Kim Askew
Rashes in children are typically benign and self-limited with only a handful of serious or potentially life-threatening rashes that require intervention, though they are commonly of great concern to parents and may prompt ED visit.
Essential information for accurate diagnosis includes associated signs and symptoms, immunization history, human and animal contacts, and environmental and medication exposures.
An exanthem is a rash involving the skin, and may have an infectious and noninfectious cause; an enanthem involves the mucus membranes.
Pediatric exanthems can be broadly classified as viral, bacterial, rickettsial, and those of unclear etiology. Rickettsial disease is covered in Chapter 99, and cutaneous anthrax is discussed in Chapter 100.
VIRAL INFECTIONS
ENTEROVIRUSES
Enteroviruses are small, single-stranded RNA viruses that include coxsackieviruses and echoviruses that commonly cause human disease and produce a wide range of clinical symptoms, typically in the summer and early fall.
Clinically enteroviral infection can cause a wide range of disease including nonspecific febrile illness, upper respiratory tract infections (common cold, croup, pneumonia), conjunctivitis, parotitis, gastroenteritis (vomiting, diarrhea, abdominal pain), hepatitis, pancreatitis, pericarditis, myocarditis, orchitis, nephritis, arthritis, meningitis, and encephalitis.
The rashes of enteroviral infections are also varied and include macular eruptions, morbilliform erythema, vesicular lesions, petechial and puerperal eruptions, rubelliform rash, roseola-like rash, and scarlatiniform eruptions.
One of the enterovirus infections that is common and has distinctive features is hand-foot-and-mouth disease. At the outset, patients typically have fever, anorexia, malaise, and mouth pain. Oral lesions appear on day 2 or 3 of illness, followed by skin lesions. The oral lesions start as painful vesicles on an erythematous base that subsequently ulcerate. The typical location is on the buccal mucosa, tongue, soft palate, and gingiva. Skin lesions start as red papules that change to gray vesicles that heal in 7 to 10 days; the distribution of lesions includes the palms, soles, and buttocks.
Differentiation between enteroviral viruses is difficult. Because there is no specific therapy, it is more important to consider and exclude bacterial diseases in the differential diagnosis.
Management is symptomatic: provide analgesia (topical or systemic, including narcotics), and ensuring adequate hydration; antipyretics may also be given.
MEASLES
Due to widespread immunizations, measles is no longer common in North America, though local epidemics do occur in unvaccinated communities. This myxovirus infection typically occurs in the winter and spring.
The incubation period is 10 days, followed by a 3-day prodrome of upper respiratory symptoms, then malaise, fever, coryza, conjunctivitis, photophobia, and cough. Patients typically appear ill.
The exanthem develops 14 days after exposure. Initially a red, blanching, maculopapular rash develops, progressing from the head to the feet and rapidly coalescing on the face. As the rash resolves over about 1 week, a coppery brown discoloration may be seen and desquamation may occur.
Koplik’s spots, tiny white to bluish-white spots on the buccal mucosa, may be seen just before the exanthem appears, and are pathognomonic for measles.
Measles is self-limited and treatment is supportive.
RUBELLA
Now quite rare due to immunizations, rubella (German measles) can occur in teenagers, typically in the spring. The incubation period is 12 to 25 days with a 1 to 5 day prodrome of fever, malaise, headache, and sore throat.
The exanthem develops as fine, irregular pink macules and papules on the face, which then spread to the neck, trunk, and arms in a centrifugal progression. The rash coalesces on the face as the eruption reaches the lower extremities and then clears in the same order as it appeared.
Lymphadenopathy typically involves the suboccipital and posterior auricular nodes. Treatment is supportive.
ERYTHEMA INFECTIOSUM
Erythema infectiosum (fifth disease) is a febrile illness, typically occurring in the spring, caused by infection with parvovirus. School-aged children 5 to 15 years old are most commonly affected.
The rash typically starts abruptly as bright red discoloration of the cheeks, giving the so-called “slappedcheek” appearance (Fig. 85-1). The lesions are closely grouped tiny papules on an erythematous base with slightly raised edges. The eyelids and chin are characteristically spared and circumoral pallor is typical. This rash fades after 4 to 5 days.
As the illness progresses, and 1 to 2 days after the facial rash appears, a nonpruritic erythematous macular or maculopapular rash appears on the trunk and limbs. This rash may last for 1 week and is not pruritic. As it fades, central clearing of the lesions yields a lacy appearance. Palms and soles are rarely affected.
