Heat stroke: implications for critical care and anaesthesia
2002; Elsevier BV; Volume: 88; Issue: 5 Linguagem: Inglês
10.1093/bja/88.5.700
ISSN1471-6771
AutoresHelen A. Grogan, Philip M. Hopkins,
Tópico(s)Climate Change and Health Impacts
ResumoHeat-related illnesses, such as heat stroke, are relatively uncommon in temperate climates. Much of the clinical experience comes from Saudi Arabia (where there is an annual pilgrimage to Mecca) and the military. Case reports and review articles are not commonly seen in anaesthesia-related journals. The intention of this article is to review the available literature on heat stroke and to discuss its relationship with other hyperthermic syndromes, such as malignant hyperthermia. Heat stroke is a medical emergency characterized by a high body temperature, altered mental status and, in classical heat stroke, hot, dry flushed skin.16Duthie DJR. Heat‐related illness.Lancet. 1998; 352: 1329-1330Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar It was first recognized by the Romans in 24 BC. But it took until 1946 for it to be shown that heat stroke could lead to multi-organ damage with haemorrhage and necrosis in the lungs, heart, liver, kidneys, brain and gut.8Bouchama A. Heatstroke: a new look at an ancient disease.Intensive Care Med. 1995; 21: 623-625Crossref PubMed Scopus (50) Google Scholar Even in the new millennium, we are not much further on in understanding the mechanisms that take a person from a hyperthermic insult through to multi-organ failure and death. There has been no real decrease in mortality from this disease, which is variably quoted as 10–50%, in the last 50 years.8Bouchama A. Heatstroke: a new look at an ancient disease.Intensive Care Med. 1995; 21: 623-625Crossref PubMed Scopus (50) Google Scholar There are several heat-related illnesses. These may take the form of heat syncope, heat cramps, heat exhaustion and heat stroke, the latter being the most severe.9Bricknell MCM. Heat illness—a review of military experience (Part 1).J R Army Med Corps. 1995; 141: 157-166Crossref PubMed Scopus (20) Google Scholar Heat syncope is fainting due to peripheral vasodilatation secondary to high ambient temperature. Heat cramp refers to muscular cramping occurring during exercise in heat, which is related to salt deficiency and is usually benign. However, there has been a case reported of a young man with post-exercise muscle cramping who subsequently fulfilled the laboratory diagnostic criteria for susceptibility to malignant hyperthermia.32Ogletree JW Antognini JF Gronert GA. Postexercise muscle cramping associated with positive malignant hyperthermia contracture testing.Am J Sports Med. 1996; 24: 49-51Crossref PubMed Scopus (36) Google Scholar Heat exhaustion occurs when the individual becomes dehydrated and weak. Nausea and vomiting occur frequently. Excessive sweating leads to a loss of predominantly water or salt. Salt-depletion heat exhaustion usually occurs when unacclimatized personnel exercise and replace only water losses. Water-depletion heat exhaustion is usually seen in acclimatized personnel who have inadequate water intake during exposure to extreme heat. Whatever the mechanism, the individual collapses from dehydration, salt depletion and hypovolaemia. The core temperature may or may not be raised and tissue damage does not occur.9Bricknell MCM. Heat illness—a review of military experience (Part 1).J R Army Med Corps. 1995; 141: 157-166Crossref PubMed Scopus (20) Google Scholar 14Dickinson JG. Exertional heat stroke‐history and epidemiology: definitions and groups at risk.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 3-19Google Scholar 35Shahid MS Hatle L Mansour H Mimish L. Echocardiographic and Doppler study of patients with heat stroke and heat exhaustion.Int J Cardiac Imaging. 1999; 15: 279-285Crossref PubMed Scopus (34) Google Scholar Heat stroke occurs when the core body temperature rises against a failing thermoregulatory system.9Bricknell MCM. Heat illness—a review of military experience (Part 1).J R Army Med Corps. 1995; 141: 157-166Crossref PubMed Scopus (20) Google Scholar 16Duthie DJR. Heat‐related illness.Lancet. 1998; 352: 1329-1330Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar The core temperature necessary for the condition to be classified as heat stroke varies but is quoted by most authors as a rectal temperature exceeding 40.6°C.35Shahid MS Hatle L Mansour H Mimish L. Echocardiographic and Doppler study of patients with heat stroke and heat exhaustion.Int J Cardiac Imaging. 