Peripheral Cold Injuries

Pathophysiology of cold injuries:

 2 mechanisms of tissue injury: architectural cellular damage from ice crystal formation and microvascular thrombosis and stasis

 1. Prefreeze Phase

- superficial tissue cooling

- microvasuclar constriction

- endothelial plasma leak

 2. Freeze-Thaw Phase

- extra-cellular fluid ice crystal formation

- intracellular dehydration and shrinkage

- cell membraine denaturation or disruption

- cell shrinkage and collapse

3. Vascular Stasis and Progressive Ischemia

 - vasospasticity

- vascular endothelial damage

- necrosis, demarcation, mummification or slough

The ultimate determinant of progressive tissue damage appears to be injury to the microvasculature. Endothelial cells are the tissue most susceptible to freezing injury.

Frostnip

- a superficial cold insult that presents with transient numbness/tingling that resolves after rewarming

*** no tissue destruction

Frostbite

- occurs when the tissue supercools well below 0 degrees Celsius

- required temperature at least -4 degrees

- symptoms usually reflect the severity of the injury (complete acute anesthesia usually suggests a severe injury)

- most commonly presents with numbness (>75% of patients)

- distal extremities most at risk

- rapid rewarming results in initial hyperemia, after thawing, partial return of sensation until blebs form

Favorable initial symptoms: normal sensation, warmth and color, early formation of clear large blebs

Unfavorable signs/symptoms: residual violaceous hue after rewarming, delayed appearance of smaller hemorrhagic blebs, lack of edema formation, early black, dry eschar

Treatment:

- Rapid rewarming: by immersion in gently circulating water that is maintained at a temperature of 37 to 39°

- continue until the part feels pliable and distal erythema is noted (usually 10 to 30 minutes of submersion)

- after rewarming, elevation and sterile dressings

**Caution: in patients with completely frozen extremities who are hypothermic can get significant fluxes in fluids and electrolytes during rewarming -> vasoconstriction, core temperature afterdrop -> can be arrhythmogenic

Non-Freezing Injuries after exposure to wet cold

Trenchfoot (immersion foot)

- results from prolonged exposure to wet cold at temps above freezing

- develops slowly over days

- results in neurovascular damage w/o ice crystal formation

- clinical presentation: varies: cool, pale feet w/ paresthesias, then can get cyanotic, cold, edematous

- hallmark:after rewarming, the skin stays red, dry and is painful to touch

- can get bullae and vesiculation/ulceration or even gangrene

from Dr. Adriana Segura