Chapter 48. Dermatologic Emergencies

To some, emergency medicine and dermatology may seem to be two of the most unrelated specialties in medicine, and in our daily practice dermatologic complaints most likely respresent a small percentage of our normal daily census but the emergency physician will encounter many patients presenting with dermatologic complaints. The astute clinician will realize that, although rare, some of these problems can be life-threatening. Some patients may even require emergency airway protection and vigorous resuscitation. This chapter reviews those special situations and discusses common and uncommon dermatologic complaints.

Initial Evaluation

The initial evaluation begins with the primary survey and vital signs. Always focus special attention on airway, breathing, and circulation (the ABCs). Note any abnormal vital signs and oxygen saturation, and be alert to subtle changes in mental status or behavior that may indicate impending airway or cardiovascular collapse. The ABCs apply to all clinical situations, and a thorough history and examination are often the most helpful tools in arriving at any diagnosis. The dermatologic examination must be performed on a disrobed patient. Inspect all areas of the skin and mucosal surfaces before addressing specific lesions.

History

Parallel to the assessment of the ABCs is a thorough history that includes potential recent exposures to foods, medications, plants, insects, and the like that may have triggered the condition. An ample history, addressing the patient's allergies, medications, medical and surgical history, last meal, and events leading up to the presentation may provide information necessary to begin appropriate management.

Angioedema and Urticaria

Angioedema

Essentials of Diagnosis

• Swelling of face, lips, tongue
• May lead to airway compromise

General Considerations

Angioedema forms in the deeper dermal and subcutaneous tissues of the distal extremities, tongue, lips, mouth, face, and neck. Particularly dangerous is the involvement of the mouth, tongue, and lower airway, which can lead to severe airway compromise. Angioedema is believed to be a similar to urticaria, which is present in half of the cases, but a deeper reaction. Two subtypes exist, the rare hereditary form and the acquired form. The autosomal dominant hereditary variant is usually due to C1-esterase deficiency or defect with 75% of patients with hereditary angioedema (HAE) having their first episode before 16 years of age. The acquired form is most commonly secondary to angiotensin-converting enzyme (ACE) inhibitors and has increased in prevalence because of widespread usage of these drugs. Patients who have been using ACE inhibitors for months or years can still develop angioedema from these agents.

Treatment

Emergency airway protection is mandated if airway compromise is impending or present. Treat shock if present. Discontinue any implicated medications or substances. Supply oxygen to maintain oxygen saturation at greater than 90%. In severe angioedema with airway compromise, administer epinephrine 0.1–0.5 mg (1:1000 solution) subcutaneously or preferably intramuscularly. This may be repeated every 5–10 minutes. Give an H1 antihistamines such as diphenhydramine HCl, 1–2 mg/kg, or in adults, 25–50 mg parenterally. Consider an H2 antihistamine such as ranitidine 50 mg intravenously. Methylprednisolone sodium succinate, 125 mg intravenously, may be repeated every 6 hours. Life-threatening HAE attacks may not respond well to epinephrine in normal dosages, antihistamines, or steroids. In these cases, airway protection is mandatory and fresh frozen plasma should be considered as it contains C1 inhibitor.

Disposition

Admit patients to an ICU if airway compromise is present; otherwise, they may need observation in a non-ICU hospital bed or in the emergency department. If a patient is thought to have experienced a reaction to a medication, instruct the patient to discontinue that medication and contact his or her primary-care physician to discuss an alternative medication.

Urticaria

Essentials of Diagnosis

• Localized areas of dermal edema
• Intense itching

General Considerations

Urticaria (hives) may be either acute or chronic and may appear in any age group. The condition represents one end of a continuum, ranging from urticaria to anaphylactic shock. Because various medications and foods are most often implicated as causes, take a thorough history of possible exposures. The lesions themselves represent localized areas of edema in the dermis. They appear as intensely pruritic, sharply demarcated raised circular or annular areas with either an erythematous or a blanched base and border. Their appearance may wax and wane, and individual lesions often resolve within an hour. With anaphylaxis (see Chapter 9), there may be an initial decrescendo of the presenting symptoms with early interventions. A late-phase response may occur hours later with a more severe presentation than the initial symptom complex.

Treatment

If airway compromise is not present, patients can be given H1-receptor blockers (see diphenhydramine dosing, above), steroids, and even epinephrine. H2-receptor blockers, such as ranitidine, may also be added. If airway compromise is present, treat on an emergency basis as for angioedema.

Disposition

Disposition is the same as for angioedema (see above). Remember the sometimes biphasic nature of anaphylactic reactions. Instruct patients to avoid any potentially responsible agents. Give any patient with a history of anaphylaxis a prescription for an autoinjector epinephrine device and instruct the patient on its proper use prior to discharge.

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

Essentials of Diagnosis

• Epidermal detachment
• Drug-induced or postviral illness
• Patients may be critically ill

General Considerations

A disorder of epidermal detachment was initially reported in 1922 when Stevens and Johnson published a description of two children with fever, erosive stomatitis, severe conjunctivitis, and a disseminated cutaneous eruption. It is now known to be a drug-induced state or one that follows a viral illness. Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are now thought to represent ends of a spectrum of reactions involving detachment of the epidermis. Both conditions share inciting factors and mucosal involvement. The range of disorders has been classified into three categories: SJS, involving less than 10% of body surface area (BSA); transitional cases, involving 10–30% of BSA; and TEN, with greater than 30% of BSA with detached epidermis. Mortality rates for SJS are approximately 5%; rates are much higher (30%) with TEN. Death is most commonly from sepsis secondary to infections from Staphylococcus aureus and Pseudomonas aeruginosa.

