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Cold injuries are divided into two general groups: those that occur without any freezing of the body tissues and those that result from the freezing of the skin or a body part. Nonfreezing injuries include hypothermia, chilblains/pernio, and trench/immersion foot. Frostnip and frostbite are considered freezing injuries.
Frostbite is defined as freezing of the tissues on exposure to temperatures below the freezing point of intact skin. It occurs at ambient temperatures below 0ï‚°C (32ï‚°F). Frostbite can occur in seconds or hours, depending on the weather and protective clothing. Usually it is the face, nose, ears, fingers and toes that get frostbitten but the shins, the corneas of the eyes, or other areas may be involved including rarely the scrotum and penis (3).
Without proper protection, cold injuries, such as frostbite, can occur even when the temperature is above freezing. This is especially true if there is a high wind or if a glove or sock gets wet. Frostbite need not happen even at extremes of altitude and temperature if adequate precautions are taken.
The condition has long been recognized. A 5,300-year-old iceman discovered in the Alps offers the earliest documented evidence of frostbite (4). Innumerable military campaigns have been affected and history reshaped because of catastrophic losses suffered due to cold injuries. It was Baron Dominique Larrey, Napoleon's surgeon who during the infamous Moscow retreat (1812) first elucidated the probable mechanisms of frostbite. He introduced the concept of friction massage with snow and described similarities with burns. Though he recognized the benefit of warming the part, he also noted the deleterious effects of the "freeze-thaw-freeze" cycle endured by the soldiers, who would warm their frozen hands and feet over the campfire at night, only to refreeze those same parts byÂ the next morning and then worsen the injury by marching on the affected feet. Frostbite affected not only the foot soldiers but also the aviators. During the World War II the commonest injury sustained by heavy bombers crew was high altitude frostbite (5). The problem of cold injury persists for modern generals, though recent Afghanistan conflict has shown declining incidence among the US troops (6).
Also seen during the World War I and II were injuries similar to frostbite but occurring at non-freezing temperatures (1.6ï‚°C-4.4ï‚°C) and caused by prolonged immersion in trenches with cold water. The term "trench foot" was coined for these injuries while "immersion foot" was noted in shipwrecked survivors on water or in life rafts. "Tropical immersion foot" was noticed in the Korean War in troops exposed to constant wetness in nonfreezing or comparatively warm water (7).
Over the next century the management of frostbite saw no significant improvement. Rapid re-warming at 37.8ï‚°C, the modern treatment of frostbite is credited to Hamill, a public health service medical officer in Alaska, who in 1956 first attempted it in a patient with hypothermia and frostbite (8).
Environmental risk factors include low ambient temperature, high humidity, wind chill, high altitude, and prolonged exposure. Degree of irreversible damage is related to the length of exposure. At the summit of Mount Everest, climbers cope with facial frostbite time of less than a minute in severe storms (9).
Anybody can develop a cold-related injury, but the young and the elderly are especially prone to this type of injury. Everyone is susceptible, even people who have been living in cold climates for most of their lives. The concept of physiological adaptation to cold is controversial. Though the Eskimo's / Sherpa's may not feel the cold as fast as inhabitants from the temperate climates, they still freeze just as quickly as the others do in the same contact situation (5,10). Others at risk of developing cold injuries include those who have underlying medical conditions such as peripheral vascular disease, atherosclerosis, arthritis, diabetes, hypothyroidism, Raynaud's disease, heart disease that requires use of beta-blocking drugs, psychiatric illness, dementia, infection, peripheral neuropathy, and those who smoke. Drug intake whether therapeutic or illicit may alter thermoregulation by direct central effect on hypothalamus. Alcohol, by causing vasodilatation can aggravate heat loss and by clouding the judgment predispose to further injury. Homelessness, fatigue, dehydration, improper clothing and history of previous cold injury are additional risk factors.
Tissue injury is greatest when cooling is slow, cold exposure is prolonged, rate of re-warming is slow, and, especially, when tissue is partially thawed and refreezes.
Four phases are described in the development of frostbite (11).
The pre-freeze phase: Begins with surface chilling at ambient tissue temperature of 3ï‚°C-10ï‚°C. Cellular changes i.e. membrane instability and plasma leakage follows. Cutaneous sensation is lost and edema due to endothelial damage is evident.
Freeze thaw phase: It is initiated by extra and intra cellular ice crystal formation, as the ambient temperature reaches -15ï‚°C to -6ï‚°C. Endothelium, bone marrow, nerve tissue, are most susceptible while muscle, cartilage and bone are less so. Cellular dehydration and shrinkage follows.
