Chronic inflammation can cause long term lymphatic obstruction. Typically, patients have disorders that present local nodes, primary lymphedema and chronic venous insufficiency. Erysipelas and trauma are major risk factors. Lymphatic edema can be developed in many acral cases accompanied by a thickening of the folds of the skin, hyperkeratosis and papillomatosis. Chronic venous edema is only partially reversible and soon becomes hard, especially confirming tenderness. All structures of the skin are affected. Dilated dermal lymphatic vessels with consequent superior organization and fibrosis result in papillomatosis. As dermal lymphatic stasis progreses, these skin changes become more marked and known as elephantiasis. Occasionally, tissue fibrosis and thickening may become so marked in the later stages of lymphedema that pitting is absent. Recurrent cellulitis, erysipelas and dermato-LAM-adenitis are complications of chronic lymphedema.

Stasis papillomatosis is a disease characterized by chronic congestion of the extremities, with blood circulation interrupted in a specific area of the body. A consequence of this congestion and inflammation is long-term lymphatic obstruction. It is also typically characterized by the appearance of numerous papules. Injuries can range from small to large plates composed of brown or pink, smooth or hyperkeratotic papules. The most typical areas where injuries occur are the back of the feet, the toes, the legs, and the area around a venous ulcer formed in the extremities, although the latter is the rarest of all. These injuries include pachydermia (thickening of the skin), lymphedema, lymphomastic verrucusis and elephantosis verracosa. The disease can be either localized or generalized; the localized form makes up 78% of cases. Treatment includes surgical and pharmaceutical intervention; indications for partial removal include advanced fibrotic lymphedema and elephantiasis. Despite the existence of these treatments, chronic venous edema, which is a derivation of stasis papillomatosis, is only partially reversible. The skin is also affected and its partial removal may mean that the skin and the subcutaneous tissue are excised. A side effect of the procedure is the destruction of existing cutaneous lymphatic vessels. It also risks papillomatosis, skin necrosis and edema exacerbation.

All etiologies lead to local dermal lymphostasis pathogenesis. A maximum variation was observed after the resection of block subcutaneous tissue in patients suffering from congenital lymphedema. Signals that the current condition are different, either in the dermis or in the subcutaneous area. In dermis, principal signs found are precollectors initial nodes, injection tank, the reticular distribution, cutaneous reflexes, and lymphatic cysts. On other hand in the subcutaneous area principal signs are; collectors, thinning, ectatic, tortuous, rest offs, reflux dermal, sclerosis, calcifications.

Pain may be the first noticed symptom. People with lipodermatosclerosis have tapering of their legs above the ankles, forming a constricting band resembling an inverted champagne bottle. In addition, there may be brownish-red pigmentation and induration.

Acroangiodermatitis of Mali (also known as "Mali acroangiodermatitis" and "Pseudo-Kaposi's sarcoma") is a rare cutaneous condition often characterized by purplish-blue to brown papules and plaques on the medial and lateral malleolus of both legs.

Acroangiodermatitis is a rare skin condition characterised by hyperplasia of pre-existing vasculature due to venous hypertension from severe chronic venous stasis. It is associated with amputees, haemodialysis (HD) patients with arteriovenous (AV) shunts, and patients with paralysed legs, hepatitis C, chronic venous insufficiency or AV malformations (AVM). Patients present with itchy, painful, confluent, violaceous or brown-black macules, papules or plaques usually at the distal lower limbs. There may be ulceration and bleeding. The histologic features are capillary proliferation and perivascular inflammation involving eosinophils in the dermis with minimal epidermal changes. Management includes compression therapy, wound care and surgical correction of AVM. Dapsone combined with leg elevation and compression, and erythromycin for HD patients with AV fistulas have also been reported. The lesions may persist for years with complications like ulceration, bleeding and infection.

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.

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.

The clinical manifestation and presentation of symptoms of lymphedema develop following a significant degree of injury. Secondary lymphedema is the lymphadenectomy and lymphatic injury following surgery, radiation, chemotherapy, and/or trauma which healing or regeneration of damaged lymphatics may occur with variable success.

Symptoms will include swelling, edema, and pain from a multitude of secondary complications (pressure, musculoskeletal disorder from asymmetry, restricted blood flow). Most patients will avoid discussing pain for many reasons, so this will require logical thinking or communication skills to assess. In advanced lymphedema, there may be the presence of skin changes such as discoloration, verrucous (wart-like) hyperplasia, hyperkeratosis, papillomatosis, and Ulcer (dermatology).

Lymphedema should not be confused with edema arising from venous insufficiency, which is not lymphedema. In addition to a compressive local environment of lymphedematous extremity, long standing venous compression potentially contributed to an increased propensity for thrombosis due to vascular changes from longstanding venous hypertension from a proximal compression or simply from a change in blood flow. However, untreated venous insufficiency can progress into a combined venous/lymphatic disorder. Proper imaging can help identify where the dysfunction is in the system, and is essential in identifying the source before treatment is decided.

