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Temperature management in critically ill patients Matthew Faulds BMedSci (Hons) MBChB FRCA Tim Meekings BMedSci (Hons) MBChB MRCP FRCA DICM FFICM Key points Disruption of thermoregulation is common in the critically ill. Severe hyperthermia should be treated promptly to avoid multiorgan failure. Hypothermia should usually be corrected no faster than 0.58C per hour. Therapeutic hypothermia can improve the outcome after cardiac arrest and perinatal asphyxia. Both hypothermic and hyperthermic patients may have underlying medical conditions that require treatment before temperature can be corrected. Thermoregulation is a dynamic part of homeostasis controlled by the anterior hypothalamus. Temperature in mammals will vary diurnally within a narrow range and temperatures outside this can have a profound effect at both a biological and clinical level. Biochemical sequelae can include acid –base disturbance, electrolyte derangement, fluid shifts, alteration of intraand extracellular enzymatic function, and variations in energy production and consumption. Clinical manifestations can also vary widely with potential neurological, cardiorespiratory, metabolic and infective compromise. In the critically ill population, thermoregulation is often disrupted. This may be inadvertent (e.g. hypothermia in a trauma patient), part of a disease process such as fever or for therapeutic benefit, such as induced hypothermia after cardiac arrest. The close monitoring, manipulation, and regulation of body temperature forms an important part of the care of the critically ill patient (Table 1). Definitions Temperature Matthew Faulds BMedSci (Hons) MBChB FRCA Specialty Registrar in Anaesthesia and Intensive Care Sheffield Teaching Hospitals Sheffield South Yorkshire S5 7AU UK Tim Meekings BMedSci (Hons) MBChB MRCP FRCA DICM FFICM Consultant in Anaesthesia and Intensive Care Critical Care Directorate Chesterfield Royal Hospital Calow Chesterfield S44 5BL UK Tel: þ44 (0)1246 512284 Fax: þ44 (0)1246 512607 E-mail: tim.meekings@chesterfieldroyal. nhs.uk (for correspondence) 75 Heat energy is the kinetic energy of the particles within a substance. Heat can be transferred from a hotter substance to a colder substance. By measuring this ability for heat to be transferred, we can quantify the heat energy. That measurement is temperature and is proportional to the mean kinetic energy of the particles in the substance. There are three major temperature scales; Kelvin, Celsius, and Fahrenheit. The International System of Units (SI) unit of temperature is the Kelvin, which has a value of 0 K at absolute zero. The Celsius scale has units of the same magnitude as Kelvin (18C¼1 K), but the values are based on properties of water, for example, the triple point of water is 0.018C or 273.16 K and the boiling point of water is 1008C or 373.15 K. Therefore, in clinical 1A01, 2C01, 3C00 practice, it is more convenient to use the Celsius scale. In some countries, notably the United States, the Fahrenheit scale is still in common use. Temperature homeostasis Heat is produced by metabolism and homeostatic mechanisms maintain core temperature. The thermoneutral zone is the ambient temperature range over which normothermia is maintained without any changes to basal metabolic rate. In humans, this has been defined as 27–318C for a naked 70 kg male. Heat production can be increased from basic metabolic rate by food consumption, exercise and, paradoxically, by an increase in body temperature. Normal muscle activity is the main method of increasing heat generation but, as a last resort, shivering in the adult can increase heat production by 2–5 times. However, there is no mechanism for reducing the metabolic rate when overheating has occurred. Heat loss occurs through five routes: radiation (40%), convection (30%), evaporation (15%), conduction (5%), and respiration (10%). Radiation, convection, and evaporation can be reduced by increasing ambient temperature and covering exposed skin—behavioural responses to low temperature. Further reductions of heat loss are achieved through reflex mechanisms such as vasoconstriction to reduce skin perfusion. The converse is true to increase heat loss; reflex vasodilation, sweating, uncovering, and reducing ambient temperature all contribute to cooling. Normothermia In humans, normal core temperature is between 35.5 and 37.58C, depending on factors such as the time of day, site, and method of measurement. In part, this is because of diurnal variation, +0.58C, with lower temperatures in the morning and higher in the evening. There is doi:10.1093/bjaceaccp/mks063 Advance Access publication 18 January, 2013 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 13 Number 3 2013 & The Author [2013]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: [email protected] Temperature management in critically ill patients Table 1 Complications of hyperthermia and hypothermia Aetiology Hyperthermia Hypothermia Dehydration Nausea and vomiting Hypotension Hyperkalaemia Tachycardia Hypercarbia and metabolic acidosis Rhabdomyolisis Renal failure Confusion Seizures