An eschar (; Greek: "eschara") is a slough or piece of dead tissue that is cast off from the surface of the skin, particularly after a burn injury, but also seen in gangrene, ulcer, fungal infections, necrotizing spider bite wounds, spotted fevers and exposure to cutaneous anthrax. The term "eschar" is not interchangeable with "scab". An eschar contains necrotic tissue, whereas a scab is composed of dried blood and exudate.

Black eschars are most commonly attributed to anthrax, which may be contracted through herd animal exposure, but can also be obtained from "Pasteurella multocida" exposure in cats and rabbits. A newly identified human rickettsial infection, "R. parkeri" rickettsiosis, can be differentiated from Rocky Mountain spotted fever by the presence of an eschar at the site of inoculation.

Eschar is sometimes called a "black wound" because the wound is covered with thick, dry, black necrotic tissue.

Eschar may be allowed to slough off naturally, or it may require surgical removal (debridement) to prevent infection, especially in immunocompromised patients (e.g. if a skin graft is to be conducted).

If eschar is on a limb, it is important to assess peripheral pulses of the affected limb to make sure blood and lymphatic circulation is not compromised. If circulation is compromised, an escharotomy, or surgical incision through the eschar, may be indicated.

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.

The primary skin lesion usually starts with a macule that is painless, round and erythematous. Then, it develops into a pustule, and then a bulla with central hemorrhagic focus. The bullae progresses into an ulcer which extends laterally. Finally it becomes a gangrenous ulcer with central black eschar surrounded by erythematous halo.

The lesion may be single or multiple. They are most commonly seen in perineum and under arm pit. However, it can occur in any part of the body.

Pressure ulcers can trigger other ailments, cause considerable suffering, and can be expensive to treat. Some complications include autonomic dysreflexia, bladder distension, bone infection, pyarthroses, sepsis, amyloidosis, anemia, urethral fistula, gangrene and very rarely malignant transformation (Marjolin's ulcer - secondary carcinomas in chronic wounds). Sores may recur if those with pressure ulcers do not follow recommended treatment or may instead develop seromas, hematomas, infections, or wound dehiscence. Paralyzed individuals are the most likely to have pressure sores recur. In some cases, complications from pressure sores can be life-threatening. The most common causes of fatality stem from kidney failure and amyloidosis.

Pressure ulcers are also painful, with individuals of all ages and all stages of pressure ulcers reporting pain.

Ecthyma gangrenosum is a type of skin lesion characterized by vesicles or blisters which rapidly evolve into pustules and necrotic ulcers with undermined tender erythematous border. "Ecthyma" means a pus forming infection of the skin with an ulcer, "gangrenosum" means the gangrene or necrosis. It is the pathognomonic of "Pseudomonas aeruginosa" bacteremia. "Pseudomonas aeruginosa" is a gram negative, aerobic, coccobacillus bacterium.

This type of skin lesion was first described in association with "Pseudomonas aeruginosa" by L. Barker in 1897. It was given the name "ecthyma gangrenosum" by Hitschmann and Kreibich.

It mostly occurs in patients with underlying immunocompromised conditions (e.g. Malignancy). Although most cases are found in "Pseudomonas aeruginosa" infection, there are recent reports of this skin lesion associated with other microorganisms, such as "Escherichia coli, Citrobacter freundii, Klebsiella pneumonia", various other Pseudomonas species, and "Morganella morganii."

An escharotic is a substance that causes tissue to die and slough off. Examples include acids, alkalis, carbon dioxide, metallic salts and sanguinarine, as well as certain medicines like imiquimod. Escharotics known as black salves, containing ingredients such as zinc chloride and sanguinarine containing bloodroot extracts, were traditionally used in herbal medicine as topical treatments for localised skin cancers, but often cause scarring and can potentially cause serious injury and disfigurement. Consequently, escharotic salves are very strictly regulated in most western countries and while some prescription medicines are available with this effect, unauthorized sales are illegal. Some prosecutions have been pursued over unlicensed sales of escharotic products such as Cansema.

Warfarin-induced skin necrosis (or, more generally, Anticoagulant-induced skin necrosis) is a condition in which skin and subcutaneous tissue necrosis (tissue death) occurs due to acquired protein C deficiency following treatment with anti-vitamin K anticoagulants (4-hydroxycoumarins, such as warfarin).

Warfarin necrosis is a rare but severe complication of treatment with warfarin or related anticoagulants. The typical patient appears to be an obese, middle aged woman (median age 54 years, male to female ratio 1:3). This drug eruption usually occurs between the third and tenth days of therapy with warfarin derivatives. The first symptoms are pain and redness in the affected area. As they progress, lesions develop a sharp border and become petechial, then hard and purpuric. They may then resolve or progress to form large, irregular, bloody bullae with eventual necrosis and slow-healing eschar formation. Favored sites are breasts, thighs, buttocks and penis, all areas with subcutaneous fat. In rare cases, the fascia and muscle are involved.

Development of the syndrome is associated with the use of large loading doses at the start of treatment.

The first skin changes in calciphylaxis lesions are mottling of the skin and induration in a livedo reticularis pattern. As tissue thrombosis and infarction occurs, a black, leathery eschar in an ulcer with adherent black slough are found. Surrounding the ulcers is usually a plate-like area of indurated skin. These lesions are always extremely painful and most often occur on the lower extremities, abdomen, buttocks, and penis. Because the tissue has infarcted, wound healing seldom occurs, and ulcers are more likely to become secondarily infected. Many cases of calciphylaxis end with systemic bacterial infection and death.

