Risk factors

Susceptibility to cold injury is increased by:^[2]

• Lower temperatures
• Infancy, elderly age, malnutrition, exhaustion
• Immobilisation, eg fracture
• Open wounds
• Prolonged exposure
• Moisture
• Peripheral vascular disease
• Impaired cerebral function: for example, alcohol, other sedatives, psychiatric illnesses^[3]
• Hypoglycaemia, diabetes, hypothyroidism
• Nicotine or other vasoconstrictive agents
• Peripheral neuropathy, autonomic neuropathy, head injury, spinal cord damage
• Infection

Presentation

• Frostnip: the mildest form of cold injury. There is initial pain, pallor and numbness of the affected area. It is reversible with rewarming and does not result in any tissue loss, unless the injury is repeated over many years, which causes fat pad loss or atrophy
• Frostbite: freezing of the tissue with microvascular occlusion and subsequent tissue anoxia. Some of the tissue damage may result from reperfusion during rewarming.
  • First-degree: hyperaemia and oedema without skin necrosis
  • Second-degree: large clear vesicle formation in addition to hyperaemia and oedema with partial-thickness skin necrosis
  • Third-degree: full thickness with subcutaneous tissue necrosis, often with haemorrhagic vesicles
  • Fourth-degree: full thickness and subcutaneous tissue necrosis, also involving muscle and bone with gangrene
• Non-freezing injury:
  • Trench foot: non-freezing injury of the hands or feet resulting from chronic exposure to wet conditions and temperatures just above freezing
  • The entire foot may appear black but deep tissue destruction may not be present. Progression to hyperaemia within 24 to 48 hours causes an intensely painful burning and dysaesthesia. Tissue damage causes oedema, blistering redness, bruising and ulceration.
  • Complications include local infection, cellulitis, lymphangitis or gangrene
  • Proper attention to foot hygiene can prevent the occurrence of most such injuries.
• Chilblains (also known as perniosis or pernio):^[4]
  • Localised inflammatory skin lesions on exposed extremities of the body which are precipitated by cold.
  • Chilblains can be classified as:^[5]
    • Acute: they develop within 12-24 hours after exposure to cold and last for 1-2 weeks.
    • Chronic: they occur with repeated exposure to cold, resulting in persistent lesions which can lead to subsequent scarring and atrophy.
  • They typically occur on the face, tibial surface, or dorsum of the hands or feet, areas poorly protected or chronically exposed to the environment.
  • There are pruritic, red purple skin lesions (papules, macules, plaques, or nodules)
  • Continued exposure leads to ulcerative or haemorrhagic lesions which progress to scarring, fibrosis, or atrophy with itching replaced by tenderness and pain.
  • Careful protection from further exposure and the use of antiadrenergics or calcium channel blockers are often helpful.

Investigations

• Investigations are mainly directed at assessment of any underlying illness, eg diabetes, anaemia, and any complications, eg cultures to check for infection, renal function tests, electrolytes, ECG.
• Technetium 99m (Tc-99m) pertechnetate scintigraphy: sensitive and specific for tissue injury. Has been shown to give good correlation with ultimate extent of deep-tissue injury.^[6]

Management of frostbite and non-freezing cold injuries

• Early management of cold-injured patients includes:
  • Adhering to the ABCDEs (Airway, Breathing, Circulation, Disability, Exposure/environment control) of resuscitation
  • Identifying the type and extent of cold injury
  • Measuring the patient's core temperature
  • Initiating a patient-care flow sheet
  • Initiating rapid rewarming techniques
  • Determining the patient's life or death status after rewarming
• Treatment should be immediate but rewarming should not be started if there is the risk of refreezing.
• Replace constricting, damp clothing by warm blankets. Give hot fluids to drink if possible.
• Place the injured part in circulating water at a constant 40°C until the pink colour and perfusion return (usually within 20 to 30 minutes).
• Avoid dry heat and do not rub or massage the area.
• Rewarming can be very painful; adequate analgesia (intravenous narcotics).
• Intravenous fluids: rarely required but patients may be dehydrated.
• Cardiac monitoring during rewarming.

Local wound care of frostbite

• Elevating the injured area, which is left open to air.
• The affected tissue should be protected by a tent or cradle and pressure spots avoided.
• The wound should be kept clean and uninfected vesicles and blisters left intact for 7 to 10 days to provide protection.
• Tetanus prophylaxis depending on immunisation status.
• Systemic antibiotics: reserved for identified infections. Tobacco nicotine and other vasoconstrictive agents must be withheld. Weight-bearing is prohibited until oedema is resolved.
• Surgery: estimation of depth and extent of tissue damage are not usually accurate until demarcation is evident. Although the surgical management of frostbite involves delayed debridement 1 to 3 months after demarcation, recent improvements in radiological assessment of tissue viability have led to the possibility of earlier surgical intervention.^[7]

Complications

When, combined with hypothermia or wound-related sepsis, localised cold injuries may lead to death. Complications are more common in those with arterial or systemic disease.^[5]

• Secondary wound infection
• Tetanus
• Fluid sequestration in damaged tissues and diuresis may cause volume depletion^[3]
• Hyperglycaemia, acidosis^[8]
• Dysrhythmias
• Gangrene
• Possible long-term sequelae of cold injury include:
  • Paraesthesias and sensory deficits, tremor
  • Hyperhidrosis or anhidrosis
  • Cracking of skin and loss of nails
  • Permanent discolouration and/or scarring
  • Vasospasm, cold sensitivity
  • Joint stiffness
  • Premature closure of epiphyses in children; osteoporosis
  • Muscle atrophy

Prognosis

The prognosis depends on the severity and duration of the cold environment and the presence of any risk factors.