Author: Jonathan Baird / Editor: Adrian Boyle / Reviewer: Mohamed Elwakil / Codes: HAP11 / Published: 17/09/2018 / Review Date: 17/09/2021
Approximately 800 heat related deaths occur annually in the UK. In 2003, a heat wave in Southern England resulted in over 1000 deaths. Not all of these deaths were due to heat stroke.(1) Sweating with dehydration causes coronary and cerebrovascular thrombosis. Mortality increases during heat waves but also decreases in the week following a heat wave. Many individuals dying during heat waves may already be close to death.
Various risk factors exist for heat related illness but those at extremes of age and individuals who participate in strenuous exercise are more vulnerable. Heat related illness ranges from mild transient oedema of the extremities to heat stroke with multi organ failure. This module focuses on the diagnosis and management of the most severe form of environmental heat related illness, namely heat stroke.
Heat oedema – Transient swelling of the peripheries
Heat syncope – Transient loss of consciousness from vasodilatation and volume depletion
Heat cramps – Painful involuntary muscle contractions
Heat exhaustion – Nausea, vomiting dizziness, mild alteration in mental status, temperature under 40 0C
Heat stroke – Marked elevation of core body temperature (>40 0C) with encephalopathy.
Heat stroke may be exertional or non-exertional.
Exertional heat stroke. Heavy physical exertion in young people combines with environmental heat exposure. Heat dissipation mechanisms are overwhelmed and heat stroke results.
Non exertional heat stroke (Classical heat stroke). More commonly encountered in elderly or debilitated patients. Classical heat stroke occurs when simple environmental heat exposure overwhelms homeostatic control mechanisms.
Heat production is determined by the general metabolic rate. Exercise and food consumption both increase metabolic rate. No mechanism exists which actively reduces body heat production.
The body can absorb heat from the environment. When the surrounding environmental temperature exceeds that of the skin heat uptake occurs through radiation and conduction.
Heat loss occurs through conduction, convection, radiation, evaporation and respiration.
For conduction to occur a temperature gradient must exist between the skin and the surrounding air. Conduction normally has very little impact as a means of losing heat. However if the layer of surrounding air which is warmed by the skin is removed and replaced by cooler air (e.g. a cool breeze) heat loss is markedly increased. This process is known as convection.
Infrared energy radiates from the body to the surrounding environment. It is less effective in hot environments.
Evaporation is most effective when the surrounding air is cool and dry. At very high humidity the body can only tolerate air temperatures up to 33 0C. In very dry environments, air temperatures up to 60 0C can be tolerated, provided salt and water are replaced.
Breathing produces heat loss by the warming and humidification of inspired air. In a warm humid environment breathing has little impact on heat loss. In a hot dry environment evaporation (by sweating) can account for 98% of heat loss. The ideal environment to maximise heat loss would be cool and dry with the presence of a breeze.(2,3)
The pathological effects of increased body heat on human tissue
Increased body temperature can produce tissue damage by a variety of mechanisms.
Body temperatures in excess of 40 0C can cause direct cellular injury. Temperatures above 42 0C can directly produce cell death.
Elevated body temperature damages vascular endothelial surfaces. This causes increased vascular permeability and the activation of the coagulation cascades. Capillary leak and coagulopathy occur.(4)
Increased core temperatures can activate numerous pro-inflammatory pathways. A systemic inflammatory response syndrome (SIRS) occurs in heat stroke leading to multiorgan failure.(5)
Dehydration through excessive sweat production combined with vasodilatation causes decreased renal and splanchnic perfusion. Renal failure and translocation of endotoxins across the gut wall results.(6)
Oedema of the hands and feet is transient and resolves spontaneously. Diuretic treatment has no role to play in the management of heat oedema.
Heat syncope results from volume depletion and peripheral vasodilatation. It is important to exclude other causes of syncope before attributing a syncopal episode to heat exposure. Patients are removed to a cooler environment. Rehydration with oral or intravenous fluids usually produces a marked improvement. Patients with reduced vasomotor tone and fixed cardiac output are more susceptible to heat syncope.
Painful involuntary muscle contractions can occur in association with prolonged exertion. Large muscle groups are often involved. Heat cramps are usually self-limiting. Management simply involves cooling, rest, analgesia and rehydration with oral fluids or intravenous saline.
Heat exhaustion is a systemic disorder. Patients complain of headache and nausea. Vomiting is common and often associated with a generalised weakness. Patients are tachycardic and tachypnoeic and often sweating profusely. Orthostatic hypotension may be present. Body temperature is elevated but usually below 40 0C. Patients are water and salt depleted.
This is the worst form of heat related illness and represents complete thermoregulatory failure. The classic presentation involves three main findings
Core body temperature above 40.0 0C.
Clinical findings vary. Sweating has been reported in cases of heat stroke and core temperature may have fallen below 40.0 0C during transfer to hospital. The key distinguishing factor that identifies heat stroke is a systemic inflammatory response. Heat stroke is heat illness associated with a systemic inflammatory response leading to multi organ problems in which encephalopathy predominates. (7) The presence of neurological problems and hot dry skin help distinguish heat stroke from heat exhaustion.
Complete thermoregulatory failure with multi organ dysfunction affects every system in the body.
