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Why Do I Have Leg Ulcers? (Venous, Arterial, and Other Causes)
Cutaneous ulcers are tissue defects that can affect the superficial layer of the skin (epidermis) and/or the deeper layers (dermis and hypodermis), and which show little tendency toward spontaneous healing. They represent a significant clinical and public health challenge, particularly in elderly and chronically ill patients.
Skin ulcers may be caused by trauma, inflammatory processes, or neoplastic conditions. They most commonly affect the legs (typically just above the ankle) and are generally chronic in nature, requiring more than 4 to 6 weeks to heal.
The symptoms and signs of a venous leg ulcer (the most common type) include:
- Swelling of the affected limb
- Discoloration of the surrounding skin (brown or reddish-brown pigmentation from hemosiderin deposits)
- Pain and itching (not always present)
- Unpleasant odor, particularly when secondary infection is present
Ulcers arising from venous insufficiency are chronic and may persist for years, sometimes recurring even after intensive treatment, particularly when the underlying circulatory problem cannot be adequately corrected. Inflammatory, infectious, and neoplastic ulcers generally respond well to targeted therapies.
The most common complications are secondary bacterial infections and allergic contact dermatitis, which can develop in ulcer patients due to prolonged exposure to a large number of topical preparations and wound dressings.
Resolution of a skin ulcer almost always results in the formation of a scar.
Causes
The possible causes of skin ulcers are numerous, although disorders of the venous circulation are by far the most common.
Veins are blood vessels that carry blood from the peripheral organs back to the heart and lungs, where carbon dioxide is released and oxygen is absorbed. The oxygenated blood is then transported from the heart and lungs back to the peripheral organs through the arteries.
Venous vessels, particularly those in the most peripheral regions of the body, such as the lower legs and feet, are equipped with valves that, working together with the pumping action of the foot and leg muscles, promote upward blood flow toward the heart. Under normal physiological conditions, these valves prevent blood from flowing backward down the leg (reflux) against gravity, thus maintaining healthy venous circulation.
The primary mechanism underlying venous insufficiency of the lower limbs is the impairment of these valves. When the valves fail to maintain correct circulation and blood accumulates in the veins, a condition called venous insufficiency develops, characterized by visible distension and bulging of the venous vessels (varicose veins).
The resulting pooling of blood in the veins leads progressively to an increase in venous pressure that can become chronic, technically defined as chronic venous hypertension. This sustained elevated pressure causes distension of the venous walls, structural damage to the vessel walls, and leakage of blood cells and fluid from the vessels into the surrounding tissue (a process called extravasation). The accumulation of these cells and fluid in the interstitial tissues (the tissue surrounding the vessels) causes local tissue damage and impairs oxygen and nutrient delivery to the surrounding skin, ultimately leading to the formation of venous ulcers.
Venous insufficiency resulting from chronic venous hypertension is both the main risk factor and the most frequent cause of leg skin ulcers, accounting for over 90% of cases.
A second important cause, less frequent than venous insufficiency but clinically significant, is impairment of the arterial circulation, which leads to the formation of arterial ulcers. Arterial circulatory insufficiency may result from various factors, most importantly:
- Atherosclerosis: Progressive degeneration of arterial walls due to the accumulation of fatty deposits (atheromatous plaques), which narrow the arterial lumen and reduce blood flow
- Diabetic angiopathy: Arterial wall changes induced by diabetes mellitus, leading to impaired peripheral perfusion
- Hypertension: Chronically elevated blood pressure causes progressive arterial wall damage
- Acute ischemia: Sudden, complete obstruction of arterial blood flow caused by an embolus, any material other than blood (such as a fatty deposit, an air bubble, or a foreign body) that travels in the bloodstream and, depending on its size, can obstruct blood vessels of varying caliber, cutting off the blood supply to a body region
Other, less frequent risk factors and causes of skin ulcers on the legs include:
- Trauma
- Pressure injuries (decubitus ulcers): In bedridden patients, prolonged pressure on bony prominences compromises tissue perfusion
- Medications:
- Hydroxyurea (a cytoreductive agent associated with leg ulcers after prolonged use)
- Chemotherapy agents
- Bacterial infections:
- Syphilis
- Leprosy
- Deep pyoderma
- Diphtheria
- Tuberculosis
- Deep fungal infections (such as sporotrichosis, actinomycosis, and deep dermatophytosis)
- Protozoal infections, such as localized cutaneous leishmaniasis
- Autoimmune diseases:
- Systemic lupus erythematosus (SLE)
- Systemic sclerosis (scleroderma)
- Inflammatory vascular diseases (vasculitis), which may be triggered by:
- Infectious causes
- Drug reactions
- Neoplastic conditions
- Hematological disorders
- Autoimmune mechanisms
- Unknown causes
- Pyoderma gangrenosum: A rare, poorly understood dermatological condition characterized by rapidly expanding, painful ulcers, often associated with systemic inflammatory diseases (such as inflammatory bowel disease or rheumatoid arthritis)
- Neoplastic conditions:
- Basal cell carcinoma
- Squamous cell carcinoma
- Melanoma
- Lymphoma
- Neurological conditions: Diseases causing peripheral nerve damage (peripheral neuropathy), especially diabetic neuropathy, lead to loss of protective sensation, predisposing to unrecognized trauma and pressure injury
Transmission and Contagiousness
Skin ulcers are only contagious when caused by infectious conditions that are not being adequately treated. In the context of venous, arterial, diabetic, or pressure ulcers, the vast majority of cases, there is no risk of transmission to other individuals. When infection (whether bacterial, fungal, or protozoal) is the primary cause of the ulcer, appropriate treatment of the infection eliminates any risk of contagion.