Vascular stasis phase: Plasma leakage and ice crystal formation continues in addition to vasospasm, dilatation, stasis coagulation and shunting.
The late ischaemic phase: ischaemia, thrombosis, continued shunting, gangrene, autonomic dysfunction and denaturation of tissue proteins characterize it.
Two distinct mechanisms are responsible for tissue damage (5)
Direct cellular damage at the time of exposure to cold
Progressive dermal ischaemia causing necrosis.
Direct Cellular damage
Extra cellular crystals form as a result of freezing of the tissues. The damage to cell membrane and change in osmotic gradient, results in intracellular dehydration. Intracellular sodium increases ten fold. Protein denaturation, enzyme destruction and cell membrane disintegration initiates cell death. With progressive fall in the tissue temperature, intracellular ice forms and as the crystals expand mechanical destruction of cells occurs (12).
Body responds by alternating cycles of vasoconstriction and vasodilatation-the "Hunter's reaction" (13). Vasodilatation results in partial thawing. This repeated partial thawing and refreezing cycle results in more damage by initiating a thrombotic phase.
Progressive dermal ischaemia
Marked similarity is noted in the inflammatory process of progressive ischaemic damage in frostbite to that of thermal burns and ischaemia/reperfusion injury. The metabolites of arachadonic acid have been heavily implicated as mediators of progressive dermal ischaemia (14). Inhibitors of eicosanoid production have been shown to have significant effects on dermal perfusion and tissue survival in both burn and frostbite animal models. Markedly elevated levels of prostaglandin F2 (alpha) and thromboxane B2 have been noted in the blister fluid in the rabbit model (15). These initiate the process of vasoconstriction, platelet aggregation, leukocyte sludging which leads to the development of micro vascular thrombosis. Ischaemia, necrosis and dry gangrene follow. Profound vasoconstriction and arteriovenous shunting is noted at the junction between the injured and non-injured tissue. The arteriovenous shunts open up to bypass the frozen part with the aim of preserving the organism at the cost of aggravating the local injury. Nitric oxide may also play important role in the pathogenesis of frostbite injury (16).
Frostbite injury shows three zones (17):
Zone of coagulation: This is the most severely affected area, located most distally and is irreversible.
Zone of hyperemia: It is superficial, located proximally, with least cellular damage and expected to recover within 10 days even without treatment.
Zone of stasis: This is the zone with severe but possible reversible cell damage, which can be salvaged with treatment.
Frostbite goes through several stages. Frostnip is the least severe and the first recognizable form of frostbite. It is a small white and waxy or gray and mottled area of skin involvement. Frostnip begins with itching and pain and eventually, becomes numb. Skin is leathery to touch. It follows intense vasoconstriction without ice crystal formation within the tissue. Characteristically it recovers within 30 minutes on re-warming. It generally does not lead to permanent damage though long-term sensitivity to cold can occur. If repeated over many years it can lead to loss of fat pad or atrophy.
A variety of frostbite classification systems have been proposed (13, 18). At the first appearance it is very difficult to categorize the injury as superficial or deep, and even more difficult to ascertain the amount of tissue damage. Classification of frostbite is conventionally applied after re-warming.
Four degrees of frostbite are recognized (19). (Table 1) Figures (1-5).
First-degree: Hyperemia and edema without skin necrosis. A numb central hard white plaque, with surrounding erythema, mild edema and sensory deficit. Capillary filling may be delayed.
Second-degree: Large, clear vesicle formation accompanies the hyperemia and edema with partial-thickness skin necrosis. Blister fill with clear or milky fluid within 24 hrs. There is no capillary filling. Skin may become hard, however, the deep tissues of the affected part are spared and remain soft and normal. They usually look worse than they are. Most of these injuries heal over 3-4 weeks. The affected area may remain sensitive to heat and cold permanently.
Third degree: Full thickness and subcutaneous tissue necrosis occurs commonly with hemorrhagic vesicle formation. The area is pale and insensate. On re-warming the pallor persists. Hemorrhagic blisters are replaced by hard black eschars in 2-4 weeks. This stage is irreversible and some tissue loss is inevitable.
Fourth-Degree: Full thickness skin necrosis including muscle and bone with gangrene. The involved area is deep purple or red and appears woody and mummified. It is this type of severe frostbite that results in lost fingers and toes. However, it can take several weeks to determine how much damage has actually occurred in the freezing process.