1999; 15: 279-285Crossref PubMed Scopus (34) Google Scholar As some cooling may take place before reaching hospital, it is probably wise not to adhere to this definition too strictly.1Akhtar MJ Al‐Nozha M Al‐Harthi S Nouh MS. Electrocardiographic abnormalities in patients with heat stroke.Chest. 1993; 104: 411-414Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar 14Dickinson JG. Exertional heat stroke‐history and epidemiology: definitions and groups at risk.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 3-19Google Scholar Heat stroke may be divided into exertional and non-exertional (classical) heat stroke.35Shahid MS Hatle L Mansour H Mimish L. Echocardiographic and Doppler study of patients with heat stroke and heat exhaustion.Int J Cardiac Imaging. 1999; 15: 279-285Crossref PubMed Scopus (34) Google Scholar Exertional heat stroke, as its name suggests, occurs in previously healthy young people exercising, usually in hot and humid climates, probably without being acclimatized. Classical heat stroke occurs during extreme heat waves, the elderly being particularly vulnerable.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar 35Shahid MS Hatle L Mansour H Mimish L. Echocardiographic and Doppler study of patients with heat stroke and heat exhaustion.Int J Cardiac Imaging. 1999; 15: 279-285Crossref PubMed Scopus (34) Google Scholar Some authors view heat exhaustion and heat stroke as different degrees of severity of a spectrum of disordered thermoregulation.14Dickinson JG. Exertional heat stroke‐history and epidemiology: definitions and groups at risk.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 3-19Google Scholar Other authors consider these two illnesses as separate entities with different aetiology, biochemistry and predisposing factors.25Howorth PJN. The biochemistry of heat illness.J R Army Med Corps. 1995; 141: 40-41Crossref PubMed Scopus (8) Google Scholar It is important for humans to maintain body temperature within a small range to avoid cellular and enzymatic dysfunction. In humans, this range is usually of the order of 36.5–37.5°C, even in the face of adverse environmental temperatures. This thermoregulation is under the control of the autonomic nervous system, which integrates afferent input and efferent responses. Central control resides in the hypothalamus, where mean body temperature is determined from peripheral and central structures and compared with a 'set point'. The efferent response is both autonomic (sweating and vasodilatation) and behavioural.11Buggy DJ Crossley AW. Thermoregulation.Br J Anaesth. 2000; 84: 615-628Crossref PubMed Scopus (182) Google Scholar There is some distinction made between exertional and classical heat stroke at this point; failure of thermoregulation (lack of sweating) may be more important in classical heat stroke and less so in exertional heat stroke, when there may be persistent sweating.28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar If heat gain is to be avoided, heat must be lost through convection, conduction, radiation and evaporation of sweat. In practice, the last is the most important mechanism. The effectiveness of sweating in cooling the body is dependent on both the environmental temperature and the humidity. Low humidity and air movements are important in allowing evaporation of sweat and convection of heat. As air temperature approaches body temperature, the effectiveness of this mechanism is lost.9Bricknell MCM. Heat illness—a review of military experience (Part 1).J R Army Med Corps. 1995; 141: 157-166Crossref PubMed Scopus (20) Google Scholar The military report three measures of environmental temperature load. Dry bulb temperature (DBT) is measured by placing a thermometer in the shade, and this represents true air temperature. A thermometer with its bulb enclosed in a wet wick measures wet bulb temperature (WBT). This can be used in the open air or shielded in a box, and measures the ability of the environment to cool by evaporation. The difference between these two measurements is proportional to the prevailing humidity (WBT<DBT until 100% humidity, when WBT=DBT). Globe temperature (GT) is measured by a thermometer placed in a globe and exposed to radiant heat. The military use the 'wet bulb globe temperature index' (WBGT), which has been modified to: 0.7 WBT+0.1 DBT+0.2 GT, and this is used to guide restrictions on training in the heat.9Bricknell MCM. Heat illness—a review of military experience (Part 1).J R Army Med Corps. 1995; 141: 157-166Crossref PubMed Scopus (20) Google Scholar 10Bricknell MCM. Heat illness—a review of military experience (Part 2).J R Army Med Corps. 