JP SMILES

Core temp < 35 °C Research limited to either mild hypothermia

in healthy subjects or case reports

Heat loss occurs through◦ Radiation◦ Conduction◦ Convection◦ Evaporation

Hypothermia results in derangement of multiple organ systems

Shivering – increases metabolic rate but only while glycogen stores last and down to temps of 30 °C

Initial tachycardia and peripheral vasoconstriction

Subsequent bradycardia (refractory to atropine), hypotension and fall in cardiac output

Osborn J waves appear < 32 °C Anti-arrythmic drugs and

inotropes/vasopressors are generally ineffective at temperatures < 30 °C

Loss of fine motors skills and co-ordination then loss of gross motor skills

Progressive decrease in GCS Cerebrovascular auto regulation is lost at 24

°C 20 °C EEG is flat and patient appears dead

as cerebral metabolism falls Temperatures at which shivering is lost

varies widely 24 °C - 35 °C Temp < 28 °C = rigidity, mydriasis, and

areflexia

Initially rise in resp rate followed by depression and basal metabolic rate slows

CO2 retention and resp acidosis can occur Significant fall in O2 consumption and CO2

production (50% at 30 °C) Apnoea can develop Initial left shift of the oxygen dissociation curve

◦ Impaired O2 delivery and tissue hypoxia

◦ Lactic acidosis If acidosis becomes severe the curve shifts

back R again

Cold induced diuresis GFR falls as CO and renal blood flow fall ARF in 40% of patients who require ICU Initial hypokalaemia due to shift of

extracellular potassium into cells Hyperkalaemia can occur with acidosis

secondary to cell death

Intestinal motility decreases below 34 °C Ileus < 28 °C Oral medication is not appropriate Hepatic impairment can occur due to

reduced CO (Raised lactate and therefore Hartmans is a bad idea)

Pancreatitis and Mesenteric Venous Thrombosis are both common

Increased blood viscosity fibrinogen and haematocrit

Coagulopathy may develop

Mild (35 °C - 32 °C) Moderate (32 °C - 28 °C) Severe (<28 °C)

Temperature measurement Accurate low reading digital of mercury

thermometer Placed 15 cm rectally of oesophageally

(better as cold faeces can effect rectal temperatures)

UEC ◦ Hypo or hyperkalaemia/ARF/low HCO3

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Glucose◦ Hypo/Hyperglycaemia

CK◦ May be elevated

FBC◦ Increased haematocrit due to cold induced diuresis and hypovolaemia◦ Thrombocytopaenia

COAG◦ Coagulopathy and DIC is common

LFT◦ Transaminitis

LIPASE◦ Pancreatitis

VBG◦ Initial respiratory alkalosis◦ Secondary respiratory and metabolic acidosis

ECG◦ Bradycardia◦ PR/QRS/QT prolongation◦ Variable ST and T wave changes◦ Osborn J waves◦ Arrythmias

AF/VT/VF/1st, 2nd, 3rd Degree HB

These waves were definitively described in 1953 by JJ Osborn

Also called J waves Delayed depolarisation Represented as ST elevation

at the QRS – ST junction < 32 °C Proportional to the degree of hypothermia Not pathognomonic

◦ SAH/Cerebral injuries/Myocardial ischaemia

ABC Remove wet clothing and insulate Gentle handling – rough handling and

invasive procedures have historically been thought to increase risk of cardiac arrythmias

Now thought these risks have been overemphasised

Consider co-existent pathology

Intubation as necessary IV Access (drugs IV only. IM SC poor absorption) Urinary catheter NGT Temperature and cardiac monitoring Fluid resuscitation

◦ Dehydration is often present◦ Warmed fluids◦ Dextrose is good

Avoid drugs until core temp 30 °C – ineffective and may accumulate until released

Rewarming – mild hypothermia Endogenous rewarming

◦ Exercise if possible Passive external warming

◦ Warm dry environment◦ Cover with warm blankets

Rewarming – moderate hypothermia Active external rewarming Warm blankets Radiant heat source Bair hugger 2°C per hour

Rewarming – severe hypothermia Includes cardiopulmonary arrest Warmed humidified inhaled oxygen Warmed IV fluids Warmed left pleural lavage Warmed Peritoneal lavage Cardiopulmonary bypass Most other methods are ineffective

Arrythmias VF may occur spontaneously in < 29 °C Sinus brady and AF with slow ventricular

response are common and can be considered physiological with hypothermia

AF usually reverts spontaneously on rewarming

Drugs and electricity are unlikely to work until temp is > 30 °C

ETT – Warmed humidified air 42 °C - 46 °C Aggressive active core warming

◦ Warmed saline/peritoneal lavage/pleural lavage/bypass VF/VT – Single defibrillation appropriate and

initial drug therapy. If no response defer further attempts or drug doses until core rises above 30 °C

PEA/Asystole – Again wait till core temp above 30°C (atropine not likely to be effective)

Many anecdotal reports of unexpected survival Not dead till they are warm and dead!!!!