The initial treatment regime is applicable to all degrees of insult and the initial classification is often not prognostically accurate. A more clinically relevant description, easier to understand, and perhaps the one that gives the best clues to outcome differentiates frost bite into superficial (first and second degree) and deep (third and fourth degree). Superficial frostbite is characteristically supple when depressed and painful after thawing. There is minimal to moderate edema, and clear blisters appear. Tissues will also show reactive hyperemia. Deep frostbite is characterized by a firm, woody feel to the tissues and is anesthetic after thawing. The extent of injury in the hands and feet can be recorded in the second, third and fourth degree frost bite as below (20):
One plus (1ï€«) - up to distal interphalangeal joint.
Two plus (2ï€«)-up to proximal interphalangeal joint.
Three plus (3ï€«) - up to metacarpo/ metatarso-phalangeal joint.
Four plus (4ï€«)- up to the middle of metacarpals or metatarsals.
Five plus (5ï€«)- up to the wrist or ankle.
Initial presentation is with a feeling of coldness, firmness and numbness in the affected part. Movements may become clumsy. Extreme pain usually follows the numbness. This gives way to throbbing sensation on re-warming and itching. This may be delayed 48-72 hrs after re-warming and can continue for weeks as the tissue demarcates. Within a week of injury, ischaemic neuritis symptoms such as residual tingling may develop which may persist with occasional electric shock type sensation. Symptoms are variable and some may have no pain at all. If no tissue is lost symptoms often resolve within a month. Tissue loss can result in months of disability.
Even in mildest forms true frostbite damages the affected tissues. Fingers, toes, tip of the nose and ear lobes are commonly affected. The reasons for this include the peripheral vasoconstriction following exposure to cold and the absence of muscles in these parts, which can generate heat. Initial signs of frostbite include yellowish-white or mottled blue extremity, possible with decreased sensation and eventually a frozen solid appearance. During re-warming, signs include immediate hyperemia, increased sensation, and subsequent blisters. At this stage the depth of freeze, superficial/ deep can be assessed. Temporarily after re-warming edema appears within 3 hours and lasts 5 days, vesicles within 6-24 hrs, eschar within 9-15 days and mummification within 22-45 days (11).
Good prognostic factors:
Preservation of sensation to pinprick
Normal skin color
Clear blister fluid rather than milky / haemorrhagic fluid
Ability of skin to deform under direct pressure, indicating dermal viability
Skin becoming pink when thawed
Poor prognostic factors
Dark fluid blisters
Non-blanching cyanosis when thawed
Hard non-deforming skin
Lab studies are not important in the initial diagnosis and management of frostbite. They may however be helpful in identifying delayed systemic complications, such as wound infection with sepsis or underlying hypothermia. Commonly encountered lab findings include evidence of hemo-concentration and depressed liver function.
Imaging Studies (5,21)
Various techniques have been used over the years for assessment of bone and tissue viability in frostbite.
Plain radiographs: Early manifestations include soft tissue swelling and loss of tissue especially at the tips of the digits, osteoporosis and periosteitis. Late manifestations include tuftal resorption of terminal phalanges, fragmentation, destruction and disappearance of epiphyseal centers. In children brachydactyly can follow premature epiphyseal fusion. Interphalaneal joint abnormalities may simulate osteoarthritis.
Doppler and Arteriography
Doppler and arteriography studies have been used, but neither can assess microcirculation and cannot be used to estimate bone cell perfusion or viability. Furthermore, arteriography is invasive, and Doppler studies are highly operator dependent. In early stages arteriography demonstrates marked slowing of blood flow, which improves after re-warming though residual occlusions become manifest. Addition of vasodilator during arteriography though reported to be useful in predicting the final pattern has not significantly altered the management or the outcome.
Laser Doppler flowmetry may offer more accurate assessment of vasomotor status. Xenon133 injections have been used experimentally, but they require highly specialized personnel for interpretation of the results, cannot assess bone perfusion, and are complicated by the presence of subcutaneous adipose tissue.