Clinical Findings

With a few exceptions, SJS/TEN results from drug exposure. The main culprits are sulfonamide antibiotics. Others on the list include aromatic anticonvulsants, β-lactam antibiotics, NSAIDs, allopurinol, tetracyclines, quinolones, and abacavir. Over 200 medications have been implicated along with vaccinations, malignancy, HIV and herpes viral infections. Patients with SJS/TEN typically present with 1- to 2-week prodrome of arthralgia, anorexia, fever, pruritus, pharyngitis, and conjunctivitis prior to skin involvement. With re-exposure of a drug, the time to onset to skin involvement is typically 1–3 days. Any mucous membrane site can be involved. Mucous membrane involvement often precedes but may accompany skin lesions. Patients with SJS/TEN present with severe, intensely painful macules and mucosal ulcerations with a truncal and occasionally facial distribution of target like lesions. The skin lesions begin as macules and are often described as burning. Over time macules coalesce into wide areas of erythema as the eruption expands. As lesions age, the skin becomes necrotic and bullae may form. The Nikolsky sign may be elicited. This refers to easy separation of the upper layers of the epidermis from the lower layers with very minor trauma, such as lateral traction or gentle rubbing on the skin. There may be eroding of the bullae, or the affected skin may slough in large sheets. This may progress over hours to days. The sloughing may involve other organ systems, including the gastrointestinal tract, genitourinary system, and the respiratory tree.

Treatment

Discontinue any potentially inciting medications. This usually requires that all nonessential medications be stopped, because no tests are available to identify the offending agents. Careful correction of electrolyte abnormalities and fluid replacement are critical, because significant fluid losses occur with loss of the protective skin barrier. Airway protection and mechanical ventilation may be necessary if the trachea and upper airway are involved. Sloughing and detachment of mucosa can lead to airway compromise. Antibiosis may be necessary to avoid sepsis-related complications. Pain control is essential. For uveitis, corneal ulceration, and/or vision loss, ophthalmologic consultation is strongly encouraged. Skin biopsy can aid in ruling out other deadly bullous diseases such as pemphigus vulgaris.

Disposition

In severe cases, treatment in a burn center may be necessary. Guard carefully against infection. Avoid steroids because they have not proved beneficial.

Exfoliation and Erythroderma

Essentials of Diagnosis

• A diffuse, generalized erythema and scaling
• Occurs secondary to many disease states

General Considerations

Many cutaneous diseases present with exfoliative erythroderma, or generalized redness and scaling. This condition is associated with a high risk for morbidity and mortality, independent of the inherent risks of the disease process it represents. Most commonly, this condition occurs secondary to psoriasis, atopic dermatitis, Hodgkin's disease, or mycosis fungoides (aka cutaneous T-cell Non-Hodgkin's lymphoma), or reactions to any of a wide range of inciting drugs. The erythrodermic state usually has a slow progression, but an acute onset may occur in patients who have cutaneous dermatoses or severe drug reactions.

Clinical Findings

Clues to the diagnosis may be from the underlying disease, such as psoriatic plaques or characteristic nail changes. Bullous pemphigoid typically exhibits tense bullae in addition to erythroderma. Long-standing erythroderma may be associated with keratoderma, alopecia, and ectropion. Peripheral edema occurs in 50% of patients. Patients with severe drug reactions may appear acutely ill with fever, malaise, and lymphadenopathy. A leukocytosis with eosinophilia, organomegaly, and hepatic or renal impairment may be present. In the most severe cases, high-output cardiac failure may occur. Severe alterations in fluid balance may occur, leading to shock. Sepsis may ensue, and hepatic necrosis may be fatal.

Treatment

Correction of derangements in fluid balance must begin early. Take care with the skin, applying moist dressings to weeping areas. Low-potency topical steroids may be used. Avoid high-potency preparations, because the large surface areas involved could lead to the absorption of large doses of steroids. Treat secondary infections.

Disposition

Hospital admission is often required, preferentially in an ICU, depending on the needs of the patient.

Staphylococcal Scalded Skin Syndrome

Essentials of Diagnosis

• Skin appears scalded and blistered
• Affects primarily children
• Skin barrier is broken and leads to S. aureus infection

General Considerations

Primarily a disease of children, staphylococcal scalded skin syndrome (SSSS) refers to a series of toxin-induced blistering dermatoses. SSSS lies within a spectrum of blistering skin disorders beginning with localized bullous impetigo. The exfoliative toxins, collectively known as exfoliatin, are primarily attributed to S. aureus, and page group 2 exotoxin-producing staphylococci are most implicated. Mortality rates are low (2–3%) in children but can reach as high as 60% in adults who have comorbidities or preexisting conditions.

Clinical Findings

The clinical presentation ranges from a milder form with localized eruption of a few fragile fluid-filled bullae surrounded by normal skin, to a more involved state. The more widespread form is often associated with fever, generalized erythema, and poor feeding in infants. Subsequently, large bullae form with a predilection for sites of friction. Erosion can occur in large areas, resulting in open, painful lesions. The Nikolsky sign is present. Unlike in SJS or TEN, mucous membranes are spared in SSSS. This may be a helpful distinguishing factor. The process is thought to result from a break in the protective skin barrier, which leads to S. aureus infection. Typical areas involved in the primary infection include the umbilicus in neonates, as well as the nasopharynx, urinary tract, and other sites.