Heat stroke Heat exhaustion Heat cramps These may occur as a continuum

Bhut Jolokia pepper

Core body temp > 40 °C Hot dry skin CNS abnormalities (delirium/coma)

Classical – Occurs due to exposure to a high environmental temperature

Exertional – Occurs in the setting of strenuous exercise

Oxidative phosphorylation stops at temperatures > 42 °C

Cell damage Loss of thermoregulatory compensatory

mechanisms Hypoxia, increased metabolic demands,

circulatory failure, coagulopathies and inflammatory response

Tachyarrythmias and hypotension Two types exist with exertional heat stroke

◦ Hyperdynamic group – high cardiac output and tachycardia

◦ Hypodynamic group – Low cardiac output, increase peripheral vascular resistance

Cardinal features of heat stroke Delirium, lethargy, coma and seizures Can be permanent (up to 33%)

Injured cells leak phosphate and calcium Hypercalcaemia and Hyperphosphataemia Hypokalaemia is seen early

◦ Secondary to heat induce hyperventilation leading to respiratory alkalosis

◦ Sweat and renal losses Hyperkalaemia is seen later

◦ Potassium losses from damaged cells and renal failure

Hyperuricaemia develops secondary to the release of purines from injured muscle

ARF in approx 30%◦ Direct thermal injury to kidneys◦ Pre-renal insult of volume depletion and renal

hypoperfusion◦ Rhabdomyolysis

Exertional heat stroke is associated with haemorrhagic complications

Petechial haemorrhages or eccyhmosis secondary to direct thermal injury or DIC

Similar to sepsis The actions of inflammatory mediators

account for the multi organ dysfunction

Consider in patients with altered mental state and exposure to heat

Classic triad of hyperthermia, neurological abnormalities and dry skin

Measure temp with rectal/oesophageal probe Sweating can still be present Hypotension and shock 25%

◦ Hypovolaemia, peripheral vasodilatation and cardiac dysfunction

Sinus tachy Hyperventilation – a universal finding in heat

stroke

UEC◦ Hypokalaemia◦ Hyperphosphataemia and hypercalcaemia◦ Hyperkalaemia and hypocalcaemia may be

present if rhabdomyolysis has occurred◦ Renal impairment

Urate – is frequently high and may play a role in the development of acute renal failure

Glucose – elevated in up to 70% LFT Almost always seen in exertional heat

stroke (AST and LDH most commonly elevated)

CK – 10000 to 1000000 in rhabdomyolysis

FBC – WCC as high as 30 -40,000 Coag – routinely abnormal and DIC may

occur Acid Base:

◦ Lactic acidosis◦ Compensatory respiratory alkalosis

Myoglobin – serum or urine myoglobin may be elevated

ECG◦ Rhythm disturbances (sinus tachy, SVT + AF)◦ Conduction defects (RBBB and intraventricular

conduction defects)◦ QT prolongation (most common secondary to low

K+ , Ca 2+ and Mg 2+)◦ ST changes (secondary to myocardial ischaemia)

CXR:◦ ARDS◦ Aspiration

If prompt effective treatment not undertaken mortality approaches 80%

A – ETT if needed◦ Consider early◦ Avoid suxamaethonium

B◦ Monitor Resp Rate and O2 sats◦ Look for evidence of aspiration if GCS decreased◦ Check for ARDS and ventilate as per lung injury

protocol C

◦ May be a large fluid deficit◦ N saline is probably best (CSL – lactate and avoid K+

containing fluids)◦ Monitor heart rate, BP, CVP and urine output◦ Picco/Swan-Ganz pulmonary artery catheter may be

indicated◦ Pressors may be needed but avoid adrenergic agents

as they can impair heat dissipation by causing peripheral vasoconstriction (dopamine)

D – Intubate if needed E – Temperature should be measured by

oesophageal or rectal probe

Mainstay of therapy and must be initiated from the onset

Use prehospital may be lifesaving Initially remove patient from heat source

and remove all clothing Evaporative cooling – tepid water on the

skin with fans Ice water immersion – most effective

method but practically difficult and cant use monitors/equipment and uncomfortable for the patient

Ice packs to axilla, groin and neck Cooling blankets and wet towels Peritoneal lavage and cardiopulmonary bypass

can be considered in severe resistant cases Shivering may occur in rapid cooling – this will

increase oxygen consumption and heat production◦ Sedate◦ paralyse

Paracetamol and aspirin are ineffective and should not be used

Mortality should be less than 10% with prompt treatment

Most recover without sequalae Residual neurological defects are reported

Heat exhaustion – mild heat stroke Same physiological process Patients can still have the capacity to

dissipate heat and the CNS is not impaired Volume depletion is still a problem

Painful involuntary spasms of major muscles

Usually in heavily exercised muscle groups Dehydration and salt loss also thought to

plat a role Rest rehydrate and replace salts