Charcot osteoneuropathy is a potentially destructive entity associated with loss of sensitivity in the feet, peripheral neuropathy secondary to diabetes mellitus is the most common cause, with an incidence of between 0.1 and 5%.1,2 However other pathological conditions can cause Charcot foot, such as neurosyphilis, multiple sclerosis, poliomyelitis, folic and vitamin B12 deficiency, HIV infection and chronic alcohol abuse, among others.1,2 The published data on the prevalence and incidence of the disease indicate that it is often not diagnosed in alcohol dependents, with figures from 0.4% to 13%, similar data to that of diabetic patients.1,2 The “rocker-bottom foot” deformity is its last and most serious manifestation.1,2 We present the case of a male patient in the fifth decade of live, non-diabetic and chronic consumer of 350g alcohol/week. He was admitted to our centre due to ulcers on both feet. When his medical history was taken, he explained symptoms over 12 months of the onset of oedema, ulcers, burning sensation in the legs, and progressive swelling of the right foot, with no previous trauma. Physical examination revealed suppurating ulcers and flat, convex deformed foot with erythema and plantar ulceration (rocker-bottom foot) CT scan (Fig. 1) showed diffuse involvement with destructuration and bone remodelling of the tarsometatarsal and scaphoid-cuneiform midfoot (straight white arrow), and radiolucent areas compatible with disuse osteopenia (dotted white arrow). Electromyography revealed sensory peripheral neuropathy. Charcot osteoneuropathy was diagnosed from the clinical and epidemiological, radiological and neurological findings. Alcohol-dependence syndrome is a chronic social disease, its most frequent neurological complication being peripheral polyneuropathy, and it is associated with nutritional deficiencies (thiamine – vitamin B1 – malabsorption), and direct neurotoxicity of ethanol as presumed risk factors for Charcot foot. The triggers for and pathogenesis of Charcot foot are not clear, but it is probably associated with mechanical and vascular factors secondary to sensory and autonomous peripheral neuropathy. In the acute phase differential diagnosis with cellulitis, osteomyelitis or deep vein thrombosis is essential. The prognosis depends on early detection, and response to treatment depends on its stage at the time of diagnosis. The initial treatment, as in the case we present, in addition to a course of antibiotics – in the event of associated infection – and nursing care, comprises immobilisation and no weight bearing on the foot by means of a full plaster, to minimise oedema and halt progression of the disease. In a second stage we used made-to-measure footwear.3,4 If this fails, for severely deformed feet, surgery is possible – to achieve a plantigrade foot and prevent bone spur causing pressure to the skin, and therefore ulcers, tendon surgery to restore muscle balance or elective reconstruction to leave the patient with a functional foot and avoid amputation3,4 which in our case, the patient refused.

Fig. 1.

CT scan of right foot: straight white arrow: diffuse involvement with destructuration and bone remodelling of the tarsometatarsal and scaphoid-cuneiform midfoot. Dotted white arrow: radiolucent areas compatible with disuse osteopenia.

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