Trophic Ulcers, what are they and how can you prevent them?

Two million people globally have trophic ulcers. Despite modern medicine’s advances, this illness is dangerous. A trophic ulcer on the leg causes significant soft tissue injury that can reach the bone and skin or mucous membrane disintegration. Chronic inflammation weakens the body’s defences, making disease treatment harder.


A trophic ulcer of the lower extremities develops when surface tissues are damaged. Reduced blood flow, infection, and other circumstances cause harm. The patient’s blood vessels enlarge, complicating treatment.

Trophic ulcer is long-lasting (up to a month or more) and periodic; the lesion penetrates deep into the tissues and bones; the ability to regenerate in the affected area may be lost; and a rough scar develops at the lesion site following therapy.

The lesion develops as a papule on the lower thigh, usually at the trauma site. It spreads swiftly, causing necrotizing pustules. Ulcers cause pain, fever, and malaise. After a few weeks, an odorous, purulent, black coating covers the ulcer.

Trophic ulcers are most common on the feet and legs because they have the least blood flow and are exposed to prolonged pressure during walking, lying down, and other activities (in more than 95 percent of cases). Foot, heel, and toe wounds are especially dangerous because they’re continually in contact with the ground, clothing, or shoes.

It’s rare in the upper limbs, trunk, and head and unrelated to vascular disease. In Europe and North America, 0.8%-1.5% of the population has lower extremity venous ulcers, and 3.6% of those over 65. 1-2 percent of the health budget is spent on ulcers.


This degenerative condition can advance from stage to stage. Symptoms include swelling, leg heaviness, warmth, and itching.

Trophic ulcer phases are:

  • First-stage pathology (exudation) is defined by skin lesions and inflammation. The earliest symptoms are red, peeling regions on the patient’s lower extremities. Some spots itch and hurt gradually.
  • In the second phase, black wounds replace red areas. A blister may leak fluid and slow wound healing. The patient complains of failing health and fever.
  • Pus flows readily from the wound in the third stage. The wound expands and swells. Ulcers can migrate to the legs, producing agonizing pain.
  • The fourth phase (repair) reduces inflammatory activity and begins recuperation.
  • In the fifth stage (epithelialization), there is no edema and the lesion narrows as surrounding epithelium multiplies.
  • In the sixth phase (scars), connective tissue replaces injured skin cells and subcutaneous tissue.
A trophic ulcer causes neuropathy, which leads to a loss of sensation and, in some circumstances, a deformed foot and uneven stride. Loss of feeling, foot deformities, and limited and uneven motion increase biomechanical foot strain.

Biomechanical strain increases pressure in some places of the foot, generating skin thickening (callus, blister), which increases load, occasionally culminating in subcutaneous bleeding and eventually trophic ulceration owing to neuropathic changes in the foot. If patients aren’t educated and preventative measures aren’t taken, these disorders can lead to poor wound healing, infection, and gangrene.


Prolonged relaxation and immobility in one posture may cause a trophic ulcer due to skin pressure that interferes with blood circulation. They’re often at the heel and knee. When ischemic skin ruptures, bacterial penetration and inflammation follow.

Statistics show that trophic ulcers are most common in varicose veins or thrombophlebitis. Blockage of venous blood outflow from the lower limbs causes blood stagnation in small veins, disturbance of capillary tone in the microvasculature, and degradation of the vascular system’s arterial connection. Arterial atherosclerosis reduces blood flow and oxygen and food availability to tissues below the plaque.

Neuropathy, defined by reduced somatic and autonomic nerve fiber function, causes most trophic foot ulcers. Diabetic peripheral neuropathy is most common.

Peripheral neuropathy is caused by metabolic disorders, including the breakdown of excess glucose into sorbitol and fructose. Diabetics often experience retinal microvascular damage, kidney damage, and nerve damage.

Neuro-osteoarthritis is more common in diabetics. Autonomic nerve dysfunction produces decreased blood supply to the foot, causing bone fragmentation and ulceration. Inactive bones and joints might deteriorate completely.

A diabetic trophic ulcer on the foot can be induced by a little injury (e.g., damage from inadequate footwear, walking barefoot, or acute injury) because it involves two or more risk factors, with peripheral neuropathy playing a key role.