Symptoms
A skin ulcer is a cutaneous tissue defect that may be painful or asymptomatic, depending on its underlying nature and any associated complications.
Venous Ulcers
The most common location for venous ulcers is the malleolar region, around or just above the ankle, on the inner (medial) surface of the lower leg. Their shape is variable, ranging from round or oval to irregular and serpiginous (with a wavy, creeping border), and their size and depth can vary considerably. The base of the ulcer may contain:
- Purulent exudate, indicating secondary bacterial infection
- Granulation tissue (moist, pink-red tissue), which signals that the repair process is actively underway
Surrounding the venous ulcer, there is typically a variable degree of edema (swelling), along with:
- Lipodermatosclerosis: Induration and fibrosis of the subcutaneous fat, giving the lower leg a characteristic inverted bottle shape
- Hemosiderin staining: Brown-to-reddish-brown skin discoloration caused by hemoglobin breakdown products from extravasated red blood cells
- Varicose eczema (stasis dermatitis): Dry, itchy, scaly skin changes in the surrounding area
Arterial Ulcers
Arterial ulcers typically affect the outer (lateral) surface of the lower leg, the dorsum of the foot, toes, and bony prominences (such as the heel). They are:
- Small and clearly demarcated, with a round or punched-out appearance
- Deep, with a pale or necrotic base (may contain dark eschar)
- Surrounded by thin, shiny, hairless, pale skin (atrophic skin due to chronic ischemia)
- Severely painful, particularly at night when the patient lies flat (rest pain), relieved by hanging the foot down
The surrounding skin may show other signs of peripheral arterial insufficiency: loss of hair, cool skin temperature, and absent or diminished peripheral pulses.
Diabetic Foot Ulcers
Ulcers in diabetic patients are characteristically located in the most distal parts of the body, typically on the plantar surface of the feet, over pressure points and bony prominences. They are often painless due to the associated diabetic peripheral neuropathy, which destroys the protective pain sensation. This painlessness is clinically dangerous, as it allows extensive tissue damage to develop unnoticed.
Vasculitic Ulcers
Ulcers caused by inflammation of blood vessels (vasculitis) may be preceded by distinctive skin lesions such as palpable purpura (non-blanching hemorrhagic spots), papules or nodules, or blisters. When these progress to ulceration, the resulting lesions can be intensely painful.
Infectious Ulcers
Ulcers caused by infections (such as syphilis, tuberculosis, or leishmaniasis) are often indolent, painless or only mildly uncomfortable, which can paradoxically delay their recognition and treatment.
Pyoderma Gangrenosum
Pyoderma gangrenosum produces characteristically exquisitely painful ulcers with a violaceous (purple-blue), undermined border, a clinical hallmark of this condition. The pain is typically disproportionate to the apparent wound appearance.
Neoplastic Ulcers
Ulcers arising from skin malignancies (such as squamous cell carcinoma, basal cell carcinoma, or melanoma) may be relatively painless in early stages and are often mistaken for chronic non-healing wounds. Any ulcer that fails to respond to standard treatment over 3 months should be biopsied to exclude malignancy.
Diagnosis
Diagnosis is primarily based on clinical examination, to which specific investigations are added as needed to better characterize the nature of the lesion and identify underlying causes.
