Numerous cutaneous problems can occur in patients admitted to hospital. Some, such as drug reactions, xerosis, decubiti, or miliaria are not specific to the surgical patient, unlike others, such as contact dermatitis induced by dressing materials (tape, tincture of benzoin) or problems with stoma maintenance. A discussion of the more common cutaneous problems follows: stomal care will be considered elsewhere. Dermatological consultation may be of value if diagnosis or management appear problematic.

Surgical patients are exposed to multiple medications in the preoperative, operative, and postoperative periods. If an adverse reaction occurs every effort should be made to attempt to identify the causative agent as specifically as possible. Time course, probability, appearance of the reaction (type), and the patient's drug allergy history are helpful in determining the most likely agent(s). Table 1 453 lists the drugs associated with specific patterns of cutaneous reaction. The generalized morbilliform eruptions (erythematous macules and papules) are not usually associated with life-threatening reactions. If medication producing this type of eruption is essential, it can frequently be continued; the eruption may or may not disappear. Close monitoring for progression of the reaction is advised.

The risk of life-threatening anaphylaxis is increased in patients who develop urticarial eruptions, and every effort should be made to identify the causative agent. Administration should be stopped if possible. Patients should be monitored for signs and symptoms of respiratory or circulatory difficulty. Treatment with drugs causing bullous erythema multiforme, or toxic erythema necrolysis should be stopped. Patients developing toxic erythema necrolysis have a mortality rate of over 50 per cent. Management in a burn centre is recommended since death usually results from fluid and electrolyte imbalance or sepsis from a cutaneous source.

The course is helpful in determining the most likely cause of the reaction: charting the onset and cessation of medications by date helps in the evaluation. Most cutaneous reactions will occur within 1 week of starting treatment, but a longer interval is seen in 50 per cent of patients who develop reactions to ampicillin and semisynthetic penicillins. Eruptions to medications which have been used for some time can occur, although they are less common than those developing in response to a newly introduced drug. Reactions can begin as long as 1 week after a medication has been stopped and can continue for 7 to 14 days: persistence of the rash for several days after discontinuation of a suspected cause does not mean that the incorrect drug has been withdrawn. The administration of high doses of corticosteroids, as is common in neurosurgical units, can mask a drug reaction, which may become apparent only when the corticosteroid doses are tapered.

Medications which frequently cause rashes include sulphonamide drugs, penicillins, and blood products; others, including digitalis preparations, antacids, vitamins, minerals, and stool softeners rarely cause cutaneous reactions. Table 2 454 lists drugs frequently associated with reactions, while Table 3 455 shows those which rarely cause cutaneous problems.

A careful drug allergy history is essential. Many patients have had a previous reaction to a similar medication. The patient may also have inadvertently been exposed to a cross-reacting drug.

Identification of the offending agent may not be possible in some patients who are receiving many drugs simultaneously. In this situation, elimination of all non-essential medication is recommended, with continuation of essential drugs and close monitoring of the patient.

Most drug reactions do not require specific treatment, other than for symptomatic relief of itch. Emollients (moisturizers) may be helpful for mildly symptomatic patients. Oral antihistamines (hydroxyzine 10–25 mg or chlorphenirimine maleate 4 mg every 4–6 h as required) may also be of help in patients for whom the drowsiness is not intolerable and other medical contraindications are absent. Oral steroids are usually not warranted.

Products employed by surgeons may produce allergic contact dermatitis in susceptible patients. The presence of vesicles or bullae, geographic location, sharp borders, and itch are features that point toward contact dermatitis rather than superficial infection (cellulitis, bullous impetigo), which it sometimes resembles. In an unsensitized individual the eruption usually starts 7 or more days after contact with the inducer, and may last up to 3 weeks. In a previously sensitized individual onset after 24 to 72 h is more typical; the duration may be 10 days to 2 weeks. A careful history of prior sensitizations should be elicited along with a record of current exposures. Common sources of contact dermatitis in surgical patients include topical preparations containing neomycin or benadryl, tincture of benzoin, metal appliances, and tape (Table 4) 456. Neomycin sensitivity is common, affecting approximately 1 per cent of the population. Sensitivity is much more common (15–30 per cent) after neomycin is applied to chronic erythematous skin, as in venous stasis dermatitis. Once sensitized, cross-reactions with other topical aminoglycosides can occur. Concomitant sensitization with bacitracin is also common. Allergy to topical sulphonamides can result in cross reactions to p-amino compounds such as p-aminobenzoic acid-containing sunblocks, benzocaine, and hair dye. Sensitization to systemic antihistamines is rare, yet topical applications commonly produce allergic contact dermatitis: the latter are ineffective and best avoided.