Trophic ulcers are caused by:

  • Heat injuries, like frostbite or burns; diabetes and its consequences; chronic dermatitis, especially allergic dermatitis; obliterating atherosclerosis of lower limb arteries
  • Autoimmune connective tissue diseases with systemic arterial, microcirculatory, and venous blood flow, including antiphospholipid syndrome; Anatomical and inflammatory lymphatic vessel disorders (acute and chronic lymphostasis); Nerve fiber injuries that compromise integrity. Antiphospholipid syndrome is an autoimmune connective tissue disorder with systemic arterial, microcirculatory, and venous blood flow.
  • Pathological problems that disrupt the blood supply and innervation of skin and subcutaneous tissue (typically the lower limbs) and trauma that causes primary injury at the site of future ulcer defect usually have the same significance in trophic ulcer formation.

Unexpected symptoms make trophic ulcers deadly. Swelling and pain in the limbs may signal a trophic ulcer.

Symptoms of trophic ulcers include:

  • Lower-limb itching.
  • During sleep, muscle spasms cause a swollen, painful skin surface.
  • Changes in skin, such as sudden hardened, glossy patches Touch-sensitive skin, an odorous ulcer purple dots that spread in volume and depth abrupt hardened areas with a shining surface
  • Symptoms arise in veins, usually on the inner thighs. The disease grows in veins, causing little lesions. The ulcer has a volcano crater shape and a purulent discharge due to inflammation. Inflammation and arterial destruction cause most artery damage.


Tropic ulcers require a medical history and a surgeon’s history and exam. Primary varicose veins usually always have hereditary or venous origins. In addition to a physical exam, various procedures are needed to diagnose the cause of the problem, such as blood vessel ultrasonography, electromyography, MR tomography, and contrast-enhanced radio angiography. Today, colour doppler vein is the most reliable diagnostic tool.


Successful ulcer therapy requires determining the cause. Before starting treatment for the disease, the patient must undergo cytological and bacteriological examinations.

Only surgery can permanently heal trophic ulcers by removing the disease’s source. When surgery isn’t an option for treating a skin condition, try to stop its spread. Ulcer treatments should be complete.

In some cases, the doctor may also propose surgery (nonsteroidal anti-inflammatory drugs, broad-spectrum antibiotics and antihistamines).

Neurotrophic and atherosclerotic ulcers with pus-filled canals require surgery. If the ulcer affects a large area of soft tissue, the doctor may propose removing it to prevent infection. Extensive ulceration is separated into numerous minor surgeries to reduce lesion size and cease inflammation. Rarely, big lesions may be treated by a skin transplant.

Conservative treatment includes regular wound cleaning and bandaging. Depending on the patient’s state, a doctor will prescribe ointments for leg trophic ulcers.

If the ulcer develops venous edema, employ compression bandages after administering ointment. They cure edema by temporarily narrowing the affected area’s diameter. Personalized socks can replace compression bandages if the disease improves.

Tubulcus is used to treat venous open wounds and conditions that put larger wounds at risk. It works on the idea of gradual pressure application, so the pressure in the tubulcus is strongest in the area of the medial maleolus and gradually lowers to the knee, assisting the veins in returning blood to the heart. As the external tubule achieves the optimum pressure, additional tissue fluid is forced into the veins and venous valves seal better. It improves cardiac circulation and decreases leg pressure. When pressure drops, skin and tissues get more oxygen. Ulcer heals.

For venous ulcers, try these steps:

  • Using properly fitted shoes and orthopedic insoles – Inflation, poor statics, and loose ligaments increase the risk of venous foot disease.
  • Gaining weight is a documented varicose vein risk factor.
  • Avoid extended standing and sitting, elevate your legs occasionally, and avoid excessive heat (saunas, solariums, thermal pools).
  • Large loads and strenuous exercise should be avoided since they raise abdominal pressure, dilating leg veins.
  • Wearing elastic stockings, daily dressing, and ulcer cleanliness


Luigi medicinal footwear improves biomechanical and medical difficulties, stimulates blood circulation, and calms wearers.

According to foot experts, anyone with joint, bone, and spine circulation issues, as well as varicose veins, should utilize Dr. Luigi products.


Prevention is easier than treatment. For prevention, it’s recommended to monitor veins, use circulation-improving gels and ointments regularly, avoid extended standing or sitting, and exercise regularly to promote circulation and stimulate the lower extremities.

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