skin vasoconstriction is the first and most important autonomic response to hypothermia, decreasing heat loss to the environment in 25%10.
Behavioral changes seem to depend more on skin temperature than on environment, allowing humans to live in places with temperature extremes11. Skin blood flow may be divided in two compartments: nutritional, represented by capillaries, and thermoregulator, represented by arterial-venous shunts. The thermoregulating flow is mediated by norepinephrine in a2-adrenergic receptors and may be decreased up to 100 times during hypothermia, especially in distal parts of the body12.
Nonshivering thermogenesis is caused by increased metabolic heat production and oxygen consumption, without muscle work increase. Its major sources are skeletal muscles and brown adipose tissue. It is the primary neonate and infant thermoregulating mechanism13, with minor contribution in adults14,16. The stimulation of a3-adrenergic receptors on brown adipose nervous terminations is responsible for the production of heat17.
Muscle shivering is an involuntary activity present only during a maximum vasoconstriction state and, as nonshivering thermogenesis, it is not enough to maintain body temperature1,18. Muscle shivering determines increase in oxygen consumption of approximately 200% to 600%, in addition to triggering sympathetic discharge, increased intracranial and intraocular pressure and myocardial ischemia19-21. Thermoregulation efficacy varies according to age. The elderly have lower vasoconstrictor response as compared to youngsters, and lower shivering threshold, being prone to hypothermia even when exposed to normal temperature22. Children and neonates, especially prematures, have limited vasoconstriction and low efficacy or even no shivering23. The lower the age, the higher the skin heat loss due to large relative body surface24.
HEAT PRODUCTION, DISTRIBUTION AND LOSS
The body produces energy and totally converts it into heat according to its metabolic need. At rest, the major tissues responsible for producing heat are the brain, the liver and the heart. Major human metabolism substrates responsible for heat production are glucose (4.1 kcal.kg-1), protein (4.1 kcal.kg-1) and lipids (9.3 kcal.kg-1). During anesthesia there is decrease in metabolic rate, oxygen consumption and heat production25.
To help understanding heat distribution in the body, it may be divided in two major thermal compartments: I. Core - made up of highly perfused tissues in which temperature remains relatively constant and higher (major body organs and CNS). It represents 50% to 60% of total body mass and is responsible for the production of all energy converted into heat26; II. Peripheral - made up of tissues with heterogeneous temperature, which varies according to the environment (upper and lower limbs, skin and subcutaneous tissue). It is the largest compartment, with temperatures in general 3 to 4 ºC below core temperature. However, this difference may increase or decrease during extreme thermal or pathological conditions27,28.
The skin is a barrier between core and peripheral compartments and the environment, and approximately 90% of all heat produced is lost through its surface. Internal redistribution of heat in the body after anesthetic induction is the main cause of perioperative hypothermia and is a function of the temperature gradient between core and peripheral compartments. Several factors can influence this gradient, including room temperature, the amount of adipose tissue and anesthetic drugs. This mechanism is responsible for 81% of the core temperature reduction during the first hour after anesthetic induction and 43% in the two subsequent hours29. Individual response intensity to heat distribution is unpredictable.
Vasoconstriction maintains core heat and decreases the loss to the environment. Conversely, vasodilatation promotes heat transfer to the periphery, which does not necessarily mean heat loss to the environment. Obese patients present lower incidence of perioperative hypothermia because they have a lower redistribution gradient due to more adipose tissue and more heat production30.
Exposure to surgical environment leads to heat loss to the environment through four mechanisms: irradiation, conduction, evaporation and convection31. Irradiation is heat loss through radiant energy to walls and solid objects. It depends on the absolute temperature difference between two surfaces to the fourth, representing 70% of total heat loss at 22 ºC32.
Conduction depends on the temperature difference between two objects in contact and on the conductance between them. One example would be heat loss to the operating table metal surface. Heat is also lost thru the evaporation of fluids applied to the skin, sweating and fluid loss by the respiratory system, surgical wound and skin. Conduction and evaporation together sum other 15% of total heat lost during anesthesia and surgery. Convection is heat loss or gain by the passage of a fluid in a certain temperature through a surface with different temperature. It is more intense when there is air shift in large spaces and is responsible for the remaining 15% heat loss from the body to the environment. Blood flow exhibits both convective and conductive components, being the former more important than the latter, especially when patients remain in operating rooms at low temperatures33.
In general, core temperature decreases 1 ºC in the first 40 minutes after anesthetic induction due to peripheral vasodilation and internal heat redistribution29. All patients submitted to procedures lasting more than 30 minutes should have their temperatures monitored and maintained in approximately 36 ºC, unless hypothermia is specifically indicated. Patients submitted to major surgeries under regional anesthesia should also have their temperature monitored34.
The site for the transducer placement should be carefully chosen according to the surgical procedure. Core temperature may be measured in the pulmonary artery, tympanic membrane, nasopharynx and distal esophagus35-38.
Oral, axillary, vesical or rectal thermometers may give reliable peripheral temperature measurements, unless patients are under extreme thermal conditions, such as during rewarming after cardiopulmonary bypass.
During liver transplantation, the exposure of receptors diaphragm muscle to the cooled graft of the donor leads to decreased esophageal temperature. In this case, a vesical thermometer provides a closer reading to pulmonary artery temperature39. In open chest procedures, esophageal temperature also does not thoroughly reflect core temperature due to cavity exposure to room temperature, being recommended the use of tympanic membrane or nasopharynx. Tympanic membrane seems to be the ideal core temperature monitoring site because it is very close to CNS and precisely reflects brain temperature, provided the sensor is well positioned37. During cardiac procedures, vesical temperature is a reasonable alternative when urinary flow is adequate. However, when it is low, measured temperature does not correspond to real temperature40. Axillary temperature corresponds to core temperature when the arm is adequately abducted. It is however less reliable than vesical and esophageal measurements41.
