Dermatologic Presentations

Background and Importance

Diseases of the skin and subcutaneous tissue account for over 5 million emergency department (ED) visits annually, approximately 3.5% of all ED visits. Dermatologic conditions often have a significant impact on quality of life. Common diagnoses among ED patients include infections, inflammatory conditions, allergic reactions, or drug reactions.

Anatomy, Physiology, and Pathophysiology

The skin is composed of three layers: the epidermis, dermis, and subcutaneous layer ( Fig. 107.1 ). The epidermis is a thin layer of stratified squamous epithelium, consisting mainly of keratinocytes, which progress through stages of differentiation as they migrate from the basal to the superficial layer. These layers are the stratum basale (base of the epithelium), stratum spinosum, stratum granulosum, stratum lucidum, and stratum corneum (superficial layer). The epidermis also includes other cells, such as melanocytes and Langerhans cells. Melanocytes produce melanin, which functions to add pigment to the skin and also to absorb ultraviolet radiation. Langerhans cells are a component of the immune system and function to ingest and process foreign antigens. The epidermis lacks direct blood supply and is dependent on the dermis for nutrients by diffusion through the dermal-epidermal junction. This junction is the site of immunologic injury resulting in separation of these layers, which appears as bullae.

The dermis consists of connective tissue, blood vessels, lymphatic vessels, nerve endings, and immune cells. The main function of the dermis is to support the epidermis and contribute to the protective functions of the skin. Fibroblasts produce procollagen and elastic fibers used to form the connective tissues that give support and elasticity to the skin. Sweat glands and the network of blood vessels in the dermis assist with thermoregulation.

The subcutaneous layer is composed of connective tissue and adipose tissue, functions to cushion the overlying skin, and contains lymph and neurovascular structures.

The skin serves several important physiologic functions. It serves as a barrier between the internal and external environment. The skin protects from external toxic and infectious materials, and assures homeostatic balance of fluids and electrolytes. The skin serves an integral role in temperature homeostasis through its barrier function, sweating mechanism, and blood vessel dilation or constriction; it functions in the absorption of ultraviolet radiation and production of vitamin D; sensory nerve endings in skin serve important functions of sensation; and finally, certain cells within the skin serve important immunologic functions, including Langerhans cells, lymphocytes, mast cells, and keratinocytes.

Impetigo

Impetigo is typically caused by Staphylococcus aureus or β-hemolytic Streptococcus. Pediatric patients are commonly affected. Streptococcal impetigo (ecthyma) is found most often on the face and other exposed areas. The eruption often begins as a single pustule and later progresses to multiple lesions, often with a golden yellow crust ( Fig. 107.2 ). Lesions may be pruritic but usually are not painful. Regional lymphadenopathy is commonly present. Lesions are contagious among infants and young children and less so in older children and adults. Postpyodermal acute glomerulonephritis is a recognized complication of streptococcal impetigo.

Staphylococcal impetigo is differentiated from streptococcal impetigo in that it is more superficial, and there is little surrounding erythema. Other diagnostic considerations include herpes simplex virus (HSV) or inflammatory fungal infections. Methicillin-resistant Streptococcus aureus (MRSA) impetigo is increasingly common. Bullous impetigo is caused by the toxin released by staphylococcus. It is seen primarily in infants and young children. The initial skin lesions are thin-walled, 1- to 2-cm bullae ( Fig. 107.3 ). When these rupture, they leave a thin serous crust and collarette-like remnant of the blister roof at the rim of the crust. The face, neck, and extremities are most often affected. The differential diagnosis includes contact dermatitis, HSV infection, superficial fungal infections, and pemphigus vulgaris.

Empirical therapy should be instituted with oral or topical antibiotics. Topical therapy is initiated with bacitracin, mupirocin, retapamulin, minocycline, or ozenoxacin. Oral antibiotics are indicated for severe or multiple lesions. Oral therapies include an agent active against S. aureus, such as dicloxacillin or cephalexin. If MRSA is suspected, doxycycline, clindamycin, or trimethoprim-sulfamethoxazole (TMP-SMX) is recommended. Therapy for bullous impetigo consists of a systemic oral antibiotic, such as dicloxacillin, erythromycin, or azithromycin. Even without treatment, impetigo generally resolves within 3 to 6 weeks (see Chapter 126 ).

