Heat stroke and sunstroke

Etiology and stages of heat stroke development

Heat stroke is an extremely severe and rapidly progressing form of hyperthermia. The primary etiological factor is the exposure of the body to high-intensity external heat. The risk of developing this pathology increases manifold when the natural mechanisms of adaptation to elevated temperatures are inefficient.

The pathogenesis of the process is characterized by its rapidity:

1. Intense overheating of the body begins.
2. A short-lived compensation stage is activated. Often, it proceeds so rapidly that it manifests no clinical symptoms.
3. A rapid and sharp breakdown of thermoregulation mechanisms occurs.
4. Transition into the decompensation stage takes place. During this period, rectal body temperature can reach life-threatening values in a very short time — 42–43 °C.

The essence of heat stroke lies precisely in this brief adaptation, which instantly gives way to profound decompensation.

Intoxication factors and systemic complications

An excessive increase in body temperature triggers a large-scale cascade of biochemical disorders, leading to severe endotoxemia. Three groups of toxic substances accumulate in the blood:

• Excess proteolysis products: ammonia, ammonia derivatives, and various peptides.
• Products of disrupted lipid metabolism: epoxides, ketone bodies, lipid peroxides, and aldehydes.
• Medium-molecular-weight molecules (MMMs): polyamines, oligosugars, glycoproteins, and oligopeptides.

This progressive intoxication exacerbates vital activity disorders. It causes erythrocyte hemolysis and a significant increase in microvessel wall permeability.

Concurrently, severe consequences develop in the hemostasis system: blood viscosity increases, systemic hypercoagulation occurs, along with microthrombosis and disseminated intravascular coagulation (DIC syndrome). Microhemocirculation is disrupted.

Mortality in heat stroke reaches 30%. The main causes of death are acute intoxication, respiratory arrest, and heart failure resulting from cardiac fibrillation or asystole.

Sunstroke: specifics of nervous system damage

Sunstroke is a typical form of a severe hyperthermic condition with a high risk of mortality. Its primary cause lies in the direct action of solar energy on the brain. The infrared part of the spectrum (thermal radiation) possesses the greatest pathogenic effect.

Unlike convection and conduction heat, infrared radiation is capable of heating both superficial and deep tissues simultaneously. It intensively heats brain tissue, including the area housing the neurons of the thermoregulation center, which accounts for the very rapid development of the pathology.

Pathogenesis consists of a combination of general hyperthermia and specific CNS damage:

1. Direct neuronal damage: metabolism and plastic processes in brain cells are disrupted.
2. Vascular and cerebrospinal fluid dynamics shifts: arterial hyperemia increases, lymph formation rises, and venous hyperemia progresses.
3. Complications: cerebral edema and multiple hemorrhages into the brain tissue develop.
4. Mechanical factor: vascular disorders lead to compression of the brain.
5. Secondary CNS damage: compression combined with impaired metabolism causes severe ischemia, hypoxia, and damage to nerve centers.

The outcome is critical vital function disorders and death.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Compensation mechanisms during overheating and the causes of their rapid breakdown.
• Biochemical cascade of medium-molecular-weight molecule formation and their toxic effects.
• Cerebrospinal fluid dynamics disorders and mechanisms of cerebral edema development in sunstroke.
• Pathogenesis of DIC syndrome development against the background of hyperthermia.
• Influence of altered lipid metabolism products on microvessel permeability.

Other topics in «Chapter 6. Body Thermal Balance Disorders»

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.