ETIOLOGY OF PERIOPERATIVE HYPOTHERMIA
Anesthetic induction is responsible for about 20% reduction of metabolic heat production, in addition to abolishing physiological thermoregulation responses normally triggered by hypothermia. If temperature is not actively maintained, hypothermia may arise. Most anesthetics have vasodilating properties and all of them change core temperature control by inhibiting thermoregulating responses against cold, such as vasoconstriction and muscle shivering42-44. Opioids45 and propofol46, for example, linearly decrease vasoconstriction and shivering threshold. Halogenate agents47,48, on the other hand, decrease the response threshold to cold in a non-linear pattern.
Consequently, thermoregulating responses of anesthetized patients will be triggered at a lower temperature as compared to non-anesthetized patients1. Care should be taken to warm patients and reduce their temperature loss to the environment before hypothermia triggers peripheral vasoconstriction. Once vasoconstriction is triggered, it becomes highly effective to prevent additional hypothermia10. Anesthetic-induced vasodilation mildly increases skin heat loss49, suggesting that this is not the major cause of post-anesthetic hypothermia. Primary mechanism is heat redistribution from the core to the peripheral compartment by circulatory conduction and convection, leading to decreased core temperature and increased peripheral temperature, however without changing mean body temperature and body heat content33,50. The same effect has been shown during regional anesthesia51.
Hypothermia during general anesthesia is developed in three stages. First there is a fast core temperature decrease by redistribution after anesthetic induction. This is followed by a linear temperature decrease (0.5 to 1 ºC/h) as long as the difference between the rates of heat metabolic production and loss to the environment persists. When the threshold temperature is reached, vasoconstriction is triggered creating a heat flow restriction between compartments, providing less internal heat distribution and heat loss to the environment.
The maintenance of metabolic heat production, in spite of continuous loss, generates a temperature plateau which is able to reestablish normal gradient between compartments. The last stage is then reached, characterized by a new thermal balance, now at a lower value52-54. When patients recover from anesthesia under hypothermia, shivering is promptly triggered to compensate intraoperative heat deficit and increase core temperature. Primary shivering consequences are increased oxygen consumption, extreme discomfort and difficult monitoring.
Spinal anesthesia inhibits central thermoregulating control through peripheral sympathetic nervous system and motor nerves block, abolishing vasoconstriction and shivering55-57. Redistribution is limited to lower limbs and remains as the major cause of perioperative hypothermia for those patients. Its magnitude varies according to patients initial thermal status and may be attenuated by warming lower limbs before anesthetic induction58.
Since there is less initial redistribution in patients under regional anesthesia, linear hypothermia will be triggered at a higher temperature, resulting in 50% less temperature decrease as compared to general anesthesia. Linear hypothermia is developed at a lower rate, since metabolic heat production rate remains close to normal. The presence and extension of sympathetic and motor blocks prevent the development of thermoregulating vasoconstriction and this linear stage is not interrupted, as seen with general anesthesia.
As a consequence, patients submitted to major procedures under regional anesthesia are at increased risk of severe hypothermia34. Body areas free from sympathetic and motor block may trigger thermoregulating responses if lower shivering threshold is reached, provided that the patient is not elderly59 or is not excessively sedated45,46. However, shivering restricted to upper extremities is relatively ineffective and insufficient to prevent additional hypothermia. Regional anesthesia-induced hypothermia is common60 and depends more on surgical procedure magnitude and duration than on patients characteristics. Temperature measurement and diagnosis of hypothermia are uncommon, unless when it is already expected.
Among different monitoring sites during spinal anesthesia, it has been observed that more accurate measures are obtained from rectal temperature due to compensatory skin vasoconstriction above blockade level61,62.
Combined anesthesia poses the highest risk of unintentional perioperative hypothermia. Initial redistribution in the four limbs promptly leads to hypothermia and the linear stage is developed at a higher rate. Regional anesthesia per se decreases vasoconstriction threshold and when superimposed to general anesthesia their effects are added. As result, vasoconstriction is lately triggered and at lower temperatures63. On the other hand, general anesthesia inhibits shivering, which could increase internal heat production during spinal anesthesia. But the most important factor of the association is the abolishment of lower limbs vasoconstriction due to peripheral nerves block. Central vasoconstriction alone is ineffective, and temperature continues to drop, reaching no plateau62,64,65.
CONSEQUENCES OF PERIOPERATIVE HYPOTHERMIA (CHART I)
Currently, perioperative normothermia is a recognized goal. However, inadvertent moderate hypothermia is often seen. Further studies are still needed to outline mechanisms of hypothermia-related complications and to develop practices to reestablish perioperative thermal balance.
Adrenergic responses to moderate perioperative hypothermia lead to energetic myocardial demand and consumption imbalance. This in turn may result in acute myocardial infarction, which is one of the major unpredictable causes of perioperative morbidity/mortality. Studies indicate that perioperative myocardial ischemia is not associated to shivering alone, but rather to hemodynamic stress produced by cold-induced sympathetic-adrenal activation19,66,67.
Even mild hypothermia increases catecholamine serum levels leading to tachycardia, hypertension, systemic vasoconstriction and myocardial oxygen supply and demand unbalance, in addition to increasing myocardial irritability19. Franck et al., in a randomized study (active warming versus routine) with 300 high risk patients to determine whether moderate perioperative hypothermia would increase the incidence of cardiovascular events, have observed that the incidence of myocardial ischemia and ventricular tachycardia was 3 times higher in hypothermal patients21. Hypothermia per se does not trigger coronary vasoconstriction, but is associated to increased cardiac work.
So, it may predispose to myocardial ischemia if the patient has some degree of coronary obstruction67. Other complication probably related to hypothermia is deep vein thrombosis (DVT) due to vasoconstriction favoring venous stases and hypoxia. Further studies are still needed to confirm this hypothesis68.
