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CHAPTER 142: Rashes in Infants and Children 925 certain strains of group A β-hemolytic Streptococcus (mucoid types 3, 5, and 18). The connective tissue of the heart, joints, CNS, and subcutaneous tissues and skin are targeted by host antibodies that develop secondary to streptococcal infection. The arthritis is characterized by synovial edema and periarticular swelling with joint effusions.  CLINICAL FEATURES The child develops the disorder 2 to 6 weeks following streptococcal pharyngitis. Although nonspecific symptoms of systemic illness pre dominate early on, physical examination eventually reveals evidence of arthritis, carditis, choreiform movements, erythema marginatum, or subcutaneous nodules, individually or in combination. Table 141-4 lists the Jones criteria for establishing a diagnosis of acute rheumatic fever. Either two major criteria or one major and two minor criteria plus evi dence of an antecedent streptococcal infection are necessary to establish the diagnosis. Of specific relevance to the musculoskeletal system, arthritis occurs in 60% to 75% of initial attacks and is characterized as a migratory, fleeting polyarticular arthritis primarily affecting the large joints.  DIAGNOSIS Diagnostic studies are used to clarify the associated antecedent infection by group A Streptococcus (a pharyngeal swab for culture, antistreptolysin titers, or streptozyme titers) or are used to identify and assess the presence and extent of carditis.  TREATMENT ED treatment is directed primarily toward the diagnosis of this condition. Admission to the hospital is generally advised in the early stages until the diagnosis is confirmed. All children with acute rheumatic fever are treated with penicillin, even if the cultures for group A Streptococcus are negative. The dose of benzathine penicillin is 600,000 units IM if <27 kg and 1.2 million units IM if >27 kg. Benzathine penicillin G can be administered in a single dose of 1.2 million units. Penicillin V administered PO is also effective. Erythromycin is substituted for the penicillin-allergic patient. Therapy is administered for 10 days. POSTSTREPTOCOCCAL REACTIVE ARTHRITIS Poststreptococcal reactive arthritis is a poorly understood clinical syndrome in which arthritis of one or more joints occurs after group A streptococcal infection of the pharynx. It is not certain whether post streptococcal reactive arthritis represents a mild or early form of acute rheumatic fever or whether it is an entirely separate entity. It falls into a group of postinfectious reactive arthritides with multiple etiologies. Poststreptococcal reactive arthritis is not associated with carditis or other major Jones criteria and is a milder illness. Poststreptococ cal reactive arthritis also begins sooner (approximately 10 days) after streptococcal infection than does acute rheumatic fever (approximately TABLE 141-4 Revised Jones Criteria for the Diagnosis of Acute Rheumatic Fever Major Criteria Minor Criteria Carditis New or changing murmurs Cardiomegaly, congestive heart failure Pericarditis Migratory polyarthritis Chorea Erythema marginatum Subcutaneous nodules Fever Arthralgia History of previous attack of acute rheumatic fever Elevated erythrocyte sedimentation rate, C-reactive protein Prolonged PR interval on ECG Rising titer of antistreptococcal antibodies Note: Diagnosis is likely when two major criteria or one major and two minor criteria are met.

m Subcutaneous nodules Fever Arthralgia History of previous attack of acute rheumatic fever Elevated erythrocyte sedimentation rate, C-reactive protein Prolonged PR interval on ECG Rising titer of antistreptococcal antibodies Note: Diagnosis is likely when two major criteria or one major and two minor criteria are met. Group A Streptococcus may be documented by a history of scarlet fever, isolation of group A Streptococcus from throat culture, or rising titers of antistreptococcal antibodies. 21 days). The arthritis in poststreptococcal reactive arthritis is generally more severe and prolonged and unusually resistant to treatment with salicylates, in contrast to the migratory salicylate-sensitive arthritis generally associated with acute rheumatic fever. The differentiation between acute rheumatic fever and poststrepto coccal reactive arthritis is clinical. The arthritis of acute rheumatic fever is classically a migratory polyarthritis, whereas the arthritis of poststreptococcal reactive arthritis is a nonmigratory mono- or oligoarthritis. Acute rheumatic fever poststreptococcal nonsuppurative sequelae are more commonly observed in younger patients (mean age, 12 ± 4 years). The typical patient with reactive arthritis is older, but it may occur in children as young as 4 years of age. Erythema nodosum and erythema multiforme are frequently associated with poststreptococcal reactive arthritis, whereas they are encountered only infrequently in cases of acute rheumatic fever. To establish the diagnosis of poststreptococcal reactive arthritis, establish antecedent infection with group A Streptococcus. If group A Streptococcus is recovered from the throat, treat with antibiotics. The diagnosis of poststreptococcal reactive arthritis should be made only after careful historical and clinical evaluation for nonsuppurative com plications or other causes of polyarthritis. Antibiotic prophylaxis may be considered on a short-term basis. If, after further evaluation, there is no evidence of carditis or chorea, prophylaxis may be discontinued. Treat ment of poststreptococcal reactive arthritis is NSAID analgesia. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Rashes in Infants and Children Michael Nguyen Amy L. Dunn INTRODUCTION This chapter describes disease processes in children for which dermatologic symptoms are diagnostic and serves as a reference for the presenting complaint of “rash” in children and young adults. Additional detailed descriptions of important skin diseases are provided in chapters in Section 20, “Dermatology, ” with Chapter 248, “Initial Evaluation and Management of Skin Disorders, ” specifically outlining principles of evaluation of rashes in both children and adults. Several important disease entities presenting with rashes are covered extensively elsewhere within this text (e.g., Lyme disease, Rocky Mountain spotted fever). In addition to the discussion below, Chapters in Section 20, “Dermatology, ” discuss diagnosis based on anatomic location of the rash. GENERAL APPROACH Most exanthems present as an isolated episode in a single child, but outbreaks can also develop in groups of children. When evaluating only a single child with a rash, the diagnosis can usually be made by routine history and physical examination. When several children develop similar-appearing skin lesions, obtain detailed contact and exposure history, and consider the need to involve specialty services or notify local public health authorities. Ask about the initial location of rash, the pattern and time frame of rash development, initial morphology, and whether any topical or systemic medications have been applied.

