Intrauterine epidermal necrosis is a cutaneous condition that is rapidly fatal, characterized by skin erosions and ulcerations only.

Although the exact cause of this condition is not known, it is an inflammatory disorder characterised by collagen degeneration, combined with a granulomatous response. It always involves the dermis diffusely, and sometimes also involves the deeper fat layer. Commonly, dermal blood vessels are thickened (microangiopathy).

It can be precipitated by local trauma, though it often occurs without any injury.

NL/NLD most frequently appears on the patient's shins, often on both legs, although it may also occur on forearms, hands, trunk, and, rarely, nipple, penis, and surgical sites. The lesions are often asymptomatic but may become tender and ulcerate when injured. The first symptom of NL is often a "bruised" appearance (erythema) that is not necessarily associated with a known injury. The extent to which NL is inherited is unknown.

NLD appears as a hardened, raised area of the skin. The center of the affected area usually has a yellowish tint while the area surrounding it is a dark pink. It is possible for the affected area to spread or turn into an open sore. When this happens the patient is at greater risk of developing ulcers. If an injury to the skin occurs on the affected area, it may not heal properly or it will leave a dark scar.

Dermatitis gangrenosa (also known as "Gangrene of the skin") is a cutaneous condition caused by infection by Clostridium resulting in a necrosis and sloughing of the skin.

A recent retrospective study of all cases of Ecthyma gangrenosum from 2004-2010 in a university hospital in Mexico shows that neutropenia in immunocompromised patients is the most common risk factor for ecthyma gangrenosum.

The cause of NME is unknown, although various mechanisms have been suggested. These include hyperglucagonemia, zinc deficiency, fatty acid deficiency, hypoaminoacidemia, and liver disease. The pathogenesis is also unknown.

The reason for its occurrence is unknown. Investigations have suspected that obesity and preceding psoriatic lesions cause local lymphatic disturbances, followed by the development of stasis papillomatosis. On the other hand, genetic or environmental factors may play a role. Some investigators have speculated that it represents an allergic response to an epidermal protein antigen created through increased hydrostatic pressure, whereas others believe that the skin has been compromised and is more susceptible to irritation and trauma.

The age is an important factor, because as some people get older the veins which carry blood from the legs back to the heart do not work as well as they use to. This causes fluid to settle in the lower legs.

The most important cause of this condition is insufficient lymphatic drainage, causing soft tissue swelling due to fluid accumulation. Obstruction of lymphatic tissue causes increased intravascular tissue protein; this will increase the production of fibroblasts and mast cells. Lymphatic obstruction due to any cause can increase the amount of proteins in the intravascular tissue, either by root osmotic pressure, or because it absorbs a little liquid. The further roteins increase the vascular fluid, fibroblasts and promote the ploriferation of mast cells which produce the clinical symptoms of nonpitting edema. The epidermis may be hyperkeratotic and warty and this predisposes to tissue cracks and allows secondary infection.

William Becker first described an association between NME and glucagonoma in 1942 and since then, NME has been described in as many as 70% of individuals with a glucagonoma. NME is considered part of the glucagonoma syndrome, which is associated with hyperglucagonemia, diabetes mellitus, and hypoaminoacidemia.

When NME is identified in the absence of a glucagonoma, it may be considered "pseudoglucagonoma syndrome". Less common than NME with glucagonoma, pseudoglucagonoma syndrome may occur in a number of systemic disorders:

- Celiac disease

- Ulcerative colitis

- Crohn's disease

- Hepatic cirrhosis

- Hepatocellular carcinoma

- Lung cancer, including small cell lung cancer

- Tumors that secrete insulin- or insulin-like growth factor 2

- Duodenal cancer

The exact cause of lipodermatosclerosis is unknown. Venous disease, such as venous incompetence, venous hypertension, and body mass ("obesity") may be relevant to the underlying pathogenesis.

Increased blood pressure in the veins (venous hypertension) can cause diffusion of substances, including fibrin, out of capillaries. Fibrotic tissue may predispose the tissue to ulceration. Recurrent ulceration and fat necrosis is associated with lipodermatosclerosis. In advanced lipodermatosclerosis the proximal leg swells from chronic venous obstruction and the lower leg shrinks from chronic ulceration and fat necrosis resulting in the inverted coke bottle appearance of the lower leg.

Lipodermatosclerosis is most commonly diagnosed in middle-aged women.

The origin of lipodermatosclerosis is probably multifactorial, involving tissue hypoxia, leakage of proteins into the interstitium, and leukocyte activation. Studies of patients with lipodermatosclerosis have demonstrated significantly decreased concentrations of cutaneous oxygen associated with decreased capillary density. Capillaries are virtually absent in areas of fibrotic scars, leading to a condition known as atrophie blanche or livedoid vasculopathy.