Coma Death Shivering Hyperglycaemia Hypovolaemia Hypokalaemia and hypomagnesaemia Bradycardia and other cardiac arrythmias Coagulopathy Reduced drug clearance Immunocompromise Pressure sores Confusion Coma Death The causes of fever in critical care patients are diverse and range in incidence from very common to extremely rare. A full account of the wide range of causes of fever in the critically ill patient is beyond the scope of this article; the focus will therefore be on some of the more commonly found causes and rarer causes that require specific treatment. also a large difference between the core (brain, thoracic, and abdominal organs) temperature and body surface temperature; the latter is lower than core temperature with a range of 32– 358C. Hypothermia Hypothermia is generally accepted to mean a core body temperature ,358C. This can then be further subdivided into mild (32– 358C), moderate (28 –328C), and severe (,288C) hypothermia. However, these terms can be confusing because of variable ranges used in the literature and guidelines. For example, during the perioperative period, the National Institute for Health and Clinical Excellence (NICE) classify normothermia as being a core temperature between 36.5 and 37.58C, with mild, moderate, and severe hypothermia defined as 35 –35.98C, 34– 34.98C, and ,348C, respectively.1 Hyperthermia This is a core temperature over 388C. Fever is a type of hyperthermia caused by an elevation of the thermoregulatory set point by a process such as infection and is defined as a core temperature .38.38C (1018F). Hyperpyrexia is a very high temperature 408C that is considered life-threatening when 41.58C. Hyperthermia Epidemiology Fever has been found to be present in a range of 15–50% of patients after surgery, in some this represents the development of infection whereas in the remainder this is simply a marker of a postoperative inflammatory response.2 A significant proportion of patients will have a core temperature .388C recorded either at admission or during their stay in critical care. As raised temperature is a contributory factor when calculating either the APACHE II and SAPS II physiology scores in critically ill patients, it is likely this demonstrates that hyperthermia is associated with adverse outcomes in these patients. 76 Systemic inflammatory response syndrome (SIRS) as a result of infection The cytokine response to infection from a variety of sources results in fever—this can occur in characteristic patterns in certain infections (e.g. the cyclical fevers of malaria). SIRS because of other causes The systemic activation of the inflammatory cascade can also be a result of other pathologies unrelated to infection. These include trauma, burns, ischaemia, and connective tissue diseases. An inflammatory response can also occur after surgery. All these processes involve a cytokine response that usually produces a fever. Malignant hyperthermia This inherited disorder of calcium metabolism in skeletal muscle results in the rapid development of an uncontrolled hypermetabolic state after exposure to succinylcholine or volatile anaesthetic agents. The clinical features include hypercarbia, sinus tachycardia, generalized muscular rigidity, and an elevated temperature. Heatstroke This is defined as altered mental status, anhydrosis, and a temperature .40.68C. Classic heat stroke is most common in the elderly and has a reported mortality five times higher in people aged 65 years and over.3 Exertional heatstroke is more common in younger, athletically active individuals. As the pathophysiology of both conditions is similar, there is a possibility that both malignant hyperthermia and a susceptibility to heatstroke are related disorders, which are both caused by abnormalities in muscle physiology. Neuroleptic malignant syndrome and serotonin syndrome These are both adverse drug reactions that include hyperthermia as a clinical feature. They can be distinguished by slightly different clinical presentations and a different onset time. Neuroleptic malignant syndrome is characterized by bradykinesia or akinesia and an onset over several days. In contrast, the serotonin syndrome typically evolves rapidly over a matter of hours and manifests as tremor, hyperreflexia, and clonus. Continuing Education in Anaesthesia, Critical Care & Pain j Volume 13 Number 3 2013 Temperature management in critically ill patients Management The sequelae of worsening multiorgan failure that results when core temperature exceeds 40.58C indicate that fever above this limit should be treated promptly and aggressively. There is controversy regarding whether milder degrees of fever secondary to infection or the systemic inflammatory response syndrome should be treated in critical care patients, as it may be part of a beneficial host response and treating it may not alter outcome.4 An elevated core temperature in certain subgroups of patients such as in traumatic brain injury and post cardiac arrest syndrome appears to be associated with poorer neurological recovery and increased mortality—patients in these subgroups may benefit from avoidance of hyperthermia and in some cases the