Decubitus ulcers

What is this condition?

Pressure sores are localized areas of damaged tissue that occur most often in the skin and tissue over bony prominences. These sores may be superficial, caused by local skin irritation, or deep, originating in underlying tissue. Deep lesions often go undetected until they penetrate the skin. By then they’ve usually caused tissue damage.

What causes them?

Pressure, particularly over bony prominences, interrupts normal circulatory function and causes most pressure sores. The severity of the sore depends on the intensity and duration of the pressure. Damage to skin and small blood vessels may eventually lead to destruction of tissue cells. In turn, dead tissue may be invaded by bacteria and become infected.

Anyone who is confined to a bed or wheelchair for a long time risks developing pressure sores. The risk is greater if movement is restricted or sensation is impaired. Pressure sores occur on those parts of the body that bear the weight of the body or rub constantly against the bedclothes. The most common sites are the elbows, knees, shoulder blades, spine, and buttocks.

Other factors that increase the risk of pressure sores include inadequate nutrition (leading to weight loss and subsequent reduction of tissue and muscle bulk), swelling, incontinence, fever, disease, and obesity.

What are the symptoms?

Early features of superficial pressure sores are shiny, red changes over the compressed area. Superficial redness progresses to small blisters or erosions and, ultimately, to necrosis (death of tissue cells) and ulceration.

An inflamed area on the skin’s surface may be the first sign of underlying damage when pressure is exerted between deep tissue and bone. Bacteria in a compressed site cause inflammation and, eventually, infection, which leads to further necrosis. A foul-smelling, pusladen discharge may seep from a lesion that penetrates the skin from beneath.

How are they diagnosed?

Pressure sores are obvious during a physical exam. In the lab, wound culture and sensitivity testing of any discharge can identifY the infecting organisms.

How are Pressure Sores Treated?

Successful Pressure Sores treatment must relieve pressure on the affected area, keep the area clean and dry, and promote healing. Antibiotics may be use to eliminate any bacterial infection.

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1. Distribution: marked predilection for the lower legs
2. Nonblanchable petechiae
3. Slightly palpable petechiae
4. Absence of ecchymoses

Clinical Presentation

The purpuric lesions of leukocytoclastic vasculitis consist entirely of petechiae; ecchymoses are not found. Moreover, since the petechiae form in association with the presence of a perivascular inflammatory infiltrate, the petechiae are usually at least slightly palpable. This accounts for one of the synonyms for this disease: palpable purpura. Other synonyms include hypersensitivity angiitis, allergic vasculitis, and necrotizing vasculitis.

The smallest lesions of neutrophilic vasculitis occur as pinpoint dots that, early in the course of the disease, are bright red. As the lesions age, they become increasingly violaceous or even blue-black. The smallest lesions may not be palpable, but they are usually accompanied by at least a few larger, palpable papules. These larger lesions are sharply marginated violaceous papules 2 to 10 mm in diameter. They are characterized by the presence of a minute centrally located blue-black infarct or a tiny hemorrhagic vesicle. Both to the small and the large lesions of neutrophilic vasculitis fail to blanch when they are compressed by a glass microscope slide. The lesions are asymptomatic.

The lesions of vasculitic purpura develop on the lower legs first and in more severe cases may then spread to the rest of the body. Some clustering of lesions, particularly over joints, is often notable.

The lesions of vasculitic purpura are easily recognizable clinically. Biopsy should be used to confirm a suspected diagnosis.

Atypical Presentations. Anaphylactoid purpura (Henoch-SchOnlein purpura) is a neutrophilic vasculitic disease occurring primarily in children. The skin lesions are quite similar, though larger (2- to 3-cm) plaques are usually intermingled with the more classical purpuric papules. Additionally, immunoglobulin A (IgA) rather than immunoglobulin G (IgG) is present around the cutaneous blood vessels. Renal and gastrointestinal lesions are regularly present.

Course and Prognosis

The prognosis of vasculitic purpura depends largely on whether or not internal organs are involved. When there is no internal involvement, there is little morbidity, and the disease runs an uneventful course over 2 or 3 weeks. On the other hand, involvement of the nervous system, kidneys, or lungs results in considerable morbidity and even the possibility of death. Intermediate syndromes with only skin, joint, and gastrointestinal involvement are also encountered.

Pathogenesis

Leukocytoclastic vasculitis is characterized by a neutrophilic inflammatory response in and around small blood vessels. This feature identifies the disease as an example of vascular wall purpura (cf. intravascular and extravascular purpura).