Clinical Signs Suggesting Secondary Infection
The following signs during examination should raise suspicion of active infection or superinfection of an ulcer:
- Purulent exudate on the wound surface
- Increased pain or a change in pain character
- Erythema and edema (redness and swelling) of the surrounding skin
- Warmth to the touch over the affected area
- Systemic signs such as fever or elevated inflammatory markers
When these features are present, a wound swab for microbiological culture and sensitivity testing should be performed to identify the causative organism and guide antibiotic selection.
Biopsy
When vasculitis, inflammatory ulcers, autoimmune disease, or malignancy is suspected, a punch biopsy of the ulcer edge (not the base, which is often necrotic and non-diagnostic) is essential for histopathological examination to define the exact cause.
Any chronic ulcer that does not improve after 3 months of appropriate standard treatment should be biopsied to exclude underlying neoplasia.
Vascular Assessment
The distinction between venous and arterial ulcers has fundamental therapeutic implications and should be established before initiating treatment. Key investigations include:
- Ankle-Brachial Index (ABI) / ABPI: A non-invasive vascular test comparing blood pressure at the ankle with that at the brachial artery (arm). An ABI below 0.9 indicates significant peripheral arterial disease and contraindicates compression therapy. This test is mandatory before applying any form of compression bandaging to a leg ulcer.
- Doppler ultrasound of the lower limb veins: Evaluates venous reflux, valve competence, and the presence of deep vein thrombosis
- Duplex ultrasound of the arteries: Assesses arterial blood flow and identifies sites of stenosis or occlusion
- CT or MR angiography: Provides detailed vascular mapping for planning revascularization procedures
Blood Tests
Relevant blood investigations depend on the clinical context and may include:
- Full blood count (to detect anemia, leukocytosis indicating infection)
- Blood glucose and HbA1c (diabetes screening and monitoring)
- Inflammatory markers (CRP, ESR, elevated in infection, vasculitis, autoimmune disease)
- Autoantibody panel (ANA, ANCA, anti-dsDNA for autoimmune and vasculitic causes)
- Coagulation studies and thrombophilia screen (in patients with recurrent ulcers without obvious cause)
Treatment
The fundamental principle of ulcer management is to identify and correct the underlying causative factor. Treating only the wound surface without addressing the root cause leads to inevitable recurrence.
Cause-Specific Treatments
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Venous ulcers: The cornerstone of treatment is compression therapy, the application of graduated elastic compression bandaging or hosiery to the lower limb. This counteracts chronic venous hypertension by promoting venous return toward the heart, reducing edema, and improving tissue oxygenation. Multiple compression systems are available (including four-layer bandaging systems and two-layer systems). The ABI must be measured before applying compression to exclude significant arterial disease. Where appropriate, surgical treatment of varicose veins (endovenous ablation or surgical stripping) is an important adjunct to reduce recurrence risk.
-
Arterial ulcers and diabetic ulcers: Treatment requires arterial revascularization to restore adequate blood supply to the ischemic tissue. Revascularization options include:
- Percutaneous transluminal angioplasty (PTA): Balloon dilation of narrowed or occluded arterial segments, with or without stent placement
- Surgical bypass grafting: Creating an alternative conduit to bypass a blocked artery
- In diabetic patients: meticulous glycemic control, offloading pressure from the wound site (using specialized footwear, total contact casting), and infection management are also essential
-
Pressure ulcers (decubitus ulcers): Reducing and redistributing pressure at the wound site is the primary intervention, through regular repositioning of the patient, use of pressure-relieving mattresses and cushions, and nutritional optimization
-
Infectious ulcers: Targeted antimicrobial therapy based on culture results, systemic antibiotics for bacterial infections, antifungals for deep fungal infections, antiprotozoal agents for leishmaniasis
-
Neoplastic ulcers: Surgical excision with appropriate margins; oncological treatment as indicated for the specific tumor type (radiotherapy, systemic chemotherapy, immunotherapy)
-
Inflammatory and autoimmune ulcers: Systemic anti-inflammatory therapy, typically with corticosteroids and disease-modifying or immunosuppressive agents, tailored to the specific underlying condition. In pyoderma gangrenosum specifically, the phenomenon of pathergy (paradoxical worsening with wound debridement) means that aggressive surgical debridement must be avoided.
-
Drug-induced ulcers: Discontinuation or substitution of the causative medication, wherever clinically possible, after discussion with the prescribing physician
Topical Wound Care
Regardless of the underlying cause, local wound management is an essential component of ulcer treatment. Modern wound care is based on the principle of moist wound healing, maintaining an optimal moist environment at the wound-dressing interface, which promotes cell migration, granulation tissue formation, and epithelialization.
