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Hypothermia / Hyperthermia / Exposure. JP SMILES. Hypothermia. Core temp < 35 ° C Research limited to either mild hypothermia in healthy subjects or case reports. Pathophysiology. Heat loss occurs through Radiation Conduction Convection Evaporation

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hypothermia
Hypothermia
  • Core temp < 35 °C
  • Research limited to either mild hypothermia in healthy subjects or case reports
pathophysiology
Pathophysiology
  • 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
cvs effects
CVS Effects
  • 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
cns effects
CNS Effects
  • 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
resp effects
Resp Effects
  • 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
renal effects
Renal Effects
  • 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
gi effects
GI Effects
  • 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
haem effects
Haem Effects
  • Increased blood viscosity fibrinogen and haematocrit
  • Coagulopathy may develop
grading of hypothermia
Grading of Hypothermia
  • 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)
investigations
Investigations
  • UEC
    • Hypo or hyperkalaemia/ARF/low HCO3-
  • 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
investigations1
Investigations
  • ECG
    • Bradycardia
    • PR/QRS/QT prolongation
    • Variable ST and T wave changes
    • Osborn J waves
    • Arrythmias
      • AF/VT/VF/1st, 2nd, 3rd Degree HB
osborn waves
Osborn waves
  • 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
management
Management
  • 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
management1
Management
  • 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
management2
Management

Rewarming – mild hypothermia

  • Endogenous rewarming
    • Exercise if possible
  • Passive external warming
    • Warm dry environment
    • Cover with warm blankets
management3
Management

Rewarming – moderate hypothermia

  • Active external rewarming
  • Warm blankets
  • Radiant heat source
  • Bair hugger
  • 2°C per hour
management4
Management

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
management5
Management

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
modification of acls for hypothermia
Modification of ACLS for hypothermia
  • 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 related illness
Heat Related Illness
  • Heat stroke
  • Heat exhaustion
  • Heat cramps
  • These may occur as a continuum

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heat stroke
Heat stroke
  • Core body temp > 40 °C
  • Hot dry skin
  • CNS abnormalities (delirium/coma)
heat stroke1
Heat stroke
  • Classical – Occurs due to exposure to a high environmental temperature
  • Exertional – Occurs in the setting of strenuous exercise
pathophysiology1
Pathophysiology
  • Oxidative phosphorylation stops at temperatures > 42 °C
  • Cell damage
  • Loss of thermoregulatory compensatory mechanisms
  • Hypoxia, increased metabolic demands, circulatory failure, coagulopathies and inflammatory response
cvs effects1
CVS Effects
  • 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
neurological effects
Neurological Effects
  • Cardinal features of heat stroke
  • Delirium, lethargy, coma and seizures
  • Can be permanent (up to 33%)
rhabdomyolysis
Rhabdomyolysis
  • 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
renal effects1
Renal Effects
  • ARF in approx 30%
    • Direct thermal injury to kidneys
    • Pre-renal insult of volume depletion and renal hypoperfusion
    • Rhabdomyolysis
haematological
Haematological
  • Exertional heat stroke is associated with haemorrhagic complications
  • Petechial haemorrhages or eccyhmosis secondary to direct thermal injury or DIC
immunological
Immunological
  • Similar to sepsis
  • The actions of inflammatory mediators account for the multi organ dysfunction
assessment
Assessment
  • 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
investigations2
Investigations
  • UEC
    • Hypokalaemia
    • Hyperphosphataemia and hypercalcaemia
    • Hyperkalaemia and hypocalcaemia may be present if rhabdomyolysis has occurred
    • Renal impairment
investigations3
Investigations
  • 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
investigation
Investigation
  • 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
investigation1
Investigation
  • 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)
investigations4
Investigations
  • CXR:
    • ARDS
    • Aspiration
management of heat stroke
Management of Heat Stroke
  • If prompt effective treatment not undertaken mortality approaches 80%
  • A

– ETT if needed

    • Consider early
    • Avoid suxamaethonium
management of heat stroke1
Management of Heat Stroke
  • 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)
management of heat stroke2
Management of Heat Stroke
  • D – Intubate if needed
  • E – Temperature should be measured by oesophageal or rectal probe
cooling methods
Cooling Methods
  • 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
cooling methods1
Cooling Methods
  • 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
outcome
Outcome
  • Mortality should be less than 10% with prompt treatment
  • Most recover without sequalae
  • Residual neurological defects are reported
heat exhaustion
Heat Exhaustion
  • 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
heat cramps
Heat Cramps
  • 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