Immersion Foot Syndrome in 6 Equids Exposed to Hurricane Floodwaters.

Prolonged exposure to water, known as immersion foot syndrome in humans, is a phenomenon first described in soldiers during World War I and characterized by dermal ischemic necrosis. In this report, we describe the pathologic findings of a condition resembling immersion foot syndrome in 5 horses and 1 donkey with prolonged floodwater exposure during Hurricane Harvey. At necropsy, all animals had dermal defects ventral to a sharply demarcated "water line" along the lateral trunk. In 5 animals, histologic examination revealed moderate to severe perivascular dermatitis with vasculitis and coagulative necrosis consistent with ischemia. The severity of the lesions progressed from ventral trunk to distal limbs and became more pronounced in the chronic cases. The pathophysiology of immersion foot syndrome is multifactorial and results from changes in the dermal microvasculature leading to thrombosis and ischemia. Prompt recognition of this disease may lead to appropriate patient management and decreased morbidity.

Immersion Foot: A Case Report.

BACKGROUND: Immersion foot (commonly called "trench foot") was originally described in the military literature during World War I. Since that time, the emergency department (ED) has become a common setting where this injury presents. However, this topic is neglected in the emergency medicine literature. The purpose of this case report is to present trench foot in a way that is relevant to emergency physicians and to provide an up-to-date summary of the history, case reports, physiology, clinical presentation, and treatment of this injury. CASE REPORT: Here we present the case of a homeless, schizophrenic patient who presented to one Midwestern ED in January for immersion foot. Photos of the actual patient are shown to illustrate the case. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Due to unfamiliarity, immersion foot can go undiagnosed during assessment of patients exposed to moist environments. In addition, patients at increased risk for developing immersion foot are frequently encountered in EDs. Most importantly, the appropriate treatment for immersion foot is different than the treatment for other freezing cold injuries.

Neuropathy in non-freezing cold injury (trench foot).

Non-freezing cold injury (trench foot) is characterized, in severe cases, by peripheral nerve damage and tissue necrosis. Controversy exists regarding the susceptibility of nerve fibre populations to injury as well as the mechanism of injury. Clinical and histological studies (n = 2) were conducted in a 40-year-old man with severe non-freezing cold injury in both feet. Clinical sensory tests, including two-point discrimination and pressure, vibration and thermal thresholds, indicated damage to large and small diameter nerves. On immunohistochemical assessment, terminal cutaneous nerve fibres within the plantar skin stained much less than in a normal control whereas staining to von Willebrand factor pointed to increased vascularity in all areas. The results indicate that all nerve populations (myelinated and unmyelinated) were damaged, possibly in a cycle of ischaemia and reperfusion.

Nature and mechanism of peripheral nerve damage in an experimental model of non-freezing cold injury.

Non-freezing cold injury (NFCI), so called trench foot, is a condition characterised by a peripheral neuropathy, developing when the extremities are exposed for prolonged periods to wet conditions at temperatures just above freezing. Classically, military personnel are affected, with 14% of casualties in the Falklands conflict afflicted. Clinically, NFCI is characterised by a well-defined acute clinical picture and chronic sequelae. Little is known regarding the pathophysiology and treatment of this condition. Opinions vary as to the type of nerve fibres most susceptible to damage and proposed mechanisms of injury include direct axonal damage, ischaemia and ischaemia/reperfusion. A series of investigations has been performed to clarify which populations of nerve fibres are more susceptible to damage, and to elucidate the exact mechanism of nerve injury. An in vivo rabbit hind limb model, subjected to 16 h of cold immersion (1-2 degrees C), provided the basis of this study. Nerve specimens were examined by semi-thin sectioning for myelin fibre counts, by electron microscopy to assess the unmyelinated fibre population, and fine nerve terminals in plantar skin were assessed immunohistochemically. The results showed that large myelinated fibres were preferentially damaged, while small myelinated and unmyelinated fibres were relatively spared. Nerve damage was found to start proximally and extend distally with time. Serial temperature measurements identified a warm-cold interface in the upper tibial region of immersed limbs. As this was the initial site of injury, this suggested that a dynamic balance exists in the cold immersed limb between the protective effects of cooling and the damaging effects of ischaemia. The non-invasive technique of near infrared spectroscopy was used to measure changes in tissue oxygen supply and utilisation and blood volume. The findings supported the hypothesis that an interface is created at the site of initial nerve damage in the upper tibia, where cyclical ischaemia-reperfusion injury occurs.

A case of bilateral trench foot.

A case of severe bilateral trench foot is presented in a patient who lived rough for 3 weeks without removing his boots. Non-operative management yielded no clinical improvement and bilateral below-knee amputation was necessary. Histology revealed subcutaneous and muscle necrosis with secondary arterial thrombosis.

Nerve conduction studies in experimental non-freezing cold injury: II. Generalized nerve cooling by limb immersion.

After immersion of the hind limb of the rabbit, up to the lower thigh, in a waterbath, at 1 degree C for 10 to 14 hours under light anesthesia, there was evidence of persistent nerve damage to the tibial nerve, which varied in severity in different animals. Nerve conduction studies, carried out within 24 hours of removal from the bath, showed that in a proportion of the motor and/or afferent fibers, there was conduction failure between the knee and ankle. This was followed, over the next 48 hours, by distal degeneration of the affected fibers. No persistent conduction block was seen. After distal degeneration had occurred, maximal conduction velocity was mildly reduced, suggesting that the fastest-conducting motor and afferent fibers had been particularly affected. Morphological studies confirmed preferential large myelinated fiber degeneration, the earliest lesions being seen in the leg at the level of the upper calf. Limb edema was not seen after cooling, and there was no histological evidence of muscle necrosis or damage to blood vessels. No abnormalities were seen in 4 control animals after hind limb immersion for 12 hours at temperatures of 30 to 35 degrees C. Possible reasons for the proximal site of myelinated nerve fiber damage during hindlimb cooling are discussed.

Recent cases of trench foot.

Two cases of cold injury to the lower extremities, 'trench foot', are presented. The management is essentially conservative, but in cases of severe damage, particularly in elderly people, amputation must be advised.