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Emergency Medicine Atlas > Part 1. Regional Anatomy > Chapter 13. Cutaneous Conditions >

Erythema Multiforme

Associated Clinical Features

Considered a hypersensitivity syndrome, erythema multiforme (EM) presents with characteristic target or iris-shaped papules and vesicobullous plaques (Fig. 13.1). These lesions are frequently cutaneous manifestations of a drug reaction, viral infection, Mycoplasma, or malignancy. These plaques are usually symmetric, pruritic, and painful, often involving the mucous membranes and extremities, including the palms and soles. The milder form of the disease has minimal mucosal involvement, no bullae, and no systemic symptoms. Fever, malaise, extensive mucosal involvement, and other constitutional symptoms are noted in the severe form of EM, known as Stevens-Johnson syndrome (see next diagnosis).

Figure 13.1

Erythema Multiforme Note the symmetric distribution of the target macules. (Courtesy of Michael Redman, PA-C.)

Differential Diagnosis

The maculopapular presentation may be confused with urticaria or fixed drug eruption, whereas the oral vesicobullous plaques resemble herpetic gingivostomatitis. However, the cutaneous target lesions and their symmetry are typical of EM.

Emergency Department Treatment and Disposition

Elimination of any possible etiology (idiopathic cause noted approximately 50%) and supportive measures to allay the burning and itching are basic to treating this disorder. Milder forms of the disease usually resolve spontaneously within 2 to 3 weeks. Corticosteroids are reserved for the severest presentations. EM minor can be treated on an outpatient basis. However, patients with significant systemic illness and additional eruptions involving the mucosal surfaces (Stevens-Johnson syndrome) may require admission and supportive care.

Clinical Pearls

1. Symmetrically distributed target lesions on the extensor surfaces of the extremities and a lack of significant systemic manifestations are classified as EM minor.

2. Drug-associated EM usually begins within 2 to 3 weeks of initiating therapy. Sulfonamides and penicillins are most often the culprits.

3. Many clinicians treat idiopathic cases empirically with a trial of acyclovir therapy owing to the high incidence of subclinical herpes simplex infection as the cause of the EM.

Stevens-Johnson Syndrome (EM Major)

Associated Clinical Features

Stevens-Johnson syndrome is a severe, rarely fatal variety of erythema multiforme. An abrupt onset of constitutional symptoms precedes the hemorrhagic bullae found on multiple mucosal surfaces and the edematous, erythematous cutaneous plaques (Fig. 13.2). The bullae erode, producing stomatitis, conjunctivitis, vulvovaginitis, or balanitis. Patients appear extremely ill and may develop pneumonia, arthritis, seizures, coma, and hepatic dysfunction. Death, when it occurs, is usually due to overwhelming sepsis.

Figure 13.2

Stevens-Johnson Syndrome Note the target lesions on the hands of this patient, as well as the mucosal involvement on the lips. (Courtesy of Alan B. Storrow, MD.)

Differential Diagnosis

Meningococcemia must be considered in the differential diagnosis. The severe involvement of mucous membranes is characteristic of Stevens-Johnson syndrome.

Emergency Department Treatment and Disposition

Patients presenting with significant evidence of toxicity should be admitted to the hospital. Supportive measures and selective use of systemic corticosteroids are the cornerstone of therapy.

Clinical Pearls

1. Stevens-Johnson syndrome is self-limited and usually resolves in approximately 1 month.

2. Sulfonamides, penicillins, and anticonvulsants are common causes of Stevens-Johnson syndrome.

Toxic Epidermal Necrolysis

Associated Clinical Features

Toxic epidermal necrolysis (TEN) is characterized by the formation of erythematous (scalded) skin followed by widespread bullae (Fig. 13.3), usually a cutaneous manifestation of a drug reaction. The epidermis eventually becomes necrotic, leading to extensive exfoliation and exposure of the raw dermis (Fig. 13.4). A prodrome of fever, fatigue, myalgias, and skin tenderness occurs in the majority of patients. The mortality rate approaches 25%, with death usually due to sepsis or gram-negative pneumonia. TEN is generally considered to be the most severe form of erythema multiforme.

Figure 13.3

Toxic Epidermal Necrolysis Note the widespread erythematous bullae and epidermal exfoliation. (Courtesy of James J. Nordlund, MD.)

Figure 13.4

Toxic Epidermal Necrolysis The initial bullae have coalesced, leading to extensive exfoliation of the epidermis. (Courtesy of Keith Batts, MD.)

Differential Diagnosis

Early in its course, TEN may resemble scarlet fever, toxic shock syndrome, or erythema multiforme. In children, staphylococcal scalded-skin syndrome closely mimics TEN; however, it involves only the superficial epidermis without extension to the dermis.

Emergency Department Treatment and Disposition

Supportive care includes debridement of necrotic tissue, pain control, aggressive hydration, appropriate antibiotic therapy, and covering exposed dermis, even with cadaver allografts, to avoid infection and reduce pain. These patients are best managed in burn treatment centers.

Clinical Pearls

1. Slight pressure causing the skin to slide laterally and separate from the dermis is a positive Nikolsky's sign.

2. The initial bullae coalesce, leading to exfoliation of the entire epidermis.

Necrotizing (Leukocytoclastic) Vasculitis

Associated Clinical Features

Necrotizing vasculitis is a hypersensitivity vasculitis in adults associated with infectious agents, connective tissue diseases, malignancy, and drugs. Symptoms may be confined to the skin in the form of symmetric petechiae and palpable purpura over the distal third of the extremities. Systemic vascular involvement occurs in the kidneys (glomerulonephritis), muscles, joints, gastrointestinal tract (abdominal pain and bleeding), and peripheral nerves (neuritis). Henoch-Schönlein purpura (HSP) (Fig. 13.5) is the classic example of vasculitis in children, consisting of a clinical triad of palpable purpura, arthritis, and abdominal pain. It is usually a benign, self-limited disease that occurs in children most commonly after a bacterial or viral infection.

Figure 13.5

Henoch-Schönlein Purpura Note the classic acral distribution of HSP. It is immunoglobulin A (IgA)–mediated and most commonly occurs in children after a streptococcal or viral infection. (Courtesy of Kevin J. Knoop, MD, MS.)

Differential Diagnosis

Idiopathic thrombocytopenic purpura (ITP), disseminated intravascular coagulation (DIC), meningococcemia, gonococcemia, Rocky Mountain spotted fever, staphylococcal septicemia, and embolic endocarditis must all be considered in the differential diagnosis; however, patients with septic vasculitis are generally more severely ill, with rapidly progressive symptoms. Also, the purpura of septic vasculitis tend to be fewer in number, asymmetric, and distal in location. Biopsy of the purpura is helpful in distinguishing necrotizing vasculitis from septic vasculitis, DIC, and embolic endocarditis.

Emergency Department Treatment and Disposition

A majority of cases are self-limited and require only rest, elevation, and analgesics. Severe cases with systemic manifestations may require admission for supportive care, corticosteroids, and cytotoxic immunosuppressive therapy. Antibiotics should be utilized if the vasculitis follows an infection.

Clinical Pearls

1. The petechiae and purpura of necrotizing vasculitis are usually localized to the lower third of the extremities.

2. A patient presenting with purpura and the signs and symptoms of serum sickness should lead the examiner to consider necrotizing vasculitis.

Rocky Mountain Spotted Fever

Associated Clinical Features

Rickettsia rickettsii is transmitted by the bite of an infected tick. Fever, rigors, headache, myalgias, and weakness occur 7 to 10 days after inoculation. The initially blanching macular eruption begins at approximately 4 days on the distal extremities and somewhat later on the palms and soles (Fig. 13.6). It soon becomes petechial as it spreads centrally to involve the trunk and abdomen. However, it can also present without obvious cutaneous manifestations.

Figure 13.6

Rocky Mountain Spotted Fever These erythematous macular lesions will evolve into a petechial rash that will spread centrally. (Courtesy of Daniel Noltkamper, MD.)

Differential Diagnosis

Viral exanthems, drug eruptions, necrotizing vasculitis, purpuric bacteremia, and meningococcemia may all resemble this potentially fatal illness.

Emergency Department Treatment and Disposition

Doxycycline or chloramphenicol is required for this potentially fatal illness. Doxycycline is the drug of choice, yet it should be avoided in pregnant or lactating women and children younger than 8 years of age. Mildly ill patients may be treated with oral antibiotics on an outpatient basis as long as close follow-up can be arranged. More severely ill patients should be admitted because their care can be complicated by circulatory collapse and coma. Approximately 20% of untreated patients will die; overall mortality is 3 to 7%.

Clinical Pearls

1. Palmar and plantar petechiae in a severely ill patient should be treated as Rocky Mountain spotted fever until proved otherwise.

2. Most cases occur between April and October, with the highest incidence occurring in the Southeast and South-Central states.

Disseminated Gonococcus

Associated Clinical Features

Disseminated gonococcus (GC) is a systemic infection, with septic vasculitis following the hematogenous dissemination of the organism Neisseria gonorrhoeae. The spectrum of disease varies from skin lesions alone to skin lesions with tenosynovitis or septic arthritis. The initial lesion is an erythematous macule that evolves into a necrotic, purpuric vesicopustule (Fig. 13.7). These purpura are few in number, asymmetric, and predominantly distal in location.

