3. HYPERTHERMIA
HEAT RELATED ILLNESSES
▸Broad range of ætiology and manifestations
▸Primary disorder due to failure of thermal homeostasis
▸But hyperthermia may be a secondary disorder
▸Major causes of hyperthermia are:
▸Exercise-associated collapse (EAC)
▸Heatstroke
▸Drug related heat illness
4. HYPERTHERMIA
PATHOPHYSIOLOGY OF
HYPERTHERMIA
▸Core body temperature >41.5°C
▸Progressive denaturing of vital cellular proteins
▸Failure of vital energy-producing processes
▸Loss of cellular membrane function
▸Organ dysfunction:
▸rhabdomyolysis, APO, DIC, cardiovascular dysfunction,
electrolyte disturbance, renal failure, liver failure, permanent
neurological damage.
5. HYPERTHERMIA
EXERCISE-ASSOCIATED COLLAPSE
▸Most common heat-related illness at sporting events
▸Manifests at end of a race
▸Muscle pump enhanced venous return ceases and cardiac
output drops.
▸Leads to collapse, often with brief LOC
▸Due primarily to failure of prompt baroreceptor responses
and not haemodynamically significant dehydration (rare).
6. HYPERTHERMIA
HEATSTROKE
▸Hallmark is failure of the hypothalamic thermostat
▸Leading to hyperthermia and organ dysfunction
▸Exertional heatstroke due to exercise in a thermally
stressful environment
▸Classic heatstroke occurs in patients with impaired
thermostatic regulation
8. HYPERTHERMIA
SEROTONIN SYNDROME
▸Serotonin toxicity: the effects are a consequence of a relative excess of central nervous system serotonin.
▸Dose related, selective serotonin re-uptake inhibitors (SSRIs), lithium, pethidine, monoamine oxidase
inhibitors (MAOIs) and amphetamines.
▸Clinical diagnosis characterised by CNS, autonomic & motor dysfunction
▸Develops after a latent period, usually of a few hours, but may be several days
▸Most patients are only mildly affected and may escape clinical detection.
▸Severe cases with hyperthermia with muscular rigidity with complications of rhabdomyolysis, DIC, and
renal failure.
▸Most cases resolve within 24–48hr once the precipitant is withdrawn.
▸Even in severe cases, the underlying biochemical abnormality rapidly improves, usually with the institution of
muscular paralysis.
▸Mortality & morbidity is due to the complications of the syndrome
9. HYPERTHERMIA
NEUROLEPTIC MALIGNANT SYNDROME
▸Neuroleptic malignant syndrome: dopamine depletion or dopamine receptor blockade is
responsible
▸Rare idiosyncratic reaction to neuroleptic agents with an incidence of between 0.02%
and 3.0% Manifests in patients who recently started or increased neuroleptic treatment
▸Associated with almost all antipsychotics (both first and second generation)
▸Reported in patients in whom a dopaminergic agent has been rapidly withdrawn (e.g. in
Parkinsonism).
▸Latent period of onset of several hours to days.
▸Four classic signs: fever, rigidity, altered mental state and autonomic instability.
▸Only the more severe cases develop hyperthermia and its complications.
10. HYPERTHERMIA
MALIGNANT HYPERTHERMIA
▸Due to exposure to volatile anaesthetic agents or suxamethonium
▸Malignant hyperthermia is a genetically inherited disorder in
which triggering agents cause a release of sarcoplasmic Ca2+
stores.
▸Elevated levels of myoplasmic Ca2+
stimulates many
intercellular processes, including glycolysis, muscle contraction
and an uncoupling of oxidative phosphorylation. Leading to
hyperthermia that is purely peripheral in origin.
11. HYPERTHERMIA
RISK FACTORS FOR
HEATSTROKE
▸ Behavioural
▸ Army Recruits
▸ Athletes
▸ Exertion
▸ Inappropriate exposure to high heat
&/or humidity
▸ Babies left in cars
▸ Manual workers
▸ Pilgrims
16. HYPERTHERMIA
PREVENTION OF HEATSTROKE
▸Education of at risk groups
▸Exertional heatstoke is most often in short, high intensity
exercise where marked dehydration is unlikely.
▸Dehydration is not as important as previously thought
▸Exercise in high heat and humidity environments should be
limited.