Often hot and dry (anhydrosis), occasionally sweating
Oliguria and renal failure
High output cardiac failure, dysrhythmia, hypotension
Disseminated intravascular coagulation with haemorrhage
Vomiting, hepatic necrosis, pancreatitis
Acute respiratory distress syndrome
Confusion, hallucination, ataxia, seizures, com
The following table highlights the haematological and biochemical abnormalities of heatstroke.
Metabolic acidosis +/- respiratory compensation, elevated lactate
Poor peripheral perfusion
Water and electrolyte loss
Elevated creatinine and urea
Reduced renal perfusion, Myoglobinuria in rhabdomyolysis
Elevated ALT and AST
Centrilobular hepatocyte necrosis
Elevated creatine kinase, hyperkalaemia and hypocalcaemia
Full blood count and
Neutrophilia, thrombocytopenia, prolonged clotting times, hypofibrinogenaemia
Disseminated Intravascular Coagulation
A patient may present with heat stroke and a body temperature below 40.0 oC, particularly if cooling has occurred during transport to hospital. A wide variety of conditions may present with elevated temperature. Paying attention to the circumstances of a patients admission and also their past medical and drug history is necessary to avoid misdiagnosis. In particular, sepsis, various endocrinopathies and drug reactions may present with hyperpyrexia. The following table indicates the main differential diagnoses.
Differential diagnosis in suspected heat stroke
Sepsis e.g. Pneumonia, UTI, meningitis, endocarditis,
Tropical infection, e.g. malaria, typhoid
Endocrinopathy, e.g. Thyroid storm, phaeochromocytoma
Intracerebral haemorrhage esp. thalamic haemorrhage
Illicit drug use, e.g. cocaine, amphetamine
Neuroleptic malignant syndrome
Heat stroke can co-exist with many of the diagnoses listed above, particularly in the elderly. For example an elderly person with urinary sepsis may also develop heat stroke during a period of hot weather. An alcoholic may collapse in a hot environment while intoxicated and present later with features of heat stroke and alcohol withdrawal.
Measurement of core temperature using a rectal thermometer or oesophageal probe (in the intubated patient) is often necessary. The core temperature may lag behind and remain elevated despite the superficial temperature (axillary/tympanic) being below 40 0C.
Management divides into cooling techniques and supportive care.
There are lots of ways to cool the hot patient. Spraying the patient with tepid water and using a fan is the most practical method.
Immersing the patients limbs or whole body in cool water is described but impractical. Simple adjuncts to cooling such as the use of cooled peripheral intravenous fluids and placing of icepacks in the groin and axillae are often used. Care must be taken with ice packs as prolonged skin contact may cause tissue damage. Cold fluid peritoneal and gastric lavage and cardiopulmonary bypass have also been described, but are not usually necessary.
The aim of cooling is not to achieve rapid normothermia, this would result in overshoot hypothermia. The target core temperature when cooling should be 38.5 0C. Once this temperature is reached active cooling measures are stopped. Rebound hyperthermia may occur after active cooling is stopped. (7)
Shivering can occur during active cooling. This can act to reduce the rate of cooling as shivering generates heat. Benzodiazepines reduce shivering, make cooling techniques more tolerable and are used to treat seizures. Dantrolene should not be used to treat environmental heat related illness.
All patients require fluid replacement alongside active cooling. Hypotension can be difficult to manage in heat stroke. Patients are often dehydrated, vasodilated and in renal failure. Although fluid is required to restore intravascular volume, very aggressive fluid resuscitation may be harmful. Central venous pressure measurement and urinary catheterisation should be established early in all patients with heat stroke. If hypotension persists despite fluid resuscitation and cooling vasopressors may be needed. Seizures should be treated with intravenous benzodiazepines.
Patients need intensive care management. Renal failure may require haemofiltration. Hepatic damage can be extensive. Liver transplantation has been required.
Management of heat stroke involves active cooling, intravenous fluids, invasive monitoring and full supportive care in an ICU setting
Prevention and risk factors for heat related illness
Prevention of heat related illness and death involves identifying those individuals most at risk. In Britain most deaths are in people over the age of 70 and occur in the first few days of a heat wave. The table below highlights risk factors for severe heat related illness.
Risk factors for severe heat related illness
Extremes of age
Underlying chronic ill health and debility (esp. cardiac, respiratory and neurological)
Drugs (diuretics, blockers alcohol, stimulants, phenothiazines, anticholinergics
Lack of air conditioning (lower socioeconomic groups)
Occupational (miners, fire fighters, military recruits)
arious strategies are required if heat related illness and death is to be prevented. A public health plan was implemented in Europe after the heat wave in 2003. Level three of the heat wave plan for England requires primary care trusts to Commission additional care and support, involving at least daily contact for at-risk individuals living at home.(8)
Prognosis & Followup strategies:
Key Learning Points:
- Active cooling can be reliably performed by use of tepid water sprays and electrical fans. (level one evidence)
- Target core body temperature when using active cooling is 38.50C. Aiming for a lower core temperature may lead to overshoot hypothermia. (level one evidence)
- Benzodiazepines play a central role in seizure control and making active cooling techniques more tolerable for the patient. (level one evidence)
- Patients with heat stroke can rapidly develop cerebral oedema and multi organ failure. Management is best conducted in an intensive care unit with invasive monitoring and support. (level one evidence)
- Dantrolene currently has no role to play in the management of heat stroke. (level three evidence)
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