Treatment

Cases of localized eruptions may be treated with oral antibiotics. The widespread form usually requires parenteral antibiotics to cover penicillin-resistant S. aureus. Treatment for adults is nafcillin, 1.5 g, or oxacillin, 2 g intravenously every 4 hours. For pediatric patients, treatment is nafcillin or oxacillin, 150 mg/kg/d intravenously in divided doses for 5–7 days. If superinfection is suspected, an aminoglycoside may be needed. Vancomycin or clindamycin should be considered. Rehydration and thermoregulation are essential, as is adequate pain control.

Disposition

Severe cases require treatment in an ICU or burn center. Because the cleavage of the epidermis and exfoliation are extremely superficial, the lesions typically heal with little or no residual scarring.

1This chapter is a revision of the chapter by: Ben H. Chlapek, DO, FACEP, FACOEP from the 6th edition.

Cellulitis and Erysipelas

Essentials of Diagnosis

Cellulitis

• Deeper infection
• Affects skin and subcutaneous tissues

Erysipelas

• Well-demarcated, superficial, erythematous infection
• Often affects face and extremities

General Considerations

Cellulitis and erysipelas refer to infections of the subcutaneous tissues. Erysipelas involves the more superficial upper dermis, and cellulitis is deeper, with more extensive involvement of the subcutaneous tissues and fat. Both conditions are acute and related to a breach in the skin's protective barrier function. This can be secondary to fissuring and maceration, burns, venous stasis, malnutrition, lymphedema, or any of a number of other factors. The primary causative agent is group A β-hemolytic streptococcus. Other causes include streptococci B, C, and G and staphylococci infection. Other causative organisms associated with cellulitis include S. aureus, H. influenzae, Streptococcus pneumoniae, and Pseudomonas. If untreated, both conditions can lead to devastating complications such as local abscesses and gangrene with severe cellulitis. Facial erysipelas may lead to cavernous sinus thrombosis. Both cellulitis and erysipelas may lead to septicemia.

Clinical Findings

Erysipelas is characterized by well-demarcated, erythematous, indurated plaques. The borders may be palpable. Primary sites include the face, scalp, and lower extremities. Patients are usually in the extremes of age. Cellulitis is usually associated with painful swelling and erythema of the involved area. The borders are usually less well defined, and the affected area is typically warm.

Treatment

Although many cases can be managed on an outpatient basis, patients may have constitutional symptoms, and those with comorbid conditions may be quite ill and require hospitalization. Antibiotics are used empirically to cover streptococci and S. aureus. Recommended therapies include penicillin G, 600,000 to 2 million units intravenously every 6 hours, for streptococci; and nafcillin, 1.5–2 g intravenously every 4 hours, for staphylococci. Treat methicillin-resistant cases with vancomycin 1.5–2 g intravenous q day. Patients who appear well and without constitutional symptoms may be given oral therapy. This includes dicloxacillin, 250–500 mg orally four times daily, or erythromycin, 0.25–0.5 g orally four times daily, in the penicillin-allergic patient. If methicillin-resistant staphylococcus is suspected treat with trimethoprim–sulfamethoxazole or minocycline. Simple measures may be helpful in both conditions, including rest, cool compresses, elevation of the affected part, and antibacterial soaks. Debridement is used in secondary abscesses.

Pemphigus Vulgaris

Essentials of Diagnosis

• Blistering of skin and mucous membranes
• Usually affects older adults

General Considerations

Pemphigus is one of several autoimmune diseases of the skin that present with blistering. The antibodies attack skin proteins and result in the inability of cells in the epidermis to hold together normally. Blisters form within the superficial epidermis. Although rare, pemphigus can be life threatening. Several subtypes exist, and pemphigus vulgaris is the most common and the most severe. Prior to newer developments in therapy, mortality rates were as high as 50% at 2 years and 100% at 5 years.

Clinical Findings

Pemphigus most often occurs in older adults. The skin and mucous membranes are usually affected, and oral lesions often appear first. All mucous membranes may eventually be affected. As described earlier, the blistering is superficial. This results in fragile, flaccid blisters. The underlying skin may be erythematous. In the oral cavity, the blisters often slough prior to presentation, and the clinician may find only ulcerations. Hoarseness may occur if the lower airway is involved. Oral involvement can be extremely painful, interfering with the patient's ability to tolerate oral intake. The blisters slough easily, and the erosions enlarge by extending their borders. Nikolsky sign is present. These erosions often crust over, but scarring is not usually a problem.

Treatment

Patients may have only isolated lesions, but more commonly there is widespread involvement. Patients may appear ill or toxic. Initial management involves fluid resuscitation, because fluid losses from the blistering are significant. Institute antibiotic therapy if secondary infection is present. Causative organisms are usually streptococci or staphylococci. This chronic disease usually mandates lifelong immunosuppressive therapy. The advent of glucocorticoids has decreased the mortality rates to approximately 5%. Start steroid therapy immediately. The suggested doses are 1–2.5 mg/kg/d of prednisone. Prednisone doses of 60 mg/d are recommended for treating isolated oral lesions. Topical high-potency steroids, such as clobetasol propionate 0.05%, can also be used in mild cases of skin involvement but should not be used on mucous membranes. Other immunosuppressive agents, such as azathioprine, cyclophosphamide, and methotrexate, are usually added to the oral steroid regimen later.

