Cold Injury

DEFINITION
Local tissue injury caused by cold temperatures, including frostnip, frostbite and non-freezing injury.
See also hypothermia.
D E A B M I M


EPIDEMIOLOGY
Cold trauma.
D E A B M I M

AETIOLOGY
Cold trauma.


D E A B M I M

BIOLOGICAL BEHAVIOUR

Pathophysiology
Severity of injury depends on T, duration of exposure, environmental conditions, protective clothing and general state of health.
- immobilisation, moisture, PVD and open wounds increase severity
- freezing or non-freezing temp important; frostbite requires freezing temps
- other terms e.g frostnip (trench-foot, chill blains) non-freezing.
Wind chill has a pronounced impact on degree of systemic chilling.
Progressive vascular thrombosis

Cold injury to vessel walls; anoxic vasculitis in microcirculation.
- direct injury to vascular epitherlial cells causes anoxic damage.


Classification

Frostnip

Mildest form.
Initial pain, pallor and numbness.
Reverses with rewarming.
No tissue loss unless repeated over many years, causing fat pad loss or atrophy.

Frostbite
Freezing of tissue due to intracellular ice formation, microvascular occlusion and tissue anoxia.
Further damage from reperfusion injury.
First-fourth degree (superficial, partial and deep thickness) similar to burn injuries.
- first: hyperaemia, oedema
- second: large vesicles with the above, partial skin necrosis
- third: tissue death from here; full thickness & subcutaneous necrosis, commonly haemorrhagic vesicle formation
- fourth: full thickness skin necrosis, muscle and bone gangrene.
Initially affected body part is cold, hard, white and anaesthetic, but changes frequently with treatment.
- initial classification may not be prognostically accurate.
- some just go for superficial vs deep.

Nonfreezing Injury
Microvascular endothelial damage, stasis and vascular occlusion.
Trench foot or cold immersion foot (or hand) is typical in soldiers, sailors or fishermen.
- results from chronic exposure to wet conditions and temps just above freezing (1.6-10oC)
- entire foot may be black, but deep tissue destruction may not be present.
Alternating vasospasm/dilation occurs
- first affected tissue is cold & anaesthetic.
- becomes hyperaemic in 24-48hrs, with intense burning dysesthesia & tissue damage charactereised by oedema, blistering, redness, echymosis and ulceration.
--> can lead to infection, cellulitis, lymphangitis or gangrene.

Chilblain (Pernio)
Dermatologic mnifestation of chronic repetitive damp cold exposure or chronic dry cold exposure
- typically face, anterior tibia or dorsum of hands and feet (poorly protected).
Pruritic red-purple lesions (papules, macules, plaques or nodules).
- ulcerative or haemorrhagic lesions may appear with continued exposure
- may scar, or atrophy with itching and tenderness.
More annoying than destructive; can be chronic.

D E A B M I M

MANIFESTATIONS

See individual conditions above.
D E A B M I M


INVESTIGATIONS
Clinical
D E A B M I M


MANAGEMENT

Principles
1. Hospitalization
2. Rewarming
3. Dressings
4. Manage blisters - debride if appropriate
5. Elevation and splinting with gentle exercise
6. Surgical intervention for demarcated tissue (may need to wait 2-3 months; usually by 3weeks.
7. Microcirculation therapy?
- (e.g. heparin, hyperbaric oxygen) = more experimental.
8. Sympathectomy?
- may benefit a subgroup, currently under Ix.

Rewarm
- do not if risk of refreezing.
Replace restrictive damp clothing with warm blankets.
Hot fluid by mouth if able to drink.
Injured part in circulating water at a constant 40oC
- until pink colour and perfusion return
- often 20-30mins.
Avoid dry heat
Do not massage / rub the area.
Adequate analgesia is essential as rewarming can hurt.
Cardiac monitoring is advised.
Prickly, itchy, painful sensation may follow.
Do NOT rub the area; acclelerates skin damage
Also no role for slow thawing

Hypothermic?
Temp <35
Remove wet clothing, dry, no rubbing, passive warming with body heat
- if too fast, may get arrhythmias.

Inflammatory response
If sufficient anoxic damage, get viscious cycle with inflammatory response
- WCCs and platelets adhere to damaged endothelial wall, release mediators, inflammation can progress vascular thrombosis.

Local Wound Care
Prevent infection, avoid opening vesicles, elvate injured area.
IV fluids are rarely required for fluid loss, but pt may be dehydrated.
Tetanus.
Antibiotics if infection identified.
Keep wounds clean and leave blebs intact for 7-10 days (sterile dressing for underlying epithelialisation).
With-hold vasoconstricive agents eg nicotine.
Weight-bearing prohibited.
Most adjuvants tried have been ineffective.
Demarcation will make extent of injury apparant over weeks.
- early debridement rarely needed unless sepsis intervenes.
Long-term, physiotherapy, neurologic rehab, care.

D E A B M I M


REFERENCES
ATLS