Folliculitis

Folliculitis is an inflammation in the hair follicle, usually caused by S. aureus. It appears as pustules with a central hair. The lesions are commonly on the buttocks and thighs, in the beard or scalp, and may cause mild discomfort. The differential diagnosis includes acne, keratosis pilaris, or fungal infection. Gram-negative folliculitis with Pseudomonas aeruginosa can occur after exposure to infected hot tubs and swimming pools, or in individuals taking antibiotics for acne.

Local treatment with an antiseptic cleanser such as povidone-iodine or chlorhexidine every day or every other day for several weeks is usually adequate. For patients with extensive involvement, a course of systemic oral antibiotics may be added, such as doxycycline or dicloxacillin (see Chapter 126 ).

Cellulitis

Cellulitis presents with localized erythema, swelling, and pain of the soft tissues ( Fig. 107.4 ). Erysipelas is a streptococcal infection of the skin and subcutaneous tissue and typically has an erythematous appearance with a well demarcated border, often with fever, malaise, or myalgias. Cellulitis may be a cause of sepsis. Ultrasound may be helpful in differentiating from abscess.

Mild cases of cellulitis may be treated with an oral antibiotic, such as a cephalosporin, dicloxacillin, or clindamycin. Moderate cases requiring IV therapy should be treated with a penicillin, ceftriaxone, cefazolin, or clindamycin. Severe cases should be treated with IV vancomycin plus piperacillin/tazobactam. Chapter 126 provides detailed management recommendations.

Abscess

Abscesses are accumulations of pus within body tissues. Furuncles are skin abscesses caused by staphylococcal infection involving hair follicles and surrounding tissue. They may present with localized soft tissue swelling, erythema, and fluctuance ( Fig. 107.5 ). Ultrasound may be helpful in differentiating abscess, which appears as a fluid-filled cavity from cellulitis, which appears as cobblestoning, with fine reticular (netlike) areas of hypoechoic stranding.

Carbuncles are large abscesses that develop in the thick, inelastic skin of the back of the neck, back, or thighs and usually involve multiple hair follicles. They may produce severe pain and fever. Septicemia may be a complication.

Abscesses should be treated with incision and drainage. Recent literature suggests higher cure rate for antibiotic treatment with TMP-SMX in addition to incision and drainage. TMP-SMX and clindamycin have demonstrated efficacy in cure rates following incision and drainage. Moderate or severe abscesses should ideally have culture and sensitivity performed. If IV antibiotics are indicated, agents may include vancomycin, daptomycin, linezolid, telavancin, or ceftaroline. Chapter 126 provides detailed management recommendations.

Hidradenitis suppurativa affects the apocrine sweat glands. Recurrent abscess formation in the axillae and groin resembles localized furunculosis. The condition tends to be recurrent and may be resistant to therapy. Ultrasound will help differentiate abscesses from vascular or lymphoid structures. Hidradenitis suppurativa may be treated with drainage of abscesses if they are fluctuant, painful, and large. Anti-staphylococcal antibiotics are useful if they are administered early and for a prolonged period. Begin treatment for mild disease with topical clindamycin for 3 months. In patients with more severe or nonresponsive disease, oral clindamycin combined with rifampin for 3 to 6 months is indicated. Antiandrogen therapy may be considered if antibiotics fail to produce improvement. Recurrent cases should be referred for surgical management.

Methicillin-Resistant Staphylococcus aureus (MRSA)

The incidence of community-associated MRSA has risen steadily since the first report in 1993. In many major cities in the United States, MRSA is now the most common pathogen cultured from ED patients presenting with skin and soft tissue infections. Hospital-acquired MRSA isolates can survive on a variety of inanimate surfaces, sometimes for weeks. Pets (including dogs and cats), livestock, and birds have been identified as MRSA carriers; their role in MRSA transmission to humans is unclear.

MRSA infections are most often manifested as skin and soft tissue suppuration, such as an abscess, furuncle, or cellulitis. Lesions frequently exhibit central necrosis and are often confused with spider bites by patients. Clinical features cannot distinguish with certainty skin and soft tissue infections caused by MRSA from those caused by methicillin-susceptible S. aureus . Although rare, MRSA infection can present as necrotizing fasciitis. Recurrences of MRSA cellulitis are common. Contagion among the close household contacts of patients as well as correctional facility, school, or sports team contacts is well recognized.

Local resistance patterns should guide therapy. Agents typically effective against MRSA include TMP-SMX, clindamycin, minocycline, or doxycycline. Cephalosporins and macrolides are typically ineffective against MRSA. Fluoroquinolones should be avoided as S. aureus resistance develops readily.

