Heat-related emergencies

Introduction

• Exercise-associated collapse (EAC) is the most common heat-related illness
  • Manifests at end of race when venous return reduces and cardiac output drops
  • Primary mechanism is failure of prompt baroceptor responses and not haemodynamically significant dehydration
• Core body temp >41.5 results in progressive denaturing of vital cellular proteins, failure of energy-producing processes and loss of cell membrane function
• At organ level, this results in rhabdomyolysis, acute pulmonary oedema, DIC, cardiovascular dysfunction, electrolyte disturbance, renal failure, liver failure and permanent neurological damage
• Hallmark of heatstroke is failure of the hypothalamic thermostat, leading to hyperthermia and pathophysiological features above
• Heatstroke can be divided into exertional and classic (impaired thermostatic mechanisms)

• Drugs
  • Serotonin syndrome (excess serotonin) and neuroleptic malignancy syndrome (central dopamine deficiency or receptor blockade) result in increased motor activity and central resetting of hypothalamic thermostat with combination resulting in hyperthermia

• Heat stroke risk factors
  • Behavioural
    • Army recruits, athletes, inappropriate clothing, elderly, babies left in cars, manual workers, pilgrims
  • Drugs
    • Anticholinergics, diuretics, phenothiazines, salicylates, stimulants/hallucinogenics
  • Illness
    • Delirium tremens, dystonia, infections, seizures

DDx of heat stroke

• Infection: Sepsis, meningitis, encephalitis, malaria, typhoid, tetanus
• Endocrine: Thyroid storm, phaeo, DKA
• Neurological: Hypothalamic bleeding or infarct, CVA, status epilepticus
• Toxicological
  • Anticholinergic syndrome
  • Sympathomimetic overdose
  • Salicylate overdose
  • Serotonin syndrome
  • Malignant hyperthermia
  • Neuroleptic malignant syndrome
  • Withdrawal syndromes esp. alcohol and benzodiazepines

Prevention

• Education of at-risk groups to prevent exertional heatstroke
• Most often reported in shorter, high-intensity exercise where dehydration is an unlikely contributor
• Adequate fluid intake is required for prolonged exercise but not a key factor in heatstroke prevention
• High ambient temperature and humidity should limit exertion

Mechanisms of heat transfer

• Heat accumulation
  • Cellular metabolism, muscle activity, radiation from sun, direct contact with hot objects. Heat absorbed from external environment when temperature higher than core body temp
• Heat dissipation
  • Radiation, conduction (direct contact), convection (air or liquid moving over surface) and evaporation
  • At ambient temp <35 degrees, radiation and evaporation dissipate most body heat
    • Insulator zone of warmed air prevents further radiative heat loss
  • Conduction of heat into water is many times more efficient than conduction into air of the same temperature
  • Wind moves heat away by convection but above 32.2 degrees and 35% humidity, convection does not remove heat well
    • This is why fans alone are not effective in preventing heat stroke during high environmental temperature and humidity
  • When ambient temp >35, body can no longer radiate heat to environment and is dependent on evaporation
    • As humidity increases, potential for evaporative heat loss dminishes
    • Sweat that drips from the skin provides no evaporative heat loss and only exacerbates dehydration

Pathophysiology

• Response to heat stress
  • Therma regulation begins to fail at core temp <35 or >40
  • Can maintain core temp 40-42 for short periods without adverse effect
  • Dilatation of blood vessels, increased sweat production, decreased heat production and behavioural heat control
  • As core temp rises, sympathetic outflow of posterior hypothalamus is inhibited, leaving unopposed sympathetic outflow from anterior hypothalamus, which leads to decreased vascular tone, particularly in cutaneous circulation
  • During exercise in conditions of hyperthermia, HR increases to compensate for decrease in stroke volume due to cutaneous vascular dilation
    • Patients with underlying CV disease or pharmacological or physiological impairment may not be able to elevate cardiac output effectively resulting in ALOC, arrhythmias, myocardial ischaemia and exacerbations of CCF
  • Increased cholinergic stimulation of the skin results in increased sweat production with sharp increase at core temp >37 up to 1.5L/hr
  • Sweating activation in older individuals begins at 1.5 degrees higher than that in younger individuals