The rash may recur intermittently in the weeks following the onset of illness and may be exacerbated by sun exposure or hot baths.
Associated symptoms include fever, malaise, headache, sore throat, cough, coryza, nausea, vomiting, diarrhea, and myalgias. Treatment is symptomatic.
Fetal injury may occur with acute infection in pregnant women, and those who have been exposed should receive appropriate counseling.
FIG. 85-1. Erythema infectiosum (fifth disease). Toddler with the classic slapped cheek appearance of fifth disease. (Photo contributed by Anne W. Lucky, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.)
HERPES VIRUS
Herpes labialis (“cold sores”) and gingivostomatitis (Fig. 85-2) are two common mucocutaneous presentations of herpes virus infection in children and young adults. Lesions may be single or clustered with herpes labialis; in gingivostomatitis, they are often distributed diffusely throughout the oral cavity including the gingiva, tongue, buccal mucosa, and palate.
Most herpetic infections are vesicular and extremely painful; lesions eventually unroof and crust over. Herpes labialis is typically localized to the vermillion border.
Treatment for oral lesions is symptomatic with antipyretics and analgesics. Narcotics may be needed to ensure adequate pain control to maintain oral intake.
For herpes labialis, oral antivirals may shorten the course of an acute outbreak and viral shedding when provided early in the disease. Topical acyclovir is ineffective. The dosing of oral acyclovir is variable based on age and location of the lesions, but is typically 25 milligrams/kg/dose every 8 hours for 5 days.
Children with an oral infection can inoculate the distal fingers, causing herpetic whitlow.
In children with existing eczema, a rare life-threatening viral infection can arise: eczema herpeticum. Herpes simplex virus is the most common etiologic agent but bacterial superinfection with staphylococci or streptococci is almost universal.
Clinical manifestations of eczema herpeticum include fever and vesicular eruptions in areas of skin contemporaneously affected by eczematous lesions (Fig. 85-3). Treatment includes acyclovir (25 milligrams/kg/dose PO every 8 hours) and either trimethoprim-sulfamethoxazole (5–10 milligrams/kg/dose twice daily) or clindamycin (5–7.5 milligrams/kg/dose three times daily) for 10 days. Inpatient treatment is recommended.
FIG. 85-2. Gingivostomatitis caused by herpes simplex virus. (Courtesy of the Centers for Disease Control and Prevention.)
FIG. 85-3. A and B. Typical appearance of eczema herpeticum. (Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006, McGraw-Hill, New York.)
VARICELLA (CHICKENPOX)
Due to immunizations, the incidence of varicella has declined dramatically. Varicella-zoster virus (VZV) is a herpes virus.
Infection typically occurs in children younger than 10 years, but it can occur at any age in susceptible individuals. Varicella occurs most often in the late winter and early spring.
Patients are highly contagious from the prodrome phase of the illness until all cutaneous lesions are crusted.
The exanthem starts as faint red macules on the scalp or trunk. Within the first day, lesions vesiculate and develop a red base, giving the characteristic appearance (Fig. 85-4). Over the next few days, crops of new lesions develop as others crust over. Lesions are usually intensely pruritic and spread is typically centrifugal (outward from the center). The palms and soles are often spared.
Low-grade fever, malaise, and headache are frequently seen but are typically mild.
Immunized children may present with atypical or limited skin involvement without systemic signs of illness when infected with VZV.
Treatment is symptomatic including antipyretics and antipruritic medication. Aspirin should be avoided as it has been associated with Reye syndrome in patients with VZV infection. Although not needed in previously healthy children, varicella-zoster immune globulin and acyclovir may be indicated for immunocompromised children.
FIG. 85-4. Typical rash of varicella (chicken pox). (Photo contributed by Lawrence B. Stack, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.)
ROSEOLA INFANTUM (EXANTHEM SUBITUM)
Roseola is a common acute febrile illness in young children, usually between 6 months and 3 years of age and is thought to be most commonly caused by human herpesvirus 6 (HHV6).
Roseola starts with the abrupt onset of high fevers for 3 to 5 days; associated symptoms are typically mild and may include irritability, cough, coryza, anorexia, and abdominal discomfort. Febrile seizures may occur. The exanthem of roseola appears as the fever abates, which is characteristic and diagnostic for this exanthem. The lesions are discrete, blanching, macular or maculopapular, rose-colored or pink and typically involve the neck, trunk, and buttocks, but may also include the face and proximal extremities (Fig. 85-5); mucous membranes are spared. The rash lasts 1 to 2 days and rapidly fades. Treatment is symptomatic.