Among the topical anaesthetics, benzocaine is a potent sensitizer, and sensitive patients will also react to procaine, tetracaine, and other agents. Safe topical anaesthetics for use in benzocaine-sensitive persons include lidocaine, pramoxine, mepivacaine, pyrrocaine, and prilocaine hydrochloride.

Treatment of contact dermatitis requires cessation of the drug and avoidance of products that may cross-react. In mild cases these efforts are sufficient. If vesicle formation is substantial or if serous drainage is prominent, wet to dry saline solution soaked gauze dressings applied for 30 min three or four times daily help dry the lesions and to remove the accumulated drainage. Topical steroids are not effective.

If the eruption is very extensive, with substantial symptoms or involvement of major structures (swollen shut eyes, oedema of genitalia), oral cortisone may help, if this is not medically contraindicated. Typical doses would be prednisone 60 mg/day with milk or antacid for 3 days, reducing the dose by 5 mg/day over a period of 2 weeks.

Surgeons have an increased risk of certain types of contact dermatitis because of their occupational exposure. Table 5 457 lists agents which may cause contact dermatitis in surgeons and surgical personnel.

Contact dermatitis can be either irritant or allergic in nature. Hexachlorophene, a preoperative scrubbing agent, is a common cause of primary irritant dermatitis, but actual allergic contact dermatitis to this agent is rare. Allergy to components of rubber gloves should be suspected in eruptions that stop abruptly above the wrist. Such sensitizers include tetramethylthiuram, mercaptobenzothiazole, and isopropyl p-phenylenediamine. Surgeons who develop such sensitivity may benefit from the use of hypoallergic gloves. Orthopaedic surgeons are exposed to acrylic bone cement, which can penetrate rubber gloves and produce sensitization. Excessive dryness and fissuring of the skin in the affected areas is accompanied by paraesthesia of the fingertips. Contact with such cement must be avoided by the sensitized individual. The double-glove technique may be successful in preventing contact dermatitis unless the sensitized individual is allergic to methyl methacrylate monomer. Starch glove powder is another source of irritant; allergic contact dermatitis can be avoided by alternative use of talc. Evaluation of potential offending agents can be performed by patch testing with standardized agents.

This superficial infection of the outer layers of the skin is characterized by the presence of honey-coloured crusts. Previously, most cases were due to infection by streptococci; occasionally mixed streptococcal–staphylococcal infection was seen. Now the majority of cases are caused by staphylococci alone; a few mixed infections are still seen. This condition is especially common in small children. The differential diagnosis includes contact dermatitis and infected atopic dermatitis.

Traditionally, treatment required a 10-day course of oral antibiotics, either penicillin VK 250 mg every 6 h (or the equivalent dose in small children) or erythromycin, 250 mg every 6 h. Topical treatment with mupirocin ointment (bactroban) three times daily has recently been used successfully, with the addition of oral antibiotics if topical therapy fails. For extensively crusted areas, wet to dry saline soaks help debride and dry the area. Complications of impetigo are unusual, but rare cases of poststreptococcal glomerulonephritis have been reported.

Moniliasis is a common problem in hospital patients, especially those who are bedridden, febrile, and diaphoretic. Other predisposing factors include obesity (deep body folds), broad-spectrum antibiotic exposure, diabetes, and oral contraceptive intake. An erythematous macerated scaly eruption is noted in intertriginous areas. Satellite pustules are present. Examination of scrapings in potassium hydroxide microscopical preparations of pustular contents, demonstrate pseudohyphae. Extensive eruptions can involve the entire back and buttocks.

Therapy is aimed at decreasing the factors producing a warm moist environment. Ambulation, where possible, is usually helpful. Applications of nystatin cream twice daily or one of the imidazole creams such as miconazole or clotrimazole twice daily usually produces improvement. Adjunctive measures include drying the area with a fan several times daily and the use of 1 per cent hydrocortisone cream lightly applied twice daily for a few days to give symptomatic relief.

Skin infections in the compromised host fall into four groups: infection originating in skin and typical in appearance to that in patients with an intact immune system; extensive infections which are usually more limited in the immunocompetent; infection from cutaneous opportunistic pathogens; and spread of infection from a non-cutaneous site to the skin.

