5.2.3 Neuropathic Ulcers

Incidence >70 per 100,000 population. Prevalence up to 50 (6-51)% in patients with diabetes during their lifetime. There are no statistics on the epidemiology of malum perforans in late-stage syphilis, leprosy or nerve injuries. Alcohol-induced malum perforans occurs exclusively in males with a distinct genetic disposition.

Ulceration through the epidermal and dermal tissue layers in areas of physical/mechanical pressure on the basis of polyetiological sensory polyneuropathy. Foot is the most common localization, but other pressure points also can be affected. Disturbance of the “trophic condition of the tissue”, not of the venous or arterial circulation.

Sensory polyneuropathy with preference of thin nerve fibers on the basis of a genetic predisposition. Dissociated sensation deficit with loss of sensorium, motor weakness, and loss of autonomic function, thermo-, pressure- and pain-sensation. Inability to withdraw the area from painful stimuli such as friction, shear forces, or traumatic processes lead to hyperkeratosis, bleeding, ulceration and necrosis.

Potential causes are:

• Metabolic disorders: diabetes; rarely amyloidosis; monoclonal gammopathy; thyroid disease, renal disease, and chronic liver disease

• Alcohol (Bureau-Barrière-syndrome)

• Inflammatory, non-infectious: sarcoidosis, Sjogren’s syndrome

• Infectious:

  • Syphilis (III/IV)

  • Leprosy

  • HIV

  • Borrelia infection (due to tick bite)

• Nerve trauma (Ischias)

• Neoplasms: Carcinoma

• Toxic: multiple vitamin deficiencies (B1, B6, B12), vitamin B6 excess, heavy metal poisoning, drug- induced neuropathy, organophosphate exposure, and alcohol

• Hereditary (Thevenard-syndrome).

Numbness, tingling, pain, and weakness starting in the toes.

Loss of thermo- and pressure sensitivity and of pain. Formation of a localized hyperkeratosis with a hemorrhagic bulla and finally ulceration. Fractures of the underlying bones (foot or toes) (acroosteopathia ulceromutilans). Hyperthermy of the involved limb with anhidrosis (diabetes) or hyperhidrosis (alcoholic polyneuropathy).

Areas of mechanical pressure; preferentially heel and ball of the foot and toes, but also all other localizations exposed to mechanical or thermal damage.

According to aetiology. In diabetic foot ulcers Wagner’s classification of diabetic foot ulcers.

Physical examination including vascular status, neurological status, and potential musculoskeletal abnormalities. Search for underlying disease.

Vascular examination: palpation of pulses in the area, ultrasound doppler, capillary refill time both peri-wound and distal to the ulceration.

Imaging methods (x-ray; MRI) to exclude bone injuries. Determination of the (severely reduced) nerve conduction velocity.

Orthopedic counseling.

Clinical picture of painless ulcer in conjunction with an underlying disorder (see aetiology). Detailed medical (trauma, surgery) and social (alcohol, infections, drugs) history.

Prevention: avoidance and treatment of the aetiopathogenetic background. Tricyclic antidepressants; voltage-gated calcium channel ligands.

Since the polyneuropathy is irreversible (vitamin B-complex may be supportive in some instances), the only effective treatment is avoidance of pressure by appropriate orthopedic shoes.

Platelet-rich plasma has been recommended for the treatment of diabetic foot ulcers. Plastic reconstructive surgery must be an exception, since the benefit is only temporarily.