Question 23

College Answer

a)

Uncoupling of oxidative phosphorylation
Failure of enzyme systems
Membrane permeability
increased Na leak into cells
ADP depleted
Sweat gland damage from heat

b)

Prognosis depends on core temp, duration of hyperthermia and presence of comorbidities.

c)

Haemoconcentration (dehydration), haemolysis
Hypernatremia
LFT derangements (cholestatic, early sign),
Renal impairment,
DIC often delayed onset and a/w worse prognosis
CK rise (exertional type),
Lactate rise.
During treatment: CXR pulmonary oedema (centralise fluid, ALI), low PO4, Ca, glucose,

d)

ABC (Airway protection if GCS low etc. ) & control of seizures if present

Remove from offending environment,

Rapid cooling to 39 C (duration of hyperthermia major determinant of outcome): remove clothing, sponge cold water, ice, fans, cooling blankets, cold intravenous fluids gastic lavage with cold solutions, immersion (young and military), cold dialysis, etc. Monitor core temp closely

Volume and electrolyte resuscitation and close monitoring
ABG,
Eectrolytes. NB Risk of cerebral oedema
CVC
 

Additional comments:
In general there was a knowledge deficit relating to the pathophysiology of heat stroke. Some candidates failed to address cooling and control of temperature in the management of heat stroke and did not recognise the need for initial rapid cooling and/ or the need for careful temperature monitoring.

Discussion

The

a) Pathophysiology of heat stroke:

• Exposure to high temperature leads to an increase in the cardiac output, cutaneous vasodilation and sweating.
• Dehydration by sweating leads to hypovolemia and salt loss
• In the absence of plentiful water and salt, sweating becomes impossible and thermoregulation is thus impaired.
• As the convective cooling is now impossible, the core body temperature increases.
• As the core temperature increase, enzyme function is altered and cellular energy production becomes impaired
• Direct heat-related tissue damage results in cytokine release
• At the same time, hypovolemia and shock lead to bacterial translocation from the gut, leading to endotoxaemia
• The cytokine response to this endotoxin load results in a systemic inflammatory response
• Due to this SIRS, the vascular endothelium is damaged, leading to multi-organ system failure and DIC.

b) Factors that affect prognosis of heat stroke:

• LDH, CK and AST levels (when extremely high) were predictive of non-survivors in a study of heat-stroked Haj pilgrims (Alzeer et al, 1997)
• Failure to decrease the core body temperature to below 38.9° within the first 30 minutes of presentation.
• A hyperdynamic circulation is protective, but a sluggish hypodynamic circulation is associated with a poorer survival
• Found collapsed at home (as opposed to public place or care facility)
• Preexisting cardiac disease
• Use of diuretics
• High body temperature
• Low Glasgow Coma Score
• Low platelet count
• Prolonged prothrombin time
• High serum creatinine
• High SAPS II score
• Use of vasoactive drugs within the first 24 hrs in the ICU

c)  List the expected changes on routine investigations in the presence of heat stroke.

• ABG: acidosis, probably mixed metabolic.
• FBC: haemolysis, thrombocytopenia and anaemia
• EUC: renal failure, hyperkalemia
• CMP: hyperphosphataemia
• LFTs: raised transaminases and bilirubin. Specifically, AST and LDH will be raised.
• CK: elevated
• Urinary myoglobin
• Coagulopathy (DIC): raised PT and APTT

d) Outline the management of a patient with heat stroke.

• Goals of therapy:
  • Early, aggressive cooling to under 39°C
  • Support of multiple failing organ systems
• Options for cooling methods:
  • Evaporation of cold water sponges
  • Ice packs
  • Immersion in ice water
  • Contact cooling by blankets and jackets
  • Iced gastric, colonic, bladder, or peritoneal lavage
  • Infusion of cold intravenous fluids
  • Invasive technique such as cooling of the dialysis circuit, or ECMO
• Supportive management:

1. Intubate to protect the airway, if unconscious
2. Ventilate with lung protective ventilation, anticipating ARDS
3. Manage haemodynamic instability aggressively, with a mixture of cold IV fluids and vasopressor agents
4. Protect from seizures (no specific evidence to recommend benzodiazepines or any other conventional agents)
5. Control hyperkalemia and hyperphosphataemia of rhabdomyolysis
6. Consider early dialysis. Watch for myoglobinuria
7. Early trophic feeds to maintain gut integrity
8. Correct the coagulopathy of DIC

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