Therapy

Milder cases of vasculitic purpura require no therapy at all. Systemically administered steroids are required when there is internal organ involvement. The response to such therapy is good, but relapse often follows cessation of steroid usage. Results of some reports suggest that nonsteroidal anti-inflammatory agents such as colchicine, indomethacin, and dapsone are of help. Antihistamines, while often administered, do not seem to be particularly effective.

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1. Distribution: face and extremities (children); groin and genitalia (adults)
2. Tendency for clustered formation
3. Central umbilication

Clinical Presentation

Molluscum contagiosum occurs as skin-colored or white papules 2-10 mm in diameter. These papules are firm, smooth surfaced, and dome shaped. Occasionally, these lesions are translucent enough to erroneously suggest vesicle formation. A central umbilication is present in about 25% of lesions and, if visible, is a pathognomonic sign. Molluscum contagiosum may develop anywhere. In children the lesions are most often found on the face, arms, and trunk, whereas in adults they are usually present on the inner thighs, lower abdomen, or genitalia. When multiple lesions are present, they are frequently in a clustered pattern. Molluscum contagiosum is almost always asymptomatic. Clinical diagnosis can be confirmed by biopsy or by the extrusion of a characteristic white globule of viral protein through a central incision.

Course and Prognosis

As befits the name and viral origin, molluscum contagiosum is capable of spreading both to the patient through autoinoculation and to others through close personal contact. If it is left untreated, the number of molluscum lesions generally increases. In children and in persons who are immunosuppressed, this increase may be explosive, with 20-50 lesions occurring in a matter of several weeks. The growth phase is followed by a period of relative stability, and this in turn is succeeded by a final phase, 12-24 months later, of spontaneous resolution. Subsequent reinfection does not commonly occur. Traumatic extrusion of viral protein into the surrounding dermis sometimes develops in one or more lesions. This leads to an inflammatory response that is occasionally brisk enough to simulate furunculosis.

Causes and Symptoms

The lesions of molluscum contagiosum are caused by two closely related DNA viruses (MCV-l and MCV-2) of the poxvirus group. Viral particles are inoculated into the epidermis as a result of cutaneous trauma during close personal contact. After an incubation period that averages about 1-2 months, viral replication begins within the cytoplasm of the midepidermal keratinocytes. This leads to epithelial cell proliferation and subsequent development of a visible papule.

The parasitized epidermal cells are recognized as a central white globule of viral protein that can sometimes be extruded through the characteristic umbilication. Presumably, spontaneous release of these cells accounts for spread of virus to other areas of skin or to other people.

The molluscum contagiosum virus cannot be cultured, and thus Koch’s postulates have not been fulfilled. Antibody response to molluscum contagiosum virus infection does occur, but resolution of the lesions probably depends on the triggering of a cell-mediated immune response.

Therapy

Molluscum contagiosum, though harmless, are usually treated because of the potential for spread. In very young children the application of cantharidin (Cantharone) results in the formation of a subepidermal blister containing the wart in its roof. Spontaneous sloughing of the roof and contained wart occurs 7-10 days later. The whole process is essentially painless. In older children and adults, cryotherapy with liquid nitrogen, application of trichloroacetic acid, incision followed by curettage, and, possibly, repeated applications of podophyllotoxin, work reasonably well. Electrosurgery, laser ablation, and excision should be avoided, as they may result in scarring.

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Bullae may occur as a part of the condition known as fixed drug eruption. Patients with this problem generally develop a single fairly large blister on an erythematous base each time they take certain medications such as sulfa-type drugs, phenolphthalein laxatives, and tetracycline antibiotics. The blisters recur in exactly the same location each time the drug is taken. In the male, fixed drug eruption is particularly likely to occur on the penis.

Trauma-induced blisters are encountered in the several genetically determined diseases of the epidermolysis bullosa group. These bullae arise from normal-appearing skin and develop following surprisingly modest degrees of friction. The diseases in this group are separately identified on the basis of inheritance pattern, histologic site of the blister, and the presence or absence of scarring at the time of healing. These diseases develop as a result of genetic defects in the various genes responsible for keratin production.

Diabetics occasionally develop blisters on the otherwise-normal skin of the lower legs and feet. Such blisters, known as diabetic bullae, seem unrelated to trauma, ischemia, or infection.