ons, obtain detailed contact and exposure history, and consider the need to involve specialty services or notify local public health authorities. Ask about the initial location of rash, the pattern and time frame of rash development, initial morphology, and whether any topical or systemic medications have been applied. Also inquire about fever and systemic symptoms, prior immunizations, potential human or animal contacts, CHAPTER Tintinalli_Sec12_p0669-0996.indd 925 8/2/19 7:57 PM

ons, obtain detailed contact and exposure history, and consider the need to involve specialty services or notify local public health authorities. Ask about the initial location of rash, the pattern and time frame of rash development, initial morphology, and whether any topical or systemic medications have been applied. Also inquire about fever and systemic symptoms, prior immunizations, potential human or animal contacts, CHAPTER Tintinalli_Sec12_p0669-0996.indd 925 8/2/19 7:57 PM 926 SECTION 12: Pediatrics recent bites or stings, travel, recent prescription or over-the-counter drug administration, and recent food and environmental exposure. Perform a complete physical exam and obtain a full set of vital signs. Completely disrobe all patients and place in a gown; examine patients in a room with good lighting to avoid missing important findings. Most rashes are self-limited and benign in children, but some rashes may be the harbinger of serious illness. An ill-appearing child or a child with a nonblanching rash raises suspicion for a serious condition. Check the scalp, ears, neck, mucous membranes, all skinfolds, digits and web interspaces, palms, and soles. Look for ticks that may be adherent in hair-bearing areas or skinfolds. Identify the morphology and determine the location and distribution of the rash. VIRUSES  ENTEROVIRUSES Enteroviruses are a very common cause of illness and rash in young children. Enteroviruses are small, single-stranded RNA viruses belong ing to the picornavirus group and include polioviruses, coxsackievirus, and echovirus. 1 The enterovirus family has been associated with a wide variety of illnesses, including polio. Enterovirus infections usually occur in epidemics, with a peak prevalence in the summer and early fall. Transmission usually occurs by the fecal–oral route and sometimes by respiratory or oral–oral transmission. The clinical signs and symptoms of infection with coxsackieviruses and echoviruses vary and can include nonspecific febrile illnesses, upper and lower respiratory infections, GI infections, aseptic meningitis, or myocarditis. Similarly, the associated skin manifestations include an array of exanthems. Diffuse macular eruptions, morbilliform erythema, vesicular lesions, petechial and purpuric eruptions, rubel liform rash, roseola-like rash, and scarlatiniform eruptions have all been reported. 2 Strict clinical–virologic associations are difficult to demonstrate, unlikely to be practical in the ED, and equally unlikely to change the course of management. Infection due to echovirus 9 or coxsackievirus A9 is common and produces typical examples of exanthems secondary to enteroviral illness. Both viruses may produce a maculopapular rash beginning on the face and neck and then extending to the trunk and feet. The palms and soles are also sometimes affected. Clinical manifestations include fever that may be accompanied by headache, GI complaints, and upper respira tory symptoms. With echovirus 9, occasionally, there are lesions on the buccal mucosa and soft palate that resemble Koplik spots. Petechiae may develop, raising concern for meningococcemia, although the petechiae due to enterovirus do not typically coalesce or progress to purpura. The exanthem persists for approximately 5 days. The exanthem of coxsackievirus A9, by contrast, may be vesicular or urticarial. Aseptic meningitis may be present. Another common rash caused by an enterovirus is hand-foot-andmouth disease. Initial signs and symptoms include fever, anorexia, malaise, and sore mouth. Oral lesions appear 1 to 2 days later, and cutaneous lesions appear shortly thereafter. The oral lesions begin as vesicles on an erythematous base, which subsequently ulcerate. The vesicles are usually 4 to 8 mm in size and are very painful. They are located on the buccal mucosa, tongue, soft palate, and gingiva (Figure 142-1). The exanthem starts as red papules that change to gray vesicles approximately 3 to 7 mm in size.

egin as vesicles on an erythematous base, which subsequently ulcerate. The vesicles are usually 4 to 8 mm in size and are very painful. They are located on the buccal mucosa, tongue, soft palate, and gingiva (Figure 142-1). The exanthem starts as red papules that change to gray vesicles approximately 3 to 7 mm in size. They are found on the palms and soles, but may occur on the dorsum of the feet and hands and on the buttocks as well (Figure 142-2). They may be oval, linear, or crescentic and may run parallel to skin lines. They heal in 7 to 10 days. Recent cases have been reported of pediatric patients presenting with onychomadesis (proximal shedding of nails due to nail matrix arrest) several weeks (average 6 weeks) after an illness consistent with hand-foot-and-mouth disease. It is helpful to be aware of this increas ingly common complication in order to reassure parents of the benign nature of the condition. A particularly severe form of hand-foot-and-mouth disease, attrib uted to enterovirus 71, has been identified in Southeast Asia and has been associated with serious illness including encephalitis and death. FIGURE 142-1. Oral lesions of hand-foot-and-mouth disease. [Reproduced with per mission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine , 4th ed. McGraw-Hill, Inc., New York. © 2016. Fig. 14-34. Photo contributed by Larry B. Mellick, MD.] Clinicians caring for patients from this region or those having trav eled to that area should be mindful of potential deterioration of these patients. Another recent strain that has circulated in many countries including the United States is enterovirus D68. This strain has been associated with more severe disease including severe respiratory com plications and acute flaccid myelitis presenting as paralysis in pediatric patients. These newer more virulent strains have prompted further research into a possible vaccine for enterovirus. A similar syndrome of fever, mouth pain, and oral ulcers is caused by other subtypes of the coxsackievirus group A and is known as herpangina. Like hand-foot-and-mouth disease, the diagnostic finding is small whitish ulcers, typically located on the soft palate and posterior pharynx, without accompanying skin lesions (Figure 142-3). The clinical differentiation of enteroviral disease is difficult, but because there is no specific therapy for enteroviral infection, it is more important to consider bacterial diseases in the differential diagnosis to exclude treatable causes of sepsis, meningitis, myocarditis, and pneu monia. Enteroviral polymerase chain reaction testing is commonly available and may be useful in cases of meningitis in which viral testing may decrease length of hospital stay and use of antibiotics. Symptomatic therapy for enteroviral infections includes hydration, antipyretics, and topical oral pain relief preparations. Combinations of Maalox® (or similar) and diphenhydramine liquids applied with a cotton swab to the painful oral lesions may be useful. This combination may be used orally as well, being mindful of weight-based dosing for both medications. Oral therapy with acetaminophen and ibuprofen has also proved helpful for pain control. Viscous lidocaine should not be used. A recent U.S. Food and Drug Administration drug safety communication advises that viscous lidocaine 2% solution should not be used in infants and children. 5 In 2014, 22 serious adverse events, including deaths, in children age 5 months to 3.5 years were attributed to the use of oral topical viscous lidocaine. Rarely, analgesia with oral narcotics is needed to prevent dehydration. Hospitalization in patients requiring this level of pain relief may be considered.  MEASLES The number of measles cases in the United States in 2013 to 2014 was the highest since 2000.