Figure 13.7

Disseminated Gonococcus A classic presentation of the asymmetric purpuric rash, vesicopustule, and polyarthritis in the hands of an individual with disseminated GC. (Courtesy of Glaxo Wellcome Pharmaceuticals.)

Differential Diagnosis

The purpura may resemble meningococcemia, staphylococcal septicemia, necrotizing vasculitis, or endocarditis with emboli. Infectious arthritis or tenosynovitis must be considered when the patient presents with joint complaints. It is important to obtain Gram's stain of the contents of the vesicopustule, as well as all other body sites and fluids.

Emergency Department Treatment and Disposition

Therapy consists of intravenous or intramuscular ceftriaxone or cefotaxime until symptoms either improve or resolve, followed by an additional 7 days of orally administered ciprofloxacin or cefuroxime. Hospitalization is recommended for noncompliant patients or cases noted to have an associated septic arthritis.

Clinical Pearls

1. The most common symptom of disseminated GC is arthralgia of one or more joints, primarily involving the hands or knees.

2. Skin lesions develop in up to 70% of cases and will resolve within 4 days regardless of antibiotics.

3. Less than one-third of patients will have urethritis.

4. The purpura of septic vasculitis (of whatever bacterial etiology) tend to be fewer in number, asymmetric, and distal in location.

Infective Endocarditis

Associated Clinical Features

Infective endocarditis is an illness characterized by fever, valve destruction, and peripheral embolization manifested by rare, usually distal purpura. Streptococcus viridans is the most common causative organism. Janeway lesions (Fig. 13.8) occur in 5% of cases and consist of nontender, small, erythematous macules on the palms or soles. Osler's nodes (Fig. 13.9) occur in 10% of cases and consist of transient, tender, purplish nodules on the pulp of the fingers and toes. Splinter hemorrhages are black, linear discolorations beneath the nail plate (Fig. 13.10). They are present in 20% of cases and are more suggestive of subacute bacterial endocarditis (SBE) if present at the proximal or middle nail plate. Murmurs, retinal hemorrhages, septic arthritis, and significant embolic episodes such as pulmonary embolism or stroke may also be present.

Figure 13.8

Janeway Lesions Peripheral embolization to the sole, resulting in a cluster of erythematous macules known as Janeway lesions. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.9

Osler's Nodes Subcutaneous, purplish, tender nodules in the pulp of the fingers known as Osler's nodes. (Courtesy of the Armed Forces Institute of Pathology, Bethesda, MD.)

Figure 13.10

Splinter Hemorrhages Note the splinter hemorrhages along the distal aspect of the nail plate, due to emboli from subacute bacterial endocarditis. (Courtesy of the Armed Forces Institute of Pathology, Bethesda, MD.)

Differential Diagnosis

Meningococcemia, gonococcemia, staphylococcal septicemia, and necrotizing vasculitis must all be considered in the differential diagnosis. Echocardiography can aid in the diagnosis.

Emergency Department Treatment and Disposition

Antibiotics must be appropriate for the infectious agent; however, therapy is often required before the diagnosis is confirmed or the infecting organism is known. All toxic patients require admission, as do all febrile patients who have prosthetic valves or who are intravenous drug abusers. These patients should receive gentamicin with nafcillin or vancomycin empirically pending the blood culture results. Patients with rheumatic or congenital valve abnormalities may receive streptomycin with penicillin or vancomycin.

Clinical Pearls

1. Janeway lesions, Osler's nodes, and splinter hemorrhages in a febrile patient with a murmur are virtually diagnostic of infective endocarditis.

2. Rheumatic heart disease is the most common predisposing factor, with the mitral valve being the most common site of damage.

3. Congenital heart disease, intravenous drug abuse, and prosthetic heart valves are additional predisposing factors to the development of infective endocarditis.

Idiopathic Thrombocytopenic Purpura

Associated Clinical Features

Idiopathic thrombocytopenic purpura (ITP) occurs as the result of platelet injury and destruction. Pinpoint, red, nonblanching petechiae or nonpalpable purpura and ecchymoses are found on the skin (Fig. 13.11) and mucous membranes, either spontaneously (platelets <10,000/mm³) or at the site of minimal trauma (platelets <40,000/mm³). Melena, hematochezia, menorrhagia, and severe intracranial hemorrhages may also occur in conjunction with the purpura. The acute form affects children 1 to 2 weeks after a viral illness; the chronic form occurs most often in adults, with women outnumbering men 3:1, and may present with an associated splenomegaly.

Figure 13.11

Idiopathic Thrombocytopenic Purpura This thrombocytopenic patient with splenomegaly has pinpoint, nonblanching, nonpalpable petechiae. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Nonhemorrhagic vascular dilatations like telangiectasia or true petechiae and purpura, as found in scurvy or posttraumatic purpura, must be differentiated from this potentially debilitating illness. Assessment of the platelet count aids in making the diagnosis.

Emergency Department Treatment and Disposition

Hospitalization at the time of diagnosis is recommended because the differential diagnosis is extensive and the bleeding risks are significant. Platelets are transfused only if there is life-threatening bleeding or the total count is <10,000/mm³. Immunosuppressive drugs, steroids, and intravenous immunoglobulin are of benefit in the acute cases; splenectomy is utilized in chronic cases.

Clinical Pearls

1. Petechiae and purpura in a thrombocytopenic patient with splenomegaly make the diagnosis.

2. The acute form of ITP has an excellent prognosis (90% spontaneous remission), whereas the course of chronic ITP is one of varying severity with little hope of remission.

Thrombotic Thrombocytopenic Purpura (TTP)

Associated Clinical Features

The diagnosis of thrombotic thrombocytopenic purpura (TTP) is characterized by the following pentad of symptoms:

1. Microangiopathic hemolytic anemia, with characteristic schistocytes on the peripheral blood smear and a reticulocytosis.

2. Thrombocytopenia with platelet counts ranging from 5000 to 100,000/L (Fig. 13.12).

3. Renal abnormalities including renal insufficiency, azotemia, proteinuria, or hematuria.

4. Fever.

5. Neurologic abnormalities including headache, confusion, cranial nerve palsies, seizures, or coma.

Figure 13.12

Thrombic Thrombocytopenic Purpura Bleeding at initial presentation is seen in about 30 to 40% of patients with TTP. (Courtesy of James J. Nordlund, MD.)

The disease affects women more than men and can affect any age group, but it occurs most commonly in ages 10 to 60.

Differential Diagnosis

Hemolytic uremic syndrome (HUS), disseminated intravascular coagulation, and the pregnancy-associated HELLP (Hemolysis, Elevated Liver enzymes, Low Platelet count) syndrome can all present like TTP. HUS and TTP appear to be closely related and may represent variants of a single disease.

Emergency Department Treatment and Disposition

The cornerstone of therapy is plasma exchange transfusion. Some patients can be treated with plasma infusions alone. It is thought that the transfusions provide a missing substrate and the exchange may remove some unknown toxic substance. Prednisone and antiplatelet therapy with aspirin may be helpful. Patients recalcitrant to standard therapy may be treated with immunosuppressives (vincristine, azathioprine, cyclophosphamide) and even splenectomy. All patients should be admitted.

Clinical Pearls

1. Platelet transfusions should be avoided unless there is life-threatening hemorrhage; they can worsen the thrombotic process.

2. Typically TTP is acute and fulminant, but it can become a chronic, relapsing form.

3. Hemoglobin less than 6 g/dL, platelet count less than 20,000, elevated indirect bilirubin and LDH, and a negative Coombs test are typically found.

Livedo Reticularis

Associated Clinical Features

Livedo reticularis presents as a macular, reticulated (lace-like) patch of nonpalpable cutaneous vasodilatation (Fig. 13.13) in response to a variety of vascular occlusive processes. This pattern predominates in the peripheral or acral areas and may or may not be associated with purpura. In time, the overlying epidermis and dermis may infarct and form ulcerations or develop palpable dermal papules or nodules. Livedo reticularis is usually representative of a severe underlying systemic disease. Inflammatory vascular diseases (livedo vasculitis, polyarteritis nodosa, lupus erythematosus), septic emboli (meningococcemia), tumors (pheochromocytoma), and systemic illnesses associated with mechanical vessel blockage (anticardiolipin antibody syndrome, polycythemia vera, sickle cell anemia, cholesterol embolus) are a few diseases associated with or responsible for livedo reticularis. It can also occur independent of any disease association.

Figure 13.13

Livedo Reticularis Note the reticulated (lace-like) blanching erythema symmetrically distributed over the lower extremities. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

The most important consideration in making this diagnosis is to rule out an associated vascular occlusion of whatever etiology.

Emergency Department Treatment and Disposition

The treatment of livedo reticularis is treatment of the underlying disorder and avoiding exposure to cold.