Presented here is an extreme case of severe unilateral hereditary lymphedema which had been present for 25 years without treatment:

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

Lymphedema affects approximately 140 million people worldwide.

Lymphedema may be inherited (primary) or caused by injury to the lymphatic vessels (secondary). It is most frequently seen after lymph node dissection, surgery and/or radiation therapy, in which damage to the lymphatic system is caused during the treatment of cancer, most notably breast cancer. In many patients with cancer, this condition does not develop until months or even years after therapy has concluded. Lymphedema may also be associated with accidents or certain diseases or problems that may inhibit the lymphatic system from functioning properly. In tropical areas of the world, a common cause of secondary lymphedema is filariasis, a parasitic infection. It can also be caused by a compromising of the lymphatic system resulting from cellulitis.

While the exact cause of primary lymphedema is still unknown, it generally occurs due to poorly developed or missing lymph nodes and/or channels in the body. Lymphedema may be present at birth, develop at the onset of puberty (praecox), or not become apparent for many years into adulthood (tarda). In men, lower-limb primary lymphedema is most common, occurring in one or both legs. Some cases of lymphedema may be associated with other vascular abnormalities.

Secondary lymphedema affects both men and women. In women, it is most prevalent in the upper limbs after breast cancer surgery, in particular after axillary lymph node dissection, occurring in the arm on the side of the body in which the surgery is performed. Breast and trunk lymphedema can also occur but, go unrecognised as there is swelling in the area after surgery and its symptoms ( peau d' orange and/or an inverted nipple ) can be confused with post surgery fat necrosis. In Western countries, secondary lymphedema is most commonly due to cancer treatment. Between 38 and 89% of breast cancer patients suffer from lymphedema due to axillary lymph node dissection and/or radiation. Unilateral lymphedema occurs in up to 41% of patients after gynecologic cancer. For men, a 5-66% incidence of lymphedema has been reported in patients treated with incidence depending on whether staging or radical removal of lymph glands was done in addition to radiotherapy.

Head and neck lymphedema can be caused by surgery or radiation therapy for tongue or throat cancer. It may also occur in the lower limbs or groin after surgery for colon, ovarian or uterine cancer, in which removal of lymph nodes or radiation therapy is required. Surgery or treatment for prostate, colon and testicular cancers may result in secondary lymphedema, particularly when lymph nodes have been removed or damaged.

The onset of secondary lymphedema in patients who have had cancer surgery has also been linked to aircraft flight (likely due to decreased cabin pressure or relative immobility). For cancer survivors, therefore, wearing a prescribed and properly fitted compression garment may help decrease swelling during air travel.

Some cases of lower-limb lymphedema have been associated with the use of tamoxifen, due to the blood clots and deep vein thrombosis (DVT) that can be caused by this medication. Resolution of the blood clots or DVT is needed before lymphedema treatment can be initiated.

The initial trauma causing the infection is often forgotten or not noticed. The infection builds at the site over a period of years, and a small red papule (skin elevation) appears. The lesion is usually not painful, with few, if any symptoms. Patients rarely seek medical care at this point.

Several complications may occur. Usually, the infection slowly spreads to the surrounding tissue while still remaining localized to the area around the original wound. However, sometimes the fungi may spread through the blood vessels or lymph vessels, producing metastatic lesions at distant sites. Another possibility is secondary infection with bacteria. This may lead to lymph stasis (obstruction of the lymph vessels) and elephantiasis. The nodules may become ulcerated, or multiple nodules may grow and coalesce, affecting a large area of a limb.

Edema and fibrinous exudate leads to fibrosis of subcutaneous tissues with localized pigment loss and dilation of capillary loops. This is called atrophic blanche. This can occur around ankles and gives an appearance of inverted champagne bottle to legs. Large ulcers may encircle the leg.

Lymphedema results from obliteration of superficial lymphatics. There is hypertrophy of overlying epidermis giving polypoid appearance, known as lipodermatosclerosis.

Chromoblastomycosis (also known as chromomycosis, cladosporiosis, Fonseca's disease, Pedroso's disease, phaeosporotrichosis, or verrucous dermatitis) is a long-term fungal infection of the skin and subcutaneous tissue (a chronic subcutaneous mycosis). The infection occurs most commonly in tropical or subtropical climates, often in rural areas. It can be caused by many different types of fungi which become implanted under the skin, often by thorns or splinters. Chromoblastomycosis spreads very slowly; it is rarely fatal and usually has a good prognosis, but it can be very difficult to cure. The several treatment options include medication and surgery.