were attributed to the use of oral topical viscous lidocaine. Rarely, analgesia with oral narcotics is needed to prevent dehydration. Hospitalization in patients requiring this level of pain relief may be considered.  MEASLES The number of measles cases in the United States in 2013 to 2014 was the highest since 2000. Recent outbreaks among adults and children in many states have been attributed to international travel and unvac cinated populations here in the United States. Thimerosal was taken out of childhood vaccines in 2001, and multiple, large, well-designed epidemiologic studies and systematic reviews have found no evidence of an association between thimerosal and autism or other developmental disorders. In fact, autism rates have continued to rise, which is the opposite of what would be expected if thimerosal caused autism. Serious complications of measles have been reported including encephalitis, bacterial infections such as pneumonia, and death. These Tintinalli_Sec12_p0669-0996.indd 926 8/2/19 7:57 PM

l disorders. In fact, autism rates have continued to rise, which is the opposite of what would be expected if thimerosal caused autism. Serious complications of measles have been reported including encephalitis, bacterial infections such as pneumonia, and death. These Tintinalli_Sec12_p0669-0996.indd 926 8/2/19 7:57 PM CHAPTER 142: Rashes in Infants and Children 927 FIGURE 142-2. Hand-foot-and-mouth disease. Typical lesions on the palms (A), soles (B), and buttocks (C). [Reproduced with permission from Shah BR, Lucchesi M, Amodio J, Silverberg M: Atlas of Pediatric Emergency Medicine, 2nd ed. McGraw-Hill, Inc., New York. © 2013. Part A: Fig. 3.66 A, B & D. Photo contributed  by Binita R. Shah, MD.] FIGURE 142-3. Herpangina. [Reproduced with permission from Wolff KL, Johnson R, Suurmond R: Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 6th ed. © 2009, McGraw-Hill, Inc., New York.] complications are more common in children under the age of 5 years than school-age and adolescent patients. All medical care providers must be able to identify the exanthem and enanthem typical of measles in any patient presenting with the undifferentiated rash. Measles virus (rubeola) is a member of the family Paramyxoviridae, genus Morbillivirus. After exposure, the incubation period for measles is approximately 10 days (range, 7 to 21 days). The prodromal period lasts approximately 3 days and is characterized by fever, malaise, and anorexia, followed by conjunctivitis, coryza, and cough. The severity of conjunctivitis is variable and may also be accompanied by lacrimation or photophobia, but is typically not exudative. The exanthem develops approximately 14 days following exposure. The rash first appears behind the ears and at the hairline of the forehead and then spreads cephalocaudally and centrifugally to involve the neck, upper trunk, lower trunk, and extremities sparing the palms and soles. It initially consists of erythematous blanching maculopapular lesions but rapidly coalesces, especially where the first lesions appeared on the face ( Figure 142-4). In general, the extent and degree of confluence of the rash correlate with the severity of the illness in children. Other rash-causing diseases often confused with measles include roseola (roseola infantum) (see Figure 142-12) and rubella (German measles) (see Figure 142-6). Search carefully for Koplik spots (Figure 142-5) in patients with suspected measles, because they are pathognomonic for measles infection and occur about 48 hours before the characteristic exanthem. However, they do not appear in all patients. Treatment is supportive. Recognition is of the utmost importance in preventing the spread of the disease and associated morbidity and mortality. Immunization remains the most important preventive measure. About 1 in 20 children who receive the measles, mumps, rubella, and varicella vaccine will develop a rash following vaccination, which may prompt a trip to the ED. The rash usually involves the trunk and face, is macular and blanching, does not involve systemic symptoms, and is self-resolving. The only treatment is reassurance.  RUBELLA Rubella, German measles, or third disease was once a common child hood disease that had its highest incidence during the spring. The incubation period is 12 to 25 days following exposure, with a 1- to 5-day prodrome of fever, malaise, headache, and sore throat. The exanthem varies and is sometimes difficult to identify. It may be a short-lived blush, or it may have a more typical and protracted 2- to 3-day course. The exanthem begins as irregular pink macules and pap ules on the face, spreading to the neck, trunk, and arms in a centrifugal distribution (Figure 142-6).

throat. The exanthem varies and is sometimes difficult to identify. It may be a short-lived blush, or it may have a more typical and protracted 2- to 3-day course. The exanthem begins as irregular pink macules and pap ules on the face, spreading to the neck, trunk, and arms in a centrifugal distribution (Figure 142-6). The rash coalesces on the face as the erup tion reaches the lower extremities and then clears in the same fashion. Forchheimer spots are pinpoint petechiae involving the soft palate that coalesce and may accompany the rash but are nonspecific. Lymphadenopathy is a clinical manifestation of rubella, with characteristic enlargement of suboccipital and posterior auricular nodes. The clinical diagnosis in an individual case is often difficult, but the epidemic nature of the illness, along with the seasonal variation and high expression rate of Tintinalli_Sec12_p0669-0996.indd 927 8/2/19 7:57 PM 928 SECTION 12: Pediatrics FIGURE 142-4. A–C. Measles. An 8-month-old child presented with fever, coryza, and marked conjunctivitis associated with intense photophobia. Confluent, erythematous, and maculopapular rash on the face developed on the fourth day of fever. He developed measles during the measles outbreak seen in New York City in 1993. [For A and B: Used with permission of Binita R. Shah, MD. Reproduced with permission from Shah BR, Lucchesi M, Amodio J (eds): Atlas of Pediatric Emergency Medicine, 2d ed. McGraw-Hill, Inc., 2013. Fig. 3.54 A&B, Pg 100. For C: Reproduced with permission from Shah BR, Laude TL: Atlas of Pediatric Clinical Diagnosis. Philadelphia, PA: WB Saunders; 2000, Pg 61.] Tintinalli_Sec12_p0669-0996.indd 928 8/2/19 7:57 PM

