Heat illness : Heat exhaustion and heat stroke
Exposure to high temperatures and high humidity, as well as strenuous exercise may lead to heat illness, a continuum of disease that encompasses disorders ranging in severity from muscle cramps, heat-syncope and heat exhaustion to heat stroke. Heat stroke is a life-threatening emergency, thus it is the most severe form of heat illness. Heat illness can affect individuals exposed to environmental conditions of high temperature such as athletes, construction workers, firefighters, military personnel, etc, or individuals staying in a hot environment, especially if they have predisposing factors reducing the body’s ability to dissipate heat.
Such
predisposing factors are:
Age extremes (children,
elderly)
Obesity
Dehydration (e.g.
gastroenteritis, inadequate fluid intake)
Cardiovascular disease, such
as congestive heart failure
Certain endocrine and
metabolic diseases, such as diabetes mellitus and hyperthyroidism
A febrile infection
Alcohol, cocaine
Treatment with some categories
of medications, such as:
MAO inhibitors,
antipsychotics, anxiolytics
Anticholinergics
Diuretics
Beta-blockers
Exertional heat illness is one of the leading
causes of death among young athletes and may be on the rise because of the
increasing popularity of mass-participation athletic events. Early recognition
and treatment of EHI is very important because it can reduce associated
morbidity and mortality.
Pathophysiology of heat illness
Heat is generated by the basal metabolism, by muscular activity and it is also absorbed from a warm environment.
The human organism has homeostatic mechanisms to maintain normal core body temperature. An increase in core temperature is detected in the hypothalamus, which reacts by sending signals to induce cutaneous vasodilation and sweating.
Under normal conditions, the body is able to dissipate heat through:
■Radiation: Transfer of heat directly from the body to a cooler environment by infrared radiation. This mechanism does not require air motion or direct contact
■Evaporation: Cooling of the skin by water vaporization (eg, sweat)
■Convection: Transfer of heat to cooler air (or liquid) that passes over exposed skin
■Conduction: Transfer of heat from the skin to a cooler surface that is in direct contact to the skin.
The contribution of each of these mechanisms depends on environmental temperature and humidity. When the environmental temperature is not high, radiation has a major role (65%), evaporation of sweat is also important (normally provides 30% of cooling). Exhalation of water vapor and production of urine and feces provide about 5% of cooling. When the environmental temperature is > 35° C, evaporation accounts for virtually all dissipation of heat because the other mechanisms can function only when the environmental temperature is significantly lower than body temperature. Radiation, convection, and conduction are decreasingly effective as the temperature of the environment approaches the skin’s temperature. Therefore, in such conditions of a hot environment, only evaporation is effective. However, evaporation is influenced by humidity and it is ineffective above a relative humidity of 75%.
Despite the compensative mechanisms of the body significant or prolonged exposure to heat may exceed the capacity of these physiologic cooling mechanisms. This will lead to an elevated core temperature. The body can tolerate modest, transient core temperature elevations, but severe elevations (> 41° C) are not well tolerated. Severe core temperature elevations can result in protein denaturation and the release of inflammatory cytokines. This causes cellular dysfunction and dysfunction of multiple organs. The activation of the inflammatory cascade apart from causing organ dysfunction may also lead to the activation of the coagulation cascade resulting in the development of disseminated intravascular coagulation (DIC). The pathophysiologic process is similar to the pathophysiology of multiple organ dysfunction syndrome, which occurs in patients with prolonged circulatory shock.
Mild forms of heat illness
Heat edema manifests by mild swelling of the feet, ankles, and hands that appears within the first few days of exposure to a hot environment. It is caused by cutaneous vasodilatation and orthostatic pooling of interstitial fluid in gravity-dependent extremities when a person is sitting or standing for a long time in a hot environment. The body’s response to a hot environment may often cause an increase in the secretion of aldosterone and antidiuretic hormone which also contributes to edema formation. Generally, edema is the clinical manifestation of an accumulation of fluid within the interstitial spaces. It develops when the normal balance between the flow of fluid out of capillaries and the return of fluid into the vascular space via capillary reabsorption and lymphatic flow is disrupted. Heat edema is mild and self-limited, usually resolving spontaneously in a few days. Elevation of the legs is usually helpful to reduce swelling. Diuretics are not used for heat edema (They are used for edema due to other causes, such as congestive heart failure or hepatic failure).
Heat stress or heat exhaustion
Heat exhaustion is a form of
heat illness of moderate severity that occurs when the body overheats exceeding
the capacity of it’s cooling homeostatic mechanisms, as a result of physical
activity in a hot environment.
Manifestations of heat
exhaustion may include thirst, cramps, dizziness, headache, vertigo, anorexia,
nausea and vomiting but there are no severe manifestations from the central
nervous system (this differentiates it from heat stroke). The patient is
flushed and sweating (with sweaty hot skin). The rectal temperature is usually 38-39°C (< 40°C).
Τachycardia and orthostatic hypotension occur as a
result of dehydration. Heat stress (heat exhaustion), if not adequately treated, may progress to heat stroke, which a is a severe condition (see below).