1996; 142: 34-42Crossref PubMed Scopus (14) Google Scholar Cases of classical heat stroke occur in response to sustained environmental heat, but this is not necessarily the case in exertional heat stroke.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar Cases have been reported in rather more temperate climates. Giercksky and colleagues describe the case of a 31-yr-old male who developed heat stroke after running 5 km at 21°C in Norway, and who subsequently developed severe liver failure.18Giercksky T Boberg KM Farstad IN Halvorsen S Schrumpf E. Severe liver failure in exertional heat stroke.Scand J Gastroenterol. 1999; 8: 824-827Google Scholar Boersma and colleagues describe the fatal case of a previously healthy 20-yr-old male who developed heat stroke after mountain-biking for 3 h in 26°C heat in a forest in the Netherlands. He died of a cerebral haemorrhage secondary to disseminated intravascular coagulation (DIC).7Boersma LVA Leyten QH Meijer JWR Strubbe EJ Bosch FH. Cerebral haemorrhage complicating exertional heat stroke.Clin Neurol Neurosurg. 1998; 100: 112-115Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar Vigorous exercise is a risk factor in the development of exertional heat stroke. This is a particular problem for military personnel, for whom training and combat may involve the wearing of protective clothing, which does not lend itself to aiding heat loss. Other groups at risk include fun runners and those taking part in other vigorous sporting activities, such as mountaineering. Those at occupational risk include foundry workers, boilermen and firemen.14Dickinson JG. Exertional heat stroke‐history and epidemiology: definitions and groups at risk.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 3-19Google Scholar Women seem curiously protected from exertional heat stroke despite their increasing participation in sports and occupations that require a degree of physical fitness. Exertional rhabdomyolysis is also rare in women. It appears that the body temperature at which thermoregulatory reflexes are activated is lower in women than in men. Thus women appear to store less heat than men for a given workload. It is not known whether this is an effect of oestrogen or simply that men are capable of generating more heat because of larger muscle bulk.28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar Other factors predisposing to heat stroke10Bricknell MCM. Heat illness—a review of military experience (Part 2).J R Army Med Corps. 1996; 142: 34-42Crossref PubMed Scopus (14) Google Scholar 15Dickinson JG. Exertional heat stroke‐predisposing factors, clinical features, treatment and prevention.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 20-41Google Scholar are listed in Table 1.Table 1Risk factors predisposing to the development of exertional heat stroke (after Dickinson)Risk factor15Dickinson JG. Exertional heat stroke‐predisposing factors, clinical features, treatment and prevention.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 20-41Google ScholarExamplesObesityCurrent upper respiratory infection orfebrile illnessRecent alcohol consumptionDehydrating illnessDiarrhoea, vomitingLack of sleep, food or waterSkin diseasesAnhidrosis, psoriasis, miliariaConditions increasing heatproductionThyrotoxicosisLack of acclimatizationLack of physical fitnessDrugsAnticholinergics (atropine,co-phenotrope)DiureticsPhenothiazinesTricyclic antidepressantsAntihistamines, cold remediesAnti-parkinsonian drugsBeta-blockersAmphetamines, EcstasyPrevious heat strokeAgeProtective clothing Open table in a new tab Heat stroke is a systemic disorder and victims can therefore display a variety of symptoms and signs concordant with multi-organ dysfunction.4Alzeer AH Al‐Arifi A Warsy AS Ansari Z Zhang H Vincent JL. Nitric oxide production is enhanced in patients with heat stroke.Intensive Care Med. 1999; 25: 58-62Crossref PubMed Scopus (37) Google Scholar The two cardinal features, however, are raised body temperature and neurological dysfunction. There is some debate about whether the clinical features of classical heat stroke are different from those of exertional heat stroke. A large observational study by Dematte and colleagues followed the course of 58 patients admitted to the intensive care unit after the 1995 Chicago heat wave.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar They showed system dysfunction similar to that already reported in exertional heat stroke. This is in contrast with other reports.8Bouchama A. Heatstroke: a new look at an ancient disease.Intensive Care Med. 1995; 21: 623-625Crossref PubMed Scopus (50) Google Scholar The cardiovascular system is commonly compromised in heat stoke. This is important because it may limit the effectiveness of heat loss mechanisms. Tachyarrhythmias and hypotension are frequently described.