Clinical Pearls

1. Livedo vasculitis is an inflammatory vascular disease usually found symmetrically on the ankles and dorsum of the feet. It consists of painful stellate-shaped ulcerations surrounded by an erythematous livedo pattern.

2. Cholesterol emboli usually occur after an intraarterial procedure. Pain often precedes the livedo pattern of purpura on the distal extremities.

3. Patients with anticardiolipin antibody syndrome have extensive livedo reticularis and recurrent arterial and venous thromboses involving multiple organ systems.

Herpes Zoster

Associated Clinical Features

Herpes zoster is a dermatomal, unilateral reactivation of the varicella zoster virus. Pain, tenderness, and dysesthesias may present 4 to 5 days prior to an eruption composed of umbilicated, grouped vesicles on an erythematous, edematous base (Fig. 13.14). The vesicles may become purulent or hemorrhagic. Nerve involvement may actually occur without cutaneous involvement. Ophthalmic zoster involves the nasociliary branch of the fifth cranial nerve and presents with vesicles on the nose and cornea (Hutchinson's sign). Ramsay-Hunt syndrome is a herpes zoster infection of the geniculate ganglion that presents with decreased hearing, facial palsy, and vesicles on the tympanic membrane, pinna, and ear canal.

Figure 13.14

Herpes Zoster This eruption consists of a dermatomal distribution of umbilicated vesicles on an erythematous base. Note the occasional cluster of hemorrhagic vesicles. Tzank smear is positive. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

The most likely differential diagnosis is herpes simplex infection, which is usually recurrent. Herpes zoster recurs in fewer than 5% of immunocompetent patients. The eruption may resemble contact dermatitis, localized cellulitis, or grouped insect bites. The prodromal pain must be differentiated from potential pleural, cardiac, or abdominal origin. Tzank smear of the floor of a vesicle demonstrating multinucleated giant cells makes the diagnosis of a herpes family infection (Fig. 13.15). Cultures may be necessary to distinguish herpes zoster forms.

Figure 13.15

Herpes Zoster A Tzank smear of both the roof and floor of a herpetic vesicle demonstrating a multinucleated giant cell. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Emergency Department Treatment and Disposition

Uncomplicated cases of herpes zoster can be managed with supportive care, especially pain control. Admission to the hospital for intravenous acyclovir is usually reserved for complicated cases involving multiple dermatomal distribution or the ophthalmic branch of the trigeminal nerve, disseminated disease, or immunocompromised patients. Acyclovir or famciclovir hasten the healing and decreases the pain if started within 72 h of appearance of the vesicles. These agents have also been shown to reduce the duration of postherpetic neuralgia. Prednisone may also prove useful. Herpes zoster keratitis requires immediate ophthalmologic consultation to avoid any potential vision loss.

Clinical Pearls

1. Dermatomally grouped, umbilicated vesicles on an erythematous base are diagnostic of herpes zoster.

2. The thorax is the most common area involved, followed by the face (trigeminal nerve).

3. The nonimmune or immunocompromised should avoid lesional contact from prodrome until reepithelialization, since the crusts can contain the varicella zoster virus.

4. Typically, an infected patient may transmit chickenpox to a nonimmune individual.

5. Zoster during pregnancy seems to have no deleterious effects on the mother or baby.

Herpetic Whitlow

Associated Clinical Features

Herpetic whitlow is a painful herpes simplex infection of the distal finger characterized by edema, erythema, vesicles, and/or pustules grouped on an erythematous base (Fig. 13.16). Fever, lymphangitis, and regional adenopathy often accompany the lesion.

Figure 13.16

Herpetic Whitlow Note the cluster of vesicles on an erythematous base located at the distal finger. Tzank smear is positive. (Courtesy of Lawrence B. Stack, MD.)

Differential Diagnosis

Paronychia, felon, and contact dermatitis must be differentiated from this contagious illness. A Tzank smear of the floor of the vesicle demonstrating multinucleated giant cells makes the diagnosis.

Emergency Department Treatment and Disposition

Acyclovir in addition to analgesics and antipyretics are useful. To be most effective, acyclovir must be started within 72 h of the appearance of the eruption. Topical antibiotic ointments help prevent secondary infection and may speed healing.

Clinical Pearls

1. Grouped, umbilicated vesicles on an erythematous base are diagnostic of a herpes family infection.

2. Wear protective gloves; herpetic whitlow is an occupational hazard in the medical and dental professions.

Erysipelas

Associated Clinical Features

Erysipelas is a group A streptococcal cellulitis involving the skin to the level of the dermis. The plaque is typically erythematous, edematous, and painful, with an elevated, well-demarcated border (Fig. 13.17). The associated edema tends to make the plaque appear shiny. Erysipelas frequently occurs on the face and lower extremities.

Figure 13.17

Erysipelas Note the well-demarcated, edematous, erythematous, shiny plaque. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Other significant illnesses—such as deep venous thrombosis, thrombophlebitis, and necrotizing fasciitis—must be ruled out.

Emergency Department Treatment and Disposition

All infections require rest, elevation, heat, and antibiotics. Mild presentations may be treated on an outpatient basis with oral dicloxacillin or erythromycin in penicillin-allergic patients. More severe illness or toxicity requires hospitalization and intravenous antibiotics.

Clinical Pearls

1. The well-demarcated, tender, shiny, erythematous plaque is diagnostic of erysipelas.

2. This same shiny, erythematous plaque on the face of a febrile child may be caused by Haemophilus influenzae, necessitating intravenous chloramphenicol or a cephalosporin.

3. Lymphatic streaking is more common in erysipelas than cellulitis.

Hot Tub Folliculitis

Associated Clinical Features

Hot tub folliculitis is a pruritic, follicular, pustular eruption confined to the hair follicle and is secondary to a cutaneous infection with Pseudomonas aeruginosa (Fig. 13.18). Headache, sore throat, earache, and fever may accompany the pustules, which usually localize to the trunk and proximal extremities.

Figure 13.18

Hot Tub Folliculitis Note the pustules localized to the hair follicles of the trunk and proximal extremity. (Courtesy of Jeffrey S. Gibson, MD.)

Differential Diagnosis

Other forms of folliculitis (including those caused by Staphylococcus aureus), acne, and miliaria rubra are usually considered in the differential diagnosis.

Emergency Department Treatment and Disposition

The folliculitis usually involutes in 7 to 10 days without treatment. Acetic acid compresses and local wound cleansing may speed recovery. In addition, the hot tub or source of exposure must be decontaminated to avoid reexposure.

Clinical Pearls

1. Pruritic pustules confined to the hair follicles of the trunk and proximal extremities is diagnostic of folliculitis.

2. This most commonly occurs in individuals who use hot tubs, whirlpools, or saunas.

3. This may also result from contact with chemicals (exfoliative beauty aids) or repetitive physical trauma (friction from tight clothing).

Ecthyma Gangrenosum

Associated Clinical Features

Ecthyma gangrenosum is a Pseudomonas aeruginosa infection that usually occurs in the septic, immunocompromised, or neutropenic patient. The initially erythematous macules develop bullae or pustules (Fig. 13.19) surrounded by violaceous halos. The pustules become hemorrhagic and rupture, forming painless ulcers with necrotic, black centers.

Figure 13.19

Ecthyma Gangrenosum A typical hemorrhagic bulla of ecthyma gangrenosum secondary to pseudomonal sepsis. (Courtesy of James Mensching, MD.)

Differential Diagnosis

Necrotizing vasculitis, fixed drug eruptions, pyoderma gangrenosum, and brown recluse spider bites must all be considered in the differential diagnosis.

Emergency Department Treatment and Disposition

These patients are usually septic and immunocompromised. Admission is usually required for the patient to receive antipseudomonal antibiotics and general supportive care.

Clinical Pearls

1. Consider ecthyma gangrenosum when examining a septic patient who presents with bullae or pustules that rupture and form painless, necrotic ulcers.

2. It is important to consider underlying immunodeficiency when making this diagnosis.

Pityriasis Rosea

Associated Clinical Features

Pityriasis rosea is a mild inflammatory, exanthematous, papulosquamous eruption. The pathognomonic finding is an oval salmon-colored papule with a central collarette of scale. It primarily occurs on the trunk with the long axis of the oval papule following the lines of cleavage in a Christmas tree–like distribution (Fig. 13.20). A herald patch, consisting of a much larger plaque with central clearing and scales, frequently precedes the exanthematous phase by 1 to 2 weeks (Fig. 13.21). The eruption usually lasts 4 to 6 weeks and is frequently pruritic.

Figure 13.20

Pityriasis Rosea An exanthematous, papulosquamous eruption, with the long axis of the oval papules following the lines of cleavage in a Christmas tree–like eruption. (Courtesy of James J. Nordlund, MD.)

Figure 13.21

Herald Patch A herald patch precedes the exanthematous phase: a larger, oval, salmon-colored patch with a central collarette of scale. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

This must be differentiated from the secondary lesions of syphilis, tinea versicolor, and some drug eruptions.

Emergency Department Treatment and Disposition

Symptomatic treatment is usually all that can be offered to the patient. Antihistamines may alleviate the associated pruritus. Ultraviolet light has also been used with some success.