Although platelet count is normal during hypothermia, morphological changes suggestive of platelet activation are obseved69, especially when the hypothermal blood is exposed to platelet activators70, such as CPB circuit and atherosclerotic plaques. Tests such as prothrombine time (PT) and activated partial thromboplastin time (APTT) remain normal because they are performed at 37 ºC regardless of patients temperature71. When performed at patients temperature, they show changes due to decreased coagulation cascade enzyme reaction speed72. Fibrinolysis is not affected at temperatures below 34 ºC and is enhanced during hyperthermia, what leads to the hypothesis that hypothermia-induced coagulopathy does not result from excessive fibrinolysis73.
Thromboelastogram studies suggest that hypothermia affects more clot formation than degradation74. Two randomized controlled studies have confirmed that a 0.5 ºC decrease in core temperature in patients submitted to hip arthroplasty under regional anesthesia is associated to higher blood loss and higher need for allogeneic transfusion56,75.
The incidence of operative wound infection is related to decreased subcutaneous oxygen tension68 and it has been proven in humans that it is decreased by thermoregulating vasoconstriction. Hypothermia has a direct effect on cell and humoral immunity50,52, and an indirect effect through decreased O2 supply to peripheral tissues76,77. Decreasing core temperature in 1.9 ºC triples the incidence of surgical wound infection after colon resection and increases in 20% hospital stay, which also increases hospital costs. It is still not well established whether hypothermia is related to other infections such as pneumonia78-80.
During hypothermia, steroid secretion is initially unchanged. However, as it persists, steroid suppression may occur81. Thyroxin production is increased due to increased thyroid-stimulating hormone (TSH) release82. The release inhibition and decreased activity of insulin, in addition to decreased renal glucose loss and increased catecholamine secretion result in hyperglycemia83. However, hypoglycemia is seen in 40% of patients. During rewarming there might be severe hypoglycemia with brain injury. So, there should be rigid glycemic control and hyperglycemia should not be treated during hypothermia84.
PHARMACOKINETICS AND PHARMACODYNAMICS (CHART II)
Atracurium duration is less dependent on core temperature because 3 ºC decrease increases its duration in 60%85. Neostigmine efficacy in reverting neuromuscular block is not changed during moderate hypothermia86. Propofol plasma concentration increases 30% during continuous infusion when patients core temperature is decreased 3 ºC. Inhalational anesthetics tissue solubility is increased in hypothermal patients and anesthesia recovery is prolonged since higher amount of anesthetics has to be eliminated. In addition, one can expect a 5% halothane and isoflurane MAC decrease for each degree of core temperature reduction87. Lenhardt et al. have published a clinical randomized double-blind trial with 150 patients submitted to major surgical procedures and have related perioperative hypothermia to prolonged anesthetic recovery and longer PACU stay, even when discharge criteria did not include normothermia74.
General anesthesia deeply inhibits body thermoregulating defenses against hypothermia and this is the reason why shivering is seldom seen in anesthetized patients. Anesthetic recovery allows the reappearance of thermoregulating responses. Shivering is then triggered to compensate intraoperative heat output and to increase core temperature at the expenses of increased metabolic rate and oxygen consumption7. This sensation is extremely uncomfortable, and would justify prevention and treatment by itself, even in the absence of other hypothermia-related complications88. Shivering is not effective during regional anesthesia, and when severe, it may interfere with the procedure or even prevent the mother of holding her child after a Cesarean section. Elderly and weak patients have less effective shivering as compared to young patients22.
Hypothermia is related to hypokalemia, hypophosphatemia and hypomagnesemia, but clinical significance of such changes is not adequately established89-91.
Bupivacaine cardiotoxicity is increased during hypothermia92. Pulse oximetry is also changed by decreased peripheral perfusion triggered by vasoconstriction93,94, which may impair monitoring.
BENEFITS OF HYPOTHERMIA
Hypothermia protects against neuronal and myocardial ischemia. Under adequately controlled conditions, it promotes well known brain protection in patients with neurological disorders. There are ongoing studies looking for adequate active cooling methods and drugs to decrease body thermoregulating responses to hypothermia, which would make cooling a fast and safe method.
Studies are still needed to confirm the benefits of hypothermia in patients with stroke, subarachnoid hemorrhage (SAH) and severe brain trauma (SBT). Minor brain temperature decrease (2 to 4 ºC) may reduce ischemia-induced neurological injury. Just as hypothermia may bring benefits, hyperthermia, even late, may worsen neurological recovery after stroke and its prevention is also important95-97.
Neurosurgery, carotid endarterectomy, cardiopulmonary bypass and hemodynamic instability may lead to brain ischemia. Some studies advocate moderate hypothermia for severe TCE. Marion et al. have shown that induced moderate hypothermia for 24 hours in patients with Glasgow comma scale between 5 and 7 has accelerated neurological recovery98. However, Hartung and Cottrell have questioned the statistical analysis of such study99. To date, there are no human studies ratifying moderate hypothermia during surgical procedures. Hindman et al. have investigated patients submitted to cerebral aorta aneurysm clipping and have observed that induced hypothermia during HSA has improved clinical recovery100.
During myocardial ischemia, changed cell metabolism associated to reperfusion injury contributes to cell death extending from necrosis epicenter to periphery. Hypothermia protects myocardium against ischemia, but the exact protection mechanism is still undefined. A possible explanation would be decrease in metabolic demand associated to myocardial ATP reserves preservation during ischemia, maintaining cell integrity101,102.
Most myocardial oxygen consumption is related to its electromechanic activity. Since cardioplegia abolishes heart contractions, hypothermia brings minor additional contribution103.
Myocardial hypothermia may be induced during cardiac procedures regardless of systemic temperature, and during reperfusion, myocardial normothermia is promptly reestablished. This way, it is possible to promote myocardial protection without exposing patients to the risk of systemic hypothermia76.
Recent studies have shown that hypothermia does not promote coronary vasoconstriction in healthy adults and, as opposed to what would be expected, an increased myocardial perfusion is observed. However, it has not been proven that acute myocardial infarction (AMI) patients benefit from hypothermia and myocardial protection has not yet been established67. There are only experimental evidences that mild hypothermia promotes post-AMI protection104-106.
