Neuropathic ulcer G63.0

A neuropathic or neurotrophic ulcer is an ulcer caused by external influences on a part of the body that is critically damaged due to a loss of afferent nerve fibers in its sensory system (Eastman etal. 2022). Basically, neuropathy can be peripheral neuropathy or central neuropathy. Peripheral neuropathy is by far the most common. The peripheral nervous system includes all parts of the motor, sensory and autonomic nerves lying outside the central nervous system with their Schwann cells and their ganglionic satellite cells, their connective tissue sheath structures (peri- and epineurium) and with the blood and lymph vessels supplying them.

Peripheral polyneuropathy usually affects only the extremities and can have multiple causes, with diabetic peripheral neuropathy being the most common (see Neuropathy, diabetic below). Unlike most other forms of polyneuropathy, diabetic polyneuropathy often involves the autonomic nervous system as well (autonomic neuropathy).

Other causes of peripheral polyneuropathy include alcoholism (alcoholic polyneuropathy) zoster (postherpetic neuralgia), B12 deficiency, autoimmune diseases, Lyme disease, syphilis, HIV, leprosy, toxin exposures, and hereditary diseases such as Charcot-Marie-Tooth and demyelinating polyneuropathy (Eastman DM et al. 2022). In some diseases, polyneuropathy also occurs as a concomitant of the actual clinical picture, such as in acute intermittent porphyria.

Exact figures are available for diabetic polyneuropathy: the prevalence of peripheral neuropathy affects up to 50% of patients with diabetes during their lifetime, with prevalence found to range from 6% to 51%, depending on several variables such as age, glycemic control, type of diabetes, and age (Eastman DM et al. 2022). Peripheral neuropathy affects men more often than women. One study showed that after the onset of a diabetic foot ulcer, mortality increased from 3.1% to 17.4%. The same study also showed that up to one-third of patients diagnosed with a diabetic foot ulcer required amputation at some point (the study covered a period of up to 14 years/Rastogi A et al. 2020).

Peripheral nerves can be divided into motor, sensory and autonomic nerves.

Damage to motor nerves leads to weakness and spasms. Damage to sensory nerves leads to numbness, tingling and pain. Damage to autonomic nerves can lead to a variety of problems, including nausea, vomiting, diarrhea and inability to regulate other body functions. Patients with advanced neuropathy usually experience all of these symptoms in some form. However, the severity of neuropathy depends on the underlying cause. Thus, it is patient-specific. There are several known causes of peripheral neuropathy that can be classified into different categories (Mayans L et al 2015).

Anatomical causes: these include compression of nerves (e.g., the sciatic nerve) or dissection of a nerve as a result of surgery or an accident.

Systemic causes: these include.

• HIV infection
• Syphilis
• carcinoma (important DD in neuropathic nasal ulcer)
• paraneoplastic syndromes
• monoclonal gammopathy
• systemic amyloidosis
• Sarcoidosis
• Sjögren's syndrome
• Borrelia infections

Metabolic neuropathies: Metabolic causes of neuropathy include:

• Diabetes mellitus
• Thyroid disorders
• acute intermittent porphyria
• renal diseases
• chronic liver disease.

Hereditary neuropathies: These include:

• Hereditary sensory neuropathy type I (syn: Acroosteopathia ulcer-mutilans familiaris).

Toxic neuropathies: Toxic causes of neuropathy include:

• multiple vitamin deficiencies (B1, B6, B12).
• Excess of vitamin B6
• Heavy metal poisoning
• Organophosphates
• Alcohol

Drug-induced neuropathies

• Chemotherapuetics (e.g. vincristine)

Neuropathic ulcers are most commonly observed on the foot, and specifically at pressure points. Thus, they affect prominent surfaces of the foot, such as the heel and ball of the foot, or areas of high friction that are prone to callus formation. Less commonly, the face (e.g., facial neuropathic ulcer) may also be affected, for example, when the trigeminal nerve is damaged (Mayans L et al. 2015).

A detailed medical history is necessary. It is important to determine the background of the disease, including the duration of the neuropathy. The patient's hemoglobin A1C laboratory value may be helpful in diabetic polyneuropathy. Furthermore, a surgical history should be obtained to include a history of foot ulcers and possible surgical procedures such as amputations, vascular surgery. A social history provides information about the patient's occupational history, gfls. about his compliance. Furthermore, drug and alcohol consumption should be inquired about.

Venous ulcers (signs of CVI, typical localizations are the ankle regions).

Arterial ulcers (signs of peripheral circulatory disorder, smoking history)

Hypertonic ulcers (ulcus hypertonicus)

Traumatic ulcerations (anamnesis)

Decubital ulcers (anamnesis, bedriddenness, localization of the ulcer - heel, coccyx region)

Carcinomas of the skin (anamnesis, bioptic tumor evidence)

Vasculitic ulcers (high painfulness)Inflammatory ulcers (pyoderma gangraenosum)

Ulcers in MGUS

Ulcers in cutaneous and systemic infectious diseases (chronic pyoderma; Buruli ulcer, tuberculosis of the skin, leprosy, leishmaniasis)

Side effects of comorbidities (e.g. Kaposi's sarcoma)

The treatment and management of neuropathic ulcers requires a multilevel approach, depending on the cause, extent and location: treatment of the underlying cause as well as the ulceration itself is necessary. Treatment strategies are multifactorial. Understanding the biomechanical causation, helps to establish guidelines for clinical practice (DiLiberto FE et al. 2016).

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