The ulcer has punched-out appearance. It is intensely painful. It has gray or yellow fibrotic base and undermining skin margins. Pulses are not palpable. Associated skin changes may be observed, such as thin shiny skin and absence of hair. They are most common on distal ends of limbs. A special type of ischemic ulcer developing in duodenum after severe burns is called Curling's ulcer.

Arterial insufficiency ulcers (also known as Ischemic ulcers or Ischemic wounds) are mostly located on the lateral surface of the ankle or the distal digits. They are commonly caused by peripheral artery disease (PAD).

A venous ulcer tends to occur on the medial side of the leg, typically around the medial malleolus in the 'gaiter area' whereas arterial ulcer tends to occur on lateral side of the leg and over bony prominences. A venous ulcer is typically shallow with irregular sloping edges whereas an arterial ulcer can be deep and has a 'punched out' appearance. Venous ulcers are typically 'wet' with a moderate to heavy exudate whereas. Arterial ulcers are typically 'dry' and scabbed. The skin surrounding a venous ulcer may be edematous (swollen) and there may be evidence of varicose veins; the skin surrounding an arterial ulcer may be pale, cold, shiny and hairless. Both venous and arterial ulcers may be painful, however arterial ulcers tend to be more painful, especially with elevation of the leg, for example when in bed.

Venous ulcers (venous insufficiency ulceration, stasis ulcers, stasis dermatitis, varicose ulcers, or ulcus cruris) are wounds that are thought to occur due to improper functioning of venous valves, usually of the legs (hence leg ulcers). They are the major occurrence of chronic wounds, occurring in 70% to 90% of leg ulcer cases. Venous ulcers develop mostly along the medial distal leg, and can be very painful with significant effects on quality of life.

The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisor Panel (NPUAP) in the United States and the European Pressure Ulcer Advisor Panel (EPUAP) in Europe. Briefly, they are as follows:

- Stage 1: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area differs in characteristics such as thickness and temperature as compared to adjacent tissue. Stage 1 may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons (a heralding sign of risk).

- Stage 2: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation.

- Stage 3: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Bone/tendon is not visible or directly palpable.

- Stage 4: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling. The depth of a stage 4 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Stage 4 ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis likely to occur. Exposed bone/tendon is visible or directly palpable. In 2012, the NPUAP stated that pressure ulcers with exposed cartilage are also classified as a stage 4.

- Unstageable: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels is normally protective and should not be removed.

- Suspected Deep Tissue Injury: A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. A deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

Signs and symptoms of PTS in the leg may include:

- pain (aching or cramping)

- heaviness

- itching or tingling

- swelling (edema)

- varicose veins

- brownish or reddish skin discoloration

- ulcer

These signs and symptoms may vary among patients and over time. With PTS, these symptoms typically are worse after walking or standing for long periods of time and improve with resting or elevating the leg.

PTS lowers a person's quality of life after DVT, specifically with regards to physical and psychological symptoms and limitations in daily activities.

Skin ulcers appear as open craters, often round, with layers of skin that have eroded. The skin around the ulcer may be red, swollen, and tender. Patients may feel pain on the skin around the ulcer, and fluid may ooze from the ulcer. In some cases, ulcers can bleed and, rarely, patients experience fever. Ulcers sometimes seem not to heal; healing, if it does occur, tends to be slow. Ulcers that heal within 12 weeks are usually classified as acute, and longer-lasting ones as chronic.

Ulcers develop in stages. In stage 1 the skin is red with soft underlying tissue. In the second stage the redness of the skin becomes more pronounced, swelling appears, and there may be some blisters and loss of outer skin layers. During the next stage, the skin may become necrotic down through the deep layers of skin, and the fat beneath the skin may become exposed and visible. In stage 4, deeper necrosis usually occurs, the fat underneath the skin is completely exposed, and the muscle may also become exposed. In the last two stages the sore may cause a deeper loss of fat and necrosis of the muscle; in severe cases it can extend down to bone level, destruction of the bone may begin, and there may be sepsis of joints.