Technetium scintigraphy: Tc-99m (Technetium 99) pertechnate scintigraphy is sensitive and specific for tissue injury and has been found to allow accurate assessment of tissue viability by doing two scans first on day 2 or 3 and second scan between days 7 to 10. (21,22). Based on intravascular injection and interval tracking of radioactive isotope, this technology can be used to identify nonviable tissue. Arterial phase, venous phase, and bone-pool images offer the treating surgeon clear visualization of tissue perfusion. Using this technique to evaluate frostbite severity, lesions may be classified similar to the classification used in myocardial scintigraphy (23). Mehta and Wilson (24) found three patterns of perfusion and delayed bone imaging: essentially normal blood and bone pool images; little or no blood pool with diminished, but clearly visible, bone pool images; and little or no flow in either the blood or bone pool images. Extremities with frostbite severe enough to result in infarction of all bone and soft tissue do not visualize at all during any phase of the scan and ultimately require amputation. It is these severely injured patients who may be candidates for consideration of salvage by immediate debridement of skin and subcutaneous tissues and immediate coverage with vascularized tissue.
Magnetic resonance imaging and magnetic resonance angiography is now advocated as a superior technique and may become the gold standard. It allows direct visualization of occluded vessels and imaging of the surrounding tissues to enable clear-cut line of demarcation to be seen early (25). The lack of significant striated muscle in fingers or toes may however limit the usefulness.
Frostbite patients have traditionally been treated conservatively, waiting 1 to 6 months from clinical demarcation to surgical amputation. The final amount of tissue destruction is proportional to the time it remains frozen, not to the absolute temperature to which it was exposed, therefore, rapid transport to a hospital is very important.
Every patient with acute frostbite must have his/her core temperature determined immediately as undiagnosed hypothermia can be rapidly fatal. Rapid thawing of the cold extremities in a hypothermic patient causes an additional drop in the core temperature (after drop), which can trigger a life-threatening Brady-arrhythmia or intractable ventricular fibrillation. A Foley catheter equipped with a thermocouple can provide continuous core temperature monitoring until the patient is normo-thermic (19).
Three phases of treatment are recognized:
Pre Thaw Field Care: Proficient field management is crucial to the final outcome in terms of function and viability because proper care is vital to preventing exacerbation of the initial exposure and injury. Hypothermia and dehydration need to be addressed as well as replacing wet, constrictive clothing with dry soft clothing to minimize further heat loss. "Folk remedies," such as rubbing the affected part with snow, exposing the area to an open flame or to a heater, and hitting the area (supposedly to restore circulation), may only make the injury worse. The injured tissue can be fragile and must be handled gently. The extremity should be padded and splinted for protection. Alcohol or sedatives, which can impair shivering and enhance heat-loss, should be avoided as also smoking. Repetitive freeze-thaw cycles are associated with increased morbidity and tissue loss caused by progressive micro vascular injury and thrombosis. If medical care is unavailable and a person has no choice but to walk out from a wilderness area, delay re-warming the frostbitten part until the person is in a protected environment. Refreezing is even more detrimental to the extremity than delay in re-warming (26).
Re-warming in the Hospital: Rapid re-warming is a keystone of therapy(13). A great deal of work has been done on rapid re-warming and the present consensus is to re-warm in a water bath at 40ï‚°C-42ï‚°C (104ï‚°F -108ï‚°F) with an antibacterial agent like povidone iodine or hexachlorophene (4). The temperature of the water should be measured with a thermometer and not with the frozen hand. Temperatures higher than this may cause burns and lower may not be as beneficial. Re-warming continues for 15-30 minutes till thawing is complete. Warming is complete when the skin is soft and pliable and sensation returns. Once thawed, the body part is elevated and splinted when possible. Cardiac monitoring during re-warming is advised (19). A cradle may be used over an injured lower extremity to avoid pressure or trauma. Massage during re-warming is to be avoided though active motion is encouraged. Clear blisters may be debrided to prevent thromboxane-mediated tissue injury. Hemorrhagic blisters are left intact to reduce risk of infection and dessication. Intravenous fluids may be required to combat dehydration and rarely if rhabdomyolysis occurs. For the face and earlobes, warm wet packs at the same temperature may be used.
Post Thaw Period After the rapid re-warming, the dermal ischaemia may seem to progress due to the inflammatory mediators released. The aim of treatment is not only to re-warm, but also to suppress the local and systemic production of thromboxane, provide analgesia, and prevent potentially catastrophic infection.
In patients with an associated dislocation, reduction should be done as soon as thawing is complete. Fractures however are managed conservatively until post thaw edema has resolved.
Elevation of the part to reduce the edema is important as this decreases the progressive dermal ischaemia. Daily hydrotherapy regime to debride the devitalized tissue and maintain active and passive range of function is important to promote functional recovery.