BR, Lucchesi M, Amodio J (eds): Atlas of Pediatric Emergency Medicine, 2d ed. McGraw-Hill, Inc., 2013. Fig. 3.54 A&B, Pg 100. For C: Reproduced with permission from Shah BR, Laude TL: Atlas of Pediatric Clinical Diagnosis. Philadelphia, PA: WB Saunders; 2000, Pg 61.] Tintinalli_Sec12_p0669-0996.indd 928 8/2/19 7:57 PM CHAPTER 142: Rashes in Infants and Children 929 the exanthem, help in establishing the diagnosis. A history of inadequate immunizations may assist in the diagnosis. There is no specific therapy.  ERYTHEMA INFECTIOSUM Fifth disease, or erythema infectiosum, is an acute, febrile illness with a unique exanthem. Outbreaks of erythema infectiosum occur primarily in the spring. During epidemics, the attack rate is highest in children 5 to 15 years of age, but all age groups can be affected. The illness is caused by infection with human parvovirus B19, a single-stranded DNA virus. The abrupt appearance of the rash is frequently the first manifestation of erythema infectiosum. It begins with a characteristic fiery red rash on the cheeks (Figure 142-7). The rash is a diffuse erythema of closely grouped tiny papules on an erythematous base. The edges are slightly raised. The erythema is most intense below the eyes and extends over the cheeks in a pattern reminiscent of butterfly wings; it is sometimes referred to as a slapped-cheek appearance. There is circumoral pallor as well as sparing of the eyelids and chin. The facial rash fades after 4 to 5 days. Approximately 1 to 2 days after the appearance of the facial rash, a nonpruritic macular erythema or erythematous maculopapular rash occurs on the trunk and limbs. It is at first localized to the deltoid areas, trunk, and forearms, but usually extends to involve a large area. This stage of the exanthem may last 1 week. A distinctive aspect of the rash is that it fades with central clearing, giving a reticulated or lacy appearance (Figure 142-8). The palms and soles are rarely affected. The exanthem may recur in the ensuing 3 weeks, sometimes briefly. The intensity of the recurrent exanthem varies and may be related to exposure to environmental factors such as sunlight, hot baths, and, perhaps, physical exertion or emotional upset. Associated symptoms frequently occur and may include fever, malaise, headache, sore throat, cough, coryza, nausea, vomiting, diarrhea, and myalgia. Arthralgia and FIGURE 142-6. Rubella. [Image used with permission of the Centers for Disease Control and Prevention.] FIGURE 142-7. Erythema infectiosum (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, Inc., New York.] FIGURE 142-5. Koplik spots. [Image used with permission of the Centers for Disease Control and Prevention.] FIGURE 142-8. Erythema infectiosum. Lacy, reticulated rash on the body of a child with erythema infectiosum. [Reproduced with permission from Shah BR, Laude TL: Erythema infectiosum, in: Atlas of Pediatric Clinical Diagnosis. Philadelphia, PA: WB Saunders; 2000.] Tintinalli_Sec12_p0669-0996.indd 929 8/2/19 7:57 PM

on.] FIGURE 142-8. Erythema infectiosum. Lacy, reticulated rash on the body of a child with erythema infectiosum. [Reproduced with permission from Shah BR, Laude TL: Erythema infectiosum, in: Atlas of Pediatric Clinical Diagnosis. Philadelphia, PA: WB Saunders; 2000.] Tintinalli_Sec12_p0669-0996.indd 929 8/2/19 7:57 PM 930 SECTION 12: Pediatrics arthritis can occur, but are more common in adolescents and adults in whom symptoms can be severe. Parvovirus infection may also be severe in patients with sickle cell disease, in whom it may precipitate aplastic crisis. Fetal anemia and hydrops may also occur with acute infection in pregnant women in the first half of pregnancy, and those who have been exposed should be counseled appropriately. In general, parvovirus infection requires only symptomatic therapy, and recovery is usually complete.  HERPES VIRUS The two serotypes of herpes simplex virus (HSV) are HSV-1 and HSV-2, which are double-stranded DNA viruses that can present variably based on the organ systems involved and the competency of the host’s immune system. Infections may be disseminated, localized to the CNS, or mucocutaneous. In the infant, HSV-2 is usually contracted during childbirth through vaginal secretions. HSV-1 is typically spread through oral secretions. The incubation period for herpes is from 2 to 14 days. With both serotypes, viral shedding may occur from an asymptomatic source. HSV-1 is the most common type identified in lesions of the skin and oral mucosa, but HSV-2 has also been identified. Autoinoculation may also occur. The clinical appearance of both serotypes is indistinguishable, and this point is important when there is concern for sexual abuse. HSV persists for life in a latent form, with the possibility of both symptomatic and asymptomatic reactivation. Visually identifiable lesions presenting to the ED may include oral lesions, skin lesions primarily of the hand or genitalia, or ocular lesions. Herpes labialis (“cold sores”) and gingivostomatitis are two com mon mucocutaneous presentations of herpes in children and young adults (Figure 142-9). A lesion may be single, or lesions may be clustered or, in the case of gingivostomatitis, may be evident diffusely throughout the oral cavity. The clinical appearance of most herpetic infections is of umbilicated vesicles that are extremely painful. They eventually unroof and crust over. Labialis is typically localized to the vermillion border. Gingivostomatitis causes erythematous edematous bleeding gums that may make eating and drinking painful. As stated earlier, viscous lidocaine preparations should not be used. Eczema herpeticum ( Figure 142-10) is the development of vesicular eruptions in the areas of the epidermis previously affected by eczema FIGURE 142-9. Primary herpetic gingivostomatitis. Typical lesions of herpes gingivostomatitis on the buccal mucosa. [Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006 by McGraw-Hill, Inc., New York.] FIGURE 142-10. Eczema herpeticum in areas of atopic dermatitis. [Photo contributed by University of North Carolina Department of Dermatology.] and may be life threatening. Although fever may present with other forms of HSV infections of children, fever is described more frequently with eczema herpeticum. Examination reveals skin with punched-out erosions, hemorrhagic crusts, or vesicles. Treatment includes oral anti biotics to treat Staphylococcus and Streptococcus (see Table 142-2 regarding antibiotics for cellulitis), as well as antiviral therapy with acyclovir, 80 milligrams/kg/d every 6 hours for 10 days. Another herpetic skin manifestation is herpetic whitlow. This infec tion of the distal fingers is usually the result of inoculation from an oral infection.