Treatment of heat exhaustion
The patient must rest in a cool environment in supine position with leg elevation. Volume and electrolyte replacement is required either with oral electrolyte solutions in patients with mild heat stress, or with IV fluids (1 - 2 L of normal saline) in patients suffering from a more severe form of heat exhaustion with vomiting or with manifestations of significant tissue hypoperfusion. Active skin cooling by sponging or spraying with water and using a fan is usually necessary.
Heat stroke
Heat stroke is a medical
emergency characterized by extremely elevated core body temperature > 40,5 °C (usually ≥ 41 °C) and central
nervous system dysfunction manifested by confusion, delirium, seizures or coma,
that occurs after exposure to a very hot environment and/or strenuous physical
activity. It is often accompanied by hepatic damage and rhabdomyolysis. If it is not treated promptly, it may lead to multiorgan dysfunction because the extremely elevated body
temperature can cause damage to the tissues.
There are two categories of heat stroke
Classic heat stroke is caused by passive exposure to a hot environment
resulting in an imbalance between heat production by and dissipation from the
body. More susceptible for heat stroke are young children, pregnant women, the
elderly and individuals with chronic underlying disease.
Exertional heat stroke is caused by high intensity physical activity
leading to an imbalance between heat production by and dissipation from the
body. It is common among healthy people who engage in intense activity during
the summer, such as athletes, soldiers, firefighters and construction workers.
Manifestations and diagnosis of heat stroke
The diagnosis of heat stroke requires not only the presence of an
extremely elevated core temperature of the body but also the presence of severe
manifestations from the central nervous system (see below) and conditions of
exposure to a hot environment and/or intense physical activity in a hot
environment.
Manifestations of heat stroke:
Elevated core body temperature > 40,5 °C (105°F)
Hot skin (due to vasodilation). The skin is often (but not always) dry.
Sweating may occasionally be present if the patient is not significantly
dehydrated.
Manifestations of severe central nervous system dysfunction (confusion,
hallucinations, delirium, seizures or coma)
Tachycardia, wide pulse pressure. Hypotension may be present. These
cardiovascular manifestations are due to peripheral vasodilation
Tachypnea
Rales may be present due to noncardiogenic pulmonary edema (acute respiratory distress syndrome-ARDS)
Hypoxemia may be present as a result of noncardiogenic pulmonary edema or
aspiration
Complications of heat stroke may include rhabdomyolysis, acute renal failure (caused by rhabdomyolysis, severe dehydration, or direct thermal injury to the kidneys ) , shock, acute respiratory distress syndrome (ARDS), reversible liver damage, disseminated intravascular coagulation ( DIC), and multiple organ failure.
Treatment of heat stroke
Priorities are the ABCs (assess and treat airway, breathing and circulation) and rapid initiation of cooling if the rectal temperature is ≥ 40 °C with a target to achieve rectal temperature of 38,5 to 39 °C . Remove clothes, spray or sponge the skin with tepid water and use a fan to encourage evaporation. Ice packs on the neck, axilla and groin are also used. Another method of cooling is immersion cooling, by placing the patient in a tub with cold water so that the torso and extremities are covered with water. In refractory cases, cold gastric or peritoneal lavage and cold intravenous fluids (cool N/S at 5-10 °C) can be used. Stop cooling therapy at 39°C (102°F) to avoid overshooting and hypothermia. In heat exhaustion or heat stroke antipyretic agents are not helpful because the elevated body temperature is not due to a change in the set point in the hypothalamus. In some cases, during cooling seizures may occur and can be treated successfully with benzodiazepines.
In patients with heat stroke or heat exhaustion rehydration is needed to replace fluid losses. Initial rehydration is accomplished with prompt administration of 0.5-1.0 L 0.9% normal saline (N/S). Aggressive fluid resuscitation is required until BP >90/60 or central venous pressure (CVP) >12 mL H2O. Avoid overhydration, which can contribute to pulmonary edema and ARDS. IV fluids should be administered at a rate that ensures adequate urinary output. Hypotension is a common initial finding in heat stroke and it usually responds to treatment with IV crystalloids (N/S). If hypotension is refractory to IV fluids, administer vasoactive catecholamines such as dopamine or dobutamine.
Endotracheal intubation and mechanical ventilation is indicated in
patients with significantly altered mental status or severe hypoxia.
GO BACK TO THE TABLE OF CONTENTS
LINK: Emergency medicine book-Table of contents
Bibliography
Liu SY, Song, JC, et al. (2020). Expert consensus on
the diagnosis and treatment of heat stroke in China. Military Medical Research
2020; 7(1). https://doi.org/10.1186/s40779-019-0229-2
Leiva DF, Church B. Heat Illness. [Updated 2021 Apr
15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553117/
Glazer JL. Management of heatstroke and heat exhaustion. Am Fam Physician. 2005;71(11):2133-2140. PMID: 15952443. LINK https://www.aafp.org/afp/2005/0601/p2133.html
Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Heat Illness: 2019 Update. LINK https://survive-student-resource.austererisk.com/environmental/wms_heat_illness.html
Bart A English W Diagnosis and management of heat stroke. LINK https://anaesthesiology.gr/media/File/pdf/WFSA_tutorial_341.pdf
No comments:
Post a Comment