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Impetigo is a contagious, superficial skin infection marked by patches of tiny blisters that erupt, exposing the skin beneath. It can occur almost anywhere but usually appears in the area around the nose and mouth.

This disorder, which usually occurs in the late summer or early fall, spreads most easily among infants, young children, and the elderly. Certain risk factors - such as poor hygiene, anemia, malnutrition, and a warm climate - may increase the likelihood of an outbreak of this infection. Impetigo can complicate chickenpox, eczema, or other skin conditions marked by open lesions.

What causes Impetigo?

Impetigo is caused by bacterial infection. Types of bacteria that produce this disorder include Staphylococcus aureus and, less commonly, group A beta-hemolytic streptococci.

What are its symptoms?

Common nonbullous impetigo typically begins with a small red macule that turns into a pus-filled vesicle. When the vesicle breaks, a thick yellow crust forms from the discharge. Smaller lesions may appear around the original lesion. Other features include itching, burning, and swollen lymph nodes in the affected region.

A rare but serious complication of streptococcal impetigo is a kidney infection called glomerulonephritis. Infants and young children may develop impetigo in the ear or an external ear infection; the lesions usually clear without treatment in 2 to 3 weeks, unless an underlying disorder such as eczema is present.

In bullous impetigo, a thin-walled vesicle opens, and a thin, clear crust forms from the discharge. The lesion consists of a central clearing surrounded by an outer rim. It commonly appears on the face or other exposed areas.

Both forms usually produce painless itching; they may appear simultaneouslyand be clinically indistinguishable.

How is it diagnosed?

When diagnosing impetigo, the doctor looks for characteristic lesions. In the lab, microscopic examination of the causative organism usually confirms bacterial infection and justifies antibiotic therapy. Culture and sensitivity testing of fluid or denuded skin may indicate the most appropriate antibiotic. Lab studies may also reveal that the person’s white blood cell count is elevated.

How is it treated?

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Generally, the doctor will prescribe systemic antibiotics (usually penicillin, a cephalosporin, or E-Mycin) for 10 days. A topical antibiotic such as Bactroban ointment may be used for minor infections. Therapy also includes removal of the discharge by washing the lesions two or three times a day with soap and water or, for stubborn crusts, warm soaks or compresses of a salt water or diluted soap solution.

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1. Distribution: anterior lower legs
2. One or several palm-sized plaques
3. Lesional pain and tenderness

Clinical Presentation

Erythema nodosum is characterized by the presence of large ( 1- to 10-cm) nonscaling, red, painful lesions on the anterior surface of the lower legs. The smaller lesions appear as slope-shouldered nodules, whereas the larger lesions appear as flat-topped plaques. Because of this bimorphic appearance, erythema nodosum is listed with the erythematous mantles, papules, and nodules (group 7) as well as with the vascular reactions. Ulceration of the plaques does not occur.

On palpation the lesions are slightly warm and very tender. The distribution may be unilateral at first, but later in the ,ourse of the disease both legs become involved. Generally, no more than six lesions are present at anyone time. Lesions usually occur on the anterior shins or around the ankles. Lesions occasionally develop above the knee, on the thigh, or posteriorly on the calf.

Ankle and knee swelling with redness and tenderness in and round the joint is rather commonly found. Erythema nodosum occurs considerably more often in women than in men.

The rapidity of onset, together with tenderness and warmth on palpation, often suggests the presence of cellulitis. However the presence of more than a single lesion, a duration of more than several days, and the failure to respond to antibiotics usually allow for differentiation. Superficial thrombophlebitis also mimics erythema nodosum, but it is rarely if ever bilateral. Biopsy can he used to confirm a clinical diagnosis of erythema nodosum.

Course and Prognosis

Individual lesions resolve over a period of 15 to 20 days, but even as the first lesions disappear, one or more new ones begin to appear. Because of this sequential development, the entire course of the disease may last for months. Recurrent episodes, following long periods of inactivity, occur in about 5% of patients. Healing is accompanied by postinflammatory hyperpigmentation, but no permanent scarring develops.

Therapy

The discomfort of erythema nodosum is due to tissue distention, which is in turn caused by the presence of inflammation . Treatment revolves around the use of nonsteroidal anti-inflammatory agents, leg elevation, and bed rest. For patients who wish to be up and around, the use of elastic wraps or support stockings may be very helpful. In some cases, nontraditional anti-inflammatory medications such as potassium iodide, hydroxychloroquine, or dapsone may be of use. In rare instances, systemically administered steroids may be necessary . Hot soaks and topically applied medications are not efficacious.