• Medications
  • Anticholinergics – Impair sweating and CV response to heat
  • Diuretics – Volume depletion and reduced CO
  • Phenothiazine – Anticholinergic effect and deplete central dopamine which interferes with hypothalamic thermostat
  • Beta-blockers – Reduce CF response to heart and reduce peripheral blood flow and ability to sweat
  • CCB – As above
  • Sympathomimetics – Cutaneous vasoconstriction and limit sweating
  • Alcohol – Inhibits secretion of ADH leading to dehydration and blunts heat-avoidance response
  • Heroin, cocaine and amphetamines disrupt endogenous endorphin and ACTH involved in heat adaptation mechanisms
  • Amphetamines and cocaine increase muscle activity leading to heat generation
  • LSD and phencyclidine produce hypermetabolic state

• Acclimation
  • Adaptation of body to environmental changes allowing withstanding of elevated heat stress
  • Lowers thermal set point in hypothalamus, which triggers sweating at lower core temperature
  • Maximal rate of sweating increases from 1.5 to 3L/hour and can be sustained for longer
  • Aldosterone secretion boosted and sodium reabsorption from sweat
  • Plasma volume expands, heart rate reduced for any given heat load and exercise tolerance improves
  • Dilation of cutaneous blood vessels occurs at lower core temperatures to promote earlier cooling
  • Can be achieved from 7 days to several weeks
  • Moderate exercise in hot, dry environment for 100 minutes each day is optimal
  • De-acclimation occurs over 1-2 weeks

Exercised-associated collapse

• Nausea, vomiting, malaise, dizziness +- collapse
• Tachycardia and orthostatic hypotension
• Core temperature <40 in these patients and neurological function rapidly returns once lying down
• Ix
  • EAC, CK, BSL, ECG +- echo
• Rx
  • Supine positioning, rest and oral fluids
  • IV N/S is only for profound dehydration
  • Routine N/S will worsen exercise-associated hyponatraemia if ongoing inappropriate ADH release

Minor heat illness

• Heat oedema
  • Mild swelling within first few days of exposure to hot environment
  • Due to cutaneous vasodilation and orthostatic pooling
  • Increased aldosterone and ADH contributes
  • Found in elderly non-acclimatised who are physically active after a period of sitting in vehicle
  • Commonly seen in healthy travellers after arrival from colder climate
  • Very rarely may be pitting but does not progress to pretibial region
  • Must differentiate from CCF or DVT
  • Resolves spontaneously over days
  • Elevation of legs and use of support hosiery may help
  • Diuretics are not effective and may predispose to volume depletion, electrolyte abnormalities and more serious heat emergencies

• Prickly heat
  • Pruritic, maculopapular and erythematous rash over normally clothed areas of the body
  • Aka lichen tropicus, miliaria rubra or heat rash
  • Acute inflammation of sweat ducts caused by blockage by macerated stratum corneum
  • Itch can be treated with antihistamine
  • Calamine lotion or topical steroids can help
  • Chlorhexidine in a light cream or salicylic acid cleaning may provide some relief
  • Light, loose clothing and avoidance of sweat-generating solutions
  • Profunda stage involves prolonged or repeated heat exposure with keratin plug of sweat duct and when duct ruptures again, it does so into deeper layers of the dermis
  • Can readily become chronic dermatitis
  • Infection with S. aureus is common
  • Can desquamate skin using 1% salicyclic acid to the affected area three times per day

• Heat cramps
  • Usually in those sweating profusely and replacing fluids with hypotonic solutions
  • Can occur during exercise, or more commonly, after exercise
  • Non-acclimated or unconditioned individuals are at risk
  • Self-limited
  • Usually short duration
  • Thought to be due to relative deficiency of sodium, magnesium, potassium or fluid at muscle level
  • Cellular hyponatraemia results in muscle cramps with calcium-dependent relaxation
  • Treatment is PO or IV fluid and salt replacement
  • Maintaining adequate dietary salt intake, drinking commercial electrolyte drinks can prevent 
  • Salt tablets by themselves are a gastric irritant and cause N&V but can dissolve in water f desired