induction of therapeutic hypothermia (TH). Initially, any potential trigger agents must be removed, for example volatile anaesthetic agents in malignant hyperthermia. The subsequent management of hyperthermia can be divided into physical and pharmacological methods of inducing cooling. Fever associated with infections on intensive care also require specific antimicrobial therapy; this should be tailored to the patient’s culture results and local resistance patterns in consultation with a medical microbiologist. Dantrolene is a skeletal neuromuscular blocking agent that acts by blocking calcium efflux from sarcoplasmic reticulum. Malignant hyperthermia is the only specific indication for dantrolene in hyperthermic patients. In this situation, an immediate i.v. bolus of 2.5 mg kg21 should be given. This is followed by 1 mg kg21 boluses as required every 5–10 min up to a maximum of 10 mg kg21. The use of dantrolene has also been described for the treatment of neuroleptic malignant syndrome. Pharmacological management of the neuroleptic malignant syndrome can also include the use of dopamine agonists such as bromocriptine. In the serotonin syndrome, 5-HT2A antagonists such as cyproheptadine may be used to provide blockade of the serotonin receptors. Hypothermia Epidemiology Physical methods of cooling Initially simple methods can be instituted, such as uncovering the patient whilst preserving their dignity and using cold towels placed across the patient or in the axillae. If ice packs are used, care must be taken to ensure that the ice does not come into direct contact with the patient’s skin and cause subsequent thermal injury. Cooling blanket systems utilize circulated cold water and a feedback control system monitoring the patient’s core temperature to achieve and maintain normothermia. In refractory cases of hyperthermia, more invasive methods of cooling may need to be implemented. This begins with rapid infusion of cooled i.v. fluids. Other invasive methods of cooling include the installation of cold fluid into body cavities such as the stomach, pleura, bladder, and peritoneum. The inherent complications and infection risks of this strategy mean that it is not widely practiced in the UK. Other invasive options for cooling include the use of intravascular cooling catheters, haemodialysis, or haemofiltration and ultimately cardiopulmonary bypass. These methods are obviously dependent upon the resources and equipment available locally. Pharmacological methods of cooling Nonspecific medication used to reduce heat production in the critically ill patient includes sedative agents and neuromuscular blocking agents. More specific antipyretic medications include paracetamol and non-steroidal anti-inflammatory drugs (NSAIDs). Paracetamol acts by selective inhibition of the cyclooxygenase-3 enzyme (COX-3); this results in reduced production of fevergenerating prostaglandins. With a relatively limited side-effect profile in most patients, paracetamol is widely used in critical care patients with fever. The other major group of antipyretics are NSAIDs—the risks of exacerbation of renal impairment and gastric ulceration with the use of these drugs mean that they are often relatively contraindicated in the critically ill population. Hypothermia is commonly found on presentation to medical care, but its true incidence is not known. Although death rates in the UK increase by 1560 per week during the winter months, little of this is thought to be directly as a result of hypothermia. It is clear that those at highest risk are the elderly, those with low socio-economic status and trauma patients. Five percent of patients over 65 years of age attending a Scottish Accident and Emergency department in winter were hypothermic and this group had a mortality of 34%.5 Around 13% of major trauma patients are hypothermic and this triples their risk of death.6 Unfortunately, hypothermia also occurs in hospital with up to 70% of postoperative patients found to be hypothermic.1 Aetiology Increased heat loss This is the most common cause of low core temperature and can cause primary or secondary hypothermia. In the United States, around 650 people each year die from primary hypothermia but these represent only the minority of cases. There is usually an underlying medical or surgical cause; of particular interest to the intensivist are trauma, immersion, burns, and the perioperative period. Trauma patients are especially at risk of hypothermia as they tend to be exposed for long periods of time both before and after arrival in hospital. They may also be wet and have obtunded thermoregulatory responses. Hypothermia is very important to recognize and control in these patients—the mortality of a patient with a core temperature of 328C is 23% but a trauma patient at the same temperature has a mortality of 100%.7 Immersion in water loses heat more rapidly than exposure to air as the thermal conductivity of water is higher and once extracted, Continuing Education in Anaesthesia, Critical Care & Pain j Volume 13 Number 3 2013 77 Temperature management in critically ill patients body temperature decreases even further