Disposition

Admit patients who appear ill to an ICU for careful management of their fluid balance.

Contact Dermatitis and Rhus Dermatitis

Essentials of Diagnosis

Rhus dermatitis

• Intense itching
• Erythema with vesicles
• Linear distribution
• Lesions appear 8–48 hours after exposure to poison ivy, poison oak, or poison sumac

General Considerations

Contact dermatitis refers to a collection of disorders resulting from an inciting environmental agent that has contacted the skin. The usual manifestation is a papulosquamous eruption, but vesicles may also be present.

A classic example is Rhus dermatitis, which is induced by plants in the Rhus genus (Toxicodendron). These include poison ivy, poison oak, and poison sumac. The culprit agent is the plant oil urushiol, and 50–70% of the U.S. population is sensitive to this substance. Factors affecting the clinical significance of any contact include the extent of exposure, the patient's age and activity level, and the patient's immunocompetence. Poison ivy, poison oak, and poison sumac are native plants of North America, rarely found at elevations above 4000 ft. Their appearance is quite variable, and they do not always exhibit the classic three-leaf morphology. The oil urushiol is widely distributed in almost all parts of the plant. The resultant dermatitis is classically described as a form of delayed hypersensitivity (type IV) reaction.

Clinical Findings

After the first exposure, lesions can erupt within 8–48 hours, and they may persist for up to 3 weeks. The presence of an intensely pruritic, erythematous, papulovesicular eruption after an environmental exposure is highly suggestive of Rhus dermatitis. The lesions are usually linear. Transfer of the allergenic urushiol can continue and produce more lesions if it is not completely removed. It must be cleansed from the fingernails, skin, and clothing and from pets. Transfer of the oil, not the vesicles or the vesicular fluid, is responsible for the development of new lesions.

Immediate eruption after exposure is not consistent with Rhus dermatitis, because it takes at least 8 hours for the cell-mediated response to develop. The most common sites for eruptions are the face and extremities. The lesions may range from erythematous papules to large bullae. Any of the commonly used rules for estimation of BSA of burns, such as the “rule of nines” or preprinted estimation sheets, may be used to estimate the percentage of BSA involved.

Treatment

The condition is self-limiting, with resolution within 3 weeks if all of the urushiol is removed. The most important therapy is prevention of exposure, but if exposure occurs, the individual should attempt to remove the oil within 10–30 minutes of exposure with warm water and soap remembering to wash under the fingernails to prevent spreading. Many new products have been introduced containing bentoquatam which binds urushiol and prevents absorption.

Treatment can decrease the severity of the symptoms, but it does not shorten the course. Oral antihistamines are effective symptomatic therapy for the intense pruritus. Topical preparations, including calamine, camphor, and cool compresses, are useful measures for comfort. Extreme caution must be used with topical antihistamines, zirconium, and benzocaine. These medications are no longer advocated, secondary to systemic absorption and sensitization. Over-the-counter steroid preparations are typically not helpful, because they contain too little steroid to be of benefit.

The backbone of therapy is usually a moderate-potency topical corticosteroid, such as triamcinolone 0.1% cream or betamethasone 0.1% cream. If the case is more severe or widespread, high-potency preparations such as clobetasol propionate 0.05% may be used. Extreme caution must be used with these creams, because systemic effects can occur secondary to steroid absorption.

Steroid therapy can also be used orally, but to be effective it must begin within 18 hours of exposure. Therapy must be tapered for 2–3 weeks. If the dose is too low or the course is too brief, intense rebound flares will often occur. A single 40-mg intramuscular dose of triamcinolone will typically produce good results in adults. Superinfection of the lesions with staphylococci or streptococci is the most common complication.

Disposition

Outpatient therapy is sufficient in all but the most severe cases, which may require parenteral steroids. Systemic glucocorticoids, such as prednisone or prednisolone at oral doses starting with 1 mg/kg/d, may be used and continued until the symptoms resolve. If prolonged steroid therapy is required, a gradually tapering dose may be advisable.

Impetigo

Essentials of Diagnosis

• Infection due to Staphylococcus or Streptococcus sp.
• Lesions appear honey-crusted
• More common in children but may affect all ages

General Considerations

Impetigo is an infection of the skin primarily due to group A streptococci and, less commonly, S. aureus. The infection is classified into bullous and nonbullous forms; the nonbullous form comprises approximately 70% of cases.

Young children are the predominant age group affected, but adults are not excluded. A break in the protective skin barrier is the inciting event. Conditions such as chick-enpox, abrasions, and burns are typically associated with impetigo. Predisposing situations include crowded living conditions, poor hygiene, and contact sports.

Clinical Findings

Impetigo is associated with the classic history of the emergence of a small vesicle or pustule. This is often in the context of one of the above-mentioned conditions. The vesicle or pustule develops into the classic honey-crusted lesion. These lesions are usually less than 2 cm in diameter and may be mildly pruritic. The lesions are usually not painful. Although in healthy individuals the lesions will usually heal spontaneously with little scarring, the potential complications can be life-threatening. Complications include septicemia, pneumonia, osteomyelitis, and glomerulonephritis.

