Heat illness occurs when there is a thermal overload and the theromoregulatory mechanisms of the body are not able to maintain homeostasis. Heat dissipation becomes less efficient and it leads to heat illness.
Hyperthermia encompasses a spectrum of disease that can range from mild - severe:
- Heat oedema - vasodilatory response causes pooling of fluid.
- Heat cramps - usually caused by exercise and dehydration/electrolyte loss.
- Heat syncope - fainting especially when standing in hot environments for too long.
- Heat exhaustion - milder form of heat illness where core temperature is normal or slightly elevated (37-40ºC).
- Heat stroke - more severe form of heat illness, characterised by elevated core temperature >40ºC + CNS dysfunction.
- Classic heat stroke - due to passive exposure so very high environmental temperatures.
- Exertional heat stroke - due to strenuous physical activity, especially in warmer environments.
We will be focusing on heat stroke mainly, and then we will touch on malignant hyperthermia.
😷 Presentation
- Temperature >40ºC
- CNS dysfunction - such as confusion, lethargy, seizures, agitation and even coma.
- Anhidrosis
- Thirst
- Syncope
- Headache
- Nausea and vomiting
⚠️ Risk factors
- Extremes of age
- Poor physical condition
- Dehydration
- Obesity
- Change of environment - i.e. lack of acclimatisation.
🔍 Investigations
- 🏆 Rectal temperature - >40ºC. Rectal thermometry measures core temperature more accurately than axillary, oral or aural thermometry. A temperature <40ºC may be due to inaccurate measuring or due to prior cooling.
- FBC - neutrophilia, anaemia, thrombocytopenia may all be present.
- LFTs - elevated ALT and AST due to heat-induced liver damage.
- Renal function tests - serum creatinine and urea may be elevated due to reduced renal perfusion.
- Blood glucose - patient may be hypoglycaemic especially with exertional heat stroke.
- Electrolytes - hyper/hyponatraemia or hyper/hypokalaemia may all be present due to volume depletion.
- ABG - metabolic acidosis and respiratory alkalosis are the most common presentations (due to poor peripheral perfusion).
- Creatine kinase - may be elevated due to rhabdomyolysis which is a common complication of heat stroke.
- Clotting profile - prolonged PT and PTT.
- ECG - arrhythmias.
🧰 Management
- Supportive care
- IV fluids
- Observation of patient
- ABC approach to stabilisation
- Rapid active cooling - wetting and fanning for classic heat stroke. Cold water/iced water immersion for exertional heat stroke. Do not cool to less than <39ºC as this will result in overshoot hypothermia.
Malignant hyperthermia is an adverse effect of anaesthetic administration in certain genetically susceptible patient.
It occurs due to excessive Ca2+ release from the sarcoplasmic reticulum of skeletal muscle.
Presentation
- Hyperpyrexia
- Muscle rigidity
Risk factors
- 🧬 Genetic susceptibility
- Defects on chromosome 19 which encode for the ryanodine receptor (RyR). It is an autosomal dominant mutation.
- 💉 Anaesthetic agents
- Halothane
- Suxamethonium
- 💊 Antipsychotic drugs
- May cause neuroleptic malignant syndrome which is similar in aetiology.
🔍 Investigations
- Creatine kinase - due to rhabdomyolysis.
- Contracture tests - a piece of muscle tissue is obtained under LA/GA and it is placed in a solution with a device that measures contractile force. It is then exposed to halothane or caffeine and the response is measured. A response is diagnostic for MH.
🧰 Management
- Dantrolene - a ryanodine receptor antagonist preventing Ca2+ release from the sarcoplasmic reticulum.
On the other hand we find hypothermia, which is a reduction of core body temperature below <35ºC.
It too can be classified as:
- Mild - 32-35ºC
- Moderate - 28-32ºC
- Severe - <28ºC
Pathophysiology
Ultimately, hypothermia occurs when heat generation < heat loss. There may be environmental exposures to cold that will rapidly accelerate it, but anyone with a reduced physiological reserve can suffer from hypothermia.
New born babies and surgical patients generally are unable to thermoregulate and require insulation to ensure they maintain their body temperature.
Heat loss from the body is primarily through radiation of infrared waves. Early on when the temperature drops, cutaneous thermoreceptors sense the low ambient temperature → regional vasoconstriction. The hypothalamus then produces TSH and ACTH to stimulate the thyroid and adrenal glands. The hypothalamus also promotes shivering at 34ºC and 36ºC.
The respiratory centre is stimulated but as time progresses, the respiratory rate and tidal volume become depressed.
Renal blood flow and GFR decreases as well. Tubular reabsorption decreases too → natriuresis and diuresis.
Insulin resistance and hyperglycaemia also occurs. Platelet dysfunction also commonly occurs → bleeding disorders.
⚠️ Risk factors
- Extremes of age
- General anaesthesia
- Substance abuse
- Hypothyroidism
- Impaired mental status
- Homelessness
🚨 Presentation
- Temperature <35ºC
- Shivering
- Cold and pale peripheries
- Frostbite - permanent skin injury due to impaired perfusion and freezing of tissue.
- Slurred speech
- Tachypnoea, tachycardia and hypertension - seen in mild hypothermia.
- Respiratory depression, bradycardia, hypotension - seen in moderate hypothermia.
- Confusion/impaired mental status
- Fixed, dilated pupils
- Increased urination
- Babies may look healthy or may look floppy and refuse to eat.
🔍 Investigations
- Core temperature measurement - done by special, low-reading rectal thermometers or thermistor probes. The patient’s temperature needs to be tracked over time to monitor improvement. Standard clinical thermometers do not typically read temperatures <34.4ºC.
- 12-lead ECG - hypothermia leads to acute ST elevation and Osborn (J) waves.
- We may also see: bradycardia, 1º heart block, long QT interval, atrial arrhythmias, ventricular arrhythmias.
- FBC - raised Hb and haematocrit due to haemoconcentration. Decreased WCC and platelets due to splenic sequestration.
- U&Es - hypokalaemia. Hyperkalaemia may occur during re-warming.
- Blood glucose - may be raised due to stress hormones suppressing insulin. May also be low due to hepatic suppression of glucose production.
- ABG -respiratory alkalosis, metabolic acidosis or a mixture of both.
- Clotting profile - prolonged PT and PTT.
- CXR - especially if the patient has an altered level of consciousness.
The J point marks the end of the QRS complex and onset of ST segment. The J wave is a positive deflection seen in precordial leads (chest leads) and true limb leads. It will also be seen as reciprocal, negative deflections in aVR and V1.
🧰 Management
- If the patient is in cardiac arrest → CPR and ALS.
- If they are not in cardiac arrest → ABC:
- A - secure the airway.
- B - monitor breathing and give humidified oxygen if SpO2 is low.
- C - warm IV fluids. We can also apply forced warm air to the patient’s body.
- Put the person into a hot bath
- Massage their limbs
- Use heating lamps
- Give alcohol