17. HYPERTHERMIA
CLINICAL FEATURES OF EXERCISE-
ASSOCIATED COLLAPSE (EAC)
▸Nausea, vomiting, malaise, dizziness
▸History of collapse
▸Tachycardia (likely) and orthostatic hypotension
▸Core temperature <40°C
▸Neurological function rapidly returns to normal
18. HYPERTHERMIA
CLINICAL FEATURES OF HEAT STROKE
▸Neurological dysfunction
▸Loss of consciousness is a constant feature
▸Core temperature >41.5°C
▸Hot dry skin
▸Profuse sweating is a more common feature than previously
believed
▸Other features include, tachycardia, hyperventilation, seizures,
vomiting and hypotension
20. HYPERTHERMIA
TREATMENT FOR EXERCISE-
ASSOCIATED COLLAPSE (EAC)
▸Rapidly responds to supine posture (lying down), rest, and
oral fluids
▸IV rehydration rarely required
▸May worsen hyponatraemia due to fluid overload
▸It increases ADH levels
21. HYPERTHERMIA
TREATMENT FOR HEATSTROKE
▸Medical emergency!!! Early recognition and early treatment
decrease morbidity and mortality.
▸Need aggressive cooling of 0.1°C/min
▸Remove clothing, fine mist spray, ice packs neck, axilla & groin
▸Iced water immersion, ice slush, cool water immersion, iced
peritoneal lavage and drugs (paralysis with ventilatory support)
▸IV fluids should be used judiciously
▸Monitor UEC & clotting closely
22. HYPERTHERMIA
TREATMENT FOR DRUG RELATED
HYPERTHERMIA
▸Serotonin syndrome
▸Cool them +/- paralysis
▸Chlorpromazine (12.5–50 mg IM/IV)
▸Cyproheptadine (4–8 mg orally 8-hourly).
▸NMS
▸Bromocriptine 2.5–10 mg tds. (May reduce the duration)
▸Malignant hyperthermia
▸Dantrolene 15-30mg/kg IV
▸Cease precipitating agent
▸Full support
23. HYPERTHERMIA
PROGNOSIS
▸Maximum core temperature and duration of temperature
elevation are predictors of outcome.
▸Prolonged coma and oliguric renal failure are poor prognostic
signs.
▸Mortality is still about 10%, but survivors will not suffer long-
term sequelae.
▸Heat stroke should be referred to ICU
▸EAC should recover in SSU of ED or onsite
25. HYPOTHERMIA
DEFINITION
▸Hypothermia: Core temperature < 35°C
▸Mild (32–35°C)
▸Thermogenesis is still possible
▸Moderate (29–32°C)
▸Progressive failure of thermogenesis
▸Severe (<29°C)
▸Poikilothermic and increasing risk of malignant cardia
arrhythmias
26. HYPOTHERMIA
ÆTIOLOGY
▸Elderly are at greater risk of hypothermia because of reduced metabolic heat
production and impaired responses to a cold environment.
▸Alcohol is a common ætiological factor and acts via:
▸Cutaneous vasodilatation
▸Altered behavioural responses
▸Impaired shivering
▸Hypothalamic dysfunction.
▸Hypothermia in the ED setting is often associated with underlying infection
27. HYPOTHERMIA
ÆTIOLOGY: “IN ANY SEASON OR
SETTING”
▸Environmental
▸Cold, wet, windy ambient conditions
▸Cold water immersion
▸Exhaustion
▸Trauma
▸Multitrauma (entrapment, resuscitation, head injury)
▸Minor trauma and immobility (e.g. #NOF, #NOH)
▸Major burns
▸Drugs
▸Ethanol
▸Sedatives (e.g. benzodiazepines) in overdose
▸Phenothiazines (impaired shivering)
▸Neurological
▸CVA
▸Paraplegia
▸Parkinson’s disease
▸Endocrine
▸Hypoglycaemia
▸Hypothyroidism
▸Hypoadrenalism
▸Systemic illness
▸Sepsis
▸Malnutrition
33. HYPOTHERMIA
CARDIAC RHYTHM IN HYPOTHERMIA
▸Shivering artefact on ECG
▸In severe hypothermia typically
this is slow atrial fibrillation
▸Extra positive deflection in the
QRS (the J or Osborn wave)
in leads II, V3–V6 with
worsening hypothermia.
▸With handling or may
spontaneously degenerate into
VF or asystole
36. HYPOTHERMIA
MANAGEMENT - FLUIDS
▸Preferential substrate to generate heat by shivering is muscle
glycogen
▸Oral glucose may be appropriate in mild hypothermia
▸In severe hypothermia, gastric stasis and ileus are common
▸Glucose IV: 5% dextrose IVI 200 ml/hr
▸Gentle warm IV fluid resuscitation due to relative dehydration as
vascular beds dilate with rewarming
▸Severe hypotension at 37°C is a normal physiological state at 27°C.