Treatment

Correction of predisposing environmental conditions is important. The honey-colored crust must be removed. Cleansing with antibacterial soaps and solutions is helpful. The only topical antibiotic therapy currently indicated for the treatment of localized lesions is mupirocin (Bactroban) ointment. Patients should apply the ointment until the lesions resolve. Scalp and oral lesions typically require oral therapy, as do disseminated cases. Effective oral therapies include cloxacillin, amoxicillin–clavulanate, or clindamycin. Cephalosporins may be used, such as cephalexin, cefaclor, cefadroxil, cefprozil, or cefpodoxime proxetil. Seven days of therapy has been demonstrated as effective. If symptoms persist beyond 7 days, cultures should be taken and further treatment should be based on the results. Treat lesions suspected of being due to S. aureus with a β-lactamase-resistant penicillin such as oxacillin or nafcillin.

Herpes Zoster

Essentials of Diagnosis

• Most cases are very painful
• Prodrome of paresthesias may occur
• Rash appears as a bandlike distribution of vesicles
• Usually has a dermatomal distribution
• Usually does not cross the patient's midline

General Considerations

Herpes zoster (HZ), or shingles, is a painful condition that results from reactivation of a latent infection with the varicella zoster virus (VZV). A patient who is naive to the virus develops chickenpox after an initial exposure. After resolution of this primary infection, the VZV remains dormant in the satellite cells of the dorsal root ganglion of the sensory nerves. It remains there for the rest of the patient's life. The triggers of subsequent reactivation in certain patients are not fully understood. Events such as trauma and exposure to ultraviolet radiation have been implicated in provoking eruptions of shingles. The incidence of HZ is increased in the elderly population. This is thought to result from diminishing immune function with increasing age. Although usually a localized process, disseminated HZ can develop in immunocompromised individuals.

Clinical Findings

The diagnosis is primarily clinical. Previous history of chickenpox and the progression of current symptoms are important points in the history.

Three phases of HZ have been described: prodrome, acute, and chronic phases. During the prodrome phase, 80% of patients feel altered sensations in the affected dermatome. These are typically described as pain, burning, or paresthesias. These feelings may be intense and will often be present several days before the appearance of any lesions. This can often make the diagnosis difficult during this phase.

Patients in the acute phase present with the eruption of vesicles, usually in a bandlike pattern, which follows a dermatomal distribution. Only rarely will the lesions cross the midline. The two most common sites are the trunk and face, respectively. The lesions will dry and form a crust within 7–10 days, and they usually resolve within 2–3 weeks.

An unfortunate subset of patients will go on to develop the chronic phase of HZ, known as postherpetic neuralgia (PHN). This is an extremely painful condition, which persists at least 30 days after the eruption resolves. PHN can be quite difficult to treat and is much more likely in the older patient. It may occur in up to 50% of elderly patients with HZ.

Several dangerous complications can develop from HZ, including ophthalmic HZ. This condition occurs when the ophthalmic branch of the trigeminal nerve is involved. Up to half of these patients will have ocular HZ. A clue to the presence of ocular HZ can be involvement of the tip of the patient's nose. Conjunctivitis, uveitis, and ulcerative keratitis can occur as a result of HZ. These serious conditions can lead to blindness if not managed properly. A complete ocular examination and urgent ophthalmologic referral are essential. Other potential complications of HZ include the Ramsay Hunt syndrome (an acute facial paralysis), meningitis, and encephalitis.

Treatment

It is important to educate patients who have HZ. They must understand that they are contagious to those who are not immune to VZV and to those who have not had chickenpox. This infective state lasts until the vesicles have dried and crusted, or approximately 1 week from the onset of the rash. During this time, patients should avoid pregnant women, those who are immunocompromised, and those who have never had chickenpox.

Pain relief is important and usually achieved with short-term combinations of oral analgesics and narcotics. Antiviral drugs are of use in the treatment of HZ, if therapy is started within 72 hours of the eruption of the rash. Oral acyclovir, 800 mg five times daily for 7–10 days, is effective in improving resolution of the rash and decreasing the incidence of PHN. Famciclovir, 500 mg three times a day for 7 days, and valacyclovir, 1 g three times a day for 7 days, are other options with similar efficacy to acyclovir. One study showed valacyclovir as having some superiority in pain control. Antiviral agents have been shown to decrease the severity of PHN but not the incidence.

Studies have shown that steroids do not prevent the development of PHN. Some authors suggest that steroids are beneficial in treating Ramsay Hunt syndrome. Treatment of ocular involvement requires the assistance of an ophthalmologist. Varicella-zoster immunoglobulin and intravenous acyclovir is recommended for immunocompromised individuals.

Herpes Simplex

Essentials of Diagnosis

• Vesicles on an erythematous base
• HSV-1: usually oral; HSV-2: usually genital
• Spread by direct contact

General Considerations

Herpes simplex virus (HSV) is a major cause of recurrent orofacial and genital lesions and causes other types of illness as well (eg, keratitis and encephalitis). Infection is spread by direct contact. Primary infection is often the most severe, although it may be asymptomatic. After the primary lesion has healed, the virus remains latent in sensory neurons in ganglion tissue, where it periodically reactivates in response to diverse stimuli.

HSV type 1 (HSV-1) tends to be associated with oral lesions and is spread through contact with saliva from an infected person, whereas HSV type 2 (HSV-2) causes mainly genital lesions and is spread primarily by sexual contact. This is classically taught, but both infections can occur in either location.