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Topically applied nitrogen mustard (mechlorethamine) is used In the treatment of mycosis fungoides. A 10-mg ampule of nitrogen mustard (Mustargen) is mixed with 50 to 100 cc of tap water, and this diluted working solution is applied to the entire surface of the skin (with the face, scalp, and skin folds excepted) daily or 3 times/week. Applications are continued until the lesions resolve, at which time tile frequency of application can be reduced to once weekly. Usually, this maintenance program must be continued indefinitely, or the disease will reappear. Allergic sensitization to nitrogen mustard occurs with some frequency and may require cessation of treatment. Keratoses and squamous cell carcinomas may occur as a result of long-term therapy. The mechanism by which nitrogen mustard treatment is effective is unknown but is more likely due to the modulation of immunologic factors rather than a direct cytotoxic effect.

Podophyllin is a cytotoxic agent used in the treatment of genital, nonkeratinizing warts. Historically, a 25% concentration in tincture of benzoin has been applied on a biweekly basis in the physician’s office. Patients were instructed to wash the product off in 2 to 8 hours. Irritation as a result of these applications was highly variable and was sometimes extremely painful. Recently, a standardized product with known amounts of active podophyllin (Condylox) has become commercially available. This preparation can be used at horne by the patient. It is applied twice daily for 3 consecutive days followed by a rest period of 4 days. The cycle is repeated for a maximum of 4 weeks. Irritation is tolerable, and cure rates in the 40% to 60% range have been reported.

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1. Distribution: face, hands, feet, and shoulders
2. Rapid growth
3. Occurrence in children, teenagers, and pregnant women

Clinical Presentation

Pyogenic granulomas are smooth-surfaced, red papules 5 to 15 mm in diameter. Most. lesions are dome shaped, but some are pedunculated. They may occur anywhere on the body but are most commonly seen over the shoulders and face. Lesions are occasionally seen on the hands and feet. Most pyogenic granulomas are found in children aged 5 to 15 years, but pregnant women are also at risk. They are asymptomat.ic except for rather easy bleeding following trauma. Previously traumatized lesions will have a partially crusted surface.

Course and Prognosis

Pyogenic granulomas first. appear as pinhead-sized papules, but t.hey grow rapidly within weeks to their final size. Left untreated, pyogenic granulomas eventually undergo spon­taneous resolution. They have no malignant potential, but their rapid growth and occasional dusky color sometimes simulate the appearance of melanoma. Such lesions should obviously be biopsied. Recurrence after treatment (occasionally with the presence of new satellite lesions) is not uncommon.

Pathogenesis

The cause of pyogenic granulomas is unknown. In spite of their name they are not granulomas, and they are not caused by infections. Histologically, they appear to be true hemangiomas. Their occurrence in late childhood and in pregnant women suggests that hormonal factors may play a role in their development.. Satellite recurrence in some patients after removal seems to indicate that a field defect involving the surrounding vascular bed may be present.

Therapy

Lesions may be removed by elliptical excision or laser ablation,or after shave removal, the base may be destroyed with electrosurgy. Cryotherapy is sometimes successful, especially if it is repeated on several occasions. Recurrences are frequently observed if the original therapy was insufficiently aggressive.

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1. Distribution: chest, back, and shoulders
2. Sharp margination
3. Confluence of central lesions; peripheral satellite macules
4. Fine scale visible only with scraping
5. Positive potassium hydroxide (KOH) preparations

Clinical Presentation

The word “versicolor” means various colors. On sun-exposed surfaces the lesions are usually white, but on covered areas they are often light brown or brown-red. The initial lesions of tinea versicolor are sharply marginated macules 3 or 4 mm in diameter. Centrifugal growth leads to enlargement and subsequent coalescence of adjacent lesions. Rather large patches may be formed. Small, isolated satellite manlles are characteristically found at the periphery of the large patches. Scale is neither visible nor palpable, but when the lesions are scraped with the edge of a scalpel blade, fine (pityriasis-type) scale can be demonstrated.

Lesions are most commonly found on the central area of the upper chest and back, but when the disease is extensive, lesions can also occur on the upper arms, antecubital fossae, lower trunk, and groin. The face is almost always spared. This distribution pattern together with the sharp margination of the lesions helps to clinically distinguish pityriasis versicolor from pityriasis alba.

