Hypothermia / Hyperthermia / Exposure

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Hypothermia / Hyperthermia / Exposure 

• JP SMILES

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Hypothermia

• Core temp lt 35 C
• Research limited to either mild hypothermia in
  healthy subjects or case reports

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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

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CVS Effects

• Initial tachycardia and peripheral
  vasoconstriction
• Subsequent bradycardia (refractory to atropine),
  hypotension and fall in cardiac output
• Osborn J waves appear lt 32 C
• Anti-arrythmic drugs and inotropes/vasopressors
  are generally ineffective at temperatures lt 30 C

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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 lt 28 C rigidity, mydriasis, and areflexia

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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

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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

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GI Effects

• Intestinal motility decreases below 34 C
• Ileus lt 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

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Haem Effects

• Increased blood viscosity fibrinogen and
  haematocrit
• Coagulopathy may develop

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Grading of Hypothermia

• Mild (35 C - 32 C)
• Moderate (32 C - 28 C)
• Severe (lt28 C)
• Temperature measurement
• Accurate low reading digital of mercury
  thermometer
• Placed 15 cm rectally of oesophageally (better as
  cold faeces can effect rectal temperatures)

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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

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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

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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
• lt 32 C
• Proportional to the degree of hypothermia
• Not pathognomonic
• SAH/Cerebral injuries/Myocardial ischaemia

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Osborn Waves
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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

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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

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Management

• Rewarming mild hypothermia
• Endogenous rewarming
• Exercise if possible
• Passive external warming
• Warm dry environment
• Cover with warm blankets

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Management

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

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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

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Management

• Arrythmias
• VF may occur spontaneously in lt 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 gt 30 C

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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
  30C (atropine not likely to be effective)
• Many anecdotal reports of unexpected survival
• Not dead till they are warm and dead!!!!

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Heat Related Illness

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

Bhut Jolokia pepper
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Heat stroke

• Core body temp gt 40 C
• Hot dry skin
• CNS abnormalities (delirium/coma)

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Heat stroke

• Classical Occurs due to exposure to a high
  environmental temperature
• Exertional Occurs in the setting of strenuous
  exercise

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Pathophysiology

• Oxidative phosphorylation stops at temperatures gt
  42 C
• Cell damage
• Loss of thermoregulatory compensatory mechanisms
• Hypoxia, increased metabolic demands, circulatory
  failure, coagulopathies and inflammatory response

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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

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Neurological Effects

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

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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

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Renal Effects

• ARF in approx 30
• Direct thermal injury to kidneys
• Pre-renal insult of volume depletion and renal
  hypoperfusion
• Rhabdomyolysis

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Haematological

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

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Immunological

• Similar to sepsis
• The actions of inflammatory mediators account for
  the multi organ dysfunction

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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

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Investigations

• UEC
• Hypokalaemia
• Hyperphosphataemia and hypercalcaemia
• Hyperkalaemia and hypocalcaemia may be present if
  rhabdomyolysis has occurred
• Renal impairment

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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

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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

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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)

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Investigations

• CXR
• ARDS
• Aspiration

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Management of Heat Stroke

• If prompt effective treatment not undertaken
  mortality approaches 80
• A
• ETT if needed
• Consider early
• Avoid suxamaethonium

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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)

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Management of Heat Stroke

• D Intubate if needed
• E Temperature should be measured by oesophageal
  or rectal probe

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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

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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

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Outcome

• Mortality should be less than 10 with prompt
  treatment
• Most recover without sequalae
• Residual neurological defects are reported

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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

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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

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The End