Heat Emergencies

Heat Emergencies

Physiology of Thermoregulation

Body temperature is controlled by the hypothalamus primarily through the preoptic anterior hypothalamus and the posterior hypothalamus. These regions receive and integrate two types of thermal input:
  • Peripheral thermoreceptors: Nociceptive neurons expressing temperature-sensitive TRP (transient receptor potential) channels. Signals are transmitted via the lateral spinothalamic tract.
  • Central thermoreceptors: Temperature-sensitive neurons located in the preoptic area, which sense core blood temperature.
These two types of signals are integrated by the thermoregulatory centre of the hypothalamus to maintain normal temperature.
A normal body temperature is maintained despite environmental variations because the hypothalamic thermoregulatory center balances :
  • Heat production: Primarily from metabolic activity in the muscles and liver.
  • Heat loss: Via the skin (radiation, convection, conduction) and lungs (evaporation)

Key Temperature Definitions

  • Fever: > 99.9°F (~99th percentile in healthy individuals)
  • Hyperpyrexia: > 106.7°F
  • Thermoneutral zone: Range of ambient temperatures where core temperature is maintained by skin blood flow alone.
    • Nude: 28–32°C
    • Lightly clothed: 14.8–24.5°C

Factors Affecting Baseline Temperature

There are mutiple causes for higher baseline body temperature:
  • Higher ambient temperature
  • Diurnal and seasonal variation
    Low levels at 8 a.m. and during summer, and higher levels at 4 p.m. and during winter.
  • Age
    Lower by 0.02°C for every 10-year increase in age
  • Demographics
    African-American women have temperatures 0.052°C higher than white men
  • Comorbid conditions
    Cancer is associated with 0.02°C higher temperatures
    Hypothyroidism is linked to temperatures lower by 0.01°C
  • Menstrual cycle
    Temperature is generally lower during the 2 weeks before ovulation, and then rises by ~0.6°C (1°F) with
    ovulation and stays at that level until menses occur.

Sites of Temperature Measurement

There are various sites of measurement:
  • Oral temperatures
    Standard reference
  • Rectal temperatures
    Generally 0.4°C (0.7°F) higher than oral readings.
  • Lower oesophagal temperatures
    Closely reflect core temperature.
  • Tympanic membrane
    Convenient but more variable

Mechanism of Fever

Harrison’s Principles of Internal Medicine (21st ed.) defines fever as
“An elevation of body temperature that exceeds the normal daily variation and occurs in conjunction with an increase in the hypothalamic set point”
An easier way to understand this is to look at it like resetting of the home thermostat to a higher level in order to raise the ambient
temperature in a room.
Once the hypothalamic set point is raised, neurons in the vasomotor centre are activated, and vasoconstriction begins.
Heat conservation occurs by:
  • Shunting blood away from the periphery to internal organs, thereby reducing heat loss from the skin
  • Behavioural adjustments such as adding clothing or blankets
Heat production occurs by:
  • Shivering, which increases heat production in muscles through ATP hydrolysis
  • Non-shivering thermogenesis
    • Heat production from the liver
    • Heat generation in muscle and brown adipose tissue via mitochondrial uncoupling (proton leak), which separates oxidative phosphorylation from ATP synthesis
These processes of heat conservation and heat production continue until the temperature of the blood surrounding the hypothalamic neurons matches the new set point. Once achieved, the hypothalamus maintains this febrile temperature using the same heat balance mechanisms as in the afebrile state.
When the hypothalamic set point is reset downward (due to reduced pyrogens or administration of antipyretics), heat loss mechanisms are activated:
  • Vasodilation
  • Sweating

Acclimatisation

Physiologic adaptations that occur as a result of repeated exposures to heat.
Daily exposure to work and heat for 100 min/day results in near-maximal acclimatisation within 7 to 14 days.
This is characterized by
  • Earlier onset of sweating
  • Increased sweat volume
  • Lowered sweat sodium concentration
  • Lower heart rate with a higher stroke volume
  • Earlier release of aldosterone
For heat- and exercise-induced adaptive responses to be maintained, heat exposure needs to continue intermittently, at least on 4-day intervals.

Models of heat injury

Heat illness spans a broad spectrum of disease
  • Heat Syncope
  • Heat Edema
  • Heat Rash (miliaria rubra / prickly heat)
  • Heat Cramp
  • Heat Exhaustion
  • Heat stroke
Symptoms present when the body is exposed to heat with inability to properly cool core body temperature.

Predisposing Factors

Non-Modifiable Risk Factors
Modifiable Risk Factors
Extremes of age
Dehydration
Autonomic disorders that cause widespread anhidrosis

• Ross syndrome
• Chronic idiopathic anhidrosis
• Sjögren syndrome
Prolonged exposure
Trauma with spine injuries
Occupational categories

• Military personnel
• Athletes
• Constructionworkers
Endocrinological disorders

• Diabetes
• Hyperthyroidism
Addictive behaviors

• Alcoholism
• Cocaine
• Amphetamine
• Heroin
Neurological disorders

• Epilepsy
Drugs

• Anticholinergics
• Beta-blockers
• Diuretics
• Neuroleptics
• Anaesthetics
• Topiramate
Skin diseases

• Scleroderma
• Burns
Infections
Hereditary disease

• Malignant hyperthermia
Obesity

Heat Stroke

Heatstroke is the most hazardous condition in a spectrum of illnesses under the broad umbrella of “Heat illness”. Clinically, heatstroke is characterised by central nervous system (CNS) dysfunction, multiorgan failure, and extreme hyperthermia (usually >40.5°C).