Clinical Pearls

1. A salmon-colored papule with central scale, negative KOH examination for hyphae, and negative serologic testing for syphilis makes the diagnosis of pityriasis rosea.

2. It frequently appears in very atypical form in dark-skinned individuals (acral, face, and genital location).

Secondary Syphilis

Associated Clinical Features

The initial papules of secondary syphilis are usually asymptomatic, although they may be painful or pruritic; they appear 2 to 10 weeks after the primary chancre. Headache, sore throat, fever, arthralgias, myalgias, and a generalized lymphadenopathy may also be present. These exanthematous papules are symmetric and nondestructive, usually forming a pityriasis rosea–like pattern on the trunk, palms, and soles (Figs. 13.22, 13.23). Later lesions are firm, pigmented papules with a coppery tint and adherent scales (Fig. 13.24). Macerated papules may form on the mucous membranes; "motheaten" alopecia may occur on the scalp; and condylomata lata may occur in the intertriginous areas.

Figure 13.22

Secondary Syphilis These eruptive, scaly, copper-colored papules on the foot may be the initial presentation of secondary syphilis. They are usually symmetric, asymptomatic, and nondestructive. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.23

Secondary Syphilis These firm, pigmented, erythematous papules are characteristic of secondary syphilis. (Courtesy of Lynn Utecht, MD.)

Figure 13.24

Secondary Syphilis These firm, pigmented papules with a coppery tint and adherent scale are characteristic. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Syphilis is "the great imitator." It may resemble psoriasis, drug eruptions, pityriasis rosea, viral exanthems, tinea corporis, tinea versicolor, and condyloma acuminata. A positive serologic test for syphilis makes the diagnosis.

Emergency Department Treatment and Disposition

Penicillin is the agent of choice for treatment, with tetracycline or erythromycin used in cases of penicillin allergy. A Jarisch-Herxheimer reaction may occur several hours after treatment with antibiotics, correlating with the clearance of spirochetes from the bloodstream. This reaction lasts approximately 24 h, yet it may be more threatening than the disease itself. Increasing fever, rigors, myalgias, headache, tachycardia, hypotension, and a drop in the leukocyte and platelet count may be encountered. Fluid resuscitation to maintain the blood pressure and supportive care may be needed.

Clinical Pearls

1. Scaly palmar and plantar papules are strongly suggestive of secondary syphilis, the incidence of which is rising.

2. These scaling red-brown papules appear 2 to 10 weeks after the spontaneous resolution of the initial painless chancre.

3. The latent stage follows the resolution of the papules; it is characterized by a positive serology and an absence of signs and symptoms.

4. Tertiary syphilis occurs in untreated or poorly treated patients and may manifest itself as general paresis, tabes dorsalis, optic atrophy, and aortitis with aneurysms.

5. It is important to consider the prozone phenomenon (falsely negative agglutination in undiluted serum) in an AIDS patient with presumed syphilis in whom the serologic test is negative.

Erythema Chronicum Migrans (ECM)

Associated Clinical Features

Borrelia burgdorferi is the tick-borne spirochete responsible for Lyme borreliosis, and erythema chronicum migrans (ECM) is the pathognomonic rash of Lyme disease occuring early in the infection. The initial prodromal symptoms of fever, myalgias, arthralgias, and headache are followed by a macule or papule progressing to a plaque at the site of the bite. This plaque expands its red, raised border as it clears centrally, leading to an annular appearance (Fig. 13.25). The plaque may burn and is rarely pruritic. On average, there are 9 days between the time of the bite and the appearance of the rash.

Figure 13.25

Erythema Chronicum Migrans (ECM) This pathognomonic eruption of Lyme disease forms at the site of the tick bite. The initial papule forms into a slowly enlarging oval area of erythema while clearing centrally. (Courtesy of Timothy Hinman, MD.)

Differential Diagnosis

This annular plaque may resemble a fixed drug eruption, tinea corporis, urticaria, or the herald patch of pityriasis rosea. The multiple secondary annular papules and plaques that may rarely form can resemble secondary syphilis. However, the Lyme-related eruption spares the palms and soles.

Emergency Department Treatment and Disposition

The duration of antibiotic treatment (10 to 30 days) depends on the severity of the symptoms. Tetracycline or doxycycline are the drugs of choice. Pregnant or lactating females and children younger than 8 years of age should be treated with penicillin or amoxicillin. Erythromycin is a suitable alternative. Patients with minimal symptoms may be treated on an outpatient basis. Those patients with significant toxicity and complications require admission, supportive care, and parenteral antibiotics.

Clinical Pearls

1. An annular plaque arising at the site of a tick bite in a patient with systemic symptoms should be treated as Lyme disease until proved otherwise.

2. Stage I of Lyme disease consists of constitutional symptoms and the characteristic rash of ECM.

3. Stage II of Lyme disease consists of neurologic (aseptic meningitis, encephalitis, bilateral Bell's palsy) and cardiac (myocarditis, conduction blocks) manifestations.

4. Stage III of Lyme disease consists of an asymmetric, episodic, oligoarticular arthritis.

Tinea Corporis, Faciale, and Manus

Associated Clinical Features

Tinea corporis includes all dermatophyte infections excluding the scalp, face, hands, feet, and groin. The dermatophytosis is pruritic and consists of well circumscribed scaly plaque with a slightly elevated border and central clearing (Fig. 13.26). This annular configuration is most commonly found on the trunk and neck. Skin scrapings viewed with a KOH preparation exhibit septate hyphae.

Figure 13.26

Tinea Corporis This dermatophytosis is known as ringworm, a well-defined, pruritic, scaly plaque with a raised border and central clearing (annular). KOH preparation is positive. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Tinea faciale is a dermatophyte infection of the facial skin. It commonly appears as a well circumscribed erythematous patch (Fig. 13.27). Tinea manus is a dermatophyte infection of the hands (Fig. 13.28).

Figure 13.27

Tinea Faciale Note the sharply marginated, polycyclic, scaly plaque with central clearing localized to the face. KOH preparation is positive. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.28

Tinea Manus This dermatophytosis is usually unilateral when it involves the hands. Note the diffuse hyperkeratosis of the left hand as well as involvement of both feet (tinea pedis). (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Pityriasis rosea, secondary syphilis, psoriasis, seborrheic dermatitis, and tinea versicolor are all usually considered in the differential diagnosis. A KOH examination of the scale demonstrating hyphae confirms the diagnosis.

Emergency Department Treatment and Disposition

Small, localized plaques may be treated with a topical antifungal cream. Extensive or resistant infection requires systemic griseofulvin or ketoconazole. It is important to treat for 2 weeks beyond the point of clinical cure to ensure successful eradication of the fungus.

Clinical Pearls

1. The scale is usually located at the leading edge of erythema and provides the best yield for scraping as part of the KOH examination.

2. The recurrence rate is high, especially for tinea manus.

Tinea Cruris

Associated Clinical Features

Tinea cruris, or "jock itch," is a pruritic dermatophytosis of the intertriginous areas, usually excluding the penis and scrotum. The scaly, erythematous plaque spreads peripherally, with central clearing (Fig. 13.29). The borders of the plaque are well defined.

Figure 13.29

Tinea Cruris This dermatophytosis is commonly called "jock itch." Note the erythematous, scaly plaque with its well-defined border. It characteristically does not involve the scrotum or penis. KOH preparation is positive. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Erythrasma, Candida albicans, seborrheic dermatitis, and psoriasis are usually considered in the differential diagnosis. A KOH examination of the scale demonstrating hyphae confirms the diagnosis.

Emergency Department Treatment and Disposition

Initial treatment consists of topical antifungal medications. Griseofulvin or ketoconazole are reserved for resistant cases. It is important to treat for 1 week beyond the point of clinical cure to ensure successful eradication of the fungus. Decreasing the amount of perspiration by using topical powders may help prevent recurrences.

Clinical Pearls

1. A less well defined, pruritic, intertriginous plaque that typically involves the scrotum is usually erythrasma. It is caused by Nocarelia minutissimus and is treated with topical erythromycin.

2. Warmth and moisture are predisposing factors.

Tinea Pedis

Associated Clinical Features

Tinea pedis, or "athlete's foot," is a pruritic dermatophytosis. It consists of erythema and scaling of the sole (see Fig. 13.28), maceration, occasional vesiculation, and fissure formation between and under the toes (Fig. 13.30). These pruritic, painful fissures may become secondarily infected with gram-negative organisms. Frequently the toenails are also affected.

Figure 13.30

Tinea Pedis A pruritic, scaling hyperkeratotic rash involving the soles of the feet and extending to the interdigital spaces is pathognomonic for tinea pedis. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Foot eczema, psoriasis, and Reiter's syndrome are considered in the differential diagnosis. A KOH examination of the scale demonstrating hyphae confirms the diagnosis.

Emergency Department Treatment and Disposition

Topical antifungal creams are the initial treatment of choice. Antibiotics may be used to treat secondary infection. Griseofulvin, then ketoconazole, are used for chronic or resistant cases. It is important to treat for 1 week beyond the point of clinical cure to ensure successful eradication of the fungus.

