Hypothermia / Hyperthermia / Exposure - PowerPoint PPT Presentation

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Hypothermia / Hyperthermia / Exposure

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Title: Hypothermia / Hyperthermia / Exposure


1
Hypothermia / Hyperthermia / Exposure 
  • JP SMILES

2
Hypothermia
  • Core temp lt 35 C
  • Research limited to either mild hypothermia in
    healthy subjects or case reports

3
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

4
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

5
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

6
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

7
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

8
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

9
Haem Effects
  • Increased blood viscosity fibrinogen and
    haematocrit
  • Coagulopathy may develop

10
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)

11
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

12
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

13
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

14
Osborn Waves
15
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

16
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

17
Management
  • Rewarming mild hypothermia
  • Endogenous rewarming
  • Exercise if possible
  • Passive external warming
  • Warm dry environment
  • Cover with warm blankets

18
Management
  • Rewarming moderate hypothermia
  • Active external rewarming
  • Warm blankets
  • Radiant heat source
  • Bair hugger
  • 2C per hour

19
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

20
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

21
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!!!!

22
Heat Related Illness
  • Heat stroke
  • Heat exhaustion
  • Heat cramps
  • These may occur as a continuum

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23
Heat stroke
  • Core body temp gt 40 C
  • Hot dry skin
  • CNS abnormalities (delirium/coma)

24
Heat stroke
  • Classical Occurs due to exposure to a high
    environmental temperature
  • Exertional Occurs in the setting of strenuous
    exercise

25
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

26
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

27
Neurological Effects
  • Cardinal features of heat stroke
  • Delirium, lethargy, coma and seizures
  • Can be permanent (up to 33)

28
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

29
Renal Effects
  • ARF in approx 30
  • Direct thermal injury to kidneys
  • Pre-renal insult of volume depletion and renal
    hypoperfusion
  • Rhabdomyolysis

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

31
Immunological
  • Similar to sepsis
  • The actions of inflammatory mediators account for
    the multi organ dysfunction

32
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

33
Investigations
  • UEC
  • Hypokalaemia
  • Hyperphosphataemia and hypercalcaemia
  • Hyperkalaemia and hypocalcaemia may be present if
    rhabdomyolysis has occurred
  • Renal impairment

34
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

35
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

36
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)

37
Investigations
  • CXR
  • ARDS
  • Aspiration

38
Management of Heat Stroke
  • If prompt effective treatment not undertaken
    mortality approaches 80
  • A
  • ETT if needed
  • Consider early
  • Avoid suxamaethonium

39
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)

40
Management of Heat Stroke
  • D Intubate if needed
  • E Temperature should be measured by oesophageal
    or rectal probe

41
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

42
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

43
Outcome
  • Mortality should be less than 10 with prompt
    treatment
  • Most recover without sequalae
  • Residual neurological defects are reported

44
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

45
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

46
The End
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