If you want to read more, Epstein & Yanovich, NEJM 2019, is a great review.
Wilderness Medical Society defines heat stroke as
“Severe heat illness characterised by a core temperature >40°C (104°F) and central nervous system abnormalities such as altered mental status, seizure, or coma resulting from passive exposure to environmental heat (classic heat stroke) or strenuous exercise (exertional heat stroke)”
As we understand from the definition, Heat Stroke is classified as
  • Classic (passive)
    Due to exposure to environmental heat and poor heat-dissipation mechanisms
  • Exertional
    Associated with physical exercise and results when excessive production of metabolic heat overwhelms physiological heat-loss mechanisms
Feature
Classic Heatstroke
Exertional Heatstroke
Age group
Extremes of age
Postpubertal and active
Occurrence
During heat waves
Any time
Concurrent activity
Sedentary
Strenuous
Health status
Chronically ill
Generally healthy
Medications
Often on prescribed medications
Usually none
Sweating
May be absent (dry skin)
Usually present (wet skin)
CNS dysfunction
Common
Common
Acid–base disturbance
Respiratory alkalosis
Metabolic acidosis
Rhabdomyolysis
Unusual
Frequent
Liver dysfunction
Mild
Marked to severe
Renal failure
Uncommon
Common
DIC
Mild
Marked to severe
ARDS
Common
Common
Creatine kinase
Mildly elevated
Markedly elevated
Calcium
Normal
Low
Potassium
Normal
Usually high

Pathophysiology

The primary pathogenic mechanism of heat stroke involves transition from a compensable thermoregulatory phase to a noncompensable phase. Consequently, core body temperature continues to rise, eventually causing multiorgan failure.
Inflammatory Response
Hyperthermia triggers a coordinated stress response involving endothelial cells, leukocytes, and epithelial cells. This response initially helps protect tissues and promote cellular repair. It is mediated by heat-shock proteins (molecular chaperones) and changes in proinflammatory and anti-inflammatory cytokines.
However, with prolonged hyperthermia, these adaptive mechanisms become overwhelmed. Acute physiological disturbances such as circulatory failure, hypoxemia, and increased metabolic demand, along with direct heat-induced cellular injury, lead to dysregulation of the inflammatory response.
Similar to septic shock, this exaggerated inflammatory response can rapidly worsen clinical status, leading to:
  • Disseminated intravascular coagulation (DIC)
  • Multiorgan failure
  • Death
Gastrointestinal Integrity
In heatstroke, reduced intestinal blood flow leads to gut ischemia, which impairs cell viability and disrupts the integrity of the intestinal barrier. This results in increased gut permeability due to oxidative and nitrosative stress, which damages cell membranes and opens tight junctions between cells. Consequently, endotoxins (and possibly pathogens) leak into the systemic circulation.
The liver normally detoxifies these endotoxins, but during heatstroke, this capacity is overwhelmed, leading to endotoxemia.
Although the association between heatstroke and endotoxemia is well established, it is often under-recognized in clinical practice.

Diagnosis

The diagnosis of heatstroke is largely clinical, based primarily on the triad of
  • Hyperthermia
  • Neurologic abnormalities
  • Recent exposure to hot weather or physical exertion

Treatment

Wilderness Medical Society Clinical Practice Guidelines (2019) divides treatment into 2 phases
1. Field treatment
The componenets of the same are
  • Remove from the heat source
    Move the victim into the shade to decrease the ambient temperature.
  • Supportive care of airway, breathing, and circulation
  • Cold water immersion
    Cold-water immersion is achieved by removing clothes and submerging the patient’s trunk and extremities in a bath of cold water or tub of ice water. Alternatively, water may be applied onto a patient covered in crushed ice and lying on a plastic sheet or tarp with its sides folded upright to keep the slurry in place (“tarp taco”).
  • Whole-body conductive cooling
    Conduction of heat from the ground can be reduced by placing the patient on a cool surface or on an insulating barrier such as a sleeping pad or sleeping bag. Loosening or removing tight-fitting clothing improves air circulation and enhances convective heat loss.
  • Intravenous hydration
    Adequate hydration helps reduce hyperthermia, as fluid losses from sweating, vomiting, diarrhea, or poor intake increase the risk of heat injury. In patients with altered mental status or seizure risk, the intravenous route is preferred to reduce aspiration risk.
    • Use 1–2 L isotonic fluids (0.9% normal saline ± 5% dextrose)
    • Avoid overhydration, especially in cardiac patients (risk of pulmonary edema)
    • Do not delay rapid cooling while establishing IV access
  • Evacuation
    Patients with heatstroke should generally be transported to a facility capable of critical care and multiorgan support.
    Exception: selected athletes or soldiers with early ice-water immersion, complete symptom resolution, and stable status may be observed in a medical station or infirmary
Other techniques to consider are
  • Evaporative cooling
  • Chemical cold packs/Ice paks
Antipyretic drugs are ineffectual and should be avoided
  1. Hospital
In the hospital setting, the primary goals are rapid reduction of core temperature and support of organ function. As with all ED patients, management begins with stabilisation of ABCs.
There 2 recommended methods of cooling in hospital
  1. Conductive cooling
    This can be achieved by cold water immersion or wetted ice packs covering the entire body can cool through conduction. This is the recommended method in both EHS and classic heat stroke.
  1. Evaporative and Convective cooling
    Evaporative and convective cooling may be considered in classic heat stroke in the hospital setting, but cooling rates with this method are inferior to those with conductive cooling. Evaporative and convective cooling is not indicated in EHS unless effective conductive cooling is not available.
Target temperature: Reduce core temperature to < 39°C
Other adjuncts to consider are
  • Cold IV fluids (4°C)
    (Shown to improve mortality when combined with other techniques)
  • Body cavity lavage with cold isotonic fluid
    (Not the recommended primary treatment)
No pharmacologic agent has been shown to be helpful as a treatment for heat stroke.