The hospitalized patient, especially if sedated, is often placed in a thermal environmental that is cooler than optimal and can exert a stressful effect.

Heat loss during a surgical procedure can be remarkable, and the administration of muscle relaxants further compromises the ability to generate heat.

Generalized Hypothermia:

Most human studies of hypothermia have been based on observation of the effects of immersion in cold water. ( Eg. German concentration camps in World War II )

Acute immersion at 40 degree C to 100 degree C results in immediate increase in both ventilatory rate and respiratory tidal volume.

The initial "gasp" response makes possible the aspiration of water, with resulting laryngospasm, asphyxia, and sudden death.

The increased respiratory rate and depth of respiration result in decreased arterial carbon dioxide concentration and a secondary constriction of the cerebral vasculature.

The reduction in cerebral blood flow, coupled with the decreased core body temperature and lower temperature of the blood perfusing the brain, results in mental confusion.

Muscle tetany makes swimming impossible. Furthermore, an increased vagal discharge leads to premature ventricular contractions, ventricular arrhythmias, and even fibrillation.

In an attempt to increase heat production, the immersed body immediately responds by increasing muscle activity and oxygen consumption. However, there are limits to the sources of energy available for sustained warming.

Within a half hour, heat loss exceeds heat production because of the combination of high direct conduction of heat from the whole skin surface and the altered muscle tone caused by decreased arterial carbon dioxide and exhaustion, and core temperature begins to fall.

Peripheral vasoconstriction is another response to conserve heat.

In addition, there is an increased sympathetic neural discharge, resulting in increased heart and basal metabolic rates and shivering.

When the core temperature approaches 35 degree C, this activity may be three to six times above normal.

Below this temperature a decline in respiratory rate , heart rate, and blood pressure ensues because of the decline in functional reserve.

With prolonged cooling, a "cold-induced" diuresis results in an increased blood viscosity.

As a result, blood flow decreases and oxygen-hemoglobin association is less effective.

Cardiac stroke volume decreases and peripheral vascular resistance increases as a direct result of both blood "sludging" and loss of plasma.

The most important factor in causing death is cardiac arrhythmia or sudden arrest.

These observations have been confirmed and extended in the last several decades, largely because the need to induce hypothermia in patients undergoing open-heart surgery.

In fact, with careful pharmocologic control, prolonged periods of decreased body temperature can be achieved with no residual harm.

During prolonged hypothermia - for example, after an accident to a mountain climber - several of the consequences of decreased body temperature are related to altered cerebrovascular function.

When the body core temperature reaches 32 degree C the individual becomes lethargic, apathetic, and withdrawn.

A characteristic response is inappropriate behavior, including disrobing, even when cold.

A further decline in temperature increases the lethargy to intermittent "stupor", and eventually coma.

Although there is no specific morphologic in those who have succumbed to hypothermia, the skin exhibits red and purple discolorations, swelling of the ears and hands, and irregular vasoconstriction and vasodilatation.

Areas of myocytolysis are seen within the heart.

The lung may display pulmonary edema and intra-alveolar, intrabronchial, and interstitial hemorrhage.

Focal Thermal Alterations:

Local reduction in tissue temperature, particularly in the skin, is associated with local vasoconstrition.

Tissue water crystallizes if blood circulation is insufficient to counter persistent thermal loss.

When freezing occurs slowly, ice crystals from within tissue cells and in the interstitial space. Concomitantly, electrolyte-rich gels are excluded.

Injury to the cellular organelles reflects the drastic changes in ionic concentrations in the excluded volume.

Denaturation of macromolecules follows, as well as physical disruption of cellular membranes by the ice.

When freezing is rapid, a gel-like structure forms within the cell that lacks the crystalloids of water. This water-solid reduces the extent of mechanical and chemical injury.

The most significant cellular damage apparently occurs on thawing, when mechanical disruption of membrane structures occurs. This may be the result of transformation of gel to crystal.

The most biologically significant cell injury appears in the endothelial lining of the capillaries and venules, an effect that alters small vessel permeability, thereby initiating extravasation of plasma, formation of localized edema and blisters, and an inflammatory reaction.

Immersion foot (trenchfoot) is caused by a prolonged reduction in tissue temperature to a point not low enough to freeze tissue.

This cooling causes cellular disruption and vascular changes that resemble those observed during the healing phase of local tissue freezing.

The target seems to be the endothelial cell.

Local thrombosis and changes caused by altered permeability are prominent.

Vascular occlusion often leads to gangrene.

Environmental Pathology- Physical Agents : click here

Environmental Pathology-Thermal Regulatory Dysfunction: click here

Environmental Pathology - Hyperthermia: click here

Environmental Pathology- Electrical Burns: click here