Hypothermia seems to be beneficial for Adult Respiratory Distress Syndrome (ARDS) patients107, as well as for patients susceptible to malignant hyperthermia (MH). An experimental study has shown lower MH incidence in susceptible patients submitted to hypothermia, in addition to less severe crises once triggered77.
PREVENTION AND TREATMENT
The risk-benefit analysis of high-risk surgical patients favors the maintenance of core normothermia in the perioperative period. Randomized studies have confirmed that normothermia decreases complications30. The most effective method to maintain normothermia is prevention by previous warming108-113. After anesthetic induction with no previous warming, hypothermia occurrence is common, even if active intraoperative warming is employed.
Redistribution hypothermia is a relatively slow and difficult to treat process. Previous warming increases peripheral compartment heat content, decreasing redistribution gradient. Skin warming with circulating air at 43 ºC for one hour transfers enough heat to decrease redistribution effects. This warming does not increase core temperature, but sweating and thermal discomfort may occur after prolonged warming114.
Warm air circulation (thermal blanket) is the most effective noninvasive warming method currently available and increases core temperature in 0.75 ºC/hour in mean. Another method to increase peripheral heat content and prevent redistribution is patients previous vasodilatation. This consists on the administration of vasodilators from 12 h up to 1 h before anesthesia (20 mg oral or 10 mg sublingual nifedipine). The administration should allow time enough for the thermoregulating system to increase peripheral temperature without the risk of decreasing core temperature115.
Room temperatures above 23 ºC will maintain or reestablish normothermia during anesthesia, however they generate thermal discomfort for the surgical-anesthetic team and worsen their cognitive performance. As a consequence, active or passive warming strategies should be adopted. Passive warming is a low cost and effective method, consisting in intraoperatively covering and warming all possible skin surfaces with sheets, blankets or plaids. It may decrease heat loss in 30%116. Blankets warming do not generate additional heat transfer, just making them more comfortable117.
Active warming, the most effective method, may revert already installed hypothermia. Total area to be covered is critical. Anterior region warming is more effective than warming the region in contact with the operating table since little heat is loss to it. Blankets or mattresses with water circulation are only beneficial when placed over the patient. Electric blankets may also be used116. Skin warming is effective when thermoregulating vasoconstriction has already been installed. Peripheral vasodilatation induced by anesthetic agents promotes intercompartment heat transfer, helping the transfer of heat applied to skin surface to the core compartment118. Warm solutions are useful when infused in a rate over 2 liters in 1 hour119. One liter of crystalloid at room temperature decreases core temperature in 0.25 ºC120. Warming and humidification of gases administered to the patient have minor impact on body temperature24.
SHIVERING PREVENTION AND TREATMENT
Normothermia is the primary method to prevent shivering, which is common in the post-anesthetic recovery unit. When present, it should always be treated due to all its previously mentioned consequences, in addition to the discomfort it brings.
Most anesthetic agents promote dose-dependent decrease of shivering threshold, even in the absence of hypothermia, which justifies shivering prevention in the post-anesthetic recovery unit, even when there has been no significant core temperature change during surgery.
Postoperative shivering is treated with active skin warming and/or opioids. Any drug decreasing shivering threshold will effectively treat it. Opioids are first choice drugs because they promote minor sedation in addition to controlling pain, which in general coexists with shivering.
Skin contains 20% of all body thermal afferents and heat transfer increases temperature above shivering threshold, leading to their abolishment. Patients recovering from general anesthesia should be submitted to warming of all possible skin surfaces. Those recovering from spinal anesthesia should have only the skin surface with preserved sensitivity warmed to prevent burnings. A limitation of this technique is its low ability to increase core temperature121. Alfentanil and sufentanil are knowingly effective, but none is to be compared to meperidine, which promotes a disproportional decrease in shivering threshold, with unknown action mechanism though. Clonidine may also be used85,86,122-124. Shivering during regional anesthesia may be treated with systemic or spinal opioids125.
Although perioperative normothermia is an accepted primary goal, unintentional hypothermia is frequent during anesthetic-surgical procedures due to several mechanisms, specially the internal heat redistribution between core and peripheral compartments, which is a direct function of their temperature gradient. Hypothermia during anesthesia develops in three stages. General anesthesia usually ends up in a thermal balance state, which may reestablish the gradient between compartments.
This balance is not reached during regional anesthesia since thermoregulating vasoconstriction and shivering are abolished due to sympathetic nervous system and motor nerves block. Combined general and regional anesthesia poses an additional risk of unintentional perioperative hypothermia.
Hypothermia triples the incidence of adverse myocardial events, significantly increases intraoperative bleeding and the need for transfusion, as well as the incidence of surgical wound infection and hospital stay. Pharmacokinetics and pharmacodynamics of most anesthetics are also changed, prolonging anesthetic recovery.
Children, elderly, obese and severely ill patients exhibit abnormal responses to hypothermia. On the other hand, deep global hypothermia is the primary brain protection technique for procedures requiring circulatory stop. The exact myocardial protection mechanism, widely used during cardiac surgeries, is still not defined, as well as it is not confirmed that AMI patients benefit from hypothermia. It is critical, then, to prevent and treat perioperative hypothermia aiming at decreasing noxious consequences and patients discomfort.
