A 48-year-old homeless man presented to the emergency department with bilateral black toes on a subzero temperature morning in January. He states that initially he felt a tingling sensation followed by clumsiness, which led to a total loss of sensation of both feet. The patient's history included tobacco smoking as well as poorly controlled diabetes mellitus. Examination revealed bilateral segments of profound, dark distal eschar, along with bullous erythema of the toes. A dusky area of mid foot tissue demarcation was apparent with segmental dark ischemic borders. Immediate amputation of the left leg was undertaken and the right foot was given a chance to demarcate over the ensuing days.
The prevalence of frostbite in the United States is unknown since no specific system for reporting cases exists.
Rare in North America with the exception of Canada, Alaska, and other northern states.
Proclivity for males aged 30 to 49 years, which probably reflects increased outdoor activity as opposed to genetic predisposition.
Young children are at greater risk of frostbite due to impaired behavioral modification.
Increased risk in the black population.
The highest-risk groups are participants in extreme sports (ie, mountaineers) and the military population.
The most affected areas are the hands, feet, face, lips, and ears.1,2
ETIOLOGY AND PATHOPHYSIOLOGY
Frostbite injury is due to the absolute temperature as well as duration of exposure. Of these two factors, the exposure duration has the greater impact on the level of injury and severity of tissue damage. The wind chill factor also influences susceptibility to and severity of frostbite.
Risk factors: malnutrition, substance abuse, mental illness, homelessness, moisture, previous cold injury, and vasoconstrictive medications.
Predisposing medical conditions: peripheral artery disease (PAD), stroke, Raynaud phenomenon, diabetes, and peripheral neuropathy.
Frostbite involves three pathophysiologic components—extracellular and intracellular ice crystallization, intracellular dehydration, and ischemia.
Extracellular ice crystal formation results in damage to the cellular membrane. Further exposure causes a shift of intracellular fluid into the extracellular matrix, resulting in intracellular dehydration and eventual intracellular ice crystal formation. Damage caused by the expansion of the ice crystals is irreversible.
Alternating vasoconstriction and vasodilation ("the hunting reaction") causes rewarming of peripheral tissues with warm core blood. Throughout this cycling, cellular mediators are released including prostaglandins and thromboxane A2, augmenting platelet aggregation, thrombosis, and vasoconstriction.
Continued exposure to colder temperatures slows the hunting reaction and eventually stops the vasodilation phase, resulting in unopposed vasoconstriction. This ultimately leads to tissue hypoxia, acidosis, venular and arteriolar thrombosis, and ischemic necrosis.
Common symptoms include paresthesias, throbbing, numbness, anesthesia, joint pain, and loss of muscle dexterity.
First degree: superficial distribution with a central pallor and surrounding edema. The surrounding skin often experiences sensory changes.
Second degree: characterized by blister formation within 48 hours of tissue exposure. At this stage there is no tissue ...
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