and Streptococcus (see Table 142-2 regarding antibiotics for cellulitis), as well as antiviral therapy with acyclovir, 80 milligrams/kg/d every 6 hours for 10 days. Another herpetic skin manifestation is herpetic whitlow. This infec tion of the distal fingers is usually the result of inoculation from an oral infection. Carefully examine the child’s eyes to ensure that no herpetic lesions are present on the cornea secondary to direct contact. Herpetic infections of the ears, thorax, and extremities have also been reported as a result of close contact sports (wrestling). Genital infections are most commonly the result of sexual transmission (consensual or abuse). Diagnosis is usually based on the clinical appearance, but viral cultures should be obtained for confirmation, particularly when sexual abuse is a consideration; obtain cultures from the fluid of an unroofed vesicle. Culture, enzyme-linked immunosorbent assay, direct fluorescent antibody testing, and polymerase chain reaction are acceptable forms of testing. Providers should confirm with their laboratories the preferred method of sampling at their institution. Treatment in the case of oral lesions is symptomatic. Oral antivirals may shorten the course of an acute outbreak and viral shedding when provided early in the disease (first 48 hours). Topical acyclovir is inef fective. Limited data suggest that children with herpetic gingivosto matitis presenting early in the course (72 to 96 hours of disease onset) who are unable to drink or have significant pain may benefit from oral acyclovir. The dosing of oral acyclovir is variable based on age, immune status, and location of lesions. A typical dosing regimen suggested by the American Academy of Pediatrics for children and adolescents is as follows: PO 80 milligrams/kg/d in four divided doses for 5 to 7 days; Tintinalli_Sec12_p0669-0996.indd 930 8/2/19 7:57 PM

dosing of oral acyclovir is variable based on age, immune status, and location of lesions. A typical dosing regimen suggested by the American Academy of Pediatrics for children and adolescents is as follows: PO 80 milligrams/kg/d in four divided doses for 5 to 7 days; Tintinalli_Sec12_p0669-0996.indd 930 8/2/19 7:57 PM CHAPTER 142: Rashes in Infants and Children 931 usual maximum dose, 3200 milligrams/d. This regimen has been shown to be helpful in shortening the duration of symptoms.7,8 When initiating antiviral medication in children <2 years old or in immunocompro mised children, dosing is more variable, and consultation with a pediatric or infectious disease specialist is appropriate. Ophthalmology should be consulted when herpetic lesions are suspected of having invaded the cornea. This may be evidenced by dendritic-appearing lesions with fluorescein staining.  VARICELLA Varicella, or chickenpox, is a result of infection with varicella-zoster virus, a herpes virus. In normal children, it is characterized by a pru ritic generalized vesicular exanthem with mild systemic manifestations. Cases generally occur in late winter and early spring. It is highly con tagious in the prodromal and vesicular stage. Varicella most frequently occurs in children <10 years old but may occur at any age. The rates of varicella and associated hospital admissions and deaths have declined dramatically in surveillance areas with significant vaccine coverage, but cases do occur in vaccinated children, although they are typically mild and more limited than in unvaccinated children. Severe side effects from the vaccine are rare. 9,10 Varicella starts on the trunk, and most lesions are clustered in this body region. Lesions are of different stages presenting simultaneously. Within 24 hours, the rash acquires the typical vesicular appearance of varicella. The rash consists of teardrop vesicles on an erythematous base, which then dry and crust over. Successive fresh crops may appear for a few days. The extent of the rash may be minimal, but usually it will spread centrifugally and become widespread ( Figure 142-11). Palms and soles are spared. Vesicles may occur on mucous membranes and go on to rupture and form shallow ulcers. Atypical and limited cutane ous involvement may occur among immunized children infected with varicella virus. Low-grade fever, malaise, and headache are frequently present but are usually mild. The diagnosis of varicella is usually made FIGURE 142-11. Varicella. [Photo contributed by University of North Carolina Department of Dermatology.] clinically based on its distinctive rash. A Tzanck smear of the vesicle contents may demonstrate varicella giant cells with inclusion bodies; polymerase chain reaction may also be performed on skin scrapings. Fluorescent antibody to membrane antigen testing is regarded as the gold standard for identification of varicella-zoster virus antibodies, but is not readily available. Complications of varicella include encephalitis, pneumonia, hepatitis, and bacterial superinfection of the ruptured vesicles with staphylococci or streptococci. Neonates born to mothers with perinatal varicella infection may develop serious illness. Uncomplicated varicella requires no specific therapy. Acetamino phen may be used as needed. Do not give aspirin because it may pre dispose to the development of Reye’s syndrome. Oral antihistamines may be useful to reduce itching. Over-the-counter oatmeal-based baths may provide temporary symptomatic relief. Clean lesions regularly to prevent secondary infection. In the absence of CNS complications, the prognosis is excellent. Routine use of antiviral therapy for uncom plicated varicella infections in immunocompetent children is not commonly recommended.

counter oatmeal-based baths may provide temporary symptomatic relief. Clean lesions regularly to prevent secondary infection. In the absence of CNS complications, the prognosis is excellent. Routine use of antiviral therapy for uncom plicated varicella infections in immunocompetent children is not commonly recommended. Oral acyclovir (80 milligrams/kg/d divided every 6 hours for 5 days; maximum dose, 3200 milligrams) may be considered if started within 24 hours of onset for children over the age of 2 years who are at increased risk of moderate to severe complications. This includes unvaccinated children over the age of 12 years, children on long-term salicylate therapy, and children on short-term steroid courses. Infants and immunocompromised children with varicella require aggressive treatment with acyclovir. Those less than 1 year of age are treated with 10 milligrams/kg every 8 hours, whereas children older than 1 year receive 500 milligrams/m 2 every 8 hours. Administration of varicella-zoster prophylaxis should be considered for patients exposed to individuals with varicella if provided within 3 days of exposure.  ROSEOLA INFANTUM Roseola infantum, or exanthem subitum, was previously called sixth disease. There is no seasonal association. The most likely cause is the human herpesvirus 6, although other viruses have been associated with a roseola-like illness. Roseola is characterized by a febrile period of 3 to 5 days, deferves cence, and the appearance of a rash for 1 or 2 days (Figure 142-12). The appearance of the rash immediately following a nonspecific febrile ill ness is characteristic and aids in the diagnosis. Primarily, young children are affected, with most patients being between 6 months and 3 years of age. The illness begins abruptly with high fever, sometimes as high as 40.6°C (105°F). The child is usually alert and active but may be irritable, especially with very high fever. Associated symptoms are usually mild and may include cough, coryza, anorexia, and abdominal discomfort. Lymphadenopathy may be present. The fever persists for 3 to 5 days, and the child rapidly becomes well. Although the exanthem in roseola usually coincides with deferves cence, the rash may follow a short afebrile interlude. The rash is an ery thematous macular or maculopapular eruption that consists of discrete, rose or pale-pink lesions 2 to 5 mm in size. It is most prominent on the neck, trunk, and buttocks, but the face and proximal extremities may also be involved. The lesions blanch with pressure. There is no mucous membrane involvement. The rash lasts 1 to 2 days but may fade rapidly, usually without desquamation. There is no specific treatment for roseola. Acetaminophen is useful for fever control. Because of the abrupt nature of the fever, febrile sei zures may occur and are treated as any febrile seizure. FUNGAL INFECTIONS Tinea refers to a broad spectrum of skin infections caused by derma tophytes. These spore-forming organisms invade the stratum corneum and proliferate by feeding on keratin. These superficial infections can affect the nails, skin, scalp, and hair and are named for the area of the body infected. Tinea capitis (scalp) and corporis (skin) are the two most common infections in younger children. Capitis is most common in children <10 years of age with a peak of 3 to 7 years old. Corporis is also Tintinalli_Sec12_p0669-0996.indd 931 8/2/19 7:57 PM