Clinical Findings

Primary Herpes Simplex Infection

The first clinical attack of HSV infection is usually the most severe. Patients may present with fever, malaise, and arthralgias. Infection is characterized at first by grouped vesicles and later by denudation, erosions, or punctate lesions on a swollen, tender, painful erythematous base. Local pain and regional adenopathy are usually marked. Gingivostomatitis is the most common manifestation of HSV-1 infection; patients with HSV-2 infection usually present with genital lesions (ie, of the vulva, vagina, penis, anus, or perineum). Patients (especially women) with genital herpes may have aseptic meningitis. The primary illness usually disappears in 2–3 weeks but may last as long as 6 weeks.

Recurrent HSV Infection

Recurrence of infection is common and may be triggered by fever, exposure to ultraviolet light, friction or trauma associated with sexual intercourse, menstruation, and possibly stress or fatigue. Focal itching, pain, or aching may precede the appearance of vesicles by hours to a few days in some patients. Vesicles usually rupture spontaneously within a few days and heal within a week without scarring. The virus may be recovered as long as lesions are moist; until the area is completely dry and healed, the patient should avoid direct skin-to-skin contact with others.

Specific Diagnosis

For either primary or recurrent herpes simplex, especially genital herpes, confirm the diagnosis by culture or antigen detection.

Treatment

Primary Infection

Antipyretics or analgesics may help to relieve systemic symptoms. Give oral acyclovir, valacyclovir, or famciclovir to all patients who have primary infection for 7–10 days. Hospitalize severely ill patients for administration of intravenous acyclovir, 10 mg/kg every 8 hours. Give other patients oral acyclovir, 400 mg threetimes daily for 10 days, valacyclovir, 1 g twice a day for 7–10 days, or famciclovir, 250 mg three times daily for 7–10 days.

Antibiotics are not necessary unless local purulence or cultures or Gram-stained smears positive for bacteria suggest concomitant bacterial infection. Candida vaginitis occurs frequently in women with primary genital herpes.

Recurrent Infection

Patients should not touch or manipulate lesions and should avoid physical contact with others around the area of moist or active lesions. Acyclovir, 400 mg orally three times daily for 5 days, valacyclovir, 500 mg twice daily for 3 days, or famciclovir, 125 mg two times daily for 5 days, will somewhat reduce healing time and the duration of virus shedding if started within a day of lesion onset.

Disposition

Hospitalization is often indicated for patients with primary genital herpes, who may have severe pain, systemic symptoms, and other complications (eg, aseptic meningitis, neuropathic bladder). Hospitalization is also required for patients with large or rapidly progressive lesions, especially if the patient is immunocompromised.

Refer pregnant patients with newly diagnosed genital herpes to an obstetrician. Order a serologic test for syphilis (eg, VDRL) for all patients to rule out the possibility of coexisting syphilis. Consider testing for HIV if risk factors are present.

Psoriasis

Essentials of Diagnosis

• Common disorder
• Well-circumscribed plaques
• Erythematous base with silvery scale
• Predilection for extensor surfaces

General Considerations

Psoriasis is a common skin condition affecting up to 2% of the U.S. population. It has been described among all age groups with a similar male-to-female ratio. Onset is usually in the third decade of life. The disease process is well described and understood, but its cause is still unknown. A family history is present in 30% of patients. Psoriasis significantly affects the patient's quality of life. It is chronic, and there is no known cure. The plaque variant of psoriasis, or psoriasis vulgaris, is the most common form.

Clinical Findings

Thorough examination reveals the characteristic erythematous, raised, scaly plaques. These are often described as having a salmon-colored base with tightly adherent silvery scales. They are typically found on the extensor surfaces of major joints, such as elbows and knees. Other sites of predilection include the scalp, ears, and umbilicus. Lesions are often found to be in various stages of plaque formation and healing. Potassium hydroxide preparations can be used to differentiate psoriasis from tinea. Classic nail findings, such as pitting and onycholysis, can also aid in the diagnosis.

Treatment

Many remedies have been tried over the years, but no cure has been found for psoriasis. Therapies often merely decrease scaling and increase the patient's comfort. The use of emollients such as petroleum jelly, Aquaphor healing ointment, or Eucerin cream should be encouraged. Tar preparations and shampoos are well-known effective keratolytics, which decrease scaling. Avoidance of skin trauma is helpful, because the Koebner phenomenon is associated with psoriasis. This phenomenon refers to a flare in symptoms and initiation of plaque formation after local skin trauma, including scratching and even surgical incisions. Judicious use of topical low-potency steroids may be helpful initially. Calcipotriene is a newer preparation that is a topical vitamin D3 analogue. Applied twice daily, effects are typically seen within 8 weeks. Oral and parenteral steroids play little or no role in the treatment of plaque psoriasis. Their use has been demonstrated as harmful in certain situations, such as the exacerbation of the more serious pustular psoriasis. Topical steroids are helpful in limited disease. Restrict the highest-potency corticosteroids, such as betamethasone, to 2 weeks of BID use. Afterwards, a midpotency corticosteroid should be considered. Narrow-band UVB light exposure three times weekly with or without tar preparations will help clear lesions over weeks, but maintenance may be needed since relapses are frequent.

Disposition

Outpatient therapy is sufficient, except in the most severe cases. Referral should be made to a primary-care physician or a dermatologist for more involved therapies, including topical preparations, ultraviolet phototherapy, and systemic agents such as methotrexate.