Sclerema neonatorum is a rare and severe skin condition that is characterized by diffuse hardening of the subcutaneous tissue with minimal inflammation. It usually affects premature, ill newborns. Prognosis is poor.

Minimal inflammation helps distinguish sclerema neonaturum from subcutaneous fat necrosis of the newborn.

The overwhelming majority of neutrophilic eccrine hidradenitis (NEH) is seen in people with cancer, especially leukaemia, who receive chemotherapy with a cytotoxic drug. These include: Bleomycin, chlorambucil, cyclophosphamide, cytarabine, doxorubicin, lomustine, mitoxantrone, topotecan, and vincristine.

NEH was first described in 1982 in a patient with acute myeloid leukaemia (AML) who had received cytarabine as chemotherapy.

Cancer itself, infections, and other medicinal drugs also can lead to NEH. NEH has been reported in patients with cancer who have not received any form of chemotherapy (i.e., as a paraneoplastic syndrome), in patients with HIV and/or AIDS, and after the use of paracetamol (acetaminophen). Also the use of targeted agents can lead to NEH, e.g. imatinib, a tyrosine kinase inhibitor.

NEH has also been described without any known reason (idiopathic cases), including idiopathic cases in children.

The exact cause of NEH is unknown. In patients receiving chemotherapy, it has been postulated that a high concentration of the cytotoxic drug in sweat has a direct toxic effect on the eccrine glands.

This disease is caused by problems in the circulatory system, so when it is presented, in the beginning it is important to follow several recommendations. The person needs to keep the legs elevated as much as possible to help the return of the blood. Whenever sitting down, the person needs to keep the legs on a foot stool. At night it is advisable to sleep with a pillow under the lower legs. In the evening, t is not unusual for legs to be swollen. The volume of the lower leg can increase to up to 100ml after a long working day or up to 200ml after a long-haul flight without moving.

In the example of the 41-year-old Japanese man the lesions were much improved by washing and topical use of corticosteroids for two months, also oral antibiotics like cephalexin are used if cellulitis is present. Moist exudative inflammation and moist ulcers respond to tepid wet compresses of Burow’s solution or just saline or water for 30 to 60 minutes several times a day. But in worse cases, edema that does not disappear spontaneously within a few hours or after a walk, is described as pathological, so it needs to have a special treatment. It is very important to say that Papillamitosis, bilateral and marked edema with few symptoms is mostly caused by the systemic circulation (heart, kidneys, liver).

Papillamitosis is associated, as has been mentioned before, with symptoms and/or clinical signs such as dilated superficial veins, varicose veins and changes in the skin. Edema and its complication Papillamitosis are only partially reversible and soon becomes hard, which is mainly confirmed on palpation. All skin structures are affected and this is characterized by the term. Lymphoedema may develop in many cases accompanied by acral thickening of the skin folds, hyperkeratosis and papillomatosis.

The organism enters directly through the breakdown of mechanical defense barriers such as mucosa or skin. Immunocompromised conditions make the patient more susceptible to this infection and septicemia. In case of septicemia, the bacteria reaches the skin via the bloodstream. Defective humoral or cellular immune system increases the risk because the organism is not able to be cleared from the bloodstream. The main mechanism of the organism that is causing the typical skin lesions is the invasion of the organism into the arteries and veins in the dermis and subcutaneous tissues of the skin. This perivascular invasion leads to nodular formation, ulceration, vasculitis and necrosis due to impaired blood supply. Perivascular involvement is achieved by direct entry of bacteria through the skin or hematogenous spreading in case of sepsis.

Alpha-1 antitrypsin deficiency panniculitis is a panniculitis associated with a deficiency of the α-antitrypsin enzyme.

Lipodermatosclerosis (also known as "chronic panniculitis with lipomembranous changes", "hypodermitis sclerodermiformis", "sclerosing panniculitis", and "stasis panniculitis") is a skin and connective tissue disease. It is a form of lower extremity panniculitis, an inflammation of the layer of fat under the epidermis.

The wounds from which ulcers arise can be caused by a wide variety of factors, but the main cause is impaired blood circulation. Especially, chronic wounds and ulcers are caused by poor circulation, either through cardiovascular issues or external pressure from a bed or a wheelchair. A very common and dangerous type of skin ulcers are caused by what are called pressure-sensitive sores, more commonly called bed sores and which are frequent in people who are bedridden or who use wheelchairs for long periods. Other causes producing skin ulcers include bacterial or viral infections, fungal infections and cancers. Blood disorders and chronic wounds can result in skin ulcers as well.

Venous leg ulcers due to impaired circulation or a blood flow disorder are more common in the elderly.

