Leg ulcers are open wounds on the lower leg that fail to heal within the expected timeframe, and the vast majority are caused by problems with blood circulation. Between 60% and 80% of all leg ulcers stem from faulty veins, making venous disease the leading cause by a wide margin. The remaining cases are split among arterial disease, diabetes-related nerve damage, and a handful of less common conditions including autoimmune disorders and, rarely, cancer.
Venous Disease: The Most Common Cause
Your leg veins carry blood back up to your heart against gravity. They rely on two systems to do this: the squeezing action of your calf muscles when you walk, and one-way valves inside the veins that prevent blood from falling back down. When those valves weaken or fail, blood pools in the lower leg. This creates sustained high pressure inside the veins, a condition called chronic venous hypertension.
That constant pressure forces proteins out of the blood vessels and into surrounding tissue, where they form a fibrous cuff around the tiny blood vessels in the skin. This cuff acts like a barrier, blocking oxygen and the growth signals cells need to repair themselves. At the same time, the body launches an inflammatory response. White blood cells flood the area, and immune cells called M1 macrophages release chemical signals that keep inflammation simmering indefinitely. Over time, this chronic inflammation actually destroys more valve tissue, creating a self-reinforcing cycle: more valve damage leads to more blood pooling, which causes more inflammation, which damages more valves.
The end result is skin that becomes thin, discolored, and fragile. Even a minor bump or scratch can open a wound that simply cannot heal in this hostile environment. These venous ulcers typically appear on the inner ankle or lower calf, and they tend to be shallow, irregularly shaped, and weepy. Roughly 0.32% of the general population has a venous leg ulcer at any given time, and healing is slow. Even with treatment, only about 57% heal within three months. By 12 months, roughly 78% have closed, meaning more than one in five people are still dealing with an open wound a full year later.
Arterial Disease and Reduced Blood Flow
While venous ulcers come from too much pressure in the veins, arterial ulcers come from too little blood reaching the tissues. The culprit is almost always peripheral artery disease (PAD), a condition where fatty deposits called plaque build up inside the arteries that supply the legs. As plaque narrows these arteries, less oxygen-rich blood gets through.
When blood flow drops low enough, the tissue at the far end of the supply line (toes, feet, and lower legs) starts to starve. This is called critical limb ischemia. At that point, the skin can break down on its own, or a small injury becomes a wound that the body simply doesn’t have the resources to repair. Arterial ulcers look different from venous ones. They tend to appear on the feet, toes, or shin rather than the inner ankle. The edges are often sharply defined, the wound bed may look pale or grayish, and the surrounding skin feels cool to the touch.
The risk factors for arterial ulcers mirror those for heart disease: smoking, high cholesterol, high blood pressure, and diabetes. A simple test called the ankle-brachial index (ABI) helps distinguish arterial from venous problems. It compares blood pressure at the ankle to blood pressure in the arm. A normal reading falls between 0.9 and 1.4. Anything below 0.9 suggests the arteries are narrowed, and the lower the number, the more severe the blockage. Below 0.5 indicates critical disease that needs specialist evaluation.
Diabetes and Nerve Damage
Diabetes creates a perfect storm for leg and foot ulcers by attacking the nerves and blood vessels simultaneously. The mechanism starts with chronically elevated blood sugar, which generates harmful molecules called reactive oxygen species. These molecules directly injure nerve fibers, starting with the smallest, unmyelinated fibers and eventually damaging the larger, insulated ones as well. The result is a progressive loss of sensation, muscle control, and automatic body functions in the feet and legs.
Sensory nerve damage is the most dangerous piece of this puzzle. When you lose feeling in your feet, you can’t detect friction from a poorly fitting shoe, the pressure of standing too long in one position, or even a sharp object underfoot. Without pain as a warning signal, you don’t shift your weight, change your shoes, or inspect the injury. A blister or small cut goes unnoticed and worsens.
Motor nerve damage compounds the problem by weakening the small muscles that maintain the arch and shape of the foot. As these muscles atrophy, the foot changes shape, creating bony prominences and new pressure points. The ball of the foot or the tips of curled toes now bear weight they weren’t designed to handle, and the skin breaks down in those spots.