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar Hypotension may result from translocation of blood from the central circulation to the periphery in an attempt to lose heat,28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar or it may result from the increased production of nitric oxide observed in heat stroke victims.4Alzeer AH Al‐Arifi A Warsy AS Ansari Z Zhang H Vincent JL. Nitric oxide production is enhanced in patients with heat stroke.Intensive Care Med. 1999; 25: 58-62Crossref PubMed Scopus (37) Google Scholar 25Howorth PJN. The biochemistry of heat illness.J R Army Med Corps. 1995; 141: 40-41Crossref PubMed Scopus (8) Google Scholar A study of Doppler and echocardiographic findings in patients with classical heat stroke and heat exhaustion was published recently by Shahid and colleagues.35Shahid MS Hatle L Mansour H Mimish L. Echocardiographic and Doppler study of patients with heat stroke and heat exhaustion.Int J Cardiac Imaging. 1999; 15: 279-285Crossref PubMed Scopus (34) Google Scholar They demonstrated a circulation that was hyperdynamic with tachycardia, resulting in high cardiac output. They also demonstrated that hypovolaemia was more pronounced in heat stroke victims. Interestingly, signs of peripheral vasoconstriction were observed more often in patients with heat stroke. Heat exhaustion patients were more likely to demonstrate peripheral vasodilatation. Whether this reflects changes in the circulation as a result of cooling or reflects progression of the disease is unclear. This supports other authors' findings of the two different types of circulatory abnormalities seen in exertional heat stroke: a hyperdynamic group, as described above, and a hypodynamic group with reduced cardiac output, elevated peripheral vascular resistance and variable pulmonary resistance.15Dickinson JG. Exertional heat stroke‐predisposing factors, clinical features, treatment and prevention.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 20-41Google Scholar Akhtar and colleagues undertook analysis of electrocardiographic changes during heat stroke, and they appear to be common.1Akhtar MJ Al‐Nozha M Al‐Harthi S Nouh MS. Electrocardiographic abnormalities in patients with heat stroke.Chest. 1993; 104: 411-414Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar All components of the ECG can be affected, including rhythm disturbances, conduction defects, prolongation of the Q–T interval and ST segment changes. Rhythm disturbances, including sinus tachycardia, atrial fibrillation and supraventricular tachycardia, have been reported. These may settle with cooling or require cardioversion. Conduction defects described include right bundle branch block and intraventricular conduction defects, which tend to persist for at least 24 h. Prolongation of the Q–T interval is the most commonly observed ECG finding, and may be related to hypocalcaemia, hypokalaemia or hypomagnesaemia. ST segment changes may be seen in localized leads, suggesting myocardial ischaemia in the territory of a particular coronary artery—in one study,1Akhtar MJ Al‐Nozha M Al‐Harthi S Nouh MS. Electrocardiographic abnormalities in patients with heat stroke.Chest. 1993; 104: 411-414Abstract Full Text Full Text PDF PubMed Scopus (68) Google Scholar 21% of patients showed these changes. It is easy to imagine how this could progress to myocardial dysfunction/infarction. Dematte and colleagues demonstrated one patient with reversible myocardial depression and normal coronary arteries. Other patients have not been so lucky—transmural myocardial infarction was reported by Knochel in 1961 in the presence of normal coronary arteries28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar and Shahid and colleagues describe one patient who showed marked global hypokinesia on echocardiography.35Shahid MS Hatle L Mansour H Mimish L. Echocardiographic and Doppler study of patients with heat stroke and heat exhaustion.Int J Cardiac Imaging. 1999; 15: 279-285Crossref PubMed Scopus (34) Google Scholar This patient then suffered an asystolic arrest and died. Neurological dysfunction is a cardinal feature of heat stroke.4Alzeer AH Al‐Arifi A Warsy AS Ansari Z Zhang H Vincent JL. Nitric oxide production is enhanced in patients with heat stroke.Intensive Care Med. 1999; 25: 58-62Crossref PubMed Scopus (37) Google Scholar Patients may present with neurological impairment of varying degrees and duration, including delirium, lethargy, coma and seizures.