• Heat stress/exhaustion
  • Occurs through water depletion and sodium depletion
    • Water depletion in elderly and those working in hot environments
    • Salt depletion tends to occur in unacclimatised individuals who replace fluids with large volumes of hypotonic solutions
  • Presents with headache, nausea, vomiting, malaise, dizziness and muscle cramps + tachycardia, orthostatic hypotension and/or near-syncope
  • Temp <40 (usually) and no signs of CNS impairment
  • If not drinking, get hypernatraemia. If drinking salt-containing fluids, get isotonic hypovolaemia
  • Treatment
    • Volume and electrolyte replacement
    • Can progress to heat stroke if not removed from hot environment
    • If do not respond to 30 minutes of fluid replacement removal from heat, should be cooled until temp <39

Confinement hyperpyrexia

• E.g. Children left in cars
• Nonventilated vehicles in hot environments may reach temperatures of 54 to 60 degrees in <10 minutes

Heatstroke

• Classic triad: Neurological dysfunction, core temp >41.5 and hot, dry skin
• Mortality 10-50%

Clinical presentation

• Altered LOC is a constant feature of heatstroke but is often improved by time they reach ED
• Must measure core temp (oral or axillary temps may mislead by normal range)
• Profuse sweating is more common than previously thought (50%)
• Tachycardia, hyperventilation, seizures, vomiting and hypotension can also occur
• Seizures can occur during cooling phase

Investigations

• Multiorgan dysfunction is the rule
• FBC, UEC, CK, Coag screen, LFT, urinalysis, serum glucose, VBG, CXR, ECG

Treatment

• True medical emergency with mortality approaching 80%  if prompt and effective treatment not undertaken
• Therapeutic goal is reduction in core temperature to <42 degrees within 15 minutes of arrival
• Early recognition and aggressive treatment can prevent substantial morbidity and mortality
• Aggressive cooling of at least 0.1 degree/min should be achievable and targeted
• Target 38-39 degrees to prevent core afterdrop of >2 degrees if cool down to 36

• Initial treatment protocol
  • Remove all clothing, spray with fine mist of tepid water (40 degrees) while gentle warm forced air is commenced
  • Vascular region packed with ice packs
  • Ice bath offers more rapid cooling but may not be practicable in ED
    • Safe in young exertional heat stroke but may increase mortality in the elderly
    • One option is body bag filled with ice slurry
  • Ice-cold IV fluids can aid in rapid cooling but can be difficult to optimally mange IV fluid and electrolyte requirements

• Further treatment
  • Diazepam 5-10mg IV (shivering, seizures must be controlled)
  • Chlorpromazine 25-50mg IV second line as lowers seizure threshold and may cause hypotension
  • Neuromuscular paralysis with NDMR if resistant to external cooling
    • Rarely require any further therapy after this
  • Urine flow must be maintained by initial fluid bolusing and later with mannitol and/or frusemide to prevent secondary renal injury
  • Close monitoring of electrolytes, acid-base and coagulation
  • Invasive cooling is rarely required once intubated and paralysed
    • Cardiopulmonary bypass/ECMO are the most rapid methods of treatment
    • Cold water gastric lavage, peritoneal/pleural/urinary bladder lavage and rectal lavage are all options but risk water intoxication, are invasive and only for extreme cases
  • Aspirin and paracetamol are not effective and should be avoided. Require intact hypothalamus to function and may have side effects (e.g. bleeding or liver respectively)
  • Dantrolene is not indicated

Serotonin toxicity

• Usually combinations of drugs
• Drugs
  • MAOi, SSRI, SNRI, St John’s Wort, TCA
  • Pethidine and tramadol
  • Amphetamines and MDMA
• Presentation
  • CNS: Agitation, anxiety, confusion, reduced LOC, seizures
  • Motor: Clonus, hyperreflexia, hypertonia, incoordination, myoclonus, tremor
  • Autonomic: Diaphoresis, diarrhoea, HTN, hyperthermia, tachycardia
• Clinical diagnosis that develops after a latent period (hours to days)
• Only the most serious will develop hyperthermia (usually in the setting of muscular rigidity) with rhabdomyolysis, DIC and renal failure
• Most cases resolve within 24-48 hours of drug cessation

• Treatment
  • In mild cases, small doses of benzodiazepines may be all that is required while awaiting spontaneous resolution
  • In severe cases, institute neuromuscular paralysis early, especially if marked alteration of mental state
  • Duration of treatment is partly judged on half-life of agents
  • Anti-serotonergic agents
    • Chlorpromazine 12.5-50mg IV/IM
    • Cyproheptadine 4-8mg PO q8h