in, scalp, and hair and are named for the area of the body infected. Tinea capitis (scalp) and corporis (skin) are the two most common infections in younger children. Capitis is most common in children <10 years of age with a peak of 3 to 7 years old. Corporis is also Tintinalli_Sec12_p0669-0996.indd 931 8/2/19 7:57 PM 932 SECTION 12: Pediatrics common and may be seen in adolescents participating in contact sports. Tinea pedis (foot) and tinea cruris (groin) also occur in children. The affected areas are typically scaly and vary with a degree of pruritus from intense (as with cruris) to barely present (corporis). Tinea corporis commonly has a ring appearance with central clearing. Tinea capitis causes patchy alopecia as the hair follicles are invaded and lose their structure, causing them to break at the base ( Figure 142-13). A more severe form of capitis, known as kerion, may occur when there is an exaggerated inflammatory response producing a painful, boggy mass FIGURE 142-12. 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, Inc., New York.] FIGURE 142-13. Tinea capitis. [Photo contributed by University of North Carolina Department of Dermatology.] FIGURE 142-14. Tinea capitis with kerion. [Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 4th ed. McGraw-Hill, Inc., New York. © 2016. Fig 13.94, Pg 415. Photo contributed by Anne W. Lucky, MD.] TABLE 142-1 Topical Antifungal Treatment for Tinea Corporis, Pedis, and Cruris* Medication Dosing Comments Clotrimazole 1% cream† Twice per day × 2–3 wk None Miconazole† Twice per day × 2–4 wk Not recommended <2 y old Tolnaftate† Twice per day × 2–3 wk Longer treatments in hyperkeratotic patients usually needed Ketoconazole Once or twice per day × 2–3 wk Pedis treated for 4–6 wk; safety in children not established Oxiconazole 1% cream Once or twice per day × 2–3 wk Pedis treated for 4 wk *Tinea capitis should not be treated topically. †Available over the counter without prescription in the United States. (Figure 142-14). Occipital and posterior auricular lymphadenopathy are common physical findings with a high positive predictive value for tinea capitis. 13 The differential diagnosis of a tinea infection includes pityriasis rosea, lichen planus, psoriasis, eczema, and contact dermatitis. Diagnosis can be aided by direct microscopic observation for hyphae. Wood lamp evaluation is not very useful, because many dermatophytes do not fluoresce. Treatment is typically topical, with the exception of tinea capitis. Some forms of tinea that do not respond to topical treatment may also require oral therapy. For topical treatment, therapy is usually continued for 7 to 10 days beyond resolution of the lesions, which may take 2 to 3 weeks to fade. Multiple topical therapies are available by prescription or over the counter ( Table 142-1). The treatment of choice for tinea capitis is griseofulvin (age >2 years old; microsize 20 to 25 milligrams/ kg/d divided every 12 hours or ultramicrosize 10 to 15 milligrams/ kg/d also divided every 12 hours). Baseline lab testing is not necessary Tintinalli_Sec12_p0669-0996.indd 932 8/2/19 7:57 PM

nter ( Table 142-1). The treatment of choice for tinea capitis is griseofulvin (age >2 years old; microsize 20 to 25 milligrams/ kg/d divided every 12 hours or ultramicrosize 10 to 15 milligrams/ kg/d also divided every 12 hours). Baseline lab testing is not necessary Tintinalli_Sec12_p0669-0996.indd 932 8/2/19 7:57 PM CHAPTER 142: Rashes in Infants and Children 933 with griseofulvin. If treatment is to extend beyond 8 weeks, then check complete blood count and liver and renal function tests. Children with a painful kerion may be treated with prednisone 1 to 2 milligrams/kg/d for 1 week in addition to systemic antifungal therapy. 14,15 Terbinafine (less effective than griseofulvin for Microsporum species), itraconazole, and fluconazole are also effective, with shorter courses of treatment, but are expensive. 16 Selenium sulfide 2.5% and ketoconazole shampoos are excellent adjunct therapy. Both should be left on the scalp for approxi mately 5 minutes to improve effectiveness. There is no recommendation for exclusion from school, because there is a high incidence of asymp tomatic carriers and spores may be spread for months. Tinea capitis and, rarely, tinea corporis may be associated with a papular hypersensitivity dermatitis (dermatophytid reaction, or “id” reaction). These papules or vesicles, having varying degrees of inflam mation, may be pruritic. The lesions are seen on the face, trunk, and extremities of children with tinea capitis at the time of the diagnosis or, more commonly, after initiation of systemic therapy. This rash is a manifestation of an immune response and is not a drug reaction. Oral antifungal treatment should be continued, and topical corticosteroids or systemic antihistamines are used as needed. BACTERIAL INFECTIONS  IMPETIGO Impetigo is a superficial infection caused by either Staphylococcus aureus or β-hemolytic streptococci (Figure 142-15). Impetigo can arise at the site of insect bites or superficial cutaneous trauma; sometimes, there is no apparent predisposing skin lesion. Lesions occur most frequently on the face, neck, and extremities. Fever and systemic signs are uncommon. Diagnosis is made on clinical appearance that takes two forms. In non bullous impetigo (more common), skin lesions start as small erythema tous macules and papules that develop into discrete, thin-walled vesicles, which become pustular and quickly rupture. As the vesicles rupture, a yellow fluid forms an exudate, which dries to form a stratified golden yellow crust that can spread the infection to other parts of the body. The crusts can be readily removed, leaving a smooth, red surface. Initially the lesions are discrete, but they may enlarge and become confluent. Local adenopathy may be present. Cultures are only necessary in patients who fail to respond to standard therapy. Ecthyma is a deeper infection than impetigo, and S. aureus and less commonly streptococci may be the cause. Lesions begin as vesicles that rupture, resulting in circular, erythematous, “punched out” ulcers with adherent crusts that can resemble a cigarette burn, often with surrounding erythematous edema. Treatment is aimed at preventing spread and eradicating the offending agent. Appropriate cleansing and general hygiene are mandatory. Mupirocin ointment (2% applied three times a day for 7 to 14 days) is the topical antibiotic of choice for localized areas of infection. FIGURE 142-15. Impetigo. [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, Inc., New York.] Cephalexin or clindamycin is given when large areas are affected or topical coverage is impractical (Table 142-2).