01. Sessler DI, Sladen RN - Mild perioperative hypothermia. New Engl J Med, 1997;336:1730-1737. [ Links ]
02. Vaughan MS, Vaughan RW, Cork RC - Postoperative hypothermia in adults: relationship of age, anaesthesia, and shivering to rewarming. Anesth Analg, 1981;60:746-751. [ Links ]
03. Sessler DI - Perioperative thermoregulation and heat balance. Ann N Y Acad Sci, 1997;813:757-777. [ Links ]
04. Hendolin H, Lansimies E - Skin and central temperatures during continuous epidural analgesia and general anaesthesia in patients subjected to open prostatectomy. Ann Clin Res, 1982;14:181-186. [ Links ]
05. Ganem F - Assistência à Parada Cardíaca, em: Auler Jr JOC, Oliveira AS - Pós-Operatório de Cirurgia Torácica e Cardiovascular, 1ª Ed, Porto Alegre, Artmed, 2004;212-215. [ Links ]
06. Neubauer RA, James P - Cerebral oxygenation and the recoverable brain. Neurol Res, 1998;20:(Suppl1):S33-S36. [ Links ]
07. Sessler DI, Rubinstein EH, Moayeri A - Physiologic responses to mild perianesthetic hypothermia in humans. Anesthesiology, 1991;75:594-610. [ Links ]
08. Lopez M, Sessler DI, Walter K et al - Rate and gender dependence of the sweating vasoconstriction, and shivering thresholds in humans. Anesthesiology, 1994;80:780-788. [ Links ]
09. Yousef MK, Dill DB, Vitez TS et al - Thermorregulatory responses to desert heat: age, race and sex. J Gerontol, 1984;39:406-414. [ Links ]
10. Kurz A, Sessler DI, Christensen R et al - Heat balance and distribution during the core-temperature plateau in anaesthetized humans. Anesthesiology, 1995;83:491-499. [ Links ]
11. Marks LE, Gonzalez RR - Skin temperature modifies the pleasantness of thermal stimuli. Nature, 1974;247:473-475. [ Links ]
12. Sessler DI, Ponte J - Shivering during epidural anesthesia. Anesthesiology, 1990;72:816-821. [ Links ]
13. Dawkins MJR, Scopes JW - Nonshivering thermogenesis and brown adipose tissue in the human newborn infant. Nature, 1963;206:201-202. [ Links ]
14. Bruck K, Baum E, Schwennicke HP - Cold-adaptative modifications in man induced by repeated short-term cold-exposures and during a 10-day and-night cold-exposure. Pflugers Arch, 1976;363:125-133. [ Links ]
15. Hynson JM, Sessler DI, Moayeri A et al - Absence of nonshivering thermogenesis in anesthetized adult humans. Anesthesiology, 1993;79:695-703. [ Links ]
16. Plattner O, Semsroth M, Sessler DI et al - Lack of nonshivering thermogenesis in infants anesthetized with fentanyl and propofol. Anesthesiology, 1997;86:772-777. [ Links ]
17. Takahashi H, Nakamura S, Shirahase H et al - Heterogeneous activity on BRL 35135, a beta 3-adrenoceptor agonist, in thermogenesis and increased blood flow in brown adipose tissue in anesthetized rats. Clin Exp Pharmacol Physiol, 1994;21:539-543. [ Links ]
18. Cohen M - An investigation into shivering following anaesthesia; preliminary report. Proc R Soc Med, 1967;60:752-753. [ Links ]
19. Frank SM, Higgins MS, Breslow MJ et al - The catecholamine, cortisol and hemodynamic responses to mild perioperative hypothermia. A randomized clinical study. Anesthesiology, 1995;82:83-93. [ Links ]
20. Motamed S, Klubien K, Edwardes M et al - Metabolic changes during recovery in normothermic patients undergoing surgery and receiving general anesthesia end epidural local anesthetic agents. Anesthesiology, 1998;88:1211-1218. [ Links ]
21. Frank SM, Fleisher LA, Breslow MJ et al - Perioperative maintenance of normothermia reduces the incidence of morbid cardiac events. A randomized clinical trial. JAMA, 1997;277:1127-1134. [ Links ]
22. Kurz A, Plattner O, Sessler DI et al - The threshold for thermoregulatory vasoconstriction during nitrous oxide/isoflurane anesthesia is lower in elderly than in young patients. Anesthesiology, 1993;79:465-469. [ Links ]
23. Bissonnette B, Sessler DI - Mild hypothermia does not impair postanesthetic recovery in infants and children. Anesth Analg, 1993;76:168-172. [ Links ]
24. Bissonnette B, Sessler DI - Passive or active inspired gas humidification increases thermal steady-state temperatures in anesthetized infants. Anesth Analg, 1989;69:783-787. [ Links ]
25. Fagher B, Monti M, Thulin T - Slective beta1-andrenoceptor blockade and muscle thermogenesis. Acta Med Scand, 1988;223:139-145. [ Links ]
26. Sessler DI - Perioperative heat balance. Anesthesiology, 2000;92:578-596. [ Links ]
27. Bristow GK, Biesbrecht GG, Sessler DI - Leg temperature and heat content in humans during immersion hypothermia and rewarming. Aviat Space Environ Med, 1994;65:220-226. [ Links ]
28. Buck SH, Zaritsky AL - Occult core hyperthermia complicating cardiogenic shock. Pediatrics, 1989;83:782-784. [ Links ]
29. Matsukawa T, Sessler DI, Sessler AM et al - Heat flow and distribution during induction of general anesthesia. Anesthesiology, 1995;82:662-673. [ Links ]
30. Schmied H, Kurz A, Sessler DI et al - Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty. Lancet, 1996;347:289-292. [ Links ]
31. English MJ, Farmer C, Scott WA - Heat loss in exposed volunteers. J Trauma, 1990;30:422-425. [ Links ]
32. Hardy JD, Milhorat AT, DuBois EF - Basal metabolism and heat loss of young women at temperatures from 22 degrees C to 35 degrees C. J Nutr, 1941;21:383-403. [ Links ]
33. Clark R, Orkin L, Rovenstine E - Body temperature studies in anesthetized man: effect of environmental temperature, humidity and anesthesia system. J Am Med Assoc, 1954;154: 311-319. [ Links ]
