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Frostbite (localized cold injury)

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Frostbite is most likely due to increased exposure to cold temperatures and/or risk-taking behavior.

Severity of frostbite injury depends on absolute temperature, wind chill, duration of exposure, wet or dry cold, immersion, clothing quality, and substance use.

Frostbite is most likely due to increased exposure to cold temperatures and/or risk-taking behavior.

The feet and hands are the most commonly affected areas and account for 90% of frostbite injuries.

Historically, frostbite was primarily seen in military populations, but it has become increasingly prevalent in homeless people, who are vulnerable to cold injuries.

In recent years frostbite has occurred in urban settings, with social disadvantage, physical disability, homelessness, substance use disorder, and psychiatric disease are the root causes of cold exposure that threatens life and limbs.

It is a localized cold thermal injury from exposure to temperatures low enough to cause ice crystal formation in tissues, resulting in damage to cell membranes and osmotically dehydrated cells.

Frostbite occurs because of 3 interlinked processes: (1) extracellular ice crystal formation as a direct injury, which (2) leads to oncotic fluid shifts and intracellular dehydration, and (3) ultimately cell death.

Cold induces indirect injury by vasoconstriction which increases blood viscosity, microvascular thrombosis, and resultant tissue hypoxia.

The indirect injury by cold-induced vasoconstriction increases blood viscosity, microvascular thrombosis, and results in tissue hypoxia.

Additionally, a growing interest in outdoor activities, such as skiing, hiking, and mountaineering, has contributed to an increased prevalence of frostbite injuries in the general population.

The final process in frostbite is the release of potent inflammatory hypoxia-related mediators during the hunting reaction and with tissue reperfusion.

These mediators include prostaglandin F2α and thromboxane A2, which trigger further vasoconstriction, platelet aggregation, and blood vessel thrombosis, leading to more endothelial cell damage and further hypoxia and cell death.

Historically, was primarily seen in military populations, but it has become increasingly prevalent in homeless people, who are vulnerable to cold injuries.

It occurs because of 3 interlinked processes: (1) extracellular ice crystal formation as a direct injury, which (2) leads to oncotic fluid shifts and intracellular dehydration, and (3) ultimately cell death.

Direct cellular damage is a result of ice crystal formation in subsequent injury to the cell membrane, combined with intracellular metabolic abnormalities.

Ischemic cellular damage follows endothelial disruption of a micro circulation, with vasoconstriction, thrombosis and inflammatory effects on re-perfusion.

The severity of frostbite is related to the degree to which frozen tissues are refused on thawing.

Stage 1:

Burning and numbness

Pallor warms to erythema

Stage2:

Insensate

Pallor warms to blistering

Perfusion after warming

Stage 3:

Insensate, frozen

Frozen warms to hemorrhagic blisters

Variable perfusion or necrosis after warming

Stage 4: the depth of injury is beneath the skin including muscle, bone, and tendon with blue gray skin discoloration, no pain with rewarming, full thickness skin wounds, necrosis of underlying bone and deep tissue

In severe frostbite frozen endothelial cells are disrupted with thawing and leads to extensive microvascular thrombosis.

The pathophysiology for cold injury is a combination of direct cellular damage from freezing and cellular ischemia from vasospasm and small vessel thrombosis.

Prevention of frostbite requires early awareness and intervention.

Warming tissues before freezing generally has good outcomes.

Frozen body parts should not be thawed if there is a risk of refreezing before arrival at a definitive warming site, as freezing-thawing-refreezing injury is worse than prolonged simple freezing injury.

Immediate care to enhance blood flow and reverse small blood vessel from thromboses should be done in patients at high risk for major tissue loss.

Treatment: admission to hospital, rapid rewarming with water immersion at 104°F to 108°F (40°C to 42°C), tetanus prophylaxis, ibuprofen for anti-inflammatory properties, narcotic analgesics for pain control, smoking cessation, limb elevation, rest, and splinting.

Early intra-arterial thrombolysis, has been used in frostbite injuries to limit ischemic effects by improving perfusion to tissues.

Thrombolysis has been shown to be effective if administered within 24 hours after rewarming frostbitten tissue.

 

Hyperbaric oxygen therapy (HBOT) treats patients with 100% oxygen at greater than 1.0 atmosphere (atm), can be used to treat selected ischemic problem wounds, wounds caused by radiation, compromised flaps and grafts, and ischemia-reperfusion disorders.

HBOT compensates for some microcirculatory failure and tissue hypoxia by increasing oxygen delivery to ischemic tissues directly via elevated arterial oxygen concentration and indirectly via angiogenesis and resolution of tissue edema.

It also may promote healing of frostbite injuries.

Side effects occurred in 77.3% of patients, with some patients experiencing multiple effects.

The most common side effect is otologic barotrauma.

In 50% of cases requiring amputation, there was a possible beneficial effect of HBOT, because the final amputation level was distal to the predicted level from pretreatment bone scans.

It has been shown to increase oxygen-sensitive fibroblast proliferation, angiogenesis, and capillary density, decrease tissue edema by promoting intermittent vasoconstriction, and modulate leukocyte bactericidal and proinflammatory activity.

Multiple studies have been published in the form of case reports with positive outcomes using HBOT.

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