Impetigo. [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, Inc., New York.] Cephalexin or clindamycin is given when large areas are affected or topical coverage is impractical (Table 142-2).  BULLOUS IMPETIGO AND STAPHYLOCOCCAL SCALDED SKIN SYNDROME Toxin-mediated erythrodermas, including bullous impetigo and staphylococcal scalded skin syndrome, are part of the spectrum of the same disease. Although the lesions of bullous impetigo are local at the site of infection, those of staphylococcal scalded skin syndrome are distant and widespread. Toxin serotypes A and B produced by Staphylococcus are the causative agents for the exfoliative presentation. 18 In bullous impetigo, the epidermolytic toxin acts locally to cause separation of the skin at the granular layer, giving rise to bullae. The infection occurs primarily in newborn infants and young children. The characteristic skin lesions of bullous impetigo are superficial, flaccid, thin-walled bullae that occur TABLE 142-2 Antibiotics for the Treatment of Staphylococcal, Streptococcal, and Soft Tissue Infections* Medication Dosing Comments Mupirocin ointment (topical) Cephalexin (PO) Apply to lesions BID

young children. The characteristic skin lesions of bullous impetigo are superficial, flaccid, thin-walled bullae that occur TABLE 142-2 Antibiotics for the Treatment of Staphylococcal, Streptococcal, and Soft Tissue Infections* Medication Dosing Comments Mupirocin ointment (topical) Cephalexin (PO) Apply to lesions BID 25 milligrams/kg PO every 12 hrs For patients with localized impetigo Use for suspected strep or methicillin-sensitive Staphylococcus aureus (diffuse impetigo) Clindamycin (PO/IV) 7 milligrams/kg IV every 8 hours; max daily dose 1800 mg/day; 4 milligrams/kg PO every 8 hrs, max 1800 mg/day Good strep and Staphylococcus coverage in MSSA (MRSA variable-inducible resistance); poor taste and insurance coverage for liquid form; well absorbed orally TMP-SMX (PO) For > 2 months old, 6 milligrams/kg TMP PO every 12 hrs; max single dose 160 mg TMP Poor strep coverage; some resistance in MRSA Doxycycline (PO/IV) 1 milligram/kg PO or IV every 12 hrs For >8 y of age; poor strep coverage; limited recent clinical experience Azithromycin (IV/PO) 10 milligrams/kg on day 1 and then 5 milligrams/kg every day for 4 d PO; max dose for entire course 10 milligrams/kg once daily IV for 5–7 d; max dose 500 mg/dose PCN-allergic patients; emerging macrolide resistance Erythromycin (ethylsuccinate or stearate (PO)) 10–20 milligrams/kg PO every 8 hrs; max dose 4000 milligrams/day PCN-allergic patients; emerging macrolide resistance Linezolid (IV/PO) 10 milligrams/kg every 12 h IV or PO for children <12 y (max, 600 milligrams BID PO/IV); > 12 y 600 milligrams every 12 hrs MRSA resistant to clindamycin and TMP-SMX; >2 weeks therapy risk of hematologic and neurologic toxicity Cefazolin (IV) 30 milligrams/kg IV every 8 hrs; max daily dose 6 grams/day PCN allergic; good strep and MSSA coverage; poor MRSA coverage Nafcillin/ oxacillin (IV) 5 milligrams/kg IV every 6 hrs; max daily dose 4000 milligrams/ day Good strep coverage; parenteral drug of choice for MSSA; inactive against MRSA Vancomycin (IV) 20 milligrams/kg IV every 8 hrs MRSA coverage; initial dosing, monitor serum concentrations for subsequent doses Abbreviations: BID = twice a day; MRSA = methicillin-resistant Staphylococcus aureus; MSSA = methicillin-sensitive Staphylococcus aureus; PCN = penicillin; strep = Streptococcus; TMP/SMX = trimethoprim-sulfamethoxazole. *Doses are not appropriate for neonates. Refer to NeoFax©2018. Tintinalli_Sec12_p0669-0996.indd 933 8/2/19 7:57 PM

