Abstract
Non-freezing cold injury develops after sustained exposure to cold temperatures, resulting in tissue cooling but not freezing. This can result in persistent sensory disturbance of the hands and feet including numbness, paraesthesia and chronic pain. Both vascular and neurological aetiologies of this pain have been suggested but remain unproven. We prospectively approached patients referred for clinical assessment of chronic pain following non-freezing cold injury between 12 February 2014 and 30 November 2016. Of 47 patients approached, 42 consented to undergo detailed neurological evaluations including: questionnaires to detail pain location and characteristics, structured neurological examination, quantitative sensory testing, nerve conduction studies and skin biopsy for intraepidermal nerve fibre assessment. Of the 42 study participants, all had experienced non-freezing cold injury while serving in the UK armed services and the majority were of African descent (76.2%) and male (95.2%). Many participants reported multiple exposures to cold. The median time between initial injury and referral was 3.72 years. Pain was principally localized to the hands and the feet, neuropathic in nature and in all study participants associated with cold hypersensitivity. Clinical examination and quantitative sensory testing were consistent with a sensory neuropathy. In all cases, large fibre nerve conduction studies were normal. The intraepidermal nerve fibre density was markedly reduced with 90.5% of participants having a count at or below the 0.05 centile of published normative controls. Using the Neuropathic Pain Special Interest Group of the International Association for the Study of Pain grading for neuropathic pain, 100% had probable and 95.2% definite neuropathic pain. Chronic non-freezing cold injury is a disabling neuropathic pain disorder due to a sensory neuropathy. Why some individuals develop an acute painful sensory neuropathy on sustained cold exposure is not yet known, but individuals of African descent appear vulnerable. Screening tools, such as the DN4 questionnaire, and treatment algorithms for neuropathic pain should now be used in the management of these patients.
Highlights
Just over 100 years ago ‘trench foot’ was described as a unique clinical syndrome observed in soldiers during World War I (Smith et al, 1915)
Our aims were to determine whether chronic Non-freezing cold injury (NFCI) was associated with a peripheral neuropathy, undertake detailed sensory phenotyping including grading of neuropathic pain and to establish if the pain associated with NFCI satisfies formal diagnostic criteria for neuropathic pain
For the first time, undertaken detailed neurological evaluation of patients with chronic NFCI defined as sensory symptoms lasting at least 3 months after cold exposure
Summary
Just over 100 years ago ‘trench foot’ was described as a unique clinical syndrome observed in soldiers during World War I (Smith et al, 1915). Trench foot was caused by exposure to cold and wet conditions, and was associated with swelling, pain and sensory disturbance of the feet. During the period of cold exposure, patients report sensory dysfunction in the extremities: numbness, paraesthesia and pain, as well as vasomotor disturbance (pallor) that may be followed by swelling, erythema and exacerbation of pain on rewarming of the affected limbs. Some patients develop chronic NFCI with persistent sensory symptoms, in particular chronic pain and cold hypersensitivity of the hands and feet. There is a lack of accepted diagnostic criteria and the aetiology of chronic pain associated with NFCI is unknown Both vascular and neuropathic causes of chronic NFCI symptoms have been posited. Animal models have suggested that cold exposure can cause injury to myelinated fibres within peripheral nerves (Denny-Brown et al, 1945). A single case report of a patient with severe NFCI resulting in gangrene and ulceration requiring surgical debridement suggested a loss of intraepidermal nerve fibres on skin biopsy these were not quantified (Irwin et al, 1997) and the severity of this one case made it unclear if this was a core feature of NFCI
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