Hyperthermia is a core (oesophageal, tympanic) temperature above 40.5°C. Hyperthermia may be an extreme form of pyrogen-induced fever associated with infection, inflammation, neoplasia or CVA
Heat Stoke is a life-threatening illness characterised by:
- Core temperature > 40°
- CNS dysfunction (delirium, convulsions, coma)
Pathophysiology of Heat Stroke
- Cellular oxidative phosphorylation becomes uncoupled at temperatures >42°C.
- Cellular damage is directly proportional to the temp and exposure time.
- Compensatory mechanisms for heat dissipation fail.
- Dehydration increases the sodium/potassium pump activity and increases metabolic rate.
- Complications may arise in multiple organ systems.
At risk - very young and elderly, obese and those undertaking unaccustomed or prolonged muscular activity, grand mal fitting, athletes, marathon runners and armed forces recruits.
Predisposing factors include:
- Alcohol use/withdrawal
- Cardiac disease
- Conditions which cause or aggravate sodium/water loss (gastroenteritis, cystic fibrosis)
- Anticholinergics - atropine, lithium, TCAs, phenothiazines
- Disrupted thermoregulation - LSD, phenothiazines
- Disrupted oxidative phosphorylation - salicylates, lithium
- Muscle activity - PCP, amphetamines, cocaine
- Malignant hyperthermia - anaesthetic agents, succinylcholine
- Neuroleptic malignant syndrome - neuroleptics
- Serotonin syndrome - SSRIs
- Dehydration (diuretics)
Clinical features Heat Stroke
- Oedema and petechial haemorrhages cause focal and generalised damage
- Skeletal muscles show widespread degeneration of fibres
- Rhabdomyolysis releases myoglobin, K+, CPK and purines (which are metabolised into uric acid) into the circulation.
- Non cardiogenic pulmonary oedema
- Oliguric acute renal failure due to renal ischaemia, muscle breakdown products, DIC, hyperuricaemia and hypovolaemia.
- Renal failure occurs in up to 35%
- DIC (poor prognosis), thrombocytopaenia, leukocytosis.
- Thermal injury to endothelium releases thromboplastins which result in intravascular thrombosis and secondary fibrinolysis.
- Metabolic acidosis, respiratory alkalosis, hypoglycaemia, hyper- or hypokalaemia
Poor Prognostic Factors in Heat Stroke
- Core temperature >41.1°C
- AST >1000 IU in first 24 hours
- Hypotension not responsive to cooling and fluid replacement
- Renal failure or hyperkalaemia
Rare, autosomal dominant, drug-induced myopathy associated with a Ca++ transfer defect in patients receiving volatile anaesthetics, muscle relaxants, antidepressants, alcohol or Ecstasy. Heat production is increased by muscle catabolism, spasm and peripheral vasoconstriction.
The neuroleptic malignant syndrome
A drug induced hyperthermic syndrome secondary to antipsychotics - especially dopamine antagonists such as haloperidol, thioridazine and chlorpromazine. It is associated with muscle rigidity, extra pyramidal signs, dyskinesia, impaired consciousness and autonomic dysfunction and continues for 1-2 weeks.
- Sweating may or may not be present - hot dry skin was previously thought to be a feature of heat stroke but patients with heat stroke may still be sweating
- Skin surface may be cool due to peripheral vasoconstriction
- Tachycardia and hypotension. Arrhythmias. Hypotension results from a combination of hypovolaemia, peripheral vasodilation and cardiac dysfunction.
- Tachypnoea is a universal finding in heat stroke
- Confusion, delirium and seizures
- Dilated pupils, oculogyric crises
- Coma with decerebrate posturing
- Cerebellar dysfunction
- Salt water depletion
- Disseminated intravascular coagulation. Purpura, conjunctival haemorrhages, melaena, haematocrit
- Heart failure with ST depression and T wave flattening
- Hypo - K+, PO4--, Ca++
- Hyper - K+ if rhabdomyolysis
- Renal impairment
- Urate - often elevated (? role in development of ARF)
- Glucose - elevated in up to 70% of cases
- LFTs Hi AST, LDH more likely in heat stroke than exhaustion
- LDH >1000 in hepatic/renal/myocardial damage
- CK usually > 10,000 (can be as low as 1,000)
- WBC up to 30-40,000
- Clotting-usually abnormal. DIC may be present
- ABG - respiratory alkalosis, metabolic acidosis
- Serum/urinary myoglobin - may be elevated
- ECG - Conduction abnormal, ST -T changes
- CXR - ? aspiration. May be signs of pulmonary oedema but significant fluid replacement may be required.
Management of hyperthermia
Mortality from heat stroke approaches 80% if prompt, effective treatment is not undertaken
- Secure the airway and give high flow oxygen. Shivering and vasoconstriction may occur during rapid cooling and increase oxygen consumption and heat production.
- Rapid cooling should be instituted for patients with temperatures >41°C. (Outcome depends on the height and duration of temperature elevation).
- Clothing should be removed and patients nursed in a cool environment.
- Use surface cooling with a fan, tepid sponging, wet sheets, ice packs or a cool bath.
- Do not give antipyretics such as aspirin (risk DIC) or paracetamol (ineffective).
- Correct hypoglycaemia with dextrose 10%.
- Active cooling measures should be stopped when temperature is <38.5°C.
- Supportive treatment includes fluid replacement and seizure control.
- Control fits with benzodiazepines.
- Saline or 0.45% saline/5% dextrose may be used (depending on U&Es, clinical assessment and haematocrit).
- Up to 4L may be required over 6-12 hours but avoid over-rapid infusion, which may cause pulmonary/cerebral oedema. Monitor CVP.
- Pressor agents may be indicated for hypotension but alpha adrenergic agents (noradrenaline, Adrenaline) should be avoided since they impair heat dissipation by causing vasoconstriction. Consider low dose dopamine (2.5mcg/kg/min)
- Insert a urinary catheter. If myoglobinuria is present aim for urine output >50ml/h and consider bicarbonate and/or mannitol. If using bicarbonate 1-2mEq/Kg boluses should be given to maintain urinary pH>6.
- Phenothiazines may be used to reduce temperature and prevent shivering (not in neuroleptic malignant syndrome).
- Muscle relaxants with non depolarising agents should be used if the patient is ventilated/resistant to external cooling
- For malignant hyperthermia the offending drug should be stopped and dantrolene 1mg/kg given i.v. every 5 minutes to a maximum dose of 10mg/kg.
- Mechanical ventilation with a high FiO2 and treatment of hyperkalaemia are required.
- The neuroleptic malignant syndrome is treated by stopping the offending drug, giving dantrolene, as above, and dopamine agonists (e.g. L-dopa or bromocriptine).
- Coagulopathy should be treated with FFP and platelets
Differential Diagnosis of Heat Stroke
- Meningitis / Encephalitis
- Intracranial haemorrhage
- Thyrotoxic crisis
- Drug induced hyperthermic syndromes
- Delirium tremens