because of evaporative losses. Similarly, burns patients may be cold as a result of initial irrigation, increased evaporative losses, and inability to effectively modulate peripheral blood flow. Both of these groups of patients have a high coincident rate of trauma, adding to their risk of being hypothermic. Inadvertent perioperative hypothermia has been of interest in recent years because of its high incidence and the increased morbidity and mortality seen in hypothermic patients. Increased heat loss is caused by both general and neuraxial anaesthesia, predominantly through vasodilatation, and also by surgical techniques that involve open body cavities or require large skin areas to be uncovered. Efforts must be made to monitor and control temperature appropriately. Decreased metabolic rate A variety of endocrinological conditions may cause decreased heat production, for example hypopituitarism, hypoadrenalism, and hypothyroidism. Rewarming may be difficult in these patients without treating the underlying pathology, for instance, with drugs such as triiodothyronine, steroids, or both. Patients who have severe malnutrition or hypoglycemia also have a low metabolic rate. Others, such as the very young and very old, do not have the ability to increase their metabolic rate because of the lack of shivering reflex or low muscle mass. Impaired thermoregulation A wide array of causes may impair thermoregulation. In general, the end result is failure of the hypothalamus to regulate core body temperature, often as a result of direct effects on the central nervous system. Examples where this occurs include brain and spinal cord trauma, stroke, intracranial haemorrhage, central nervous system tumours, Parkinson’s disease, Wernicke’s encephalopathy, and multiple sclerosis. Sepsis and uraemia may also alter the hypothalamic set point resulting in hypothermia. Drugs such as general anaesthetic agents, beta-blockers, neuroleptics, and meperidine may disrupt thermoregulation. Ethanol, sedatives, and phenothiazines obtund the responses to low ambient temperatures. Therapeutic hypothermia Therapeutic hypothermia aims to improve the outcome by reducing metabolic oxygen demands. In the operating theatre, TH can be instituted for neuroprotection before primary insult, for example in aortic root repair when the cerebral circulation is interrupted. Postoperatively, these patients require specialist management on the cardiac intensive care unit. TH to ameliorate the secondary insult is more common, with the best evidence for its use after either cardiac arrest or perinatal hypoxia. Trials looking at TH in traumatic brain injury and ischaemic stroke have produced equivocal results to date and consequently use in these conditions is not recommended at present. 78 In 2002, two studies of TH after out-of-hospital cardiac arrest demonstrated significantly improved outcome with a number needed to treat (NNT) of 6– 7. Consequently, the International Liaison Committee on Resuscitation (ILCOR) recommended that the management of all unconscious patients who have suffered an out-of-hospital cardiac arrest with a shockable rhythm should include 24 h of TH at 32 –348C, initiated as soon as possible after return of circulation.8 However, building on the ILCOR statement, the 2010 Resuscitation Council (UK) Guidelines now stipulate that non-shockable and in-hospital arrests should also be considered for TH although there is limited evidence to support this. Perinatal hypoxia occurs in around 2 in 1000 births and causes major morbidity and mortality. Ten randomized controlled trials of TH in these neonates showed a reduction in poor outcome with 72 h of TH at 33– 348C (NNT¼9) and its use is recommended by NICE (IPG347).9 Management Therapeutic hypothermia Induction of TH should be achieved as quickly as possible and in most cases will begin before arrival on the ICU. Initial strategies include covered ice packs and peripheral infusion of cold i.v. fluids unless there are signs of significant fluid overload. Further cooling and maintenance of TH is achieved using devices that provide either surface or core cooling, often using an automated feedback control system that responds to changes in the patient’s temperature. Most commonly, these are water-filled cooling blankets or suits, but there are also methods of providing localized cooling to the brain. These include the use of cooling helmets or caps in newborn infants with perinatal hypoxia and nasal probes designed to provide rapid intranasal cooling in adult patients suffering cardiac arrest. Shivering must be prevented during TH as it increases oxygen demand and generates heat. This is achieved using sedation and boluses or infusions of neuromuscular blocking agents until the temperature is ,33.58C when the shivering reflex itself is obtunded.10 The hypothermic patient Hypothermia affects nearly all the systems of the body. Cardiac irritability increases as temperature decreases and arrhythmias are frequently seen ,308C. Maintenance of intravascular volume and electrolytes is important as hypovolaemia, hypokalaemia, and hypomagnesaemia are common especially in head injuries