Clinical Pearls

1. If it scales, scrape it and look for hyphae.

2. Macerated areas may become secondarily infected by bacteria.

Tinea Capitis

Associated Clinical Features

Tinea capitis is scalp ringworm, or a dermatophytosis of the scalp. It presents as a pruritic, erythematous, scaly plaque with broken or missing hairs frequently referred to as "gray patch" or "black dot" ringworm (Fig. 13.31). This may develop into a kerion. A kerion is a delayed-type hypersensitivity reaction to the fungus, where the initial erythematous, scaly plaque becomes boggy with inflamed, purulent nodules and plaques (Fig. 13.32). The hair follicle is frequently destroyed by the inflammatory process in a kerion, leading to a scarring alopecia.

Figure 13.31

Tinea Capitis This dermatophytosis is characterized by a pruritic, circular area of hair loss covered by adherent scales. KOH preparation is positive. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.32

Kerion This collection of boggy, inflamed, purulent nodules and papules is the result of a delayed-type hypersensitivity reaction to the fungus. Scarring alopecia will follow as a result of the actual destruction of the hair follicle. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Various inflammatory follicular conditions—such as folliculitis, impetigo, psoriasis, alopecia areata, and seborrheic dermatitis—may resemble tinea capitis. The diagnosis is made by a KOH examination of a scraping of the area, revealing hyphae and spores.

Emergency Department Treatment Disposition

Systemic griseofulvin is usually required for several weeks to treat tinea capitis successfully. Systemic antibiotics and corticosteroids are usually added when treating a kerion. Selenium sulfide lotion used as a shampoo may actually decrease the duration of the infection. It is important to treat for 2 weeks beyond the point of clinical cure to ensure successful eradication of the fungus. Ketoconazole is reserved for resistant cases.

Clinical Pearls

1. Tinea capitis is a disease of childhood; it is rare in immunocompetent adults.

2. It is epidemic in many African American communities.

3. The KOH scrape is aided by using a disposable urethral brush or similar device.

Onychomycosis

Associated Clinical Features

Onychomycosis is an invasion of the nails by any fungus. Four clinical subtypes are noted. Distal subungual presents as discolorations of the free edge of the nail with hyperkeratosis leading to a subungual accumulation of friable keratinaceous debris (Fig. 13.33). White superficial consists of sharply outlined white areas on the nail plate which leave the surface friable. Proximal subungual presents as discolorations which start proximally at the nail fold. Candidal onychomycosis encompasses the entire nail plate, leaving the surface rough and friable.

Figure 13.33

Onychomycosis Note that multiple nail beds have been invaded by the fungus, leading to chronic hyperkeratosis and subungual accumulation of friable keratinaceous debris. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Psoriasis and various other nail dystrophies, such as distal onycholysis caused by excessive water exposure or drugs, must be differentiated from this fungal infection. Pseudomonal nail infection is characterized by the subungual accumulation of green debris. A KOH examination of the keratinaceous debris demonstrating hyphae confirms onychomycosis.

Emergency Department Treatment and Disposition

The most common treatment consists of oral griseofulvin, fluconazole, lucenazole, or terbinafine. Candidal infections require oral ketoconazole. Toenail onychomycosis is very difficult to eradicate.

Clinical Pearls

1. All that causes the nail plate to separate from the nail bed is not necessarily fungus.

2. Distal subungual is the most common type of onychomycosis.

Tinea Versicolor

Associated Clinical Features

Tinea versicolor is a chronic, superficial fungal infection that involves the trunk and extremities with little or no involvement of the face. The fungus is part of normal skin flora. Finely scaling brown macules are present in fair-skinned patients (Fig. 13.34), whereas scaly hypopigmented macules are often noted in the dark-skinned (Fig. 13.35). These sharply demarcated macules are intermittently pruritic.

Figure 13.34

Tinea Versicolor This chronic superficial fungal infection leads to the formation of multiple well-defined, scaly brown macules on the trunk and extremities. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.35

Tinea Versicolor An example of hypopigmented areas on dark skin. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Pityriasis rosea, secondary syphilis, and some drug eruptions must all be considered in the differential diagnosis. A KOH examination of a scraping of the area revealing hyphae and spores makes the diagnosis (see Fig. 21.16).

Emergency Department Treatment and Disposition

Treatment consists of short applications of selenium sulfide lotion, topical antifungal creams, or topical ketoconazole. Resistant cases require oral ketoconazole. Ultraviolet exposure is required to regain any lost pigment.

Clinical Pearls

1. Tinea versicolor is more common in adolescents and young adults.

2. Clinically active areas or areas colonized with the fungus may be identified by orange fluorescence noted on Wood's light examination.

Basal Cell Carcinoma

Associated Clinical Features

Basal cell carcinoma is a malignancy of the basal cell layer of the epidermis, presenting as a translucent, pearly papule with central ulceration and rolled borders with fine superficial telangiectasias (Fig. 13.36). It is most frequently located on the head, neck, and upper trunk. The patient frequently notes easy bleeding of the papule with poor to nonhealing. There are several variants of basal cell carcinomas. Pigmented basal cell carcinoma consists of a brownish-black, firm nodule with irregular surface and central ulceration (Fig. 13.37). Superficial multicentric basal cell carcinoma is psoriasiform in nature, consisting of a flat, erythematous, scaly translucent plaque without central ulceration or raised border (Fig. 13.38).

Figure 13.36

Basal Cell Carcinoma Nodular basal cell carcinoma consists of a firm, centrally ulcerated (rodent ulcer) nodule with a raised, rolled, pearly, telangiectatic border. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.37

Pigmented Basal Cell Carcinoma This pigmented basal cell carcinoma consists of a firm, translucent, brownish-black ulcerated nodule with an irregular surface and asymmetry of its border. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.38

Basal Cell Carcinoma A superficial multicentric basal cell carcinoma is frequently psoriasiform in nature. Note the flat, erythematous, scaly plaque with its elevated, irregular border. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Pigmented basal cell carcinoma resembles nodular melanoma. Superficial multicentric basal cell carcinoma resembles psoriasis, tinea corporis, and squamous cell carcinoma in situ.

Emergency Department Treatment and Disposition

Excisional surgery, cryosurgery, or electrosurgery are recommended forms of treatment. If there is a potential for disfigurement, radiation therapy is usually instituted instead of surgery. Prompt dermatologic consultation must be arranged when evaluating any suspicious lesion. Up to half of patients will develop a recurrence.

Clinical Pearls

1. Basal cell carcinoma is the most common form of skin cancer.

2. This malignancy forms in the epidermis that has developing hair follicles; therefore, it is not found on the vermilion border of the lips or the genital mucosal membranes.

3. The pearly, rolled, telangiectatic border with central ulceration is diagnostic of basal cell carcinoma.

4. Despite being locally invasive, basal cell carcinoma does not metastasize.

Squamous Cell Carcinoma

Associated Clinical Features

Squamous cell carcinoma varies from erythematous, hyperkeratotic, sharply demarcated plaques to elevated, ulcerative nodules (Fig. 13.39). It may be sun-induced or related to ionizing radiation or industrial carcinogens. Invasive squamous cell carcinoma is characterized by a discrete elevated plaque or nodule with thick keratotic scale and ulceration.

Figure 13.39

Squamous Cell Carcinoma Note the single erythematous, scaly plaque on the dorsal aspect of this sun-exposed hand. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Squamous cell carcinoma must be differentiated from a benign lesion such as tinea corporis, psoriasis, impetigo, wart, seborrheic keratosis, or keratoacanthoma (Fig. 13.40).

Figure 13.40

Keratoacanthoma This rapidly evolving neoplasm consists of an erythematous nodule with a hyperkeratotic core. It most closely resembles a squamous cell carcinoma although it is a benign epithelial neoplasm. Biopsy serves to differentiate these two conditions. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Emergency Department Treatment and Disposition

Excisional surgery is required, with radiation therapy utilized in potentially disfiguring cases. All suspicious lesions require prompt dermatologic consultation.

Clinical Pearls

1. Squamous cell carcinoma is the second most common type of skin cancer.

2. This malignancy develops more commonly in fair-skinned people with a significant history of sun exposure.

3. Most lesions are found on the lips or other sun-exposed areas.

4. A rapidly evolving (2 to 4 weeks) nodule or plaque with a dense hyperkeratotic core is a keratoacanthoma. It is closely related to squamous cell carcinoma and frequently occurs at a site of trauma. Treatment is the same.

5. Risk of metastasis is related to size, location, and histology.

Melanoma

Associated Clinical Features

Melanoma is a malignancy involving the melanocytes of the epidermis. Asymmetry, an irregular border, a mottled display of color, a diameter greater than 5 to 6 mm, and an elevation or distortion of the surface are five signs that a lesion may be a melanoma (Fig. 13.41). Melanoma may or may not occur in sun-exposed areas.