Management of blisters: The management and excision of blisters is open to discussion. Keeping them in place for as long as possible diminishes the risk of sepsis and facilitates the daily manipulations by reducing pain. In contrast, excising the blisters allows earlier visualization and assessment of the underlying tissue. White or clear blisters represent superficial injury. Conventionally they are aspirated or debrided to prevent further contact with high levels of PGF2 and TX A2 in the exudates, especially if they are on weight bearing areas. Hemorrhagic blisters represent structural damage to superficial dermal plexus. They may be aspirated but risk of desiccation increases therefore should be left intact if they do not interfere with the range of motion.
The goals of medical management of frostbite are pain control and prevention of complications, such as further tissue damage or infection. There are widely disparate views on the use of drugs in frostbite, a tacit admission that few are really effective.
Anti-inflammatory therapy: Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase activity and prostaglandin synthesis as well as inhibit leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil and platelet aggregation, and various cell-membrane functions. Ibuprofen (400 mg PO q6-8h) is preferable to aspirin, which irreversibly blocks synthesis of prostaglandins needed for normal cell function and integrity (27).
Antibiotics - Wound infection may be the result of Staphylococcus aureus, beta-hemolytic streptococci, gram-negative rods, or anaerobes. Use for wound infection prophylaxis is controversial and not recommended by some experts unless signs of infection develop.
Topical agents - Topical Aloe Vera is applied to the debrided clear blisters and intact hemorrhagic blisters to minimize further thromboxane synthesis (28). Topical Aloe Vera in conjunction with oral vasodilator pentoxyfylline has been reported to lead to 30% improvement in tissue survival (29).
Toxoids - Booster injection in previously immunized individuals is recommended. It should be supplemented with tetanus Immunogloblins (250 U IM), if patient was never fully immunized.
Analgesics- There may be quite a bit of pain when the injured area is re-warmed. Analgesics, such as acetaminophen, aspirin, ibuprofen, morphine sulfate, may be needed for pain. Epidural analgesia has been reported to be highly effective in patient management (30).
Conventional teaching in the management of frostbite has been "Frost bite in January-Amputate in July". Gradual mummification of the dead tissue would take place over 8-12 weeks and then decision would be made to debride and reconstruct or allow auto amputation. Surgical management of frost bite involves delayed amputation 1-3 months after demarcation as accurate early assessment of tissue viability is difficult and is compounded by discrepancy between the limit of skin lesions and the extent of damage to deeper structures. Delayed amputation also has a positive effect on psychological acceptance. Recent advances in the radiological assessment of tissue viability may allow earlier surgical intervention (21,31).
The only indication for early surgical intervention has been a compartment syndrome warranting fasciotomy. Active early debridment has however been shown to reduce time to recovery and decrease post op pyonecrotic complications. With improvement in radiological assessment of tissue viability, early aggressive and proactive approach is being used at some centers. When such injury can be identified early, (within 7 to 10 days), using triple-phase scanning, debridment of metabolically active tissues (skin, subcutaneous tissue) is done. The devascularized, metabolically less active tissues (bone, tendon, ligament) is then covered with vascularized tissue (21, 22).
Adjunctive therapies to diminish the progressive dermal ischaemia
Low molecular weight dextran. It has been used to counteract erythrocytic clumping in microcirculation and increased blood viscosity seen in cold injuries. Though useful in protecting against tissue loss in experimental studies clinical results are equivocal (5).
Anticoagulation: Superficial dermal plexus thrombosis is known to follow thawing. Heparin may help though anticoagulants have not been shown to alter the natural history of frostbite.
Vasodilators: Since their first use in Korean war, vasodialtors have been controversial adjuncts in frostbite treatment (32, 33). Intra-arterial injection of reserpine though successful in reducing vasospasm on arteriography has not translated to reduction in tissue loss. Several drugs have been tried to help prevent frostbite. One of the most commonly used drugs is Nifedipine which increases circulation to the extremities by dilating the blood vessels (34). Another commonly recommended drug is prostacyclin (0.5 to 2 ng of iloprost per kilogram of body weight per minute for 6 hours for up to 8 days (35).