Autonomic nerve damage adds a third layer. These nerves normally regulate sweating and blood flow in the skin. When they fail, the skin becomes dry, cracked, and less able to regulate temperature, all of which makes it more vulnerable to breakdown. Combine all three types of nerve damage with the poor circulation that diabetes also causes, and you get wounds that form easily and heal poorly.
Less Common Causes
About 10% to 20% of leg ulcers don’t fit neatly into the venous, arterial, or diabetic categories. These atypical ulcers have a wide range of underlying causes, and they’re important to recognize because treating them as ordinary ulcers won’t work.
Pyoderma gangrenosum is an inflammatory skin condition where the immune system attacks healthy tissue, creating rapidly expanding, painful ulcers. The wound often has a distinctive purple or lilac-colored border. It’s linked to autoimmune conditions like inflammatory bowel disease, rheumatoid arthritis, and certain blood cancers. Diagnosing it requires ruling out other causes first, and a tissue sample typically shows a dense concentration of a specific type of white blood cell in the deeper layers of skin.
Vasculitis, or inflammation of the blood vessel walls, can also produce leg ulcers. When blood vessels become inflamed, they may narrow or close entirely, starving the tissue they supply. The ulcers are painful and often appear alongside other signs of vessel inflammation: purplish discoloration, tiny red dots from broken capillaries, and blisters.
In rare cases, a long-standing chronic ulcer or old scar can undergo cancerous transformation. This is known as a Marjolin’s ulcer, and it occurs in roughly 1.7% of chronic skin wounds. The cancer that develops is usually squamous cell carcinoma. Any ulcer that has been present for years and suddenly changes in appearance, starts growing faster, or develops raised, irregular edges warrants a biopsy.
Key Risk Factors
Certain factors raise the likelihood of developing a leg ulcer regardless of the specific type:
- Age: The risk climbs steadily after 60, as veins lose elasticity, arteries accumulate plaque, and skin becomes thinner and more fragile.
- Obesity: Excess weight increases pressure in the leg veins, reduces mobility, and is closely associated with diabetes, heart disease, and stroke, all of which feed into ulcer development.
- Immobility: Your calf muscles act as a pump to push blood back toward the heart. Prolonged sitting, bed rest, or limited mobility from any cause allows blood to pool and pressure to build.
- Previous leg ulcers: Once the venous system is damaged, recurrence is common even after successful treatment.
- Smoking: Accelerates plaque buildup in arteries and impairs wound healing by reducing oxygen delivery to tissues.
- Deep vein thrombosis (DVT) history: Blood clots damage vein valves directly, often triggering the chain of venous hypertension that leads to ulceration years later.
How Ulcer Type Affects Treatment Approach
Identifying the underlying cause isn’t academic. It determines treatment, and getting it wrong can cause serious harm. Venous ulcers are treated with compression, which squeezes blood back up toward the heart and reduces the pressure causing the problem. But applying compression to a leg with severely blocked arteries would cut off the little blood flow that remains, potentially leading to tissue death. This is why an ABI measurement matters: compression is only safe when the reading is above 0.5, and full-strength compression generally requires a reading above 0.8.
Venous ulcers respond best to sustained compression, leg elevation, and sometimes procedures to close off the faulty veins. Arterial ulcers require restoring blood flow, often through procedures to open or bypass the blocked arteries. Diabetic ulcers need aggressive pressure relief (called offloading), careful blood sugar control, and regular inspection since the patient may not feel the wound getting worse. Inflammatory ulcers like pyoderma gangrenosum are treated with medications that calm the immune system rather than wound care alone.
Most leg ulcers develop from conditions that build gradually over years. The skin changes that precede a venous ulcer (darkening around the ankles, eczema-like itching, a feeling of heaviness in the legs) are warning signs that the venous system is struggling. Addressing circulation problems, managing blood sugar, staying active, and maintaining a healthy weight won’t eliminate all risk, but they target the root mechanisms behind the vast majority of leg ulcers.