A 43-year-old woman presented with severe pain, burning, and swelling of the feet. Her symptoms began 2 days prior after returning from a 7-day camping and hiking trip. She reported that her boots were soaked during this period. Examination revealed that both feet were swollen, acrocyanotic, and cold with decreased capillary refill in all 10 toes; pedal pulses were palpable bilaterally. There were dried up blisters in the bilateral feet and ankles (Figure 88-1). Arterial duplex documented normal posterior tibial and dorsalis pedis arteries. A diagnosis of bilateral immersion foot was made. She was initially treated with bed rest, intravenous antibiotics, elevation, and hydration. Her swelling improved over the next few weeks, but she continued to have symptoms of pain and discomfort which were treated with gabapentin therapy. There was no tissue or limb loss due to early detection and treatment.
Immersion foot syndrome (IFS) is a clinical syndrome that results from damage to peripheral tissues in the extremities exposed to cold in a wet environment for prolonged periods at temperatures just above their freezing point (0-15°C).
It has also been referred to as nonfreezing cold injury (NFCI) to differentiate clinically and pathologically from frostbite, which is a freezing cold injury.1
It is not uncommon to have both freezing and nonfreezing injuries in the same individual when exposed to harsh conditions for a prolonged period.
IFS, besides trench foot, also includes less recognized conditions like warm water immersion foot, shelter limb, and paddy foot (tropical immersion foot). Trench foot is considered a serious military problem for soldiers exposed to cold and wet conditions during battle time,2 but due to infrequent reporting in civilian personnel, it has remained rather obscure as a civilian medical problem.
Trench foot was described in World War 1 when trench warfare was employed and soldiers wore wet boots and socks for prolonged periods under cold conditions. Cold injuries have been described as early as the Crimean War of 1853 in the men stuck in trenches filled with mud.
During the Second World War, American forces sustained 11,000 cases of trench foot, and the German army performed more than 15,000 am-putations for cold-related injuries.3
African Americans are more susceptible to cold weather injury as observed in the American Civil War and also during the cold winter conflict of Ardennes in 1944.
Hikers exposed to cold and wet conditions for prolonged periods are at risk if they do not take appropriate care of wet boots and socks. Civilian cases of IFS have also been reported in homeless, older adults, and alcoholics where environmental factors and decreased alertness can lead to injury. Injury to mountaineers has also been reported in the context of inappropriate clothing, incorrect equipment, and lack of knowledge of cold injuries.4
Skin is a major thermoregulatory organ and functions to either conserve or dissipate heat according to the individual’s body temperature.
The vascular anastomosis of the skin is under dual neural control.
Under cold conditions the increased central sympathetic tone causes vasoconstriction.
Direct local control of the vasculature causes vasoconstriction in cold and dilation in warm conditions.5
An important protective mechanism of the skin is cold-induced vasodilation (CIVD), where the vasoconstrictive response in cold conditions is interrupted by periods of vasodilation and increased heat flow. Maximal vasoconstriction and minimal cutaneous blood flow occurs when skin is cooled to 15°C or below. If, however, cooling continues to lower temperatures, CIVD is observed in 5- to 10-minute cycles. CIVD results from a cessation of vasoconstrictor transmitter release from adrenergic nerve endings and also as a direct cold-induced relaxation of vascular smooth muscle. The thermoprotective nature of CIVD is evidenced by the fact that Eskimos and Nordics have a very strong CIVD response occurring at much shorter intervals than others.
Vasoconstriction—Prolonged vasoconstriction leads to vasospasm of the vessels that supply blood to nerve and muscle cells. Exposure to cold stimulates the release of norepinephrine in the peripheral circulation, which acts on the alpha-2 adrenergic receptors, causing constriction of vascular smooth muscle.6
Increased sympathetic drive—The degree and severity of cold injury depends on duration of cold exposure. Pain and fear can activate the sympathetic nervous system, leading to vasoconstriction.
Cold-induced ischemia—Leads to injury to the endothelium, resulting in platelet and leukocyte accumulation leading to tissue hypoxia.
Reperfusion injury—Results in free radical generation, which leads to further endothelial damage and eventually edema.7
CIVD—Absence of CIVD with prolonged cold exposure is an additional factor contributing to IFS.
Nerve injury—Ischemia of the nerves causes hypoxia and results in primary nervous system injury. Thick, large, myelinated fibers (C fibers) are most susceptible to injury after prolonged cold exposure. However, the full extent of nerve fiber involvement depends on the actual duration and severity of the cold exposure. Cold exposure also results in nerve conduction blockade and associated cessation of axoplasmic transport.6