An ulcer is defined as a loss of skin substance involving the epidermis, dermis, and sometimes even the hypodermis. It can be phagedenic, spreading in size, or tenebrous, deepening over time. Although consensus is lacking, it is considered chronic if not healed within 6 weeks.
Regarding etiology, multiple factors may contribute, such as secondary bacterial infection. Patient history is crucial for assessing concurrent diseases, ulcer evolution, and initiating factors. Small traumas are common initial causes, with arterial ulcers typically showing slow, gradual progression, while venous ulcers develop rapidly. Analyzing accompanying symptoms is equally important.
• Unilateral or bilateral edema
• Joint mobility
• Presence of varicose veins
• Trophic skin changes
• Ulcer location and number
• Characteristics of edges, base, and surrounding skin
• Distal pulses (note that thickened skin and edema can hinder pulse examination, particularly in venous ulcers. T/B index aids in such cases)
In many instances, clinical evaluation alone may be insufficient, necessitating additional diagnostic tests.
They are the most common among all leg ulcers, resulting from chronic venous hypertension caused by insufficiency of the deep venous system, occasionally associated with insufficiency of the superficial and/or perforating venous system. Rarely do ulcers arise exclusively due to perforating system insufficiency. The calf muscle pump plays a crucial role in preventing ulcers, and any condition that affects this mechanism worsens and accelerates the disease’s progression. Venous hypertension leads to capillary changes, including elongation and thickening, pericapillary fibrin deposition, increased plasma viscosity, and other alterations (see details in the venous ulcer chapter).
Diagnosis is generally not difficult due to symptoms from the medical history (intermittent claudication), current complaints (rest pain), and physical examination (absence of pulse with decreased index). Arterial ulcers tend to occur in areas more prone to trauma or pressure, such as the toes, bony prominences, pre-tibial regions, or lateral malleolus. Regardless of size, these ulcers are painful, with increased pain when the limb is elevated.
Differential diagnosis can be complicated in cases of associated lipodermatosclerosis and hyperpigmentation with the absence of palpable pulses. It is estimated that 10 to 20% of patients with venous ulcers also have associated arterial disease.
They can be congenital or acquired, localized or diffuse, and are more common in the lower limbs. In congenital cases, the presence of nevi or associated vascular changes is frequent. These cases exhibit an enlarged affected limb, peripheral edema, increased skin temperature, prominent and/or pulsating veins, thrill, and bruit. Similar to varicose ulcers, they differ in their location and heal when the fistula is corrected. Treatment options include embolization, ligation of involved branches, and even amputation for cases where other treatment options fail with intractable ischemic pain.
Rarely occurring, they are only seen in advanced lymphedema cases, characterized by typical lymphatic edema with no varicose veins.
Ulcers related to rheumatoid arthritis are relatively common, accounting for up to 8% of leg ulcers. They can occur anywhere on the leg but are more frequent around the ankle region. The presence of characteristic hand and foot changes aids in the differential diagnosis. These ulcers are challenging to treat.
Among collagen diseases, scleroderma is the most common cause of ulcers. Raynaud’s phenomenon, arthritis, dysphagia, and facial changes suggest the disease, especially when associated with elevated ESR and ANA titers. These ulcers are small, usually multiple, painful, deep with minimal signs of healing, and can be localized but may extend to the foot.
In systemic lupus erythematosus (SLE), multiple, small, chronic, and recurrent ulcers occur anywhere on the leg, associated with high lupus antibody titers.
Pyoderma gangrenosum is a non-infectious, chronic, and recurrent ulcer leading to skin destruction and necrosis. Initially presenting as a nodule, pustule, or hemorrhagic blister, it rapidly progresses to ulceration with irregular, multiloculated necrotic edges and a slightly elevated, erythematous halo. The base is granular, usually covered by necrotic crust. When it heals, it leaves an atrophic scar that may recur. Pyoderma gangrenosum is often associated with ulcerative colitis, Crohn’s disease, monoclonal gammopathies, and leukemia.
Necrobiosis lipoidica is a condition found in diabetics, involving necrosis of subcutaneous fat and skin, of unknown cause.
Gout can cause ulceration due to skin necrosis caused by compression from a gouty tophus, where uric acid crystals act as a foreign body.