34. Frank SM, Beattie C, Christopherson R et al - Epidural versus general anaesthesia, ambient operating room temperature, and patient age as predictors of inadvertent hypothermia. Anesthesiology, 1992;77:252-257. [ Links ]
35. Webb GE - Comparison of oesophageal and tympanic temperature monitoring during cardiopulmonary bypass. Anesth Analg, 1973;52:729-733. [ Links ]
36. Mekjavic IB, Rempel ME - Determination of esophageal probe insertion length based on standing and sitting height. J Appl Physiol, 1990;69:376-379. [ Links ]
37. Sato K, Kane N, Soos G et al - Reexamination of tympanic membrane temperature as a core temperature. J Appl Physiol, 1996;80:1233-1239. [ Links ]
38. Stone JG, Young WL, Smith CR et al - Do temperature recorded at standard monitoring sites reflect actual brain temperature during deep hypothermia? Anesthesiology, 1991;75: A483. [ Links ]
39. Russell SH, Freeman JW - Prevention of hypothermia during orthotopic liver transplantation: comparison of three different intraoperative warming methods. Br J Anaesth, 1995;74:415-418. [ Links ]
40. van Westing J, Clinton CW - Use of intravesical temperature as a monitor of core temperature during and following general anaesthesia. S Afr J Surg, 2001;39:133-136. [ Links ]
41. Lefrant JY, Muller L, De La Coussaye JE et al - Temperature measurement in intensive care patients: comparison of urinary bladder, oesophageal, rectal, axillary, and inguinal methods versus pulmonary artery core method. Intensive Care Med, 2003;29:414-418. [ Links ]
42. Stoen R, Sessler DI - The thermoreglatory threshold is inversely proportional to isoflurane concentration. Anesthesiology, 1990;72:822-827. [ Links ]
43. Hynson J, Sessler DI - Intraoperative warming therapies: a comparison of three devices. J Clin Anesth, 1992;4:194-199. [ Links ]
44. Young CC, Sladen RN - Temperature monitoring. Int Anesthesiol Clin, 1996;34:149-174. [ Links ]
45. Kurz A, Go JC, Sessler DI et al - Alfentanil slightly increases the sweating threshold and markedly reduces of vasoconstriction and shivering thresholds. Anesthesiology, 1995;83:293-299. [ Links ]
46. Matsukawa T, Kurz A, Sessler DI et al - Propofol linearly reduces the vasoconstriction and shivering thresholds. Anesthesiology, 1995;82:1169-1180. [ Links ]
47. Xiong J, Kurz A, Sessler DI et al - Isoflurane produces marked and nonlinear decreases in the vasoconstriction and shivering thresholds. Anesthesiology, 1996;85:240-245. [ Links ]
48. Annadata R, Sessler DI, Tayefeh F et al - Desflurane slightly increases the sweatinhg threshold but produces marked, nonlinear decreases in the vasoconstriction and shivering thresholds. Anesthesiology, 1995;83:1205-1211. [ Links ]
49. Sessler DI - Sweating threshold during isoflurane anesthesia in humans. Anesth Analg, 1991;73:300-303. [ Links ]
50. Bissonnette B, Nebbia SP - Hypothermia during anesthesia: phisiology and effects of anesthetics on thermorregulation. Anesthesiol Clin North America, 1994;12:409-455. [ Links ]
51. Hynson JM, Sessler DI, Glosten B et al - Thermal balance and tremor patterns during epidural anesthesia. Anesthesiology, 1991;74:680-690. [ Links ]
52. Burton AC - Human calorimetry: The average temperature of thetissues of the body. J Nutr, 1935;9:261-280. [ Links ]
53. Cooper TE, Trezek GJ - Correlation of thermal properties of some human tissue with water content. Aerosp Med, 1971;42:24-27. [ Links ]
54. Orkin FK - Physiologic Disturbances Associated with Induced Hypothermia, em: Orkin FK, Cooperman LH - Complications in Anesthesiology. Philadelphia, JB Lippincott Company, 1983;626. [ Links ]
55. Emerick TH, Ozaki M, Sessler DI et al - Epidural anesthesia increases apparent leg temperature and decreases the shivering threshold. Anesthesiology, 1994;81:289-298. [ Links ]
56. Kurz A, Sessler DI, Schroeder M et al - Thermoregulatory response thresholds during spinal anesthesia. Anesth Analg, 1993;77:721-726. [ Links ]
57. Leslie K, Sessler DI - Reduction in the shivering threshold is proportional to spinal block height. Anesthesiology, 1996;84:1327-1331. [ Links ]
58. Glosten B, Hynson J, Sessler DI et al - Preanesthetic skin-surface warming reduces redistribution hypothermia caused by epidural block. Anesth Analg, 1993;77:488-493. [ Links ]
59. Vassilieff N, Rosencher N, Sessler DI et al - Shivering threshold during spinal anesthesia is reduced in the elderly patients. Anesthesiology, 1995;83:1162-1166. [ Links ]
60. Frank SM, Nguyen JM, Garcia C et al - Temperature monitoring practices during regional anesthesia. Anesth Analg, 1999;88:373-377. [ Links ]
61. Frank SM, Shir Y, Raja SN et al - Core hypothermia and skin-surface temperature gradients. Epidural versus general anaesthesia and the effects of age. Anesthesiology, 1994;80:502-508. [ Links ]
62. Bonica JJ, Berges PU, Morikawa K - Circulatory effects of peridural block: I. Effects of level of analgesia and dose of lidocaine. Anesthesiology, 1970;33:619-626. [ Links ]
63. Joris J, Ozaki M, Sessler DI et al - Epidural anesthesia impairs both central and peripheral thermoregulatory control during general anesthesia. Anesthesiology, 1994;80:268-277. [ Links ]
64. Valley MA, Bourke DL, Hamill MP et al - Time course of sympathetic blockade during epidural anesthesia: laser Doppler flowmetry studies of regional skin perfusion. Anesth Analg, 1993;76:289-294. [ Links ]