37. HYPOTHERMIA
MANAGEMENT - INTERVENTIONS
▸Intubation where needed allows protection of the airway and an avenue of rewarming via the
ventilator
▸AF - should correct with warming alone
▸no need for chemical correction
▸Pulse VT/VF; manage along conventional pathways
▸If DC shocks do not work; repeat every 1°C warmer
▸Mg2+ may be the anti arrhythmic of choice
▸Pacing
▸Transcutaneous pacing may be indicated in a bradycardic patient whose blood pressure is too
low to allow arteriovenous rewarming
▸Due to cardiac irritability, transvenous pacing is contraindicated in hypothermia
38. HYPOTHERMIA
MANAGEMENT - DRUGS
▸Pharmacokinetics/Pharmacodynamics change with temperature.
ie insulin is inactive <30°C, thus hyperglycaemia is common in
hypothermia
▸Drug metabolism of drugs is decreased and protein binding may
be increased in hypothermia.1
▸With rewarming drugs may become bioavailable at toxic levels.
▸It may be prudent not to give vasoactive drugs to a patient with
core temperature less than 30C
39. HYPOTHERMIA
MANAGEMENT - WARMING
▸Stop them becoming cold/colder
▸Remove wet clothing
▸Avoid drafts, and multiple
exposures of the patient once
warming has begun
▸Endogenous rewarming
▸Warm, dry, wind-free environment
▸Warmed intravenous fluids (to
prevent cooling)
▸External exogenous rewarming
▸Hot bath immersion
▸Forced-air blankets
▸Heat packs
▸Body-to-body contact
▸Core exogenous rewarming
▸Warmed, humidified inhalation
▸Left pleural cavity lavage
▸Extracorporeal circulation
43. HYPOTHERMIA
SUMMARY
▸Minimise further heat loss
▸Begin rewarming of hypothermic patients early
▸Some patients are cold and dead but other cold patients who appear dead can
be resuscitated with full neurologic recovery
▸Endogenous rewarming should occur in moderate-severe hypothermia
▸Rewarming with forced-air rewarming blankets in most cases of moderate-to-
severe hypothermia can be done without the need to resort to more aggressive
techniques.
▸Rewarming should be with cardiopulmonary bypass or warm left pleural lavage
in the arrested hypothermic patient.
44. HYPERTHERMIA/HYPOTHERMIA
REFERENCES
▸Rogers, Ian. Heat-related illness, draft chapter TEXTBOOK OF ADULT EMERGENCY MEDICINE
▸Heat-Related Illness Emergency Medicine Clinics of North America. Atha, Walter F., MD.. Published
November 1, 2013. Volume 31, Issue 4. Pages 1097-1108.
▸Drug-Induced Hyperthermic Syndromes. Bryan D. Hayes PharmD, Joseph P. Martinez MD and Fermin
Barrueto MDEmergency Medicine Clinics of North America, 2013-11-01, Volume 31, Issue 4, Pages 1019-
1033,
▸Hyperthermia Caused by Drug Interactions and Adverse Reactions. Mary S. Paden MD, Lucy Franjic MD and
S. Eliza Halcomb MD. Emergency Medicine Clinics of North America, 2013-11-01, Volume 31, Issue 4, Pages
1035-1044
▸TEXTBOOK OF ADULT EMERGENCY MEDICINE. 4th Ed. Churchill Livingstone 2015 Elsevier Ltd
▸Out-of-Hospital Evaluation and Treatment of Accidental Hypothermia. Ken Zafren. Emergency Medicine
Clinics of North America, 2017-05-01, Volume 35, Issue 2, Pages 261-279,
▸https://www.pharmacytimes.com/contributor/patrick-wieruszewski-bs-pharmd-candidate-
2016/2016/03/pharmacokinetic-and-pharmacodynamic-considerations-for-patients-undergoing-therapeutic-
hypothermia
Notes de l'éditeur
In severe serotonin toxicity and neuroleptic malignant syndrome, increased motor activity and central resetting of the hypothalamic thermostat combine to produce hyperthermia.
Serotonin toxicity: the effects are a consequence of a relative excess of central nervous system serotonin.
Dose related, selective serotonin re-uptake inhibitors (SSRIs), lithium, pethidine, monoamine oxidase inhibitors (MAOIs) and amphetamines.
Neuroleptic malignant syndrome: dopamine depletion or dopamine receptor blockade is responsible
Rare idiosyncratic reaction to neuroleptic agents with an incidence of between 0.02% and 3.0%
Malignant hyperthermia is a genetically inherited disorder in which triggering agents cause a release of sarcoplasmic Ca2+ stores.
Elevated levels of myoplasmic Ca2+ stimulates many intercellular processes, including glycolysis, muscle contraction and an uncoupling of oxidative phosphorylation. Leading to hyperthermia that is purely peripheral in origin.