Hypothermia a decrease in body temperature below 35
degree C can result in systemic or focal injury. Example of focal
injury is trenchfoot or immersion foot. In localized hypothermia of
these types, actual tissue freezing does not occur. Frostbite, by
contrast, involves the crystallization of tissue water.
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
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Environmental Pathology-Thermal Regulatory
Dysfunction: click here
Environmental Pathology - Hyperthermia: click here
Environmental Pathology- Electrical Burns: click
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