Patients with large abscesses, abscesses in high-risk locations, fever, signs of systemic infection, young age, or immunodeficiency should be considered for inpatient treatment. Vancomycin is considered the parenteral drug of choice for patients with invasive S. aureus infection, although clinical failures have been reported. It is reasonable to combine vancomycin with another effective anti-staphylococcal agent as many antibiotics have better bactericidal activity. In severely ill patients, carbapenems such as meropenem, panipenem, and ertapenem are recommended, because they are active against MRSA and synergistic with vancomycin. Other effective parenteral agents may include clindamycin, linezolid, daptomycin, tigecycline, or telavancin. Chapter 126 provides detailed management recommendations.

Although decolonization strategies have been recommended by some, neither the indications for their use nor their effectiveness in reducing the risk of recurrences has been established. Common antiseptics appear to retain reasonable activity against MRSA, although the results of studies are somewhat conflicting. Good personal hygiene, including appropriate handwashing techniques, separation of infected patients, and routine cleaning of shared equipment, remain essential to limiting MRSA spread.

Erythema Migrans

Lyme disease is caused by the organism Borrelia burgdorferi and is transmitted by the deer tick bite ( Fig. 107.6 ). Most cases occur in the spring and early summer. Endemic areas in the U.S. include the Northeast, Midwest, West, and scattered other areas. Although 36 to 48 hours of tick attachment is necessary to transmit disease, less than 33% of patients recall a tick bite. The incubation period is 3 to 30 days.

Clinical presentations include three disease stages. Stage I occurs early and is manifested by malaise, headache, fever, lymphadenopathy, and arthralgias. Stage I typically resolves in 4 weeks. Erythema migrans occurs in 60% to 80% of cases and manifests as erythematous annular, non-scaling lesion with central clearing ( Fig. 107.7 ). Stage II presents with secondary annular lesions, fever, lymphadenopathy, neurologic manifestations, or cardiac conduction abnormalities that may last weeks to months. Stage III manifests as chronic arthritis, dermatitis, or central nervous system (CNS) disease.

Diagnostic tests may include a nonspecific elevated ESR and serologic tests, which are helpful in establishing the definitive diagnosis but are not typically available acutely. Serologic testing includes a two-tiered serologic analysis consisting of an enzyme-linked immunoassay or immunofluorescence assay, followed by reflexive immunoblotting.

Management should include appropriate antibiotic administration. The antibiotic regimen may include doxycycline or amoxicillin, for 10 to 21 days, or as alternates, cefuroxime, clarithromycin, erythromycin, or azithromycin. ^, Chapter 123 provides detailed management recommendations.

Necrotizing Fasciitis

Necrotizing fasciitis should be considered with skin and soft tissue infection with signs of systemic toxicity, or severe infection ( Figs. 107.8, 107.9, and 107.10 ). The etiology is often polymicrobial (mixed aerobic/anaerobic microbes) or monomicrobial (group A streptococci, community-acquired MRSA). Radiographic tests may demonstrate soft tissue air. Prompt surgical consultation is indicated.

Empirical antibiotic treatment should be instituted with broad coverage, such as vancomycin or linezolid plus one of the following: piperacillin-tazobactam, carbapenem, or a combination of ceftriaxone and metronidazole. Chapter 126 provides detailed management recommendations.

Meningococcal Infection

Meningococcal infection is caused by the organism Neisseria meningitides, typically transmitted by respiratory secretions. Meningococcal disease may manifest as one of three syndromes: meningitis, bacteremia, or pneumonia. Meningococcal disease typically affects healthy children and adolescents, and it may result in significant morbidity and mortality. Infection is fatal in approximately 10% of cases.

Clinical presentation may include fever, malaise, arthralgias, nausea, and vomiting. Cutaneous findings of macules, papules, vesicles, or petechiae and purpura may be present.

Ten percent of cases may present with Waterhouse-Friderichsen syndrome characterized by shock with intracutaneous hemorrhage.

The diagnosis should be suspected clinically and treated promptly. Confirmatory tests may include blood cultures, cerebrospinal fluid (CSF) cultures, or skin scrapings.

Empirical therapy should be instituted with agents, such as a third-generation cephalosporin (e.g., ceftriaxone or cefotaxime) plus vancomycin. Alternative antibiotics may include penicillin G, chloramphenicol, a fluoroquinolone, or aztreonam. Dexamethasone should also be considered for suspected or proven meningitis. ^, Immunization against meningococcal infection is recommended for groups at increased risk for infection, including adolescents. Chapter 118 provides detailed management recommendations.