FIG. 85-5. An infant with roseola infantum. (Photo contributed by Raymond C. Baker, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.)
FUNGAL INFECTIONS
Tinea infections are common in infants and children and named for the body parts affected: tinea capitis (scalp), corporis (skin), pedis (foot), and cruris (groin). Tinea infections typically manifest as scaly patches, usually circular with central clearing, and with pruritus of varying intensity (intense with cruris, barely present with corporis).
Successful treatment for all but tinea capitis is usually accomplished with topical antifungal creams including those available over-the-counter (clotrimazole, miconazole, tolnaftate) or by prescription (ketoconazole, oxiconazole, ciclopirox, terbinafine) and should be continued for 7 to 10 days after resolution of the lesions, which may take 2 to 3 weeks to fade.
Tinea capitis ranges from mild scalp lesions with patchy alopecia, to a painful, boggy mass known as kerion. Tinea capitis is treated with oral griseofulvin (ultramicrosize 15 milligrams/kg/dose once daily) and selenium sulfide shampoo. Treatment is usually continued for at least 8 weeks and close follow up to monitor response and liver function is important. Consider adding a 10-day course of cephalexin (8.3–3.16 milligrams/kg/dose given every 8 hours) for painful kerions that appear secondarily infected. The role of steroids is controversial.
BACTERIAL INFECTIONS
IMPETIGO
This superficial infectious exanthem is typically caused by group A β-hemolytic streptococci or Staphylococcus aureus and commonly affects young children. Outbreaks in daycare or school settings can occur.
Lesions can occur in areas of minor trauma or insect bites, but there may be no apparent preceding injury. The lesions start as red macules and papules that subsequently form vesicles and pustules. Rupture of the vesicles results in the formation of a characteristic golden crust and lesions may become confluent. The most common sites include the face, neck, and extremities.
With the exception of lymphadenopathy, fever and systemic signs are rare with impetigo. Diagnosis is based on the clinical appearance of the rash (Fig. 85-6).
Localized areas of infection can be treated with topical mupirocin. Larger areas usually require oral antibiotics; appropriate choices include cephalexin, erythromycin, clindamycin, amoxicillin-clavulanate, and dicloxacillin.
FIG. 85-6. A young girl with crusting impetiginous lesions on her chin. (Photo contributed by Michael J. Nowicki, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.)
BULLOUS IMPETIGO AND STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)
Bullous impetigo occurs primarily in newborns and young children, while SSSS predominantly occurs in children <6 years of age, with most cases in children <2 years of age. Both are toxin-mediated erythrodermas, caused by toxin serotypes A and B produced by Staphylococcus.
In bullous impetigo, lesions are superficial, thin-walled bullae filled with clear fluid that characteristically occur on the extremities, rupture easily, leave a denuded base, dry to a shiny coating, and contain fluid, which harbors staphylococci.
Diagnosis is usually made by the appearance of characteristic bullae (Fig. 85-7).
Treatment includes local wound care and oral antistaphylococcal agents such as cephalexin, and topical agents such as mupirocin. Coverage for community acquired methicillin resistant Staphylococcus aureus (CA-MRSA) may be indicated in certain communities.
In SSSS, the rash progresses from erythroderma to extensive areas of exfoliation, and Nikolsky sign is usually present. Symptoms such as fever, malaise, irritability, and tenderness of the skin are often present.
Patients with diffuse SSSS often require admission for IV fluids and parenteral antibiotics, with treatment in a burn unit sometimes required. Antibiotics such as nafcillin, penicillin G, amoxicillin-clavulanate, and cephalexin are acceptable therapies; vancomycin should be used when CA-MRSA is suspected.
FIG. 85-7. A child with bullous impetigo. (Courtesy of the Centers for Disease Control and Prevention.)
SCARLET FEVER
Scarlet fever typically occurs in school-aged children and is diagnosed by the presence of exudative pharyngitis, fever, and a characteristic rash. Associated symptoms include sore throat, fever, headache, vomiting, and abdominal pain.
Scarlet fever is usually caused by group A β-hemolytic streptococci (recently group C streptococci have been implicated as well).