The appearance of infectious processes may be altered in the immunocompromised patient, and diagnosis may only be possible through histopathological examination of tissue, using both routine stains, and special stains for yeast, fungi, and acid-fast organisms, or by culture of biopsy tissue for routine and unusual organisms. Table 6 458 describes the gross morphology of cutaneous lesions and some of the associated organisms found in these patients.

Skin problems frequently seen in transplant patients fall into three categories: accelerated development of malignancies; increased frequency, extent, and recalcitrance of cutaneous infections; and medication-related problems.

The most common cutaneous malignancies are of the non-melanoma types, including squamous cell carcinoma, basal cell carcinoma, and keratoacanthoma (benign). These tumours appear earlier in life than anticipated, but do arise in sites commonly exposed to the sun. There is an increased incidence of squamous cell carcinoma in transplant patients compared with the population at large. Management is similar to that in non-transplant patients. Some keratoacanthomas behave in a more aggressive fashion in transplant patients. They may best be treated as squamous cell carcinomas.

Table 7 459 lists the cutaneous infections which are seen more often in transplant patients. Opportunistic systemic infections may present on the skin. Histopathological examination of specially stained biopsy specimens and culture should be performed on undiagnosed cutaneous lesions in these patients.

Cutaneous side effects of medication include those related to oral steroids, such as thinning of skin, increased bruising, striae, acne, moon facies, and hirsuitism. Cyclosporin, one of the immunosuppressants, also produces hirsutism in some patients.

Surgical patients in hospital often suffer from dry, scaly, and itchy skin (xerosis); this is often a pre-existing problem which is exacerbated by the hospital environment, with increased bathing, use of antibacterial soaps, and low humidity. Xerosis can be at least partially overcome by frequent application of emollients to the affected area, use of oil or superfatted soaps, decreased frequency of bathing, and an increased environmental humidity (30–40 per cent).

Miliaria or ‘prickly heat’ is a common problem in febrile, diaphoretic patients in overheated hospital rooms. It results from blockage of the sweat orifices, resulting in a sweat-containing vesicle appearing on the skin (miliaria crystallina); the duct may rupture and become inflamed, forming erythematous papules (miliaria rubra). Polymorphonuclear leucocyte influx produces the third stage, miliaria pustulosa. The differential diagnosis includes moniliasis, folliculitis, and drug-induced eruptions. Reduction of temperature and humidity and ambulation are usually sufficient to resolve the condition. Symptomatic improvement may be hastened by application of agents such as 2 to 3 per cent salicylic acid in 70 per cent isopropanol, which remove the top layers of the stratum corneum and reopen the ducts.

No one measure or combination of measures is effective in preventing or healing all decubitus ulcers. The primary pathophysiological event is chronic pressure on skin over a bony prominence. Tissue ischaemia follows, producing areas of necrosis that are susceptible to infection. Friction and prolonged contact with urine or faeces are additional predisposing factors. Resection of an underlying bony prominence may be necessary to allow healing to occur.

The most common sites of decubitus ulcers are the sacrum, tibial crest, ischial tuberosities, greater trochanters, iliac spine, spinous processes, heels, malleoli, knees, and elbows. Decubiti may also occur over the occiput and on the ears. Elderly, debilitated, paralysed, and unconscious patients are at greatest risk.

Prevention is the best approach to decubitus care. Frequent repositioning of the patient (every 1–2 h) usually prevents the development of such ulcers. Ambulation, when possible, also diminishes the risk. Good nutrition is essential to the maintenance of cutaneous integrity and also to facilitate healing once decubiti have developed. Correction of anaemia is an additional adjunctive measure. The ulcer per se is managed in the same way as any cutaneous ulcer.

Skin in areas at risk should be examined frequently for the presence of localized erythema, which indicates the presence of increased pressure and is a forerunner to ulceration. Alternating pressure mattresses, water-filled mattresses, and ‘egg-crate’ pads (thick papillated foam) are helpful in prevention and treatment of ulcers.

Incision and drainage of any infected space and removal of necrotic tissues is an important first step in treatment. Various topical powders, creams, and semipermeable dressings have been used with varying degrees of success. When medical approaches to ulcer healing have failed, several surgical approaches are possible. Complete excision of the ulcer with split thickness skin graft coverage may heal ulcers which have poor granulation tissue, necrotic edges, and lack of epithelial ingrowth. Full thickness grafts or rotational flaps and pedicles are helpful when bone and periosteum have been damaged or when little subcutaneous support is present. The use of myocutaneous flaps is gaining in popularity.