Chronic ulcers may be painful. Most patients complain of constant pain at night and during the day. Chronic ulcer symptoms usually include increasing pain, friable granulation tissue, foul odour, and wound breakdown instead of healing. Symptoms tend to worsen once the wound has become infected.

Venous skin ulcers that may appear on the lower leg, above the calf or on the lower ankle usually cause achy and swollen legs. If these ulcers become infected they may develop an unpleasant odour, increased tenderness and redness. Before the ulcer establishes definitively, there may be a dark red or purple skin over the affected area as well as a thickening, drying, and itchy skin.

Although skin ulcers do not seem of great concern at a first glance, they are worrying conditions especially in people suffering from diabetes, as they are at risk of developing diabetic neuropathy.

Ulcers may also appear on the cheeks, soft palate, the tongue, and on the inside of the lower lip. These ulcers usually last from 7 to 14 days and can be painful.

Signs and symptoms of CVI in the leg include the following:

- Varicose veins

- Itching (pruritus)

- Hyperpigmentation

- Phlebetic lymphedema

- Chronic swelling of the legs and ankles

- Venous ulceration

CVI in the leg may cause the following:

- Venous stasis

- Ulcers.

- Stasis dermatitis, also known as varicose eczema

- Contact dermatitis. Patients with venous insufficiency have a disrupted epidermal barrier, making them more susceptible than the general population to contact sensitization and subsequent dermatitis.

- Atrophie blanche. This is an end point of a variety of conditions, appears as atrophic plaques of ivory white skin with telangiectasias. It represents late sequelae of lipodermatosclerosis where the skin has lost its nutrient blood flow.

- Lipodermatosclerosis. This is an indurated plaque in the medial malleolus.

- Malignancy. Malignant degeneration is a rare but important complication of venous disease since tumors which develop in the setting of an ulcer tend to be more aggressive.

- Pain. Pain is a feature of venous disease often overlooked and commonly undertreated.

- Anxiety.

- Depression.

- Inflammation

- Discoloration

- Skin thickening

- Cellulitis

These ulcers have punched-out edge and slough in floor, resembling gummatous ulcer. Surrounding area might have loss of sensation.

Different types of discharges from ulcer are:

- Serous, usually seen in healing ulcer

- Purulent, seen in infected ulcer. Yellow creamy discharge is observed in staphylococcal infection; bloody opalescent discharge in streptococcal infection, while greenish discharge is seen in pseudomonas ulcer

- Bloody (sanguineous), usually seen in malignant ulcers and in healing ulcers with healthy granulation tissue

- Seropurulent

- Serosanguinous

- Serous with sulphur granules, seen in actinomycosis

- Yellowish, as seen in tuberculous ulcer

Pressure ulcers, also known as pressure sores, pressure injuries, bedsores, and decubitus ulcers, are localized damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of pressure, or pressure in combination with shear and/or friction. The most common sites are the skin overlying the sacrum, coccyx, heels or the hips, but other sites such as the elbows, knees, ankles, back of shoulders, or the back of the cranium can be affected.

Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. Shear is also a cause, as it can pull on blood vessels that feed the skin. Pressure ulcers most commonly develop in individuals who are not moving about, such as those being bedridden or confined to a wheelchair. It is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development.

These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis, diabetes or infection), smoking or medications such as anti-inflammatory drugs.

Although often prevented and treatable if detected early, pressure ulcers can be very difficult to prevent in critically ill people, frail elders, and individuals with impaired mobility such as wheelchair users (especially where spinal injury is involved). Primary prevention is to redistribute pressure by regularly turning the person. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the person in the bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is very important.

The rate of pressure ulcers in hospital settings is high; the prevalence in European hospitals ranges from 8.3% to 23% and 26% in Canadian healthcare settings. In 2013, there were 29,000 documented deaths globally, up from 14,000 deaths in 1990.

Stasis dermatitis refers to the skin changes that occur in the leg as a result of "stasis" or blood pooling from insufficient venous return; the alternative name of varicose eczema comes from a common cause of this being varicose veins.