Dermatosis neglecta is a skin condition in which accumulation of sebum, keratin, sweat, dirt and debris leads to a localized patch of skin discoloration or a wart-like plaque. It is caused by inadequate hygiene of a certain body part, usually due to some form of disability or a condition that is associated with pain or increased sensitivity to touch (hyperesthesia) or immobility.

Dermatosis neglecta typically develops several months after a disability or other affliction leads to improper cleaning. Patients may deny that negligence is the cause of the lesion, even though it completely resolves on vigorous rubbing with alcohol swabs or water and soap (which provides both diagnosis and treatment). Recognizing the diagnosis avoids unnecessary skin biopsies.

Examples of case reports from the literature include a man who avoided washing the skin area surrounding an artificial pacemaker out of fear it might be damaged; a woman who didn't clean the right side of her chest due to hyperesthesia following an amputation for breast cancer (mastectomy); a girl who was afraid to wash the area around an abdominal scar; and a man with multiple fractures, shoulder dislocation and radial nerve palsy which significantly reduced his mobility.

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.

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.

Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.

Pretibial myxedema is almost always preceded by the ocular signs found in Graves' disease.

It usually presents itself as a waxy, discolored induration of the skin—classically described as having a so-called "peau d'orange" (orange peel) appearance—on the anterior aspect of the lower legs, spreading to the dorsum of the feet, or as a non-localised, non-pitting edema of the skin in the same areas. In advanced cases, this may extend to the upper trunk (torso), upper extremities, face, neck, back, chest and ears.

The lesions are known to resolve very slowly. Application of petroleum jelly on the affected area could relieve the burning sensation and the itching. It occasionally occurs in non-thyrotoxic Graves' disease, Hashimoto's thyroiditis, and stasis dermatitis. The serum contains circulating factors which stimulate fibroblasts to increase synthesis of glycosaminoglycans.

Pretibial myxedema (myxoedema (UK), also known as Graves' dermopathy, thyroid dermopathy, Jadassohn-Dösseker disease or Myxoedema tuberosum) is an infiltrative , resulting as a rare complication of Graves' disease, with an incidence rate of about 1-5% in patients.

Many other conditions can lead to localized scaling or hyperpigmentation.

This condition should firmly be distinguished from dermatitis artefacta, which is the "factitious" creation of a skin lesion, whereas dermatosis neglecta results from unconscious avoidance of cleaning due to pain or immobility.

Other skin conditions which should not be mistaken for dermatosis neglecta include: terra firma-forme dermatosis (in which there is no history of inadequate cleaning); confluent and reticulated papillomatosis of Gougerot and Carteaud; several forms of ichthyosis; acanthosis nigricans; and Vagabond's disease.

Superficial thrombophlebitis is a thrombosis and inflammation of superficial veins which presents as a painful induration with erythema, often in a linear or branching configuration forming cords.

Superficial thrombophlebitis is due to inflammation and/or thrombosis, and less commonly infection of the vein. It is generally a benign, self-limited disorder, however, it can be complicated by deep vein thrombosis (DVT) and even pulmonary embolism (PE). Migratory superficial thrombophlebitis is known as Trousseau's syndrome.

Findings of tenderness, induration, pain and/or erythema along the course of a superficial vein usually establish a clinical diagnosis, especially in patients with known risk factors. In addition, there is often a palpable, sometimes nodular cord, due to thrombus within the affected vein. Persistence of this cord when the extremity is raised suggests the presence of thrombus.

Papillomatosis is skin surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae. These papillary projections of the epidermis form an undulating surface under microscopic examination.

The characteristic eruption is of multiple warty papules and nodules beginning on acral skin, especially the hands and wrists, and disseminating onto the skin of the entire body. These skin lesions develop on the trunk, extremities, and face, and are almost twice as common in men than in women, especially individuals aged 53–72 years. Pruritus is also associated.

Florid cutaneous papillomatosis (also known as the Schwartz-Burgess syndrome) is an obligate paraneoplastic syndrome.

FCP begins as the sudden onset of numerous cutaneous papillomas that are clinically indistinguishable from viral warts. The papillomas range from 1 to 3 mm in diameter may spread to involve the entire body, including the face. Pruritus, which may sometimes precede the onset of FCP, is evident in the affected regions in about half of patients. Evaluation of a skin biopsy clearly distinguishes FCP from viral warts.

FCP is associated with underlying cancer of the breast, bladder, ovary, uterus, prostate, and lung. Other associated underlying malignancies include squamous cell carcinomas and lymphomas such as non-Hodgkin's lymphoma.

FCP is sometimes seen together with other signs of internal cancer, especially malignant acanthosis nigricans, tripe palms, Leser–Trélat sign, and hypertrichosis lanuginosa acquisita. FCP tends to improve in association with surgical or chemotherapeutic therapy of the underlying internal cancer. A recurrence or exacerbation of FCP may be linked with tumor regrowth or metastatic spread.