This inflammatory suppurative condition of unknown cause involves the apocrine glands and is frequently seen as a tetrad of hidradenitis suppurativa, severe cystic acne (acne conglobata), pilonidal sinus, and perifolliculitis capitis (dissecting folliculitis). While medical management can frequently be helpful early in the disease process, patients with extensive and persistent disease can only be managed effectively by surgery. Since apocrine glands are not fully developed until puberty, prepubertal patients are uncommon. Once developed, hidradenitis may persist into older adult life. The condition affects areas in which the apocrine glands are found: axillae, groin, buttocks, scrotum, perineum, submammary, areolar, and periumbilical skin. Lesions initially present as tender, erythematous to flesh-coloured subcutaneous nodules. Treatment at this stage includes incision and drainage and oral antibiotics, but severe scarring may result. Progression of the condition results in the development of multiple, large, interconnected, chronic deep-seated abscesses with sinus tracts between the lesions and to the overlying skin. Treatment is surgical, and may include the unroofing of sinus tracts to allow healing by granulation, or total excision of the apocrine-containing tissues (this is more successful in the axilla than in the groin).

Early in the course of the disease histopathological examination of the skin shows a perifolliculitis with infiltrating cells composed of lymphocytes, polymorphonuclear leucocytes, and histocytes. The primary abnormality may be apocrine follicular occlusion. The pilosebaceous structures are destroyed by resulting abscesses; sinus tracts lined with epidermis and extensive scar formation are late findings. Differential diagnosis includes fistulae of regional ileitis, furunculosis, infected cysts, developmental fistulae, cystic acne, and lymphogranuloma venereum.

Non-specific measures, including weight reduction for obese individuals, improved hygiene, and incision and drainage or intralesional steroids are helpful early in the infection. Short courses of antibiotics may also be successful (oral erythromycin or oral tetracycline in divided doses, a total of 1 g daily for 1–2 weeks). Chronic low-dose antibiotic therapy may help reduce flares of the condition in patients with multiple, recurrent lesions. Oral 13- cis retinoic acid has produced temporary improvement in some severely affected patients, but side-effects include malformed fetuses in women receiving the drug during pregnancy, calcium deposits in tendon and bone, increased blood lipids, night blindness, and severe dryness.

Surgical treatments include unroofing of sinus tracts with healing by secondary intention and wide excision of apocrine gland-containing areas that are chronically affected. Good results can be achieved in the axilla following wide excision and primary closure (Pollock procedure). Squamous cell carcinoma occasionally arises in chronically scarred areas.

This cutaneous non-suppurative infection of the connective tissue (dermal) and subcutaneous layers of the skin may be caused by several types of bacteria, of which haemolytic streptococci are the most common. These are usually group A organisms, but &bgr;-haemolytic streptococci of groups B, C, or G may also be responsible.

Erythema, swelling, and tenderness spreads rapidly with sharp or vaguely defined borders. A defined portal of entry into the skin may or may not be present (puncture site, cutaneous ulcer, surgical wound, fissures in skin secondary to tinea pedis). Moderate to high fever may be present, with or without local adenopathy. Predisposing conditions include saphenous venectomy, chronic lymphoedema, and phlebitis. The inflammation may be relatively superficial with well demarcated borders. Patients with swollen arms or legs after proximal regional lymph node dissections should be given a prescription for penicillin V or another antibiotic in anticipation of need, so that they can treat themselves at the first sign of erysipelas.

Differential diagnoses include contact dermatitis, superficial thrombophlebitis, and postinjection chemical inflammation.

Oral antibiotics are the most important single component in treatment; admission to hospital may be necessary for non-compliant, diabetic, immunosuppressed, or septicaemic patients. Penicillin G, 2 million units IV every 4 h and oxacillin 1 g every 6 h (staphylococcal coverage) is one recommended programme for the in-patient. Oral penicillin VK 250 to 500 mg or erythromycin 250 mg every 6 h are reasonable alternatives for outpatient therapy. Treatment should be continued for 10 days. Adjunctive measures include application of heat to the area by warm moist compresses, elevation of the area, and rest. Failure to respond in 48 to 72 h may indicate the presence of an abscess which may require incision and drainage.