The characteristic rash typically starts in the neck, groin, and axillae, with accentuation in flexural creases (Pastia’s lines). The rash is red and punctate, blanches with pressure, and has a rough sandpaper feel (Fig. 85-8). Early in the course of illness, the tongue has a white coating through which hypertrophic, red papillae project (the “white strawberry tongue”); hemorrhagic spots may be seen on the soft palate. The exanthem typically develops 1 to 2 days after the onset of illness and facial flushing and circumoral pallor are characteristic. Desquamation usually occurs with healing in about 2 weeks.
The diagnosis is generally made on clinical grounds, though throat culture, if obtained, reveals group A β-hemolytic streptococci or group C streptococci.
Treatment is penicillin (azithromycin in the penicillin-allergic patient) which shortens the course of the illness and reduces the incidence of rheumatic fever and nephritis.
FIG. 85-8. Scarlatiniform rash of scarlet fever; texture is typically sandpaper-like. (Photo contributed by Lawrence B. Stack, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.)
ERYSIPELAS AND CELLULITIS
Erysipelas is a cellulitis and lymphangitis of the skin caused by group A β-hemolytic streptococci. Fever, chills, malaise, headache, and vomiting are common.
The face is the most common site, and the lesion typically forms in an area of prior injury or inflammation. The rash begins as a red plaque that rapidly enlarges. Increased warmth, swelling, and a raised, sharply demarcated indurated border are characteristic (Fig. 85-9). Diagnosis is clinical.
Initial parenteral treatment with penicillin G procaine (300,000 U/d IM for <30 kg, 600,00–1 million U/d IM >30 kg) is usually warranted (erythromycin, clarithromycin, or clindamycin in the penicillin-allergic patient). Outpatient treatment includes cephalexin (6.25–25.12 milligrams/kg/dose four times daily), erythromycin (10–15 milligrams/kg/dose three times daily), or clindamycin (5–7.5 milligrams/kg/dose three times daily). Rapid clinical improvement is expected with treatment.
Other forms of cellulitis are treated similarly, however, CA-MRSA is an increasingly common cause of cellulitis in children, and treatment should be based on local sensitivities.
Traditionally, oral cephalexin (8.3–3.16 milligrams/kg/dose three times daily) has been the antibiotic of choice. With the rise of CA-MRSA, clindamycin (5–7.5 milligrams/kg/dose three times daily) or trimethoprim-sulfamethoxazole (5–10 milligrams of trimethoprim component/kg/dose twice daily) are more common choices.
FIG. 85-9. Erysipelas. (Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine. © 2006, McGraw-Hill, New York.)
INFESTATIONS
Scabies and lice infestations are covered in Chapter 157.
COMMON NEONATAL RASHES
Erythema toxicum is a benign, self-limited rash that occurs in up to 50% of newborns in the first and sometimes second week of life. Characteristic erythematous macules on the trunk, face, and extremities with central pustules suggest the diagnosis. No treatment is needed and lesions resolve in about a week.
Neonatal acne typically appears around the third week of life and affects boys more commonly than girls. Erythematous papules and pustules on the face and trunk suggest the diagnosis in the older neonate, and reassurance of spontaneous clearing is all that is needed.
Seborrheic dermatitis affects neonates and infants and is thought to be the result of genetic and environmental factors. In newborns, greasy yellow or red scales on the scalp, around the ears, eyebrows, and cheeks develop in the second to sixth week of life and are treated with topical application of oils and removal of scales with a fine comb.
Atopic dermatitis is a chronic, recurrent inflammatory disorder with a strong genetic predisposition. Characteristic dry skin and erythematous papular or papulovesicular lesions and plaques appear in the second to sixth months of life (later than seborrheic dermatitis), are usually pruritic, and may become weeping. The typical flexural distribution seen in older children may not be seen in young infants. Therapy is aimed at reducing drying of the skin, application of emollients, and treatment of inflammation with topical steroid ointments.
DIAPER RASH
A complaint specific to neonates and infants, there are two common forms of diaper rash: contact (irritation from reducing substances in stool and irritants in urine) and candidal dermatitis.
Contact diaper dermatitis is an erythematous, macular or maculopapular rash with well-demarcated borders that spares skin folds. Treatment includes good hygiene, air-drying, and use of barrier creams/ointments such as zinc oxide.