where mannitol may worsen the effects of cold diuresis. Although the coagulation cascade and platelet function are impaired during hypothermia, reports of spontaneous bleeding are rare. However, if surgical intervention is planned or if spontaneous bleeding occurs, supportive treatment in the form of blood products and related therapies may be required. Other complications include respiratory secretion retention as a result of ciliary dysfunction and pressure sores. Continuing Education in Anaesthesia, Critical Care & Pain j Volume 13 Number 3 2013 Temperature management in critically ill patients the period after rewarming and may have been an underlying cause of the hypothermia. Table 2 Methods of warming the hypothermic patient Non-invasive Invasive Ensure dry Cover skin Cover/close wounds Raise ambient temperature Radiant warmer Forced air warmer Warmed IV fluids Luminal lavage Haemodialysis/haemofiltration Cardiopulmonary bypass Cardiac arrest in a hypothermic patient presents several problems; ventricular fibrillation and ventricular tachycardia may be refractory to defibrillation and drugs may have unpredictable efficacy, even becoming toxic secondary to reduced metabolism and clearance. Below 308C it is advised to deliver a total of three shocks and withhold inotropic or antiarrhythmic drugs until the core temperature increases to .308C. The drug administration interval time should be doubled between 30 and 358C. If the arrest is survivable, declaration of death is not possible until a core temperature of 328C has been achieved unless rewarming attempts fail. Summary Temperature is not only an important clinical marker of severity of illness but also an independent predictor of morbidity and mortality in critically ill patients. Close monitoring and regulation to avoid extremes of body temperature is particularly important in the critically ill patient. This will prevent the uncontrolled disruption of homeostasis and associated subsequent organ dysfunction and failure. Declaration of Interest None declared. References 1. Perioperative hypothermia (inadvertent). Clinical guidelines CG65. National Institute for Health and Clinical Excellence 2008 2. Barone JE. Fever: fact and fiction. J Trauma 2009; 67: 406–9 Rewarming In general, rewarming (Table 2) should not be faster than 0.58C h21 to avoid localized temperature differences (cerebral thermopooling), cerebral hypoxia, and impaired cerebrovascular reactivity. An initial decrease in core temperature may be seen on commencement of rewarming as peripheral tissues become reperfused and colder blood returns to the core. In practice, this is only clinically significant when treating severe hypothermia. Hypotension secondary to vasodilatation is countered by the administration of fluid boluses and vasoconstrictor infusions. As rewarming progresses, particular attention must be given to potassium and glucose levels. Hyperkalaemia caused by shifts from the intracellular to the extracellular compartment is common. Insulin sensitivity may increase rapidly because of both a decrease in insulin resistance and the return of pancreatic function. Hypoglycaemia may result if blood glucose and insulin infusion rates are not monitored closely. Once the core temperature is 338C, the level of sedation and muscle relaxation in place will require additional consideration as activation of the shivering response increases oxygen consumption and may lead to systemic hypoxaemia and metabolic acidosis. Once normothermia is reached, active maintenance of this temperature is necessary to avoid rebound hyperthermia. Temperature control is further complicated by infection, which is common in 3. Ellis FP. Mortality from heat illness and heat aggravated illness in the United States. Environ Res 1972; 5: 1– 58 4. Gozzoli V, Schottker P, Suter PM, Ricou B. Is it worth treating fever in intensive care unit patients? Arch Int Med 2001; 161: 121– 3 5. Pedley DK, Paterson B, Morrison W. Hypothermia in elderly patients presenting to accident and emergency during the onset of winter. Scott Med J 2002; 47: 10– 11 6. Ireland S, Endacott R, Cameron P, Fitzgerald M, Paul E. The incidence and significance of accidental hypothermia in major trauma—a prospective observational study. Resuscitation 2011; 82: 300–6 7. Tsuei BJ, Kearney PA. Hypothermia in the trauma patient. Injury 2004; 35: 7– 15 8. Nolan JP, Morley PT, Vanden Hoek TL, Hickey RW, ALS Task Force. Therapeutic hypothermia after cardiac arrest. An advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Resuscitation 2003; 57: 231– 5 9. Edwards AD, Brocklehurst P, Gunn AJ, Halliday H, Juszczak E, Levene M, Strohm B, Thoresen M, Whitelaw A, Azzopardi D. Neurological outcomes at 18 months of age after moderate hypothermia for perinatal hypoxic ischaemic encephalopathy: synthesis and meta-analysis of trial data. Br Med J 2010; 340: c363 10. Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: Practical considerations, side effects, and cooling methods. Crit Care Med 2009; 37: 1101–20 Please see multiple choice questions 5– 8. Continuing Education in Anaesthesia, Critical Care & Pain j Volume 13 Number 3 2013 79