Neuroleptic malignant syndrome

• Rare idiosyncratic reaction to neuroleptic agents
• Incidence of 0.02-3%
• Occurs in response to single agents, usually at therapeutic doses (unlike serotonin syndrome)
• At risk groups:
  • Patient: Agitation, dehydration, male 2:1, organic brain disease
  • Drug: Depot, high initial dosing, high potency (e.g. haloperidol), rapid dose increases
• Usually drug just initiated or dose increased
• Associated almost all antipsychotics including first and 2^nd generation
• Also seen in rapid withdrawal of dopaminergic drugs e.g. in parkinsonism
• Four classic signs: Fever, rigidity, altered mental status and autonomic instability
• Difficult to distinguish from serotonin syndrome without good medication history
• Only the more severe cases suffer hyperthermia and its complications

• Treatment
  • Early recognition and treatment is key
  • Dopamine agonists
    • Bromocriptine 2.5-10mg TDS (PO or NG)
    • May reduce the duration

Malignant hyperthermia

• Triggering agents
  • Inhalational anaesthetics e.g. halothane, isoflurane, enflurane
  • Succinylcholine and ketamine
  • First signs
    • Failure to achieve muscle relaxation
    • Tachypnoea and tachycardia
    • If not recognised and treated
      • Acidosis, rhabdomyolysis and hyperthermia
  • Sometimes can be delayed or even reappear after apparently successful treatment e.g. post-operative fever
  • Untreated mortality 70% but only 7% if appropriately managed
  • Treatment
    • Full supportive care
    • Dantrolene 2.5mg/kg IV, q15min up to 30mg/kg
    • Inhibits Ca release from sarcoplasmic reticulum

Complications of heat stroke

• Early
  • Vascular – Hypotension, cardiac failure, APO
  • Temp – Hypothermic overshoot, Hyperthermic rebound
  • Muscular – Rhabdomyolysis
  • Neurological – Delirium/comam, Seizure
  • Renal – Oliguria
  • Metabolic – Hypokalaemia, Hypo/hypernatraemia

• Late
  • Neurological: Cerebral oedema, encephalopathy, persistent neuro deficit
  • Cardiac: Myocardial injury
  • Pulmonary: ARDS
  • Renal: Renal failure
  • GI: Intestinal ischaemia, pancreatic injury, hepatic dysfunction
  • Metabolic: Hyperkalaemia, hypocalcaemia, hyperuricaemia
  • Haematological: Thrombocytopaenia, DIC

• Hypotension
  • Fluid bolus and ongoing cooling
  • If low CO and raised CVP, dopamine or dobutamine
  • Potent vasoconstricting agents may impede cooling by redirecting blood flow away from skin
• Thermal injury to liver is common
  • Peak at 24-72 hours due to centrilobular necrosis
  • Almost always reversible
• Hypotension, low CO and falling cardiac index are poor prognostic findings

Prognosis and disposition

• Heatstroke
  • Max core temp and duration of elevation predict outcome
  • Prolonged coma and oliguric renal failure are poor prognostic indicators
  • Mortality 10%
  • Most survivors will not suffer long-term sequelae
  • Refer all suspected heatstroke to ICU
  • Mortality corresponds to degree of temp elevation, time to cooling initiation, number of organs involved, anuria, coma and cardiovascular failure

• Exercise-associated collapse
  • Most short stay or treatment on-site at event
• Drug-related
  1. Prognosis depends on complications before treatment initiated
  2. Early referral to ICU in most cases
  3. Malignant hyperthermia mortality 7% even with treatemnt
  4. Re-assess medication regime
  5. In neuroleptic malignant syndrome, may be able to initiate low-dose agent in future
  6. Malignant hyperthermia will warrant modification of future anaesthetics and family member susceptibility testing

Recommendations for prevention

• Decrease or reschedule strenuous activity
• Light and loose-fitting clothing
• Increasing carbohydrate intake and decreasing protein intake to decrease endogenous heat production
• Drinking plenty of fluids even if not thirsty
• Avoid alcohol
• Using salt tablets as well as fluids
• Avoid direct sunlight
• Take advantage of the shade

Last Updated on November 23, 2021 by Andrew Crofton