Available wound dressing categories include:
- Exudate-absorbing dressings: Hydrofibres, alginates (derived from seaweed), and polyurethane foam dressings, ideal for moderately to heavily exuding wounds
- Hydrocolloid dressings: Promote granulation tissue formation in wounds with low to moderate exudate; provide an occlusive, moist environment
- Collagen and hyaluronic acid-based dressings: Stimulate cellular proliferation and support the wound healing cascade
- Antimicrobial dressings (such as silver-containing or iodine-based dressings): Used when wound infection or heavy bacterial colonization is present; should not be used indefinitely
- Negative Pressure Wound Therapy (NPWT): Application of controlled sub-atmospheric pressure to the wound via a sealed foam dressing and suction device, reduces edema, stimulates granulation, and draws wound edges together; used in selected complex or cavity wounds
Wound debridement, the removal of necrotic, devitalized, or infected tissue from the wound, is often necessary to allow healing. Methods include:
- Sharp surgical debridement (most rapid and effective for large amounts of necrotic tissue)
- Enzymatic debridement (using topical enzymatic preparations)
- Autolytic debridement (using occlusive or moisture-retentive dressings to allow the body’s own enzymes to soften and liquefy necrotic tissue)
- Larval (maggot) therapy: Application of sterile medicinal maggots, which selectively debride necrotic tissue and have antimicrobial properties
In selected cases, skin grafting (transplanting thin sheets of the patient’s own skin from a donor site, autologous split-thickness skin grafts, or bioengineered skin substitutes) may be used to cover large or recalcitrant ulcers and accelerate healing.
It is important to note that healing of chronic leg ulcers frequently requires prolonged treatment over months and sometimes years. Regular reassessment and adjustment of the treatment plan are essential.
Prevention
Prevention of skin ulcers is achieved primarily by preventing or effectively managing the underlying disease that causes them. In patients with established risk factors or active disease, prevention consists of halting disease progression through adequate and timely treatment.
Venous Ulcer Prevention
- Graduated elastic compression of the lower limbs is indispensable for correcting chronic venous hypertension in patients with venous insufficiency, both for ulcer prevention and for preventing recurrence after healing. Compression stockings should be prescribed at an appropriate compression class (typically 23-32 mmHg or higher) and replaced regularly.
- Surgical treatment of varicose veins (endovenous thermal ablation, foam sclerotherapy, or surgical stripping) should be considered as a preventive measure in patients with significant venous insufficiency, to reduce venous hypertension and the risk of ulceration.
- Leg elevation: Elevating the legs above heart level when resting reduces venous hypertension and edema.
- Regular physical activity (particularly walking) activates the calf muscle pump and promotes venous return.
- Weight management: Obesity significantly worsens venous insufficiency.
Arterial Ulcer Prevention
- Optimal management of cardiovascular risk factors: blood pressure control, glycemic control in diabetes, lipid-lowering therapy, and smoking cessation
- Regular monitoring of peripheral arterial pulses and ABI in high-risk patients
- Careful foot care in diabetic patients (daily inspection, professional podiatry, protective footwear)
General Wound Prevention
- Regular repositioning and use of pressure-relieving equipment in bedridden or wheelchair-dependent patients to prevent pressure injuries
- Prompt and thorough treatment of any skin infections before they can progress to ulceration
- Patient education regarding warning signs (non-healing wounds, color changes, increased pain) that require prompt medical evaluation
Sources and Bibliography
- Cainelli T., Giannetti A., Rebora A. Manuale di dermatologia medica e chirurgica. McGraw-Hill, 4th edition.
- Wounds UK. Best Practice Statement: Compression Hosiery (2nd edition). London: Wounds UK, 2018.
- NICE Guideline NG200. Chronic wounds: advanced wound dressings and antimicrobial dressings. National Institute for Health and Care Excellence, 2021.
- O’Meara S, et al. Antibiotics and antiseptics for venous leg ulcers. Cochrane Database of Systematic Reviews. 2014.
- Alavi A, et al. What’s new: Management of venous leg ulcers. Treating venous leg ulcers. Journal of the American Academy of Dermatology. 2016;74(4):643-664.
- Hinchliffe RJ, et al. Management of peripheral arterial disease in patients with diabetes. Diabetes/Metabolism Research and Reviews. 2020.