65. Modig J, Malmberg P, Karlstrom G - Effect of epidural versus general anesthesia on calf blood flow. Acta Anaesthesiol Scand, 1980;24:305-309. [ Links ]
66. Frank SM, Fleisher LA, Olson KF et al - Multivariate determinants of early postoperative oxygen consumption in elderly patients. Effects of shivering, body temperature, and gender. Anesthesiology, 1995;83:241-249. [ Links ]
67. Frank SM, Satitpunwaycha P, Bruce SR et al - Increased myocardial perfusion and sympathoadrenal activation during mild core hypothermia in awake humans. Clin Sci, 2003;104: 503-508. [ Links ]
68. Tayefeh F, Kurz A, Sessler DI et al - Thermoregulatory vasodilation decreases the venous partial pressure of oxygen. Anesth Analg, 1997;85:657-662. [ Links ]
69. Schmied H, Schiferer A, Sessler DI et al - The effects of red-cell scavenging, hemodilution, and active warming on allogeneic blood requirements in patients undergoing hip or knee arthroplasty. Anesth Analg, 1998;86:387-391. [ Links ]
70. Winkler M, Akca O, Birkenberg B et al - Aggressive warming reduces blood loss during hip arthroplasty. Anesth Analg, 2000;91:978-984. [ Links ]
71. Leslie K, Sessler DI, Bjorksten AR et al - Mild hypothermia alters propofol pharmacokinetics and increases the duration of action of atracurium. Anesth Analg, 1995;80:1007-1014. [ Links ]
72. Melling AC, Ali B, Scott EM et al - Effects of preoperative warming on the incidence of wound infection after clean surgery: a randomised controlled trial. Lancet, 2001;358:876-880. [ Links ]
73. Hines R, Barash PG, Watrous G et al - Complications occurring in the postanesthesia care unit: a survey. Anesth Analg, 1992;74:503-509. [ Links ]
74. Lenhardt R, Marker E, Goll V et al - Mild intraoperative hypothermia prolongs postanesthetic recovery. Anesthesiology, 1997;87:1318-1323. [ Links ]
75. De Witte J, Sessler DI - Perioperative shivering: physiology and pharmacology. Anesthesiology, 2002;96:467-484. [ Links ]
76. Bert A, Stearns G, Feng W et al - Normothermic cardiopulmonary bypass. J Cardiothorac Anesth, 1997;11: 91-99. [ Links ]
77. Iaizzo PA, Kehler CH, Carr RJ et al - Prior hypothermia attenuates malignant hyperthermia in susceptible swine. Anesth Analg, 1996;82:803-809. [ Links ]
78. Haley RW, Culver DH, Morgan WM et al - Identifying patients at high risk of surgical wound infection. A simple multivariate index of patient susceptibility and wound contamination. Am J Epidemiol, 1985;121:206-215. [ Links ]
79. Greif R, Akca O, Horn EP et al - Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. N Engl J Med, 2000;342:161-167. [ Links ]
80. Salo M - Effects of anaesthesia and surgery on the immune response. Acta Anaesthesiol Scand, 1992;36:201-220. [ Links ]
81. Macphee IW, Gray TC, Davies S - Effects of hypothermia on the adrenocortical response to operation. Lancet, 1958;2:1196-1199. [ Links ]
82. Reichlin S, Martin JB, Mitnick M et al - The hypothalamus in pituitary-thyroid regulation. Recent Prog Horm Res, 1972;28:229-286. [ Links ]
83. Curry DL, Curry KP - Hypothermia and insulin secretion. Endocrinology, 1970;87:750-755. [ Links ]
84. Piccioni MA, Auler Jr JOC - Termorregulação e Hipotermia Induzida, em: Yamashita AM, Takaoka F, Auler Jr JOC et al - Anestesiologia SAESP, São Paulo, Atheneu, 2001;631-642. [ Links ]
85. Joris J, Banache M, Bonnet F et al - Clonidine and ketanserin both are effective treatments for postanesthetic shivering. Anesthesiology, 1993;79:532-539. [ Links ]
86. Alfonsi P, Sessler DI, Du Manoir B et al - The effects of meperidine and sufentanil on the shivering threshold in postoperative patients. Anesthesiology, 1998;89:43-48. [ Links ]
87. Vitez TS, White PF, Eger EI 2nd - Effects of hypothermia on halothane MAC and isoflurane MAC in the rat. Anesthesiology, 1974;41:80-81. [ Links ]
88. Kurz A, Sessler DI, Narzt E et al - Postoperative hemodynamic and thermoregulatory consequences of intraoperative core hypothermia. J Clin Anesth, 1995;7:359-366. [ Links ]
89. Polderman KH, Peerdeman SM, Girbes AR - Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury. J Neurosurg, 2001;94: 697-705. [ Links ]
90. Piccioni MA, Auler JO - Equilíbrio ácido-base durante hipotermia. Rev Bras Anestesiol, 1992;42:297-302. [ Links ]
91. Luz HLM, Auler Jr JOC - Temperatura e alterações no equilíbrio ácido-base de pacientes submetidos à cirurgia cardíaca com circulação extracorpórea, sob normotermia e hipotermia Rev Bras Anestesiol, 2002;52:197-208. [ Links ]
92. Freysz M, Timour Q, Mazze RI et al - Potentiation by mild hypothermia of ventricular conduction disturbances and reentrant arrhythmias induced by bupivacaine in dogs. Anesthesiology, 1989;70:799-804. [ Links ]
93. Lawson D, Norley I, Korbon G et al - Blood flow limits and pulse oximeter signal detection. Anesthesiology, 1987;67:599-603. [ Links ]
94. Kober A, Scheck T, Lieba F et al - The influence of active warming on signal quality of pulse oximetry in prehospital trauma care. Anesth Analg, 2002;95:961-966. [ Links ]
95. Reith J, Jorgensen HS, Pedersen PM et al - Body temperature in acute stroke: relation to stroke severity, infarct size, mortality, and outcome. Lancet, 1996;347:422-425. [ Links ]
96. Marion DW, Obrist WD, Carlier PM et al - The use of moderate therapeutic hypothermia for patients wth severe head injuries: a preliminary report. J Neurosurg, 1993;79:354-362. [ Links ]