Calciphylaxis is characterized by the following histologic findings:

1. systemic medial calcification of the arteries, i.e. calcification of tunica media. Unlike other forms of vascular calcifications (e.g., intimal, medial, valvular), calciphylaxis is characterized also by

2. small vessel mural calcification with or without endovascular fibrosis, extravascular calcification and vascular thrombosis, leading to tissue ischemia (including skin ischemia and, hence, skin necrosis).

Many conditions mimic or may be mistaken for warfarin necrosis, including pyoderma gangrenosum or necrotizing fasciitis. Warfarin necrosis is also different from another drug eruption associated with warfarin, purple toe syndrome, which usually occurs three to eight weeks after the start of anticoagulation therapy. No report has described this disorder in the immediate postpartum period in patients with protein S deficiency.

Calciphylaxis, or calcific uremic arteriolopathy (CUA), is a syndrome of calcification of the blood vessels, blood clots, and skin necrosis. It is seen mostly in patients with stage 5 chronic kidney disease, but can occur in the absence of kidney failure. It results in chronic non-healing wounds and is usually fatal. Calciphylaxis is a rare but serious disease, believed to affect 1-4% of all dialysis patients.

Calciphylaxis is one type of extraskeletal calcification. Similar extraskeletal calcifications are observed in some patients with hypercalcemic states, including patients with milk-alkali syndrome, sarcoidosis, primary hyperparathyroidism, and hypervitaminosis D.

Respiratory infection in humans is relatively rare and presents as two stages. It infects the lymph nodes in the chest first, rather than the lungs themselves, a condition called hemorrhagic mediastinitis, causing bloody fluid to accumulate in the chest cavity, therefore causing shortness of breath. The first stage causes cold and flu-like symptoms. Symptoms include fever, shortness of breath, cough, fatigue, and chills. This can last hours to days. Often, many fatalities from inhalational anthrax are when the first stage is mistaken for the cold or flu and the victim does not seek treatment until the second stage, which is 90% fatal. The second (pneumonia) stage occurs when the infection spreads from the lymph nodes to the lungs. Symptoms of the second stage develop suddenly after hours or days of the first stage. Symptoms include high fever, extreme shortness of breath, shock, and rapid death within 48 hours in fatal cases. Historical mortality rates were over 85%, but when treated early (seen in the 2001 anthrax attacks), observed case fatality rate dropped to 45%. Distinguishing pulmonary anthrax from more common causes of respiratory illness is essential to avoiding delays in diagnosis and thereby improving outcomes. An algorithm for this purpose has been developed.

African tick bite fever is often asymptomatic or mild in clinical presentation and complications are rare. The onset of illness is typically 5–7 days after the tick bite, although in some cases it may take up to 10 days for symptoms to occur. Symptoms can persist for several days to up to three weeks. Common presenting symptoms include:

- Fever

- Headache

- Muscle aches

- Inoculation eschar, which is dead, often black, tissue around a bite site (see photo above)

- Eschars may or may not be present. "Amblyomma" ticks actively attack cattle or humans and can bite more than once. In African tick bite fever, unlike what is typically seen with other Rickettsial spotted fevers when only one eschar is identified, multiple eschars may be seen and are considered pathognomonic.

- Swollen lymph nodes near the site of the bite

- Maculopapular and/or vesicular rash

Signs and symptoms include fever, headache, muscle pain, cough, and gastrointestinal symptoms. More virulent strains of "O. tsutsugamushi" can cause hemorrhaging and intravascular coagulation. Morbilliform rash, eschar, splenomegaly, and lymphadenopathies are typical signs. Leukopenia and abnormal liver function tests are commonly seen in the early phase of the illness. Pneumonitis, encephalitis, and myocarditis occur in the late phase of illness.

Acute scrub typhus appears to improve viral loads in patients with HIV. This interaction is challenged by an "in vitro" study.

Cutaneous anthrax, also known as Hide porter's disease, is when anthrax occurs on the skin. It is the most common form (>90% of anthrax cases). Cutaneous anthrax is also the least dangerous form of anthrax (less than 1% mortality rate with treatment). Cutaneous anthrax presents as a boil-like skin lesion that eventually forms an ulcer with a black center (eschar). The black eschar often shows up as a large, painless, necrotic ulcer (beginning as an irritating and itchy skin lesion or blister that is dark and usually concentrated as a black dot, somewhat resembling bread mold) at the site of infection. In general, cutaneous infections form within the site of spore penetration between two and five days after exposure. Unlike bruises or most other lesions, cutaneous anthrax infections normally do not cause pain. Nearby lymph nodes may become infected, reddened, swollen, and painful. A scab forms over the lesion soon, and falls off in a few weeks. Complete recovery may take longer.

Cutaneous anthrax is typically caused when "B. anthracis" spores enter through cuts on the skin. This form is found most commonly when humans handle infected animals and/or animal products.

Cutaneous anthrax is rarely fatal if treated, because the infection area is limited to the skin, preventing the lethal factor, edema factor, and protective antigen from entering and destroying a vital organ. Without treatment, about 20% of cutaneous skin infection cases progress to toxemia and death.

Complications are rare and are not life-threatening. No deaths due to African tick bite fever have been reported. Reported complications include:

- Prolonged fever > 3 weeks in duration

- Reactive arthritis

- Moderate to severe headache

Scrub typhus or bush typhus is a form of typhus caused by the intracellular parasite "Orientia tsutsugamushi", a Gram-negative α-proteobacterium of family Rickettsiaceae first isolated and identified in 1930 in Japan.

Although the disease is similar in presentation to other forms of typhus, its pathogen is no longer included in genus "Rickettsia" with the typhus bacteria proper, but in "Orientia". The disease is thus frequently classified separately from the other typhi.