The so-called heat injuries are due to both the sudden changes in temperature – rapid rise, and the slower conditioning of the body to the temperature changes. They are generally divided into two groups – mild heat injuries and conditions and severe heat injuries. The first group includes heat edema, miliaria rubra, sunburn, heat cramps, heat tetany, and heat (“parade”) syncope. The second group includes heat exhaustion, heatstroke, and sunstroke.
Heat edema is the appearance of swelling in the area of the feet, wrists, and fingers during prolonged sitting or standing in non-acclimatized persons, in the first days of residence in hot climatic conditions.
The pathophysiological mechanism is subcutaneous vasodilatation, increased intravascular hydrostatic pressure, and fluid collection in the extremities. Patients complain of tight shoes and discomfort. The symptoms disappear in a few days with the process of acclimatization. Treatment for this self-limiting condition is elevation of the extremities to improve venous edema, wearing elastic stockings, and local cooling of the affected area.
Heat rash – miliaria rubra is a common condition when living in countries and areas with hot and humid climates. It is due to a blockage of the openings of the sweat glands, which is often complicated by a secondary staphylococcal infection. The skin with a military rash cannot effectively participate in the body’s thermoregulation, and the risk of developing heat stroke increases according to the area affected by the rash.
Treatment consists of drying the skin and treating the lesions with chlorhexidine lotions/creams in combination with or without salicylic alcohol, an antibiotic against staphylococcal infection. Hydrocortisone cream or menthol alcohol is applied topically against itching.
Sunburn of the skin also impairs the body’s thermoregulation by reducing sweating in the affected areas, and can also lead to an increase in body temperature.
Cramps are short-term, periodically recurring, and painful spasms of muscles from the most physically active muscle groups (shoulders, thighs, lower legs). They occur as a result of profuse sweating with salt (Na, Cl) deficiency after the end of vigorous physical activity in non-acclimatized persons subjected to heat stress. Objectively, “twitches” of the affected muscles are observed lasting up to 2-3 minutes.
Heat syncope is a temporary circulatory disorder due to the pooling of blood in the peripheral veins, especially in the lower extremities during prolonged standing, combined with a high temperature. It manifests itself with a short-term loss of consciousness, as a result of cerebral hypoperfusion, and often occurs with poor acclimatization.
Heat exhaustion is the most common form of heat injury and is not usually associated with organ damage. It occurs when the blood pushed by the heart is insufficient to cover the increased needs of the skin blood vessels. Consciousness, unlike heat stroke, is unchanged.
In turn, heatstroke is a serious, life-threatening condition that requires immediate action. It is characterized by an increase in central body temperature above 40 °C and the appearance of quantitative and/or qualitative changes in consciousness. In its classic form, heat stroke occurs with anhidrosis (sweating is stopped). At the same time, the presence of sweating should not exclude the diagnosis.
These patients are at high risk of developing rhabdomyolysis and acute renal failure. In the beginning, non-specific symptoms such as nausea, vomiting, general weakness, and headache appear. At a later stage, the characteristic changes in consciousness develop – drowsiness, disorientation, lethargy, irritation, ataxia, to acute psychoses with progression to sopor and coma. Seizures may occur.
The clinical manifestations of sunstroke are similar to those of heat stroke. It develops as a result of the direct impact of heat from the sun’s rays on the unprotected head and a subsequent increase in temperature in the cranial cavity. As a result, vasodilatation and increased vascular permeability of cerebral vessels occur, which leads to the development of cerebral edema and an increase in intracranial pressure.
Bibliography:
1. Damage caused by heat, E. Taneva
2. TB MED 507/ NAVMED P-5052-5/ AFP 160-1. Prevention, treatment and control of heat injury
The material is informative and cannot replace consultation with a doctor. Before starting treatment, you must consult a doctor.