Figure 13.41

Melanoma Note the asymmetry, irregular border, and focal hyperpigmentation in this melanoma. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Lentigo maligna is characterized by a single, flat, freckle-like macule with an irregular border, usually on the face (Fig. 13.42). This melanoma in situ is often confused with a solar lentigo or a seborrheic keratosis and has about a 5% risk of being malignant. Superficially spreading melanoma is the most common form of melanoma. It usually presents as a brown macule with irregular borders and variegation in color. Nodular melanoma usually starts as a papule which becomes an elevated nodule with irregular borders and variegation in color (Fig. 13.43). It must be differentiated from a hemangioma, angiokeratoma, or pigmented basal cell carcinoma. Acral lentiginous melanomas, which are agressive and metastasize easily, are often mistaken for plantar warts or subungual hematomas; they are flat, pigmented, irregularly bordered macules of the palms, soles, and subungual areas (Fig. 13.44).

Figure 13.42

Lentigo Maligna Melanoma This long-lived melanoma in situ has now invaded the dermis, forming a black nodule classified as lentigo maligna melanoma. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.43

Nodular Melanoma This melanoma has progressed to an exophytic tumor, which was deeply invasive histopathologically. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Figure 13.44

Acral Lentiginous Melanoma The finding of a pigmented, irregularly bordered macule involving the proximal nail fold is called Hutchinson's sign. It represents melanoma of the nail matrix and is therefore classified as an acral lentiginous melanoma. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Emergency Department Treatment and Disposition

A melanoma must be surgically excised with adequate margins. Prompt dermatologic consultation is required of all suspicious lesions, because the prognosis of melanoma correlates directly with early detection and treatment.

Clinical Pearls

1. Prognosis of melanoma is most dependent on the depth of invasion, therefore, early detection and treatment are essential.

2. Only 20% of melanomas arise from preexisting moles, so the appearance of a new mole, especially after the age of 30, is particularly significant.

3. Most benign moles have symmetry, one color, and are less than 7 mm in diameter.

Pyogenic Granuloma

Associated Clinical Features

Pyogenic granuloma is characterized by a solitary, violaceous, pedunculated or sessile vascular nodule which usually forms at the site of cutaneous injury (Fig. 13.45). The well demarcated nodule consists of exuberant granulation tissue ("proud flesh") which may be erosive and encrusted. Pyogenic granuloma commonly occurs on the digits and is particularly common in pregnancy.

Figure 13.45

Pyogenic Granuloma This solitary, violaceous, pedunculated, vascular nodule formed at the site of an injury. Note that the nodule is well demarcated by a thin rim of epidermis. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

This benign vascular neoplasm resembles a hemangioma; however, it must be differentiated from amelanotic melanoma, squamous cell carcinoma, and metastatic renal cell carcinoma.

Emergency Department Treatment and Disposition

Since this neoplasm usually does not resolve spontaneously, it may be shaved off with electrodessication of the base.

Clinical Pearls

1. A fine collarette of scale surrounding an exophytic vascular neoplasm is diagnostic.

2. The lesion may exhibit recurrent bleeding episodes.

3. Nearly 25 to 33% of these benign lesions follow some form of minor trauma.

Fixed Drug Eruption

Associated Clinical Features

A fixed drug eruption is a cutaneous reaction to an ingested drug, usually an over-the-counter laxative, barbiturate, tetracycline, or sulfa drug. The reaction occurs at the identical site with repeated exposure to the same drug, usually on the genital skin or proximal extremity. It presents as a round, pruritic, erythematous, sharply demarcated plaque that may evolve into a painful bulla with secondary erosion (Fig. 13.46). Residual hyperpigmentation frequently follows healing.

Figure 13.46

Fixed Drug Eruption This red to violaceous, pruritic, sharply demarcated patch is a cutaneous reaction to a drug. Repeated exposure will cause a similar reaction in the same location. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Early cellulitis, erythema multiforme, arthropod assault, and genital herpes are usually considered in the differential diagnosis.

Emergency Department Treatment and Disposition

The etiology must be identified and removed before the plaque will resolve. Symptomatic treatment includes antihistamines and analgesics.

Clinical Pearls

1. The identical recurrence of a painful, pruritic, well-demarcated violaceous plaque makes the diagnosis.

2. This reaction occurs with repeated exposure to the same drug.

3. Some patients have a refractory period following exposure.

Exanthematous Drug Eruptions

Associated Clinical Features

Exanthematous drug eruptions are an adverse hypersensitivity reaction to a drug. This symmetric, pruritic, morbilliform, blanching, erythematous eruption is the most frequent of cutaneous drug eruptions (Fig. 13.47). The initially pruritic macules or papules usually become confluent and may progress to an exfoliative dermatitis.

Figure 13.47

Exanthematous Drug Eruption This symmetric, morbilliform, blanching eruption may eventually become confluent, leading to an exfoliative dermatitis. (Courtesy of GlaxoWellcome Pharmaceuticals.)

Differential Diagnosis

Viral exanthem, secondary syphilis, atypical pityriasis rosea, and scarlet fever must all be considered in the differential diagnosis. A serologic test for syphilis, antistreptolysin O titer, and a good history are usually sufficient to make the diagnosis. Severe drug eruptions may be accompanied by eosinophilia, lymphadenopathy, and liver function abnormalities.

Emergency Department Treatment and Disposition

The eruption may resolve despite the drug's continued use. The drug should be discontinued if considered to be the cause of the rash. It may take as long as 2 weeks for the eruption to fade after discontinuation of the causative drug. Symptomatic management includes antihistamines and topical corticosteroids.

Clinical Pearls

1. Drug eruptions are usually symmetric and pruritic as opposed to viral eruptions, which are usually asymmetric and asymptomatic.

2. Mononucleosis patients taking amoxicillin or AIDS patients taking sulfa drugs frequently experience this reaction.

Erythema Nodosum

Associated Clinical Features

Erythema nodosum is a delayed hypersensitivity reaction, usually to certain drugs, infections, or systemic illnesses. This panniculitis (inflammation of the fat) consists of painful, nonulcerated, poorly marginated nodules with overlying erythematous, warm, shiny skin. (Fig. 13.48). The lower legs are the most common site; the face is rarely involved. Fever, malaise, and arthralgias often accompany the cutaneous manifestations.

Figure 13.48

Erythema Nodosum These multiple painful nodules with overlying erythematous, warm and shiny skin were associated with coccidioidomycosis and are typical of erythema nodosum. (Courtesy of GlaxoWellcome Pharmaceuticals.)

Differential Diagnosis

Erythema induratum, syphilitic gummas, and nodular vasculitis are considered in the differential diagnosis.

Emergency Department Treatment and Disposition

Identify and treat the underlying etiology. Oral contraceptives, sulfa drugs, tuberculosis, sarcoidosis, fungal infections, and inflammatory bowel disease are common predisposing factors. Symptomatic treatment includes nonsteroidal anti-inflamatory drugs (NSAIDs), bed rest, and compressive dressings.

Clinical Pearls

1. Erythema nodosum most commonly presents in young women secondary to oral contraceptives or sulfa drugs.

2. Its appearance in association with systemic fungal infections (coccidioidomycosis) indicates a likely recovery from the disease.

Urticaria and Angioedema

Associated Clinical Features

Urticaria, a vascular reaction localized to the skin, is composed of transient, erythematous, edematous, pruritic papules or plaquelike wheals (Figs. 13.49, 13.50). It tends to favor the covered areas (back, chest, buttocks). Angioedema comprises thicker plaques that result from fluid shift into the dermis and subcutaneous tissues. It generally affects the distensible tissues (lips, eyelids, earlobes, Fig. 13.51) and is usually nonpruritic. There are countless causes of urticaria; the most common being food, medications, and underlying infection. Cholinergic urticaria involves micropapular lesions induced by exercise or heat. Dermatographism presents as linear hives at the site of skin stroking. Cold urticaria (Fig. 13.52) can be diagnosed with the ice cube test, and solar urticaria occurs in areas exposed to sunlight. Urticaria may also occur as a result of exposure to pressure, heat, and water. Hereditary angioedema is an autosomal dominant disorder with systemic manifestations secondary to edema of the subcutaneous and mucosal tissues of the respiratory and gastrointestinal tract in addition to the face and extremities. Mortality rates approach 30%, usually from airway obstruction. There is also an acquired form of angioedema secondary to an underlying malignancy, usually lymphoreticular. The use of angiotensin converting enzyme (ACE) inhibitors is a frequent cause of angioedema.

Figure 13.49

Urticaria Note the edematous papules and wheals covering the skin of the neck. (Courtesy of Alan B. Storrow, MD.)

Figure 13.50

Urticaria Note the classic raised plaques on the lower extremity of this patient with urticaria. (Courtesy of James J. Nordlund, MD.)

Figure 13.51

Angioedema Prominent lip involvement in a young woman with ACE inhibitor–induced angioedema. (Courtesy of Alan B. Storrow, MD.)

Figure 13.52

Cold Urticaria Plaque formation after placement of an ice cube on the skin confirms cold urticaria. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Bacterial or viral exanthems, erythema multiforme, and drug eruptions must be considered in the differential diagnosis of urticaria. Edema of any etiology (congestive heart failure, glomerulonephritis, chronic liver disease) must be differentiated from the soft tissue swelling associated with angioedema.