97. Clifton GL, Miller ER, Choi SC et al - Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med, 2001;344:556-563. [ Links ]
98. Marion DW, Penrod LE, Kelsey SF et al - Treatment of traumatic brain injury with moderate hypothermia. N Engl J Med, 1997;336:540-546. [ Links ]
99. Hartung J, Cottrell J - Statistics and hypothermia. J Neurosurg Anesthesiol, 1998;10:1-4. [ Links ]
100. Hindman BJ, Todd MM, Gelb AW et al - Mild hypothermia as a protective therapy during intracranial aneurysm surgery: a randomized prospective pilot trial. Neurosurgery, 1999;44:23-32. [ Links ]
101. Carrier M, Tourigny A, Thoribe N et al - Effects of cold and warm blood cardioplegia assessed by myocardial pH and release of metabolic markers. Ann Thorac Surg, 1994;58:764-767. [ Links ]
102. Ning XH, Xu CS, Song YC et al - Temperature threshold and modulation of energy metabolism in the cardioplegic arrested rabbit heart. Cryobiology, 1998;36:2-11. [ Links ]
103. Hearse D, Stewart D, Braimbridge M - The additive protective effects of hypothermia and chemical cardioplegia during ischemic cardiac arrest in the rat. J Thorac Cardiovasc Surg, 1980;79:39-43. [ Links ]
104. Dae MW, Gao DW, Sessler DI et al - Effect of endovascular cooling on myocardial temperature, infarct size, and cardiac output in human-sized pigs. Am J Physiol Heart Circ Physiol, 2002;282:H1584-H1591. [ Links ]
105. Dae MW, Gao DW, Ursell PC et al - Safety and efficacy of endovascular cooling and rewarming for induction and reversal of hypothermia in human-sized pigs. Stroke, 2003;34:734-738. [ Links ]
106. Dixon SR, Whitbourn RJ, Dae MW et al - Induction of mild systemic hypothermia with endovascular cooling during primary percutaneous coronary intervention for acute myocardial infarction. J Am Coll Cardiol, 2002;40:1928-1934. [ Links ]
107. Villar J, Slutsky AS - Effects of induced hypothermia in patients with septic adult respiratory distress syndrome. Resuscitation, 1993;26:183-192. [ Links ]
108. Hynson JM, Sessler DI, Moaiery A et al - The effects of preinduction warming on temperature and blood pressure during propofol nitrous oxide anesthesia. Anesthesiology, 1993;79:219-228. [ Links ]
109. Glosten B, Sessler DI, Faure EA et al - Central temperature changes are poorly perceived during epidural anesthesia. Anesthesiology, 1992;77:10-16. [ Links ]
110. Just B, Trevien V, Delva E et al - Prevention of intraoperative hypothermia by preoperative skin-surface warming. Anesthesiology, 1993;79:214-218. [ Links ]
111. Vanni SM, Braz JR - Hipotermia perioperatória: novos conceitos. Rev Bras Anestesiol, 1999;49:360-367. [ Links ]
112. Vanni SM, Braz JR, Modolo NS et al - Preoperative combined with intraoperative skin-surface warming avoids hypothermia caused by general anesthesia and surgery. J Clin Anesth, 2003;15:119-125. [ Links ]
113. Sessler DI, Schroeder M, Merrifield B et al - Optimal duration and temperature of prewarming. Anesthesiology, 1995;82:674-681. [ Links ]
114. Vassilieff N, Rosencher N, Sessler DI et al - Nifedipine and intraoperative core body temperature in humans. Anesthesiology, 1994;80:123-128. [ Links ]
115. Sessler DI, Moayeri A - Skin-surface warming: heat flux and central temperature. Anesthesiology, 1990;73:218-224. [ Links ]
116. Reis Jr A, Linde H - Temperatura corpórea central durante e após garroteamento de membros inferiores em crianças. Rev Bras Anestesiol, 1999;49:27-34. [ Links ]
117. Sessler DI, Schroeder M - Heat loss in humans covered with cotton hospital blankets. Anesth Analg, 1993;77:73-77. [ Links ]
118. Clough D, Kurz A, Sessler DI et al - Thermoregulatory vasoconstriction does not impede core warming during cutaneous heating. Anesthesiology, 1996;85:281-288. [ Links ]
119. Sessler DI - Consequences and treatment of perioperative hypothermia. Anesthesiol Clin North America, 1994;12:425-456. [ Links ]
120. Pisani IS - Prevenção da hipotermia per-operatória e a utilidade do forno de microondas. Rev Bras Anestesiol, 1999;49:399-402. [ Links ]
121. Cheng C, Matsukawa T, Sessler DI et al - Increasing mean skin temperature linearly reduces the core-temperature thresholds for vasoconstriction and shivering in humans. Anesthesiology, 1995;82:1160-1168. [ Links ]
122. Kurz A, Ikeda T, Sessler DI et al - Meperidine decreases the shivering threshold twice as much as the vasoconstriction threshold. Anesthesiology, 1997;86:1046-1054. [ Links ]
123. Ikeda T, Sessler DI, Tayefeh F et al - Meperidine and alfentanil do not reduce the gain or maximum intensity of shivering. Anesthesiology, 1998;88:858-865. [ Links ]
124. Horn EP, Standl T, Sessler DI et al - Physostigmine prevents postanesthetic shivering as does meperidine or clonidine. Anesthesiology, 1998;88:108-113. [ Links ]
125. Brownridge P - Shivering related to epidural blockade with bupivacaine in labour, and the influence of epidural pethidine. Anaesth Intensive Care, 1986;14:412-417. [ Links ]
Dr. José Otávio Costa Auler Júnior
Address: Av. Dr. Enéas de Carvalho Aguiar, 44, 2° andar, Bloco I, Cerqueira César
ZIP: 05403-900 City: São Paulo, Brazil
for publication June 10, 2005
Accepted for publication October 21, 2005
* Recebido da Received from Disciplina de Anestesiologia da Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP