Leg ulcers start when something disrupts the normal flow of blood or oxygen to the skin of the lower leg, weakening it to the point where even minor damage can’t heal. The process is almost never sudden. In most cases, the skin deteriorates over weeks or months before an open wound appears, and the underlying cause has often been building for years. About half of all chronic leg ulcers are venous, meaning they stem from problems with blood flowing back up toward the heart. The rest are caused by arterial disease, diabetes, or a combination of factors.
How Venous Ulcers Begin
Venous leg ulcers, the most common type (accounting for roughly 51% of chronic leg wounds), start with a problem inside the veins of your legs. Veins have one-way valves that push blood upward against gravity. When those valves weaken or fail, blood pools in the lower leg, creating sustained high pressure inside the veins. This condition is called chronic venous insufficiency, and it sets off a chain of damage that eventually reaches the skin surface.
The high pressure forces fluid and proteins out of the veins and into the surrounding tissue. A layer of protein called fibrin builds up around the tiny blood vessels near the skin, forming a barrier that blocks oxygen and nutrients from reaching skin cells. At the same time, the body launches an inflammatory response. White blood cells flood into the tissue, releasing substances that break down the structural framework of the skin. This inflammation becomes self-sustaining: it damages the vein walls further, which worsens the pooling, which increases the pressure, which drives more inflammation.
Over time, this cycle produces visible changes you can see and feel. The skin around the ankles starts to look thin or tissue-like. A brownish discoloration appears, caused by iron deposits from red blood cells that have leaked out of damaged vessels. The skin gradually becomes thickened, hard, and waxy, a condition called lipodermatosclerosis. At this stage, the skin is extremely fragile. A small bump, scratch, or even the pressure of a shoe can break it open, and because the underlying blood flow is compromised, the wound simply cannot heal on its own.
Venous ulcers characteristically appear around the inner ankle bone. They tend to have sloping edges and a wound bed covered in a yellowish film called slough. The surrounding skin often shows eczema-like irritation and that telltale brown staining.
How Arterial Ulcers Begin
Arterial ulcers follow a different path. Instead of blood pooling from below, the problem is blood not arriving from above. Narrowed or blocked arteries, usually from atherosclerosis (the same plaque buildup that causes heart attacks), reduce the amount of oxygen-rich blood reaching the lower legs and feet. When tissue doesn’t get enough oxygen, it begins to die.
Three mechanisms can restrict arterial flow: pressure from outside the artery (like swelling compressing a vessel), thickening of the artery wall itself, or blockage inside the artery from plaque or clots. All three result in the same outcome: starved tissue that breaks down.
Arterial ulcers look distinctly different from venous ones. They typically form over the toes, heels, and bony parts of the foot rather than around the ankle. The wound has a “punched out” appearance with sharply defined edges and a pale, non-healing base that may contain dead tissue. The skin around the ulcer is often cool to the touch, hairless, shiny, and thin. In severe cases, the tissue turns black as gangrene sets in.
How Diabetes Leads to Ulcers
Diabetic ulcers start through a particularly dangerous combination: nerve damage removes your ability to feel injury, while poor circulation slows your ability to heal from it. Peripheral neuropathy, which affects the nerves in the feet and lower legs, means you may not notice a blister, cut, or area of pressure. You keep walking on it, keep wearing the same shoes, and the damage compounds.
The triad behind diabetic foot ulcers is neuropathy, foot deformities (which create abnormal pressure points), and repetitive trauma. Diabetes also impairs wound healing at a cellular level, so once the skin breaks, the wound tends to stall rather than progress through normal repair stages. These ulcers most commonly appear on the bottom of the foot, under the ball or the heel, where pressure from walking is greatest.
The Role of Swelling
Chronic leg swelling, regardless of its cause, is a direct threat to skin integrity. Persistent edema stretches the skin, reduces the number of tiny blood vessels supplying it, and measurably lowers oxygen levels in the tissue. Research shows a clear correlation between the severity of swelling and the decline in skin oxygen content.
Swelling also creates a vicious cycle with infection. Fluid-logged tissue is more vulnerable to bacterial skin infections like cellulitis, and infection causes more inflammation, which causes more swelling. In cases where the tissue becomes hardened and fibrotic from long-standing swelling, the increased skin tension alone can be enough to trigger ulceration. This is different from the softer, more diffuse swelling seen in heart failure or lymphedema, where ulceration is less common but still possible.
Risk Factors That Set the Stage
Leg ulcers rarely appear in otherwise healthy people. A large study of 1,000 patients with chronic leg ulcers found that more than half had high blood pressure, 45% had obesity, 27% had type 2 diabetes, and about 24% had high cholesterol. Nearly one in five met the criteria for metabolic syndrome, meaning they had at least three of those conditions simultaneously. Each of these conditions damages blood vessels in its own way, and together they accelerate the process dramatically.
Obesity plays a particularly outsized role. It increases pressure in the leg veins, promotes inflammation, reduces physical activity (which normally helps pump blood back up the legs), and can cause lymphatic congestion. In the same study, over 90% of patients with lymphedema-related ulcers were also obese. A history of deep vein thrombosis (blood clots in the leg veins) is another major risk factor, since clots directly damage the vein valves and set up the conditions for venous pooling.
Early Warning Signs Before a Wound Opens
Leg ulcers give warning signs, often for months or years before the skin actually breaks. Recognizing these signs is the best opportunity to intervene before an open wound develops.
- Skin discoloration: A brownish or reddish-brown tint around the ankles, caused by iron deposits from leaking blood cells. This is one of the earliest visible signs of venous disease.
- Persistent swelling: Ankles that swell daily and don’t fully return to normal overnight suggest the venous or lymphatic system is struggling.
- Skin texture changes: The skin may become dry, itchy, flaky (venous eczema), or gradually harden into a tight, woody texture.
- Leg pain or heaviness: Aching that worsens with standing and improves with elevation points to venous insufficiency. Pain that worsens with walking and improves with rest suggests arterial disease.
- Shiny, hairless skin on the lower legs: This signals poor arterial circulation and typically appears on the feet and shins.
These changes represent skin that is already compromised. At this point, the tissue has reduced oxygen supply, weakened structural integrity, and an impaired ability to repair itself. A minor injury that would heal in days on healthy skin can become a chronic wound that persists for months or years.
Why These Wounds Don’t Heal on Their Own
What makes leg ulcers different from ordinary wounds is that the underlying cause keeps working against the healing process. In venous ulcers, the sustained inflammation breaks down new tissue as fast as the body can build it. Inflammatory cells that should transition from a “destroy damaged tissue” mode to a “rebuild” mode get stuck in the destructive phase. The proteins responsible for dissolving old tissue remain overactive, chewing through the scaffolding that new skin cells need to grow across the wound.
In arterial ulcers, the tissue simply doesn’t receive enough blood to fuel the energy-intensive process of wound repair. And in diabetic ulcers, both impaired circulation and altered immune function combine to stall healing. This is why treating a leg ulcer requires addressing the root cause, not just the wound itself. Compression therapy restores healthier blood flow in venous disease. Procedures to open blocked arteries restore oxygen delivery in arterial disease. Blood sugar management and pressure offloading protect diabetic wounds. Without correcting what started the process, the ulcer will persist or recur even after it closes.