Emergency Department Treatment and Disposition

This involves the identification and elimination of any potential etiology. Antihistamines can be effective for urticaria, often requiring both H₁ and H₂ blockers and steroids for stubborn cases. Life-threatening attacks of hereditary angioedema do not respond well to antihistamines, epinephrine, or steroids. Admission for supportive care and active airway management is the mainstay of treatment. Danazol may be utilized for prophylactic management.

Clinical Pearls

1. Both urticaria and angioedema are acute and evanescent.

2. Urticaria is pruritic and responsive to antihistamines, epinephrine, and steroids.

3. Angioedema is only rarely pruritic and minimally responsive to epinephrine; it may require danazol for long-term treatment.

4. Doxepin may be considered for refractory cases due to its potent H₁ and H₂ blocking effect.

Dyshidrotic Eczema (Pompholyx)

Associated Clinical Features

Dyshidrotic eczema is a papulovesicular plaque involving the epidermis of the fingers, palms, and soles. The dermatosis initially consists of pruritic, deep-seated vesicles grouped in clusters (Fig. 13.53). Scaling and painful fissure formation are late complications, as is secondary bacterial infection. Spontaneous remissions and recurrent attacks are usually the rule. The bullous form is called pompholyx.

Figure 13.53

Dyshidrotic Eczema Note the cluster of deep-seated vesicles along the sides of the fingers. Scaling and painful fissure formation may also occur. No overlying erythema is present. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Acute contact dermatitis must be considered in the differential diagnosis of the acute eruption. Psoriasis and dermatophytosis are considered in the differential diagnosis of the chronic eruption.

Emergency Department Treatment and Disposition

Burow's wet dressings should be utilized during the early vesicular stage. High-potency topical steroids are used in all stages of the eruption. Systemic corticosteroids should be avoided except for the most severe cases. Antihistamines treat the pruritus. Dicloxacillin or erythromycin are used to treat secondary bacterial infections. Minimal exposure to water and generous emolliation also hasten healing.

Clinical Pearls

1. Deep-seated, tapioca-like vesicles on the sides of the digits, followed by scaling and fissure formation, are typically seen in this disease.

2. Dyshidrotic eczema is frequently associated with psychosocial stressors.

3. The "id reaction," due to fungal infections and drug eruptions, may have similar clinical presentations.

Atopic Dermatitis

Associated Clinical Features

Atopic dermatitis is a broadly defined pruritic inflammation of the epidermis and dermis, with approximately 60% of the cases occurring during the first year of life. The characteristic pattern is erythema, papules, and lichenified plaques with excoriation and exudation of wet crusts (Fig. 13.54). Its distribution is the face (sparing of the mouth), the antecubital and popliteal fossae, and the dorsal surfaces of the forearms, hands, and feet. This is generally considered a lifelong condition with gradual improvement toward adulthood.

Figure 13.54

Atopic Dermatitis Lichenfied plaques, erosions, and fissures are characteristic of atopic dermatitis. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Nummular eczema, allergic contact dermatitis, impetigo, dermatophytosis, and psoriasis are usually considered in the differential diagnosis. A KOH examination of the scale rules out dermatophytosis. A biopsy may help differentiate this condition from nummular eczema and contact dermatitis.

Emergency Department Treatment and Disposition

Antihistamines treat the pruritus. Unscented emollients prevent xerosis (dry skin). Topical corticosteroids treat the underlying inflammation. Systemic corticosteroids should be avoided except for the most severe cases. Since these patients are frequently colonized with Staphylococcus aureus, antistaphylococcal antibiotics are also used during flares of the condition.

Clinical Pearls

1. Scaly plaques on the flexural surface with excoriation and exudation of crusts is diagnostic of atopic dermatitis.

2. Asthma and allergic rhinitis may develop as the atopic dermatitis improves.

Nummular Eczema

Associated Clinical Features

Nummular eczema is a pruritic, eczematous dermatitis consisting of closely grouped vesicles that coalesce into coin-shaped, erythematous plaques with poorly defined borders (Fig. 13.55). These plaques may become encrusted or dry and scaly. They are usually found on the trunk and extremities (especially the hand) of a middle-aged or elderly patient.

Figure 13.55

Nummular Eczema An example of multiple erythematous, coin-shaped plaques with fine scales, representative of this pruritic, eczematous dermatitis. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Allergic contact dermatitis, impetigo, dermatophytosis, and psoriasis must all be considered in the differential diagnosis. If it scales, scrape it and look for hyphae to differentiate a dermatophytosis. A biopsy may help differentiate contact dermatitis from nummular eczema.

Emergency Department Treatment and Disposition

Antihistamines treat the pruritus. Unscented emollients prevent xerosis. Topical corticosteroids treat the underlying inflammation. Systemic corticosteroids should be avoided except for the most severe cases.

Clinical Pearls

1. Coin-shaped, pruritic, eczematous plaques not responsive to antibiotics are diagnostic of nummular eczema.

2. Recurrences tend to appear in previously involved sites.

Allergic Contact Dermatitis

Associated Clinical Features

Allergic contact dermatitis is an acute or chronic delayed-type hypersensitivity reaction caused by contact exposure to a variety of agents. The acute form is characterized by multiple, closely grouped vesicles with exudative erosions and crust formation on a well defined erythematous, edematous base (Fig. 13.56). Subacute contact dermatitis consists of dry, scaly patches with areas of desquamation, whereas the chronic form consists of hyperkeratosis and pigmentation. All forms of allergic contact dermatitis are pruritic.

Figure 13.56

Contact Dermatitis Note that the erythematous, edematous base of the eruption corresponds to the posterior surface of the watch. Superimposed on the erythematous base are multiple vesicles with exudate and crust. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Differential Diagnosis

Atopic dermatitis, nummular eczema, impetigo, and dermatophytosis are included in the differential diagnosis. If it scales, scrape it and look for hyphae to differentiate a dermatophytosis. A positive patch test is diagnostic of an allergic contact dermatitis. Contact exposure of the skin to the allergen leading to erythema and vesicle formation is considered a positive test.

Emergency Department Treatment and Disposition

Identify and remove any potential allergen. Antihistamines relieve the pruritus. Topical corticosteroids treat the underlying inflammation. Systemic corticosteroids should be avoided except for the most severe cases.

Clinical Pearls

1. Well-defined, pruritic areas of erythema superimposed on exudative vesicles and a recent history of exposure to a specific allergen are diagnostic of allergic contact dermatitis.

2. Poison ivy and oak are the most common causes of allergic contact dermatitis.

3. In treating dermatitis with topical ointments, worsening may signify an allergic reaction to the medication.

Phytophotodermatitis and Drug-Induced Photosensitivity

Associated Clinical Features

Phytophotodermatitis is a pruritic, linear dermatitis that occurs when skin exposed to certain plants becomes exposed to sunlight. Bizarre patterns of pruritic erythema convert into vesicles and bullae that undergo involution, leaving behind a residual intense hyperpigmentation (Fig. 13.57).

Figure 13.57

Phytophotodermatitis This linear, photodistributed, eczematous plaque resulted from contact with a plant-derived photosensitizer (lime juice). This frequently resolves with hyperpigmentation. (Courtesy of the Department of Dermatology, Wilford Hall USAF Medical Center and Brooke Army Medical Center, San Antonio, TX.)

Drug-induced photosensitivity is an adverse skin reaction due to simultaneous exposure to certain drugs and ultraviolet radiation. The rash is erythematous and edematous, much like sunburn (Fig. 13.58).

Figure 13.58

Drug-Induced Photosensitivity Erythematous reaction to ultraviolet radiation associated with carbamazepine use. (Courtesy of the Department of Dermatology, Naval Medical Center, Portsmouth, VA.)

Differential Diagnosis

Rhus dermatitis is most often mistaken for this eruption. Photosensitivity can be caused by other diseases.

Emergency Department Treatment and Disposition

Symptomatic treatment includes wet dressings, antihistamines, calamine lotion, and corticosteroid creams. For drug-induced photosensitivity, the offending drug should be discontinued. Counsel patients about the use of sunscreens and sun avoidance to prevent recurrences.

Clinical Pearls

1. Linearly distributed, pruritic vesicles in a photodistribution with a history of plant exposure make the diagnosis.

2. The distribution of the rash is limited to sun-exposed areas.

3. Common drugs causing drug-induced photosensitivity are carbamazepine, amiodarone, doxycycline, furosemide, phenothiazines, and sulfonamides.

Pemphigus Vulgaris

Associated Clinical Features

Pemphigus vulgaris is a bullous autoimmune disease of the skin and mucous membranes caused by IgG autoantibodies. Previously, mortality was high, but now it only occurs in 10% of cases, usually secondary to steroid complications. This disease typically affects middle-aged adults. Vesicles and bullae arise on the skin of the scalp, chest, umbilicus, and intertriginous areas (Fig. 13.59).

Figure 13.59

Pemphigus Vulgaris Classic vesiculobullous lesions of pemphigus vulgaris throughout the chest and abdomen. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Pemphigus vulgaris must be distinguished from all other bullous diseases by a skin biopsy.