The mortality for toxic epidermal necrolysis is 25-30%. People with SJS or TEN caused by a medications have a better prognosis the earlier the causative medication is withdrawn. Loss of the skin leaves patients vulnerable to infections from fungi and bacteria, and can result in sepsis, the leading cause of death in the disease. Death is caused either by infection or by respiratory distress which is either due to pneumonia or damage to the linings of the airway. Microscopic analysis of tissue (especially the degree of dermal mononuclear inflammation and the degree of inflammation in general) can play a role in determining the prognosis of individual cases.

Calciphylaxis most commonly occurs in patients with end-stage renal disease who are on hemodialysis or who have recently received a renal (kidney) transplant. Yet calciphylaxis does not occur only in end-stage renal disease patients. When reported in patients without end-stage renal disease, it is called non-uremic calciphylaxis by Nigwekar et al. Non-uremic calciphylaxis has been observed in patients with primary hyperparathyroidism, breast cancer (treated with chemotherapy), liver cirrhosis (due to alcohol abuse), cholangiocarcinoma, Crohn's disease, rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE).

Lipodermatosclerosis is a form of panniculitis associated with chronic venous insufficiency that presents with brown indurations on the front of the shins. It may be associated with pain and other signs of chronic venous insufficiency. The exact cause is unknown.

Other forms include:

- Subcutaneous fat necrosis of the newborn, a form of panniculitis occurring in newborns that is usually self-resolving, that may be a result of hypoxic injury to relatively high levels of brown fat.

- Sclerema neonatorum, affecting premature births.

- Weber–Christian disease, a symmetrical form of the disease of unknown origin occurring in middle-aged women.

- Lupus erythematosus panniculitis, panniculitis associated with lupus erythematosus.

- Forms associated with use of high doses of systemic corticosteroids during rapid corticosteroid withdrawal, and from the injection of silicone or mineral oils.

Cutaneous vasculitis can have various causes including but not limited to medications, bacterial and viral infections or allergens. It is estimated that 45-55% of cases are idiopathic, meaning the cause is unknown. In cases where a cause can be determined, medications and infectious pathogens are most common in adults, while IgA vasculitis (Henoch-Schönlein purpura) frequently affects children. Other etiologies include autoimmune conditions and malignancies, usually hematologic (related to the blood).

The small vessels in the skin affected are located in the superficial dermis and include arterioles (small arteries carrying blood to capillaries), capillaries, and venules (small veins receiving blood from capillaries). In general, immune complexes deposit in vessel walls leading to activation of the complement system. C3a and C5a, proteins produced from the complement system, attract neutrophils to the vessels. Once activated, neutrophils then release preformed substances, including enzymes causing damage to vessel tissue. Evidence of this process can be seen with a sample of removed skin tissue, or biopsy, viewed under a microscope. Neutrophils are seen surrounding blood vessels and their debris within vessel walls, causing fibrinoid necrosis. This finding on histological examination is termed “leukocytoclastic vasculitis”.

Considering the wide range of potential causes leading to cutaneous small vessel vasculitis, there are subtle variations in the underlying pathophysiology for each cause. For example, medications are metabolized to smaller molecules that can attach to proteins in the blood or vessel walls. The immune system senses these altered proteins as foreign and produces antibodies in efforts to eliminate them from the body. A similar process occurs with infectious agents, such as bacteria, in which antibodies target microbial components.

Cutaneous small-vessel vasculitis, also known as hypersensitivity vasculitis, cutaneous leukocytoclastic vasculitis, hypersensitivity angiitis, cutaneous leukocytoclastic angiitis, cutaneous necrotizing vasculitis and cutaneous necrotizing venulitis, is inflammation of small blood vessels (usually post-capillary venules in the dermis), characterized by palpable purpura. It is the most common vasculitis seen in clinical practice.

"Leukocytoclastic" refers to the damage caused by nuclear debris from infiltrating neutrophils in and around the vessels.

OFG is uncommon, but the incidence is increasing. The disease usually presents in adolescence or young adulthood. It may occur in either sex, but males are slightly more commonly affected.

Neutrophilic eccrine hidradenitis (NEH) usually is a cutaneous complication of chemotherapy, but it can also occur for other reasons. It consists of fever and non specific skin lesions. It is rare, and self-limited.

While recent case series (n=9-80) studies have found a mortality rate of 20-40%, a large (n=1641) 2009 study reported a mortality rate of 7.5%.

More than 70% of cases are recorded in people with at least one of the following clinical situations: immunosuppression, diabetes, alcoholism/drug abuse/smoking, malignancies, and chronic systemic diseases. For reasons that are unclear, it occasionally occurs in people with an apparently normal general condition.

The infection begins locally at a site of trauma, which may be severe (such as the result of surgery), minor, or even non-apparent.