A clinical diagnosis should be confirmed by use of a KOH preparation. The microscopic appearance of the KOH preparation in pityriasis versicolor is described . Culture of the organism in ordinary clinical laboratories is not possible.

Course and Prognosis

Pityriasis versicolor occurs at any age, but it is found most commonly in teenagers and young adults. Left untreated, the infection persists indefinitely with varying degrees of exacerbation and remission. When the lesions are treated, scale formation stops and the KOH becomes negative. The white color present at the site of the lesions remains for several months, however, before normal skin color gradually returns. Patients should be forewarned that this persistence of hypopigmentation is not necessarily an indication of treatment failure. The disease has a marked tendency for recurrence even after adequate treatment has been administered.

Pathogenesis

Pityriasis versicolor is caused by the mycelial form of the yeast Pityrosporum orbicular. This organism, in its spore phase, is a normal inhabitant of the stratum corneum of human skin. The trigger that converts the spore phase to mycelial growth is unknown, but environmental factors are probably important. For instance, the prevalence of the disease correlates well with climatic conditions of high heat and high humidity and also correlates with work environments that favor the production of copious sweating. Other factors such as pH and variations in skin lipid formation, which may be genetic, may also playa role. Treatment presumably reconverts growth of the organism to the spore phase without eradicating it from the skin. This probably explains the great predilection for periodic recrudescence of the disease. The cause of the hypopigmentation in this disease is not known, but the presence of fungal products such as dicarboxylic acids are hypothesized to influence melanin production.

Therapy

Pityriasis versicolor responds to a variety of different treatment programs. Selenium sulfide shampoo (Exsel and Selsun), used as a soap daily for 3 weeks, is commonly prescribed. Imidazole preparations such as clotrimazole (Lotrimin) or miconazole (Micatin, Monistat), although more expensive, are also quite effective when they are applied twice daily for several weeks. Ketoconazole, in a dose of 200 mg each morning for as little as 2 to 7 days, is increasingly used because of convenience; fluconazole, a related drug, may also be effective. Orally administered griseofulvin and topically applied tolnaftate (Tinactin, Aftate) are not effective in the treatment of this disease. Patients should be forewarned that the whiteness will remain for months following treatment. Since the recurrence rate is very high, patients are well advised to re-treat themselves each spring prior to the “tanning season.”

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1. Distribution: anterior shins
2. Violaceous border
3. Central atrophy or ulceration

Clinical Presentation

Necrobiosis lipoidica diabeticorum (NLD) occurs as one or more yellow plaques on the anterior lower legs. Rarely, lesions may be found on the arms, face, and dorsal surface of the feet. Most of the plaques are 2 to 10 cm in diameter. The center of the plaque has a yellow, waxy appearance; the borders of the plaques are dusky red or violaceous. Palpation reveals a sense of firmness in the deep tissue.

Atrophy is present, and therefore, underlying veins can usually be seen more easily throughout the lesion than within the surrounding normal skin. Occasionally, the atrophic areas break down and ulcerate. The lesions are asymptomatic unless ulcerated, in which case pain may occur. Sometimes, there is overlap between the clinical appearance of granuloma annulare and NLD. Lesions of morphea often have a yellow waxy hue that can mimic that of NLD. Round and oval plaques of morphea rarely occur on the lower leg, but sometimes biopsy is required to differentiate these two diseases.

Course Prognosis

The lesions of NLD remain present for long periods of time. Usually, there is some element of slow centrifugal expansion. Approximately 60% of the patients with NLD have overt diabetes mellitus. Conversely, only about 0.5% of patients with diabetes develop these lesions.

Pathogenesis

The cause of NLD is unknown, although some clinicians believe that the plaques occur as the result of the same microangiopathy that is responsible for other complications of diabetes. There is considerable histologic similarity between NLD and the lesions of granuloma annulare and rheumatoid nodules. The significance of this observation is unknown.

Therapy

Therapy is not very effective. Some improvement may be seen following the use of topical steroids when they are used under occlusion. Intralesionally injected steroids are more effective, but there is some risk that the injected steroids will create more atrophy and increase the likelihood of ulceration. There has been some recent enthusiasm for the use of oral agents that affect blood flow (pentoxitilline) or interfere with platelet aggregation and activation (dipyridamole), but proof of efficacy has not been shown.

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