Emergency Department Treatment and Disposition

High-dose steroids are the mainstay of therapy. Other immunosuppressives—such as azathioprine, methotrexate, and cyclophosphamide—can be helpful. Plasmapheresis is used in cases resistant to standard treatment.

Clinical Pearls

1. Nikolsky's sign can be seen—dislodging of the epidermis with lateral finger pressure on the edge of the bulla.

2. Ulcers and erosions of the oral mucosa are the presenting sign in up to 90% of patients.

Vitiligo

Associated Clinical Features

Vitiligo is an acquired loss of pigmentation that commonly involves the backs of the hands, the face, and body folds (Fig. 13.60). There is a positive family history in 30% of the cases. Initially the disease is limited, but it then slowly progresses over years. Vitiligo is secondary to absence of epidermal melanocytes, which may be due to an autoimmune phenomenon against melanocytes. Approximately half of these cases begin in patients less than 20 years of age.

Figure 13.60

Vitiligo Note the hypopigmented areas characteristic of vitiligo. (Courtesy of James J. Nordlund, MD.)

Differential Diagnosis

Vitiligo must be differentiated from tinea versicolor (which has scale and a positive KOH scraping), postinflammatory hypopigmentation, leprosy, and pityriasis alba.

Emergency Department Treatment and Disposition

Vitiligo requires referral to a dermatologist for PUVA (psoralen plus ultraviolet A), topical therapy, or skin grafting. The best results from therapy occur on the face and neck.

Clinical Pearls

1. Vitiligo occurs at sites of trauma (Koebner's phenomenon).

2. Wood's lamp examination helps identify hypopigmented areas in patients with light complexions.

3. Tinea versicolor has a scale and positive KOH prep.

Scabies and Norwegian Scabies

Associated Clinical Features

Transmission of scabies occurs after direct skin contact with an infected individual and possibly from clothing and bedding infested with the mite. The female mite burrows into the individual's skin and deposits two to three eggs daily. Fecal pellets (scybala) are also deposited in the burrow and may be responsible for the localized pruritus. Nocturnal pruritus is characteristic of scabies. The pink-white, slightly elevated burrows (Fig. 13.61) are typically found in the web spaces of the hands and feet, penis, buttocks, scrotum, and extensor surfaces of the elbows and knees. Norwegian scabies (Fig. 13.62) tends to cause asymptomatic crusting—rather than the typical inflammatory papules and vesicles—as well as nail dystrophy and keratosis.

Figure 13.61

Scabies A burrow on the heel of a pediatric patient with scabies. (Courtesy of Briana Hill, MD.)

Figure 13.62

Norwegian Scabies Gray scales and crusting consistent with Norwegian scabies. In these patients, many thousands (versus a few dozen) mites are present. (Courtesy of Lynn Utecht, MD.)

Differential Diagnosis

Infestation by lice, eczema, and insect bites can be confused with scabies.

Emergency Department Management and Disposition

Topical permethrin or lindane are commonly used to treat scabies. Each of these products should be applied thoroughly and then, after 8 to 12 h washed from the skin. Lindane should be avoided during infancy and pregnancy because of reports of infant neurotoxicity following systemic absorption through the skin.

Clinical Pearls

1. Ivermectin given as a single 200-mg/kg dose or a 5% sulfur ointment can also be used for treatment.

2. Oral antipruritic therapy and analgesics will help alleviate discomfort.

3. Intimate contacts and all family members in the same household should be treated.

Cutaneous Larva Migrans

Associated Clinical Features

Cutaneous larva migrans (CLM) presents as a serpiginous, red, raised, wavy rash that is approximately 3 mm wide (Fig. 13.63). The lacy rash is moderately to severely pruritic as a result of larval secretion of proteolytic enzymes. Infection is most frequent in warmer climates and occurs when the ova of adult hookworms penetrate the skin of a person walking in contaminated soil. Symptoms begin days to weeks after infestation. The nematodes prefer to infect cats or dogs; humans are infected accidentally. The goal of the larva is to eventually penetrate the intestines of its prey. However, owing to physiologic limitations in humans, penetration deeper than the basal layer of the epidermis is prevented.

Figure 13.63

Cutaneous Larva Migrans Note the elevated tracks caused by migration of the larva through the epidermis. (Courtesy of the Department of Dermatology, National Naval Medical Center, Bethesda, MD.)

Differential Diagnosis

The appearance of CLM and its associated pruritus can resemble an allergic reaction, but the lacy border usually distinguishes it.

Emergency Department Treatment and Disposition

Topical application of thiabendazole is the treatment of choice. It is applied two or three times per day for a total of 5 days. Thiabendazole is also available in an oral form; however, it is less effective. Albendazole is an alternative. Symptoms should improve in 48 h. Untreated CLM will usually resolve in 2 to 8 weeks.

Clinical Pearls

1. Löffler's syndrome can occur in patients with severe CLM infestation. In this condition, larval invasion of the bloodstream is manifest as a patchy infiltrate of the lung and eosinophilia of the blood and sputum.

2. The larval track represents an allergic reaction; the larva itself stays slightly ahead of the track.

3. Freezing the skin with ethyl chloride is a simple, effective treatment used in endemic areas.

Uremic Frost

Associated Clinical Features

Uremic frost is a classic manifestation of chronic renal failure; it is rarely seen today. It develops as a result of accumulation of urea in sweat. In advanced uremia, the accumulation of urea in sweat may reach such a critical level that, upon its evaporation, a fine white powder is left on the skin surface (Fig. 13.64). Associated hyperkalemia may also be present owing to renal failure.

Figure 13.64

Uremic Frost Note the fine white powder on the skin of this patient with end-stage renal disease. (Courtesy of Richard C. Levy, MD.)

Differential Diagnosis

Dried sweat from a patient with cystic fibrosis forms fern-like crystals that may resemble this condition. In an individual without known renal disease, uremic frost may be mistaken for a dermatologic problem or chemical exposure. However, in a patient with known end-stage renal disease, the differential of a white precipitate on the skin surface is limited.

Emergency Department Management and Disposition

Treatment of the underlying condition that resulted in the patient's uremia may prevent further accumulation of uremic frost. Typically, urgent dialysis is indicated.

Clinical Pearls

1. Although rare today, this condition may be seen in patients without adequate air conditioning who are poorly controlled on dialysis.

2. For patients presenting with altered mental status, attention to the airway, oxygenation, and rapid assessment and treatment of associated metabolic disorders such as hyperkalemia are indicated.

Bacillus Anthracis (Anthrax)

Associated Clinical Features

Anthrax is usually a disease of herbivores; humans are infected when they come into contact with infected animals or contaminated animal products. Recently, anthrax has received increased international attention as a potential biological warfare agent. There are three distinct clinical manifestations of anthrax.

Cutaneous anthrax accounts for about 95% of human cases. After direct contact on exposed skin, the infection begins as a pruritic papule. It enlarges into an ulcer surrounded by vesicles in 1 to 2 days and then eventually becomes a characteristic black, necrotic central eschar surrounded by nonpitting edema (Fig. 13.65). Systemic manifestations (fever, hypotension, tachycardia) may accompany cutaneous involvement.

Figure 13.65

Anthrax Note the early ulcer of cutaneous anthrax on the right of the lower lip. (Courtesy of Thea James, MD.)

Respiratory anthrax (woolsorters' disease) occurs after exposure to anthrax spores and presents as an upper respiratory infection. Within 1 to 4 days, the disease progresses to severe respiratory distress, hypoxia and hypotension. Death uniformly occurs within 24 h after the onset of the fulminant phases of the infection.

Gastrointestinal anthrax is rare and occurs 3 to 7 days after exposure to contaminated animal meat. Initially it presents as a nonspecific gastroenteritis with fever, vomiting, diarrhea, and malaise. The disease then progresses to hematemesis, bloody diarrhea, sepsis and shock. Death usually occurs 2 to 5 days after symptom onset.

Differential Diagnosis

Cutaneous anthrax resembles staphylococcal infection, tularemia, and plague. Inhalation and gastrointestinal anthrax may initially be similar to a viral upper respiratory infection or gastroenteritis, respectively.

Emergency Department Treatment and Disposition

Admission is indicated for patients with anthrax. Intravenous penicillin is the primary treatment for all forms. Ciprofloxacin or doxycycline are alternatives. Oral ciprofloxacin is recommended for postexposure prophylaxis.

Clinical Pearls

1. Gastrointestinal and inhalation anthrax are almost uniformly fatal, even with antibiotic therapy.

2. Human killed vaccine is available and recommended for mill workers and veterinarians at high risk for exposure.

3. The virulence of anthrax is derived from its edema toxin, lethal toxin, and capsular material.

4. A classic pathologic finding for inhalation anthrax is hemorrhagic mediastinitis; this may be manifested on chest radiography as a widened mediastinum.

5. Decontamination of suspected anthrax spore exposure consists of removal of exposed clothing (place in a sealed plastic bag) and washing of the exposed area with soap and water.

Acknowledgments

The author acknowledges Christopher R. Sartori, MD, and Michael B. Brooks, MD, for portions of this chapter written for the first edition of this book.

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