Malignant transformation of a previous ulcer (Marjolin’s ulcer) can occur, typically squamous cell carcinoma. Primary neoplastic processes presenting as leg ulcers are rare and usually involve basal cell carcinoma and some sarcomas, such as dermatofibrosarcoma.
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Ecthyma is a pyodermatitis caused by strepto or staphylococcus, characterized by a pustule that ruptures and deepens, forming a smooth, reddish, or purulent ulcer. The edge has a slightly erythematous, minimally edematous halo. Typically 1 to 2 cm in size, round, and preferably located on the legs. Poor hygiene and malnutrition are significant factors.
Caused by non-hemolytic streptococcus associated with staphylococcus, gram-negative bacillus, or clostridium, progressing rapidly. It has a bluish, undermined edge, reaching the skin and subcutaneous tissue, with thrombosis of small skin vessels, leading to gangrene.
Occur in Bazin’s indurated form as nodules that liquefy and fistulate, especially in the calves of young white women. Usually occurring in outbreaks, they are almost always symmetrical and located in the subcutaneous tissue. They evolve by adhering to the epidermis, becoming indurated, and rupturing in 30% of cases, with the expulsion of necrotic material. In these cases, shallow ulcers form, with a red, granular base. Healing leaves atrophic, depressed, and hyperpigmented areas. Histopathologically, there are tuberculoid granulomas with caseous necrosis, but no bacilli are present. There is also vasculitis with thickening of the tunics, thrombosis, and necrosis. PPD is usually strongly reactive.
More common than estimated. They are more common in children, especially those who have not received BCG vaccination. Most often, inoculation occurs through plant trauma. They form ulcers with detached, painless, and cool edges, with a necrotic base. If multiple lesions are present, they are usually intercommunicating. History is the most facilitating diagnostic element, but in doubtful cases, ulcer biopsy typically reveals bacilli.
Frequently occur on the feet, especially on the soles, dorsum, or proximal phalanx of the hallux, but can also be seen on the legs. It is associated with sensory deficits. Secondary ischemia due to capillary occlusion by immune complex deposition (Lucio’s phenomenon) can occur. Ulcers are multibacillary, rarely occurring in the indeterminate form and rarely in the tuberculoid form. General disease characteristics (leonine facies, madarosis, hansenomas, etc.) aid in diagnosis.
Rarely diagnosed in their classic nodular form. There is early malignant syphilis, which occurs concurrently with HIV, producing ulcers, although more commonly seen on the face and scalp.
It is a phagedenic ulcer with rapid evolution and mixed flora. They are painful ulcers associated with poor hygiene conditions, usually solitary, with raised edges and a necrotic base. They can progress to deeper planes, affecting fascia, muscle, and tendons.
Ulcerated lesions with a granular red base, although almost always covered by serous or purulent secretion, with raised “frame” edges. Diagnosis is made by observing leishmania through direct examination or histopathology. Montenegro’s intradermal reaction should be performed, but its positivity does not necessarily indicate disease.
Occurs due to fungal inoculation from trauma, usually cat scratches. After an incubation period of 7 to 180 days, an infiltrated and erythematous-based ulcer appears at the site of trauma. This lesion remains solitary for several weeks, then a chain of painless nodules forms, which may or may not ulcerate, characterizing the lymphatic form of the disease. Direct microscopy is not useful; only culture, which takes 5 days for optimal growth, can provide a diagnosis.
Sickle cell anemia tends to occlude distant capillaries where there is low oxygen pressure.
This is because in hypoxic or dehydrated conditions, it tends to change its shape, taking on a sickle form. This occurs in the retina, kidneys, heart, and lower limbs, leading to leg ulcers. It is believed that 25 to 50% of patients will develop leg ulcers at some point in their lives. They are resistant to treatment, tend to recur, and can lead to osteomyelitis, cellulitis, and lymphadenitis.
They occur in pressure areas associated with neuropathy. They are more common under the first metatarsophalangeal joint, the base of the 5th metatarsal, and the heel. They are painless, deep, and surrounded by hyperkeratosis.
Burns, accidents, or iatrogenic causes lead to leg ulcers. Hot water bags in anesthetized patients and subcutaneous injections (as in sclerotherapy) can cause them.