Scabies

Essentials of Diagnosis

• Human parasite
• Causes intense itching
• Spread by contact
• May affect entire households

General Considerations

Scabies have been known to affect the human condition for thousands of years. The culprit organism in scabies is a mite, Sarcoptes scabiei. This mite is found in varying stages of development in the epidermis of the infested individual. There it makes tunnels, leaving behind eggs and feces. The mites are obligate parasites of humans and are spread by skin-to-skin contact between persons. This includes both sexual and nonsexual interactions.

Clinical Findings

The diagnosis of scabies is primarily a clinical one, with the usual history of intense pruritus that is especially worse at night. Consider scabies when entire households complain of the onset of pruritus. The classic physical findings are tiny burrows in the web spaces between the fingers, in intertriginous areas, and in flexor creases. Burrows may not always be seen. Only excoriations and impetiginization may be found. The lesions may be difficult to differentiate from atopic dermatitis. In the most extreme cases, heavy mite loads may result and lead to the crusted or Norwegian variant. This is usually limited to individuals with severe disabilities or in immunocompromised states. The diagnosis of scabies is confirmed by microscopic visualization of mites or eggs in skin scrapings.

Treatment

Adults

The treatment for adults (except pregnant or lactating women) and older children includes permethrin 5% cream (Elimite). It should be applied after a shower or bath over the entire body from the neck down. It should be left on for 8 hours, after which it should be carefully washed off. A 60-g tube is usually sufficient to treat one to two people. All clothing and bed linens should be laundered in hot water to kill all remaining mites.

Alternative regimens include lindane cream or lotion. Used for many years, it is effective but some strains of lindane-resistant scabies exist. Also, dangerous central nervous system side effects have occurred in the elderly and in immunocompromised patients, or in normal hosts after repeated uses.

Sulfur in petrolatum 6% is another treatment option. It should be applied to the entire body from the neck down for three consecutive nights. Patients should bathe between applications and 24 hours after the final treatment. Although it has no dangerous systemic effects, this remedy has an unpleasant odor. Crotamiton 10% cream may be applied for two consecutive nights and then washed off 24 hours after the last application.

Children

The treatment for infants, children younger than 10 years of age, and pregnant or lactating women is permethrin 5% cream, crotamiton 10% cream, or sulfur and petroleum as described above. The lindane preparation should not be used due to potential toxicity.

Pediculosis

Essentials of Diagnosis

• Lice infestation
• Different distributions: head, body, pubic area
• Spread by direct contact or sharing of personal items

General Considerations

Pediculosis refers to infestation of the body with lice. Similar to scabies, pediculosis results from a parasite. These organisms feed on the blood of humans. Several variants exist, and the organisms are named in reference to the area of the body they inhabit. These include Pediculus humanus capitis (head lice), P. humanus corporis (body lice), and Pediculosis pubis (pubic lice). Head lice are the most common, with the classic scenario of outbreaks in school children seen in all levels in society. The lice are transmitted by direct contact as well as by sharing of hats, brushes, and other personal items. Body lice predominantly affect adults of lower socioeconomic standing such as the homeless and those in refugee situations. Pubic lice are spread by sexual contact, and they often occur in conjunction with other sexually transmitted diseases.

Clinical Findings

Recognition of the lice as described above is essential in the diagnosis. Pruritus may lead to excoriations that may become secondarily infected. Infestation of head lice is diagnosed by visualizing live lice or nits (eggs) attached to the proximal portion of the hair shaft. Body lice and eggs are found in the clothing of the affected individual, with excoriations over the body. A body louse does not attach to hair but in clothing, coming out to feed on blood. Pubic lice are intensely pruritic, and the lice themselves may be transferred to other hair-bearing areas of the body. Remember to screen these patients for other sexually transmitted diseases. When pubic lice are found in children, they have often resulted from nonsexual contact; however, abuse should be considered in the differential.

Treatment

For the treatment of pediculosis capitis, corporis, and pubis, permethrin 1% cream rinse can be used. It can be applied to the groin, armpit, or scalp for 10 minutes and then washed off. Lindane 1% shampoo may be used as an alternative regimen. It is applied as above but is left on for 8 hours before washing off. For pediculosis capitis, it may be used as a shampoo, left on for 4 minutes, and then rinsed. Lindane should never be used on pregnant or lactating women, or on children younger than 10 years of age. Clothes should be washed in hot water and dried with high heat. Since Pediculus corporis resides in clothing, discarding or sealing clothing for 2 weeks leads to eradication.

Cutaneous Dermatophytes/Tinea

Essentials of Diagnosis

• Superficial fungal infections
• Flat, scaly patches

General Considerations

Dermatophytes include a group of fungi that infect the skin. The organisms themselves survive on the dead keratin found in the uppermost layer of the epidermis. The infections are limited to this superficial distribution in immunocompetent individuals. The dermatophytoses are classified by the distribution of the lesions.

Clinical Findings

Tinea Corporis

Tinea corporis refers to tinea of the body. Some authors and clinicians include the face in this category, but the American Academy of Dermatology refers to tinea of the face separately as tinea faciei. The most common causative organisms are Trichophyton rubrum, Microsporum canis, and Trichophyton mentagrophytes. Classic ring-worm (tinea circinata) is the most common form of tinea corporis. It usually begins as a flat scaly patch with a raised, palpable border. It enlarges by advancing its border outward, leaving an area of central clearing.