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar Neurological damage is presumably attributable to metabolic disarray, cerebral oedema or ischaemia.7Boersma LVA Leyten QH Meijer JWR Strubbe EJ Bosch FH. Cerebral haemorrhage complicating exertional heat stroke.Clin Neurol Neurosurg. 1998; 100: 112-115Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar These deficits are common to both classical and exertional heat stroke, although the latter are said to have more transient symptoms.31Macnamee T Forsythe S Ndukwu IM. Central pontine myelinolysis in a patient with classic heat stroke.Arch Neurol. 1997; 54: 935-936Crossref Scopus (21) Google Scholar The central nervous system is particularly vulnerable to heat, the cerebellum being the most susceptible.2Albukrek D Bakon M Moran DS Faibel M Epstein Y. Heat‐stroke‐induced cerebellar atrophy: clinical course, CT and MRI findings.Neuroradiology. 1997; 39: 195-197Crossref PubMed Scopus (84) Google Scholar 15Dickinson JG. Exertional heat stroke‐predisposing factors, clinical features, treatment and prevention.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 20-41Google Scholar A case of exertional heat stroke-induced cerebellar atrophy in a 45-yr-old man has been described.2Albukrek D Bakon M Moran DS Faibel M Epstein Y. Heat‐stroke‐induced cerebellar atrophy: clinical course, CT and MRI findings.Neuroradiology. 1997; 39: 195-197Crossref PubMed Scopus (84) Google Scholar In this case, early computed tomography (CT) imaging of the brain was normal, and moderate cerebellar atrophy was first noticed on magnetic resonance imaging (MRI) 10 weeks after the hyperthermic insult (Fig. 1). This proved to be progressive during the subsequent year—it was clearly not transient. Other cases of neurological insult have been described, including a 20-yr-old male who died as a result of an intracerebral haemorrhage. He developed a mild coagulopathy secondary to exertional heat stroke.7Boersma LVA Leyten QH Meijer JWR Strubbe EJ Bosch FH. Cerebral haemorrhage complicating exertional heat stroke.Clin Neurol Neurosurg. 1998; 100: 112-115Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar Rarer still, McNamee and colleagues reported possibly the first case of central pontine myelinolysis in a patient with classical heat stroke during the 1995 Chicago heat wave.31Macnamee T Forsythe S Ndukwu IM. Central pontine myelinolysis in a patient with classic heat stroke.Arch Neurol. 1997; 54: 935-936Crossref Scopus (21) Google Scholar Guillain–Barré syndrome has also been reported; in this case anticholinergic agents had been prescribed to reduce sweating in a 28-yr-old drug addict withdrawing from opiates.33Pfeiffer G Steffen W. Guillain–Barré syndrome after heat stroke.J Neurol Neurosurg Psychiatry. 1999; 66: 408Crossref PubMed Scopus (10) Google Scholar These cases illustrate that neurological injury may not necessarily be transient. In one series, 24% of patients had no neurological impairment and 43% had minimal impairment, but 33% had moderate to severe impairment of neurological function at discharge from hospital.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar Some authors speculate that this neurological injury may be related to hypernatraemic cerebral damage.5Ayus JC Arieff AI. Features and outcomes of classic heat stroke.Ann Intern Med. 1999; 130: 613Crossref PubMed Scopus (18) Google Scholar The changes are well described in exertional heat stroke.28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar Lactic acidosis may occur even as a normal response to severe exertion, but lactate is rapidly cleared by the liver and converted to glucose. In heat stroke the patient is shocked, this mechanism is less efficient, and restoration of the circulating volume may lead to worsening lactic acidosis as skeletal muscle is reperfused. The body compensates with acute respiratory alkalosis secondary to increased respiratory effort. This may in itself lead to heat-induced tetany. After several hours, the situation changes from a mixed picture of acidosis and alkalosis to predominant metabolic acidosis because of sustained tissue damage. The patient may develop rhabdomyolysis. Injured cells leak phosphate, which reacts with extracellular calcium. This process leads to hyperphosphataemia and hypocalcaemia. Hypokalaemia is commonly seen early, and this may be a direct catecholamine effect or may occur secondary to heat-induced hyperventilation, leading to respiratory