Candidal diaper dermatitis is characterized by erythematous papules and pustules with scaling margins and associated small pustules beyond the margins of the main rash known as satellite lesions.Diagnosis is clinical and treatment involves antifungal agents, such as nystatin (100,000 U/gram as cream, ointment, or powder applied 3–4 times daily for 10–14 days). Barrier creams (zinc oxide after nystatin application) can be useful. Topical steroids (1%-2% hydrocortisone cream) may be useful if severely inflamed. Oral thrush may be associated with candidal diaper dermatitis and should be treated with oral nystatin.
EXANTHEMS OF UNKNOWN ETIOLOGY
Erythema multiforme, Stevens–Johnson syndrome, and toxic epidermal necrolysis are covered in Chapter 156, Dermatologic Emergencies.
KAWASAKI’S DISEASE
Kawasaki’s disease (KD), or mucocutaneous lymph node syndrome, is a generalized vasculitis of unknown etiology that peaks around 18 to 24 months of age, and rarely occurs <4 months or >5 years.
Children may present with classic (complete) findings or incomplete findings; younger children and infants are more likely to have atypical or incomplete features and are at higher risk for complications, which include coronary artery aneurysms and sudden cardiac death.
Classic KD is diagnosed in patients who have fever for at least 5 days and at least four of the following clinical features: (1) bilateral non-exudative conjunctivitis; (2) rash (variable in nature); (3) cervical lymphadenopathy >1.5 cm; (4) mucous membrane changes, including injection of the pharynx and lips with prominent papillae of the tongue (strawberry tongue); and (5) erythema or edema of the extremities, with peeling in the convalescent stage.
The rash of KD is variable, and may be erythematous, morbilliform, urticarial, scarlatiniform, or erythema multiforme–like. Perineal rash is common.
Incomplete KD is defined by fever for 5 days, plus at least two of the classic clinical symptoms listed above, plus a CRP >3.0 milligrams/L and or ESR >40 mm/h plus three or more of the following laboratory findings: (1) albumin <3 grams/dL; (2) anemia for age; (3) elevated ALT; (4) sterile pyuria (obtained by clean catch or bag rather than catheterization); (5) WBC >12,000/mm3; (6) platelets >450,000/mm3 after 7 days of fever onset.
Patients with either classic or incomplete KD are often irritable, and may have associated arthralgias, refusal to bear weight, and desquamation.
If complete or incomplete KD is suspected, admission and specialty referral is indicated. Treatment consists of intravenous gamma globulin (IVIG) and aspirin. The use of steroids is typically not indicated unless patients do not improve with IVIG.
HENOCH–SCHÖNLEIN PURPURA
Henoch–Schönlein purpura (HSP) is the most common vasculitis in childhood.
There are four main clinical features to HSP: palpable purpura ranging in size from 2 to 10 mm primarily involving the buttocks, thighs, legs, and arms; gastrointestinal symptoms including vomiting, diarrhea, abdominal pain, and GI bleeding; polyarthralgias; and hematuria and proteinuria (nephritis).
Children with HSP are generally well appearing and afebrile. Diagnosis can be made clinically in the presence of the characteristic rash (Fig. 85-10) and requires no laboratory evaluation other than urinalysis to assess for hematuria (if present, renal function tests are indicated).
Treatment is symptomatic for arthralgias or arthritis with analgesics (typically NSAIDs), though prednisone (1 milligram/kg/dose PO) for 2 weeks followed by a 2-week taper may reduce severe joint and gastrointestinal symptoms.
HSP is usually self-limited, but may be recurrent. Follow-up for repeat urine testing should be assured in patients with nephritis.
FIG. 85-10. Henoch–Schönlein purpura. (Photo contributed by Kevin J. Knoop, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.)
PITYRIASIS ROSEA
Pityriasis rosea is characteristically seen in older school-aged children and young adults in the spring and fall. It is not contagious and does not appear to occur in epidemics.
The rash evolves over weeks: it begins with a “herald patch,” one red lesion with a raised border, typically on the trunk, which may not be noted by parents; 1 to 2 weeks later, a widespread eruption of pink macu-lopapular oval patches erupts on the trunk in a pattern following the ribs (the so-called “Christmas tree distribution”). Lesions may be pruritic. There may be mucous membrane involvement.
Pityriasis rosea typically lasts 3 to 8 weeks. In adolescents, the differential diagnosis includes secondary syphilis, which has a similar appearance.
Treatment is symptomatic and includes antihista-mines for itching.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 134, “Rashes in Infants and Children,” by Gary Bonfante and Alexander M. Rosenau.