Tinea Pedis

Also known as athlete's foot, tinea pedis is a common condition. It affects up to 70% of adults. It is divided into three subtypes. The most prevalent is the interdigital type. It is chronic and occurs with fissuring and maceration between the toes. Moccasin-type tinea pedis has a plantar distribution. The plantar surface is tender and erythematous. It is usually covered with a silvery scale. The third type is the wet, vesicular type.

Tinea Cruris

Tinea cruris, commonly called “jock itch,” affects the groin area, sparing the genitalia. Men are affected more commonly than women, and the condition has a predilection for summer months.

Tinea Versicolor

Tinea versicolor affects a deeper layer of the skin than the previously described tineas. It is caused by the yeast Malassezia furfur. It often is associated with multiple hypopigmented macular lesions distributed over the trunk and extremities. Exposure to sunlight accentuates the lesions, because they do not tan normally like the surrounding skin. A fine scale is often present.

Treatment

Tinea Corporis

Mild cases of tinea corporis can usually be treated with over-the-counter topical preparations, such as miconazole nitrate or clotrimazole. Prescription agents include ketoconazole 2% cream or econazole nitrate. All topical remedies should be used for 1–2 weeks after resolution of symptoms. Extensive disease or difficult cases may require oral therapy. Agents include griseofulvin, itraconazole, terbinafine, and fluconazole.

Tinea Pedis

Most mild cases of tinea pedis can be treated successfully with 1–4 weeks of therapy with an over-the-counter preparation, in conjunction with the use of drying powders. Severe cases may require oral therapy. Drugs such as griseofulvin, fluconazole, and itraconazole are effective. Cases are often recurrent if concomitant nail disease is present.

Tinea Cruris

Tinea cruris can often be treated with topical antifungal therapies used for 2–3 weeks (see as for tinea corporis). The area should be kept dry, because moisture and maceration are problems with this disease. Antifungal powders and loose-fitting clothing are often useful adjuncts. A mild topical corticosteroid may be used cautiously for a short time to help relieve the pruritus, which is often severe. Corticosteroids may be used only for 48–72 hours; longer use is contraindicated. As with tinea corporis, resistant disease may require oral therapy.

Tinea Versicolor

Limited tinea versicolor can be treated with topical selenium sulfide 2.5%. Daily application of ketoconazole to the affected areas for 3 days is an alternative regimen. Recurrence of the disease may be prevented with the use of a once-monthly bedtime application of selenium sulfide 2.5%.

Pityriasis Rosea

Essentials of Diagnosis

• Herald patch is initial lesion
• Rash is usually truncal and has a “Christmas tree” distribution
• May be pruritic

General Considerations

Pityriasis rosea is a common rash that may easily be confused with tinea corporis. It is a papulosquamous eruption that most commonly affects patients in the second to the fourth decades of life. Pityriasis rosea affects men and women equally. Although its cause is thought to be related to a viral exanthem associated with reactivation of human herpesvirus 7 (HHV-7) and sometimes HHV-6, the exact cause of pityriasis rosea is unknown.

Clinical Findings

The classic progression of the exanthem begins with the appearance of a herald patch. This is an isolated salmon-colored macule usually found on the trunk. It is typically oval shaped and can be as large as 10 cm in diameter. It usually has an erythematous scaling border, and there may be central clearing. The subsequent lesions usually develop within 1–2 weeks, and their distribution has been described as resembling the shape of a Christmas tree. The individual lesions are smaller than the herald patch, are usually of a lighter shade, and have a scaly border.

Treatment

The lesions are self-limiting and usually disappear within 6–8 weeks. The initial lesions regress, and new lesions develop during this time. No effective treatment has been found for pityriasis rosea. If pruritus is present, it may be treated symptomatically with oatmeal baths, antihistamines, or topical hydrocortisone 1% ointment. Patients should be reassured that recurrences are uncommon, occurring in only approximately 3% of cases.

Molluscum Contagiosum

Essentials of Diagnosis

• Viral infection
• Pearly pink papules with central umbilication

General Considerations

Molluscum contagiosum is a viral infection of the skin. It is associated with multiple lesions, typically papules, spread over the skin. Molluscum contagiosum is present worldwide and is a member of the poxviruses. In normal hosts, it is a self-limited disease and usually resolves within 8 weeks. Recently there has been increased prevalence in the immunocompromised population, especially in patients with HIV. In this population, the disease presentation can be dramatic, with large, widespread lesions and a longer duration.

Clinical Findings

The diagnosis is made by the identification of the lesions. They are typically flesh-colored papules. The lesions may also appear pearly pink. The papules are rounded with a distinctive central umbilication and are firm to palpation. They usually are 1–5 mm in diameter, but in certain situations they may be quite large. The lesions may be distributed anywhere on the body, but they are rarely found on the palms or soles. They are usually found in groups, and usually fewer than 20 lesions are present. Molluscum contagiosum is spread by close contact with infected persons, by contact with contaminated surfaces, or by autoinoculation with scratching or shaving. It can also be spread by sexual contact.

Treatment

Most lesions resolve without treatment in immunocompetent patients. Lesions involving the perineum and genitalia should be treated to avoid spread via sexual contact. If lesions require treatment, the two most commonly used modalities are cryosurgery and curettage. Various topical therapies have had varying levels of success, including lactic acid, podophyllin, cantharidin, and silver nitrate. In pediatric patients, use of a topical anesthetic, such as lidocaine plus prilocaine, should be considered prior to curetting. Instruct patients to avoid contact sports, swimming pools, and other such activities until the lesions have resolved.