Thrombolysis: Early thrombolytic therapy can theoretically limit microvascular thrombosis and help prevent reperfusion injury. Risk benefit ratio has to be considered before recommending tPA. Thrombolysis is indicated in patients who have less than 24hrs exposure to cold, with no multiple freeze/thaw cycles, clinically have absent capillary refill and absent Doppler pulses and show objective evidence of perfusion deficit (arteriography/bone scan), with no contraindications to tPA (36). Bruen, et al. reported a 10% amputation rate among those treated with intra-arterial tPA within 24 hours of injury (vs. 41% in those not receiving tPA) (37). For intra-arterial use initial bolus of 2-4 mg is given, followed by infusion of 1 mg/hr; (If two extremities involved = 0.5 mg/hr per extremity, etc.). Heparin is given at 500 mg/hr concurrently through the access sheath. tPA is continued until there is evidence of tissue reperfusion, 48 hours have passed, or the attending surgeon and interventional radiologist feel there is no further therapeutic gain by continuing the infusion. Heparin is continued for 72-96 hours (36,37).
Twomey et al showed equal effectiveness of intra-arterial and intravenous administration of tPA (38). Intravenous tPA is recommend as 0.15 mg/kg bolus with a 0.15 mg/kg/hr infusion over 6 hours up to a maximum of 100 mg and heparin therapy (defined as PTT twice control values) for 3-5 days (38). Over the last few years, use of tPA has become standardized in the treatment of severe frostbite (39, 40)
Sympathectomy: Immediate sympathectomy within few hours after injury may increases the edema and accelerates tissue death. However if performed after 24-48 hrs of thawing it speeds the resolution of edema. Digital surgical sympathectomy has been used for chronic vasospasm and pain in the hand (41).
Hyperbaric oxygen (HBO): Though the potential benefits are debated, a number of case reports are available indicating good response. Experimental evidence indicates that immediate HBO treatment for 2 hrs a day decreased the mean tissue loss, however if started after 24 hrs and given for less than 1 hr / day the benefit was considerable less (5,42,43).
Recommended standard management protocol for patients with frostbite is as elucidated in Table 2.
Long-term sequel (44,45,46,47,48)
It is extremely difficult to predict the outcome in the first few days after frostbite. 65% of people will suffer long-term symptoms because of their frostbite. The late squeals are autonomic, trophic and pigmentary changes. Long-term squeal include paraesthesias and sensory deficits, hyperhidrosis or anhidrosis, cracking skin and loss of nails, abnormal color changes indicative of vasospasm, cold sensitivity, joint stiffness, tremor, premature closure of epiphyses in children, osteoporosis, intrinsic muscle atrophy, and phantom pain of amputated extremities. Motor nerve conduction studies have revealed prolonged terminal latency suggesting possible demylination. Sialo-proteinuria, Achilles peritendinosis Auricular ossificans (ectopic ossification of the auricle) and frostbite arthritis have also been reported. The area remains vulnerable to further thermal damage for an indefinite period. Sensitization of neurons located in the superficial as well as the deep dorsal horn contributes to hyperalgesia following freeze injury to the skin.
Non-Freezing cold injuries
Chilblains or pernio is primarily a dermatological manifestation of chronic repetitive exposure to above freezing temperature in high humidity in susceptible individuals. It typically occurs on the face, anterior tibial surface or dorsum of the hands and feet, areas poorly protected or chronically exposed to the environment. The affected area may typically itch, turn reddish-blue, are swollen and painful (papules, macules, plaques or nodules). With time, blisters containing clear fluid may form. Pressure areas are vulnerable. The injured area may be very sensitive to the cold in the future though there is usually no other permanent damage. It is a self-limiting condition and management is supportive. It is more annoying than destructive. Reassurance, immersion in a warm water bath, keeping the part warm and dry, elevation and moisturizing lotion application should suffice. Use of calcium channel blockers like Nifedipine (20mg three times a day) gives some relief (34). Though majority of the cases are idiopathic, association with conditions like SLE, cryoglobulinemia and antiphospholipid syndrome have been suggested. (49)
Trench foot or cold immersion foot (or hand)
It results from exposure of wet feet (or hands) to cold temperatures at or above freezing. It develops over hours to days and damages the nerves and muscles. Like frostbite, immersion injury causes permanent damage. The symptoms of immersion injury are similar to those of chilblains, but the damage is usually more serious. Areas affected by immersion injury are first red then turn pale and swollen, and later may develop blisters. The blisters are deeper and resemble the blisters that form after a burn. The affected tissue is first cold and anesthetic progressing to hyperemia in 24-48 hours associated with intense painful burning and dysesthesia. Complications of local infection, cellulitis, lymphangitis, or gangrene can occur. Skin breakdown, or even liquefaction of the affected tissues can follow. Management is on lines of frostbite.
Cornerstone of management of cold injuries is prevention. A large number of guidelines are available on preventive strategies to be adopted (20, 50,51).