Scarlet Fever

Scarlet fever results from group A strep infection. The illness presents with fever, chills, malaise, and sore throat, followed within 12 to 48 hours by a distinctive rash that begins on the chest and spreads rapidly, usually within 24 hours. Circumoral pallor may be noted. The skin has a rough sandpaper-like texture due to a multitude of tiny papules. The pharynx is typically injected, and there may be erythematous lesions or petechiae on the palate. After the resolution of symptoms, desquamation of the involved areas may occur. Erythema marginatum may be seen in 10% of cases and presents with annular erythematous lesions that may be transient and reappear over days, weeks, or months ( Fig. 107.11 ).

Complications include the development of a streptococcal infection of lymph nodes, tonsils, middle ear, or respiratory tract. Late complications include rheumatic fever or glomerulonephritis.

Treatment should be initiated with oral penicillin VK (children <27 kg: 250 mg twice daily or three times daily for 10 days; adolescents and adults: 250 mg four times daily or 500 mg twice daily for 10 days) or IM benzathine penicillin (given as Bicillin C-R (<27 kg: 600,000 units as a one-time dose; ≥27 kg: 1,200,000 units as a one time dose). In patients allergic to penicillin, treatment may be initiated with erythromycin, other macrolides, or a cephalosporin.

Syphilis

Syphilis is the third most common sexually transmitted infection in the United States (following chlamydia and gonorrhea) and is transmitted by direct contact with an infectious lesion. The incidence of reported cases has risen steadily since 2001. The causative organism is the spirochete Treponema pallidum. After an incubation period of 10 to 90 days, the primary lesion appears, which lasts 3 to 12 weeks and heals spontaneously. If untreated, in 6 weeks to 6 months after exposure, the secondary stage may be manifest. These lesions also heal spontaneously in 2 to 6 weeks as the disease enters the latent phase. Tertiary syphilis or latent syphilis may occur in months to years after untreated secondary syphilis.

The chancre is the dermatologic manifestation of primary syphilis. Chancres usually appear as single lesions but may be multiple. They appear at the site of spirochete inoculation, usually the mucous membranes of the mouth or genitalia. The chancre begins as a papule and characteristically develops into an ulcer approximately 1 cm in diameter with a central base and raised borders ( Fig. 107.12 ). The chancre is typically painless unless it is secondarily infected, and it may be accompanied by painless lymphadenopathy. Many patients do not recall the primary chancre.

The secondary stage usually follows the primary stage by 6 weeks or more. There are a number of cutaneous manifestations of secondary syphilis. Lesions may be erythematous or pink macules or papules, usually with a generalized symmetric distribution. Secondary syphilis should be considered in the differential diagnosis of any maculopapular rash. Pigmented macules and papules may appear on the palms and soles ( Fig. 107.13 ). Generalized lymphadenopathy and malaise accompany the skin lesions. Moist, flat, verrucous condyloma latum may appear in the genital area. These lesions are highly contagious.

The diagnosis of primary or secondary syphilis should be made in the ED based on clinical presentation. Definitive diagnosis is made by the identification of spirochetes with darkfield microscopy and by serologic testing. The result of the Venereal Disease Research Laboratory (VDRL) test, the most commonly used diagnostic nontreponemal serologic test, is positive in approximately three-fourths of patients with primary syphilis but may be negative early in the course of the disease. The VDRL test result is positive in cases of secondary syphilis. Rapid plasma reagin (RPR) is an alternative nontreponemal test. The most specific and sensitive serologic test is the fluorescent treponemal antibody absorption (FTA-ABS) test.

Current guidelines for syphilis treatment, including in penicillin allergic individuals, are available at www.cdc.gov. Treatment should be initiated in the ED based on clinical diagnosis. Primary and secondary syphilis is treated with benzathine penicillin G in a dose of 2.4 million units IM. Pregnant women should be treated with the regimen appropriate for their disease state. Doxycycline or azithromycin are alternatives in patients with penicillin allergy. Patients with early latent syphilis are treated the same as patients with primary disease, whereas late latent syphilis and tertiary syphilis are treated with benzathine penicillin G, three doses of 2.4 million units IM at weekly intervals for a total of 7.2 million units. Treatment of neurosyphilis requires infusion of aqueous crystalline penicillin, 3 to 4 million units IV every 4 hours for 10 to 14 days. Following antibiotic therapy, patients may experience a Jarisch-Herxheimer reaction, with symptoms of fever, headache, and myalgia.