Insufficient venous return results in increased pressure in the capillaries with the result that both fluid and cells may "leak" out of the capillaries. This results in red cells breaking down, with iron containing hemosiderin possibly contributing to the pathology of this entity.

The cracks and poor skin-condition of this disorder predisposes for the entry of bacterial infection causing spreading cellulitis infection in the leg. If the skin condition deteriorates further and breaks down, a venous ulcer (also known as a stasis ulcer) may form.

Diabetic foot ulcer is a complication of diabetes. Diabetic foot ulcers are classified as either neuropathic, neuroischaemic or ischaemic.

Assessment of diabetic foot ulcer includes identifying risk factors such as diabetic peripheral neuropathy, noting that 50 percent of people are asymptomatic, and ruling out other causes of peripheral neuropathy such as alcohol abuse and spinal injury.

The location of the ulcer, its size, shape, depth and whether the tissue is granulating or sloughy needs to be considered. Further considerations include whether the there is malodour, condition of the border of the wound and palpable bone and sinus formation should be investigated. Signs of infection require to be considered such as development of grey or yellow tissue, purulent discharge, unpleasant smell, sinus, undermined edges and exposure of bone or tendon.

Identification of diabetic foot in medical databases, such as commercial claims and prescription data, is complicated by the lack of a specific ICD-9 code for diabetic foot and variation in coding practices. The following codes indicate ulcer of the lower limb or foot:

- 707.1 Ulcer of lower limbs, except pressure ulcer

- 707.14 Ulcer of heel and midfoot

- 707.15 Ulcer of other part of foot

- 707.19 Ulcer of other part of lower limb

One or more codes, in combination with a current or prior diagnosis of diabetes may be sufficient to conclude diabetic foot:

- 250.0 Diabetes Mellitus

- 250.8 Diabetes with other specified manifestations

Malum perforans (also known as neurotrophic ulcer and trophic ulcer) is a long-lasting, usually painless ulcer that penetrates deep into or through the skin, usually on the sole of the foot (in which case it may be called malum perforans pedis). It is often a complication in diabetes mellitus and other conditions affecting the nerves.

The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage.

Most varicose veins are reasonably benign, but severe varicosities can lead to major complications, due to the poor circulation through the affected limb.

- Pain, tenderness, heaviness, inability to walk or stand for long hours, thus hindering work

- Skin conditions / dermatitis which could predispose skin loss

- Skin ulcers especially near the ankle, usually referred to as venous ulcers.

- Development of carcinoma or sarcoma in longstanding venous ulcers. Over 100 reported cases of malignant transformation have been reported at a rate reported as 0.4% to 1%.

- Severe bleeding from minor trauma, of particular concern in the elderly.

- Blood clotting within affected veins, termed superficial thrombophlebitis. These are frequently isolated to the superficial veins, but can extend into deep veins, becoming a more serious problem.

- Acute fat necrosis can occur, especially at the ankle of overweight people with varicose veins. Females are more frequently affected than males.

Chronic venous insufficiency (CVI) is a medical condition in which blood pools in the veins, straining the walls of the vein. The most common cause of CVI is superficial venous reflux which is a treatable condition. As functional venous valves are required to provide for efficient blood return from the lower extremities, this condition typically affects the legs. If the impaired vein function causes significant symptoms, such as swelling and ulcer formation, it is referred to as chronic venous disease. It is sometimes called "chronic peripheral venous insufficiency" and should not be confused with post-thrombotic syndrome in which the deep veins have been damaged by previous deep vein thrombosis.

Most cases of CVI can be improved with treatments to the superficial venous system or stenting the deep system. Varicose veins for example can now be treated by local anesthetic endovenous surgery.

The prevalence of CVI is far higher in women than in men. The Tampere study, which examined the epidemiology of varicose veins in a large cohort of 3284 men and 3590 women, demonstrated that the prevalence of varicose veins in men and women was 18% and 42%, respectively. The condition has been known since ancient times and Hippocrates used bandaging to treat it.

Post-thrombotic syndrome (PTS), also called postphlebitic syndrome and venous stress disorder is a medical condition that may occur as a long-term complication of deep vein thrombosis (DVT).

