1. JP SMILES

2.  Core temp < 35 ° C  Research limited to either mild hypothermia in healthy subjects or case reports

3.  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

4.  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

5.  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

6.  Initially rise in resp rate followed by depression and basal metabolic rate slows  CO 2 retention and resp acidosis can occur  Significant fall in O 2 consumption and CO 2 production (50% at 30 ° C)  Apnoea can develop  Initial left shift of the oxygen dissociation curve ◦ Impaired O 2 delivery and tissue hypoxia ◦ Lactic acidosis  If acidosis becomes severe the curve shifts back R again

7.  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

8.  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

9.  Increased blood viscosity fibrinogen and haematocrit  Coagulopathy may develop

10.  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)

11.  UEC ◦ Hypo or hyperkalaemia/ARF/low HCO 3 -  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

12.  ECG ◦ Bradycardia ◦ PR/QRS/QT prolongation ◦ Variable ST and T wave changes ◦ Osborn J waves ◦ Arrythmias  AF/VT/VF/1 st, 2 nd, 3 rd Degree HB

13.  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

15.  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

16.  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

17. Rewarming – mild hypothermia  Endogenous rewarming ◦ Exercise if possible  Passive external warming ◦ Warm dry environment ◦ Cover with warm blankets

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

19. 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

20. 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

21.  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!!!!

22.  Heat stroke  Heat exhaustion  Heat cramps  These may occur as a continuum Bhut Jolokia pepper

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

24.  Classical – Occurs due to exposure to a high environmental temperature  Exertional – Occurs in the setting of strenuous exercise

25.  Oxidative phosphorylation stops at temperatures > 42 ° C  Cell damage  Loss of thermoregulatory compensatory mechanisms  Hypoxia, increased metabolic demands, circulatory failure, coagulopathies and inflammatory response

26.  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

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

28.  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

29.  ARF in approx 30% ◦ Direct thermal injury to kidneys ◦ Pre-renal insult of volume depletion and renal hypoperfusion ◦ Rhabdomyolysis

30.  Exertional heat stroke is associated with haemorrhagic complications  Petechial haemorrhages or eccyhmosis secondary to direct thermal injury or DIC

31.  Similar to sepsis  The actions of inflammatory mediators account for the multi organ dysfunction

32.  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

33.  UEC ◦ Hypokalaemia ◦ Hyperphosphataemia and hypercalcaemia ◦ Hyperkalaemia and hypocalcaemia may be present if rhabdomyolysis has occurred ◦ Renal impairment

34.  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

35.  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

36.  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)

37.  CXR: ◦ ARDS ◦ Aspiration

38.  If prompt effective treatment not undertaken mortality approaches 80% AA – ETT if needed ◦ Consider early ◦ Avoid suxamaethonium

39. BB ◦ Monitor Resp Rate and O 2 sats ◦ Look for evidence of aspiration if GCS decreased ◦ Check for ARDS and ventilate as per lung injury protocol C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)

40.  D – Intubate if needed  E – Temperature should be measured by oesophageal or rectal probe

41.  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

42.  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

43.  Mortality should be less than 10% with prompt treatment  Most recover without sequalae  Residual neurological defects are reported

44.  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

45.  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