Disseminated Gonococcal Infection

Gonococcal infections are the second most common notifiable condition in the U.S., following Chlamydia trachomatis infections. The incidence of reported gonococcal infection has risen consistently since 2009. Disseminated gonococcal infection (DGI) occurs in less than 2% of patients with gonorrhea, affecting women primarily. Symptoms typically include fever and migratory asymmetric polyarthralgias, tenosynovitis, or skin lesions. The lesions have a predilection for periarticular regions of the distal extremities. The lesions typically begin as erythematous or hemorrhagic papules that evolve into pustules and vesicles with an erythematous halo ( Fig. 107.14 ). They may be tender and may have a gray necrotic or hemorrhagic center. Healing with crust formation usually occurs within 4 or 5 days, although recurrent crops of lesions may appear even after antibiotics have been started. Rare complications may include perihepatitis, endocarditis, or meningitis.

The organism may be cultured from the cutaneous lesions. A more reliable diagnostic technique is immunofluorescent antibody staining of direct smears from pustules.

Treatment should be initiated with ceftriaxone, 1 g IV q 24 hours, and treatment for chlamydia with doxycycline 100 mg bid for 7 days. Alternatives include cefotaxime or ceftizoxime, plus doxycycline. Patients allergic to β-lactam antibiotics or those with severe penicillin allergies may be treated with spectinomycin. Ciprofloxacin and ofloxacin are not recommended owing to increasing resistance patterns. Hospitalization is recommended for patients with DGI. Chapter 84 provides detailed management recommendations.

Staphylococcal Scalded Skin Syndrome

Staphylococcal scalded skin syndrome (SSSS) typically occurs in children 6 years old or younger. It is caused by an infection with phage group 2 exotoxin-producing staphylococci. The illness begins with erythema and crusting around the mouth. The erythema then spreads down the body, followed by bulla formation and desquamation. Mucous membranes are typically spared. After desquamation occurs, the lesions dry up quickly, with clinical resolution in 3 to 7 days.

Treatment should be initiated promptly with intravenous antibiotics, such as nafcillin, oxacillin, or vancomycin. For patients allergic to penicillin, alternatives may include clarithromycin or cefuroxime. Chapter 126 provides detailed management recommendations.

Toxic Shock Syndrome

Toxic shock syndrome (TSS) is an acute febrile illness characterized by a diffuse desquamating erythroderma. Clinical presentation may include high fever, hypotension, constitutional symptoms, multiorgan involvement, and rash. The syndrome gained notoriety in the early 1980s because of association with tampon use. However, it is also well known in men and children. Its appearance has often been linked to exotoxin-producing S. aureus. Approximately 50% of cases are associated with menstruation. Other cases occur in the postoperative setting, or related to burns, postpartum infection, osteomyelitis, arthritis, empyema, fasciitis, septic abortion, pharyngitis, peritonsillar abscess, sinusitis, or subcutaneous abscess.

TSS is typically caused by Staphylococcus aureus or Streptococcus pyogenes . It has been reported in previously healthy patients, immunocompromised patients, and elders. Fatigue, localized pain, and nonspecific symptoms herald the onset of this disease, followed by septic shock and multisystem organ failure.

Diagnosis of TSS requires the presence of (1) temperature of at least 38.9°C; (2) hypotension, with a systolic blood pressure of 90 mm Hg or less; (3) rash; and (4) involvement of at least three organ systems. Systemic involvement may include the gastrointestinal tract, muscular system, or CNS and laboratory evidence of renal, hepatic, or hematologic dysfunction. Headache, myalgias, arthralgias, alteration of consciousness, nausea, vomiting, or diarrhea may be present.

The rash is typically a diffuse, blanching, macular erythroderma. Accompanying nonexudative mucous membrane inflammation is common. Pharyngitis, sometimes accompanied by a “strawberry tongue,” conjunctivitis, or vaginitis, may be seen. As a general rule, the rash fades within 3 days of its appearance. This is followed by a full-thickness desquamation, most commonly involving the hands and feet.

Initial treatment of TSS consists of IV fluid replacement, ventilatory support, pressor agents, antibiotics covering S. aureus (including MRSA) and S. pyogenes . Initial empirical antibiotic regimens may include clindamycin, vancomycin, linezolid, imipenem, meropenem, ticarcillin-clavulanate, or piperacillin-tazobactam. Chapter 126 provides detailed management recommendations.