alkalosis. Hypokalaemia may also be related to sweat losses and renal wasting resulting from the physiological hyperaldosteronism induced by training in the heat. Within hours, the situation can be reversed. Sustained hyperthermia, hypoxia and hypoperfusion lead to failure of the Mg2+-dependent Na+/K+-ATPase pump, leading to cellular leak of K+. Hyperkalaemia is made worse by hypocalcaemia and acute renal failure. ECG monitoring remains the most useful tool in determining the timing of intervention. Acute hypophosphataemia is also observed and is probably related to the increased glucose phosphorylation seen in alkalotic conditions. Hyperuricaemia develops secondarily to release of purines from the injured muscle. Excretion of uric acid is also reduced in the presence of lactic acidaemia. It is hard to believe that similar processes, albeit less striking ones, do not occur in classical heat stroke. Indeed, Dematte and colleagues reported acid–base abnormalities in 45% of their patients.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar The picture was of mixed non-anion gap metabolic acidosis/respiratory alkalosis vs mixed positive anion gap metabolic acidosis/respiratory alkalosis, and 60% of their patients required mechanical ventilation: 10% went on to develop acute respiratory distress syndrome. Renal dysfunction is well documented in exertional heat stroke and the incidence of acute renal failure is approximately 30%.28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar The cause is usually multifactorial, including direct thermal injury, the pre-renal insults of volume depletion, and renal hypoperfusion, rhabdomyolysis and disseminated intravascular coagulation.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar The literature is inconsistent as to how common renal dysfunction is in classical heat stroke. In one series, 53% of patients with classical heat stroke developed moderate to severe renal insufficiency, and 19% of this subset died.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar In these patients, although creatine kinase levels were elevated to levels below those seen in exertional heat stroke, elevation of this enzyme did occur despite a lack of history of exercise. Abnormal liver function tests may be seen. Mild elevations in aspartate aminotransferase (AST), lactate dehydrogenase (LD) and total bilirubin have been described. Concentra tions of AST, alanine aminotransferase (ALT), γ-glutamyl transpeptidase (γ-GT), LD and total bilirubin increased over time, with peaks on the third day after the heat insult.13Dematte JE O'Mara K Buescher J et al.Near‐fatal heat stroke during the 1995 heat wave in Chicago.Ann Intern Med. 1998; 129: 173-181Crossref PubMed Scopus (345) Google Scholar The course may be more severe in exertional heat stroke. Liver damage is almost always seen and is probably related to direct thermal injury and hypoxia secondary to splanchnic redistribution.18Giercksky T Boberg KM Farstad IN Halvorsen S Schrumpf E. Severe liver failure in exertional heat stroke.Scand J Gastroenterol. 1999; 8: 824-827Google Scholar 34Saissy JM. Liver transplantation in a case of fulminant liver failure after exertion.Intensive Care Med. 1996; 22: 831Crossref PubMed Scopus (26) Google Scholar Fulminant liver failure, however, is rare. There have been three reports of severe liver failure; two of the three patients required liver transplantation. Both patients who were transplanted died, one at 41 days and the other at 11 months, from chronic rejection.34Saissy JM. Liver transplantation in a case of fulminant liver failure after exertion.Intensive Care Med. 1996; 22: 831Crossref PubMed Scopus (26) Google Scholar The third patient, a 31-yr-old male, developed heat stroke after running 5 km in 21°C heat. He progressed to severe liver failure and a biopsy on day 5 showed extensive liver cell necrosis. He was referred for consideration of liver transplantation but recovered completely with conservative treatment.18Giercksky T Boberg KM Farstad IN Halvorsen S Schrumpf E. Severe liver failure in exertional heat stroke.Scand J Gastroenterol. 1999; 8: 824-827Google Scholar Exertional heat stroke is usually associated with haemorrhagic complications.28Knochel JP. Exertional heat stroke‐pathophysiology of heat stroke.in: Hopkins PM Ellis FR Hyperthermic and Hypermetabolic Disorders. Cambridge University Press, Cambridge1996: 42-62Google Scholar These may be petechial haemorrhages and ecchymoses, which may represent direct thermal injury or may be r
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