Curling's ulcer (stress ulcer) or a Curling ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The condition was first described in 1823 and named for a doctor, Thomas Blizard Curling, who observed ten such patients in 1842.

These stress ulcers (actually shallow multiple erosions) were once a common complication of serious burns, presenting in over 10% of cases, and especially common in child burn victims. They result in perforation and hemorrhage more often than other forms of intestinal ulceration and had correspondingly high mortality rates (at least 80%).

A similar condition involving elevated intracranial pressure is known as Cushing's ulcer.

A stress ulcer is a single or multiple mucosal defect which can become complicated by upper gastrointestinal bleeding during the physiologic stress of serious illness. Ordinary peptic ulcers are found commonly in the gastric antrum and the duodenum whereas stress ulcers are found commonly in fundic mucosa and can be located anywhere within the stomach and proximal duodenum.

Up to 50% of people with PAD may have no symptoms. Symptoms of PAD in the legs and feet are generally divided into 2 categories:

1. Intermittent claudication—pain in muscles when walking or using the affected muscles that is relieved by resting those muscles. This is due to the unmet oxygen demand in muscles with use in the setting of inadequate blood flow.

2. Critical limb ischemia, consisting of:

Medical signs of PAD in the legs, due to inadequate perfusion, include:

- Noticeable change in color – blueness, or in temperature (coolness) when compared to the other limb.

- Buerger's test can check for pallor on elevation of limb and redness (rubor) on a change to a sitting position, in an assessment of arterial sufficiency.

- Diminished hair and nail growth on affected limb and digits

PAD in other parts of the body depends on the organ affected. Renal artery stenosis can cause renovascular hypertension.

Carotid artery disease can cause strokes and transient ischemic attacks.

The mean age at presentation is thirty-seven years with a reported range of nineteen to sixty-four years. The mean age of onset since diagnosis of diabetes is fifteen years. The female:male ratio is 1.3:1. Other diabetic complications such as nephropathy, neuropathy, retinopathy and hypertension are usually present. Its major symptom is the acute onset muscle pain, usually in the thigh, in the absence of trauma. Signs include exquisite muscle tenderness and swelling.

Varicose veins are veins that have become enlarged and twisted. The term commonly refers to the veins on the leg, although varicose veins can occur elsewhere. Veins have pairs of leaflet valves to prevent blood from flowing backwards (retrograde flow or venous reflux). Leg muscles pump the veins to return blood to the heart (the skeletal-muscle pump), against the effects of gravity. When veins become varicose, the leaflets of the valves no longer meet properly, and the valves do not work (valvular incompetence). This allows blood to flow backwards and they enlarge even more. Varicose veins are most common in the superficial veins of the legs, which are subject to high pressure when standing. Besides being a cosmetic problem, varicose veins can be painful, especially when standing. Severe long-standing varicose veins can lead to leg swelling, venous eczema, skin thickening (lipodermatosclerosis) and ulceration. Although life-threatening complications are uncommon, varicose veins may be confused with deep vein thrombosis, which may be life-threatening.

Non-surgical treatments include sclerotherapy, elastic stockings, leg elevation and exercise. The traditional surgical treatment has been vein stripping to remove the affected veins. Newer, less invasive treatments which seal the main leaking vein are available. Alternative techniques, such as ultrasound-guided foam sclerotherapy, radiofrequency ablation and endovenous laser treatment, are available as well. Because most of the blood in the legs is returned by the deep veins, the superficial veins, which return only about 10% of the total blood of the legs, can usually be removed or ablated without serious harm.

Secondary varicose veins are those developing as collateral pathways, typically after stenosis or occlusion of the deep veins, a common sequel of extensive deep venous thrombosis (DVT). Treatment options are usually support stockings, occasionally sclerotherapy and rarely, limited surgery.

Varicose veins are distinguished from reticular veins (blue veins) and telangiectasias (spider veins), which also involve valvular insufficiency, by the size and location of the veins. Many patients who suffer with varicose veins seek out the assistance of physicians who specialize in vein care or peripheral vascular disease. These physicians include vascular surgeons, phlebologists or interventional radiologists.