This is a superficial pustular eruption localized to the hair follicle opening, commonly caused by Staphylococcus aureus infection. Predisposing factors include obesity, diabetes, moist humid climate, and tight or occlusive clothing. A small pustule with a hair emerging is the typical clinical finding. Healing usually occurs without scarring. Contact with mineral oils or tar products may produce a sterile folliculitis; a similar sterile folliculitis may occur beneath adhesive plasters or adhesive dressings. Differential diagnoses includes miliaria pustulosa (see above), inflammatory tinea, and moniliasis.

Folliculitis is often self-limited. Improvement in hygiene and the use of antibacterial scrubs such as 3 per cent hexachlorophene or chlorhexidine gluconate may clear the infection; wearing of loose fitting cotton clothing often helps. If the infection is persistent or extensive, treatment with dicloxacillin or erythromycin (each 250 mg four times daily for 7 days) is usually sufficient. Recurrence is common.

An abscess is a localized collection of pus within the skin associated with erythema, tenderness, and showing marked infiltration by polymorphonuclear leucocytes. An abscess which involves the hair follicle is termed a furuncle. Staphylococcus aureus is the most common causative organism; streptococci and Gram-negative organisms may also be present.

Furuncles are uncommon in children except in those with atopic dermatitis; the incidence increases at puberty, becoming common in adolescents and young adults. Men are more frequently affected than women. Most patients have intact immune systems. Local mechanical factors participate in the pattern of distribution of lesions.

The earliest lesion is a small tender inflammatory nodule in a follicular location. Pustulation occurs, followed by necrosis and discharge. Healing results in scar formation. Furuncles may be single or multiple. Common sites are the buttocks, anogenital area, face, neck, arms, wrists, and fingers. Cystic acne, hidradenitis supprativa, and inflamed epidermal inclusion cysts are the most common lesions which need to be distinguished from furuncles.

Since the course of furuncles is often self-limited, therapy may not be necessary. Large lesions should be treated by incision and drainage. Antibiotic therapy such as dicloxacillin or erythromycin (each 250–500 mg every 6 h for 7 days) is also warranted in this situation. Patients who show persistent recurrences may be nasal or perineal carriers of the causative organism.

A carbuncle is a suppurative extension of several contiguous furuncles into the subcutaneous fat. The maintenance of fascial attachments to the skin results in the production of multilocular compartments, particularly in the nape of the neck, upper back, hips, and thighs. Men in middle to late life are most commonly affected; predisposing factors include malnutrition, diabetes, cardiac failure, prolonged steroid therapy, and generalized dermatoses. Staphylococcus aureus is the most common cause.

The initial lesion is a painful dome-shaped nodule, which may increase in size over several days to 10 cm or more. After about 1 week pus-draining follicular orifices are noted, followed by necrosis of skin and deep ulceration. Fever and malaise may precede or accompany the development of the lesion.

Wide excision therapy is necessary to prevent spread. In addition, a penicillinase-resistant antibiotic such as dicloxacillin (250–500 mg every 6 h) should be administered.

Herpes zoster and herpes simplex are both common in hospital patients. The latter appears clinically as grouped vesicles on an erythematous base and may be provoked by febrile episodes. Herpes zoster may appear as clusters of vesicles located unilaterally in the distribution of a single dermatome. The differential diagnosis includes contact dermatitis and cellulitis. Confirmation of diagnosis can be made by viral culture or, more rapidly and less expensively, by staining a smear of the vesicle base with Giemsa dye and examining the microscopic preparation for the presence of multinucleated giant cells.

Therapy is aimed at pain reduction, promoting healing, and decreasing the potential for secondary bacterial infection. Local measures, such as wet to dry saline dressings, three or four times daily may be all that is required. Large doses of medication may be needed initially for pain relief in patients with herpes zoster. Secondary bacterial infection, if it develops, can be treated with appropriate antibiotics, selected on the basis of the results of Gram-staining or culture. Persistent localized herpes simplex in AIDS patients may require treatment with oral acyclovir in doses of 200 to 400 mg five times daily until the lesions are completely healed. Relapses are common.

Disseminated herpes zoster is rare in healthy people but more common in patients with lymphoma. This condition will usually respond to intravenous acyclovir in doses of 10 mg/kg every 8 h (if renal function is normal).

Topical acyclovir is ineffective in altering the clinical outcome of herpes simplex virus infections in individuals with normal immunological capabilities.

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