Above a certain thermal limit, denaturation of enzymes and precipitation of other proteins occur. In addition, "melting" of the lipid bilayers of cell membranes takes place.

Systemic hyperthermia:

Elevation of the body core temperature occurs because of increased heat production, decreased elimination of heat from the body (reflecting an aberrant response of the thermoregulatory center), or a disturbance of the thermal regulatory center itself.

It can also alter because heat is being conducted into the body faster than the system can clear the additional "thermal load".

During infectious processes and inflammatory responses, a circulating factor derived from macrophages apparently resets the body's "thermostat" to permit a higher body core temperature level. This small polypeptide, interleukin-1, may exert a direct effect or may have a prostaglandin intermediate. However, it may not be the sole thermal factor.

There is a definite level to which core temperature can rise, above which survival of the individual is no longer possible.

A blood temperature higher than 42.5 degree C leads to profound functional disturbances, including general vasodilatation, inefficient cardiac function, and altered respiration.

Isolated heart-lung preparations fail at about the same temperature, suggesting an inherent temperature limitation in the cardiovascular system and perhaps in the myocardial cells themselves.

In general, systemic temperature elevations above 41 degree to 42 degree C are not compatible with life.

Systemic temperature elevations associated with infections are commonly designated "fever".

There are few, if any, defined pathologic changes that are associated with fever alone.

Physical findings include increased heart and respiratory rates, peripheral vaso- dilatation, and diaphoresis, all recognized mechanisms for thermoregulation.

The central nervous system responds with irritability, restlessness, and particularly in children, convulsions. The temperature at which convulsions occur differs for each individual, and may change during life.

Nocturnal temperature elevations with "night-sweats" are a feature of pulmonary granulomatous infections (especially tuberculosis) and are also seen lympho-proliferative diseases. Infectious Granuloma of the Lung

Prolonged temperature elevation can produce wasting, principally because of an increased metabolic rate.

A peculiar thermal alteration that occurs during surgery in susceptible persons is designated malignant hyperthermia.

The cause of this prolonged temperature elevation (over 40 degree C) is not known, but it may be a hypersensitivity response to anesthetic agents.

Localized Hyperthermia:

Cutaneous burns are the most frequent form of localized hyperthermia.

Both the elevated temperature and the rate of temperature change are important in determining the patterns of the tissue response.

A temperature of 70 degree C or higher for several seconds causes necrosis of the entire dermal epithelium, where as a temperature of 50 degree C may be sustained for 10 minutes or more without killing the cells.

Cutaneous burns have been separated into three categories of severity : First ; Second ; and Third - degree burns.

A more contemporary classification refers to full thickness (third-degree) and partial thickness (first and second-degree) burns.

First-degree burns : First-degree burns, such as a mild sunburn, are recognized by congestion and pain, but are not associated with necrosis.

Mild endothelial injury produces vasodilatation, increased vascular permeability and slight edema.

Second-degree burns : Burns that cause necrosis of the epithelium but spare the dermis are termed second-degree burns.

Clinically, these are recognized by blisters, in which the epithelium is separated from the dermis.

Third-degree burns : Third-degree burns char both the epithelium and the underlying dermis.

Histologically, the epidermis and the dermis are carbonized and the cellular structure is lost.

The extent of anatomical change is related to the intensity of the thermal exposure and the rapidity of dissipation of heat energy.

Flash burns resulting from atomic bomb explosions are associated with carbonization of the epithelial fragments, but show little evidence of deep thermal injury.

One of the most serious systemic disturbances caused by cutaneous burns arises from the fact that the denuded skin surfaces "weep" plasma. People with third-degree burns can lose about 0.3 ml body water per square centimeter of burned area a day. The resulting hemoconcentration and poor vascular perfusion of the skin and other viscera complicate the recovery of these individuals.

The healing of cutaneous burns is related to the extent of the tissue destruction.

First-degree burns, by definition, display little if any cell loss, and healing requires only repair or replacement of the injured endothelial cells.

Second-degree burns also heal without a scar because the basal cells of the epidermis are not destroyed and serve as a source of regenerating cells for the epithelium.

Third-degree burns, in which there is destruction of the entire thickness of the epidermis, pose a separate set of problems.

If the destruction spares the skin appendages, reepithelialization can arise from these foci. Initially, islands of proliferation at the orifices of these glands grow and coalesce to cover the surface.

Saprophytic infection of the charred tissue is common, and poses another difficulty for healing.

Deeper burns that destroy the skin appendages require new epidermis to be grafted to the debrided area to establish a functional covering.

Burned skin that is not replaced by a graft heals with the formation of a dense scar.

Since this connective tissue lacks the elasticity of normal skin, contractures which limit motion may be the eventual result.

Environmental Pathology- Physical Agents : click here

Environmental Pathology-Thermal Regulatory Dysfunction: click here

Environmental Pathology - Hypothermia: click here

Environmental Pathology- Electrical Burns: click here

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