BID = twice a day; MRSA = methicillin-resistant Staphylococcus aureus; MSSA = methicillin-sensitive Staphylococcus aureus; PCN = penicillin; strep = Streptococcus; TMP/SMX = trimethoprim-sulfamethoxazole. *Doses are not appropriate for neonates. Refer to NeoFax©2018. Tintinalli_Sec12_p0669-0996.indd 933 8/2/19 7:57 PM 934 SECTION 12: Pediatrics FIGURE 142-16. Bullous impetigo. [Image used with permission of the Centers for Disease Control and Prevention.] a burn unit for further care. Patients with localized infection may be discharged to home with appropriate follow-up. Parental nafcillin, oral dicloxacillin, penicillin G procaine, amoxicillin-clavulanate, cefazolin, and cephalexin are all acceptable therapies. For methicillin-resistant S. aureus, options include clindamycin, trimethoprim-sulfamethoxa zole, or vancomycin. Coverage is often provided for both methicillinsensitive and methicillin-resistant S. aureus (Table 142-2). 18,19  SCARLET FEVER Second disease, or scarlet fever, is an acute febrile illness, primarily affecting young children, caused by group A β-hemolytic streptococci. Group C Streptococcus has been implicated as well. Clinical manifesta tions include acute onset with fever, sore throat, headache, vomiting, and abdominal pain followed by a distinctive exanthem in 1 to 2 days. There is both an enanthem and an exanthem associated with scarlet fever, caused by an erythrogenic toxin elaborated by the streptococcal organism. The tonsils and pharynx are red and covered with exudate, although, occasionally, pharyngeal findings are minimal. The tongue may develop a white coating through which red and hypertrophied papillae project, creating the appearance of a “white strawberry tongue. ” The white coating disappears by day 4 or 5, and the tongue acquires a bright-red appearance, the “red strawberry tongue” ( Figure 142-18). Bright-red or hemorrhagic spots may be seen on the soft palate or anterior pillars of the tonsillar fossa. The exanthem of scarlet fever begins 1 or 2 days after the onset of the illness. It starts on the neck, axillae, and groin and spreads to the trunk and extremities (Figure 142-19). The rash is red and finely punctate, consisting of 1- to 2-mm papules that blanch and have a characteristic rough, sandpaper feel. It is sometimes easier to identify the rash by palpation. Linear petechial eruptions, Pastia lines, are often present in the antecu bital and axillary folds. There is facial flushing with circumoral pallor. A brawny desquamation occurs at 2 weeks, yielding fine flakes of dry skin. The diagnosis of scarlet fever is readily made on clinical grounds. Throat swabs usually culture group A β-hemolytic streptococci, although FIGURE 142-17. Staphylococcal scalded skin syndrome. [Photo contributed by Judith C. Bausher, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, Inc., New York.] most often on the extremities but can occur anywhere. Bullae range in size from 0.5 to 3.0 cm. They can arise from normal skin or may have a thin, red halo. The bullae are filled with a clear, pale-to-yellow fluid and rupture easily, leaving a moist, denuded base that dries rapidly with a shiny coating (Figure 142-16). Extensive areas of skin may be involved if left untreated. The clinical appearance of the lesions usually makes diagnosis less complicated. The rash is localized to one area of the body and these children are not typically systemically ill. In most cases, bul lous impetigo may be treated locally and as an outpatient. Topical or oral agents directed at both methicillin-sensitive S. aureus and Streptococcus are recommended. Treatment consists of oral dicloxacillin, a cephalo sporin, or clindamycin if methicillin-resistant S.

not typically systemically ill. In most cases, bul lous impetigo may be treated locally and as an outpatient. Topical or oral agents directed at both methicillin-sensitive S. aureus and Streptococcus are recommended. Treatment consists of oral dicloxacillin, a cephalo sporin, or clindamycin if methicillin-resistant S. aureus (MRSA) is sus pected (Table 142-2). Staphylococci cultured from the fluid of aspirated bullae will establish the diagnosis. Staphylococcal scalded skin syndrome occurs primarily in children under the age of 5 years, and outbreaks in nurseries have been reported. Children are irritable and febrile, as compared to bullous impetigo where systemic symptoms are lacking. The rash appears as generalized, tender, macular erythema that is most prominent on the skin around the mouth and nose and in intertriginous areas. Within 1 or 2 days, the rash begins to peel. The large superficial flaccid bullae are then unroofed, revealing areas of erythematous and shiny skin, which then crust and heal (Figure 142-17). Nikolsky sign (separation of the epidermis when pressure is applied) is present with staphylococcal scalded skin syndrome. 17,18 Obtain cultures of blood, urine, nasopharynx, and cutaneous lesions; treatment often requires inpatient therapy, fluid resuscitation, and par enteral antibiotics. Patients with diffuse disease should be admitted to Tintinalli_Sec12_p0669-0996.indd 934 8/2/19 7:57 PM

sent with staphylococcal scalded skin syndrome. 17,18 Obtain cultures of blood, urine, nasopharynx, and cutaneous lesions; treatment often requires inpatient therapy, fluid resuscitation, and par enteral antibiotics. Patients with diffuse disease should be admitted to Tintinalli_Sec12_p0669-0996.indd 934 8/2/19 7:57 PM CHAPTER 142: Rashes in Infants and Children 935 FIGURE 142-19. Sandpaper-like rash of scarlet fever. [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, Inc., New York.] FIGURE 142-18. Scarlet fever: white and red strawberry tongue. [Reproduced with permission from Wolff K, Johnson RA, Saavedra AP (eds): Fitzpatrick’s Color Atlas and Synopsis of Clinical Dermatology, 7th ed. McGraw-Hill, Inc., 2013, Fig. 25-42.] FIGURE 142-20. Erysipelas. [Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006, McGraw-Hill, Inc., New York.] group C may be cultured as well. Treatment with antibiotics is necessary to reduce the incidence of rheumatic fever and may ameliorate the clinical course of the disease, although the effect on other complications such as nephritis remains unclear. Penicillin and amoxicillin are antibiotics of choice. For penicillin-allergic patients, alternatives include cephalexin and clindamycin; macrolide antibiotics remain an option, although resistance of group A streptococci to macrolides is increasing. 19,20  ERYSIPELAS AND CELLULITIS Erysipelas, or St. Anthony’s fire, is cellulitis and lymphangitis of the skin caused by group A β-hemolytic streptococci. Infection is frequently accompanied by fever, chills, malaise, headache, and vomiting. The rash is characterized by local redness, heat, swelling, and a raised, indurated border. There is marked involvement of the superficial der mal lymphatics. The rash starts as an erythematous plaque that rapidly enlarges by peripheral extension. At first, it is scarlet, hot, brawny, swollen, and tender. The edge is raised and sharply demarcated. The rash can vary in appearance from a transient hyperemia to intense inflammation, vesiculation, and bulla formation. The rash may have the appearance of an orange peel. The face was commonly the most frequent site (Figure 142-20) of infection, but more recently, infections in children have been more common on the extremities. 19 A skin wound, fissure, or ulcer may act as a portal of entry. The diagnosis is clinical, and cultures of the blood or from aspi ration of the leading edge of the lesion are rarely helpful. 21 A brief course of parenteral penicillin G procaine is usually warranted because of the rapid advancement of the infection, the acutely toxic state of the patient, and the possibility of suppurative complications. Rapid clinical response is usually obtained. Cephalosporins, clindamycin, or Tintinalli_Sec12_p0669-0996.indd 935 8/2/19 7:57 PM

enteral penicillin G procaine is usually warranted because of the rapid advancement of the infection, the acutely toxic state of the patient, and the possibility of suppurative complications. Rapid clinical response is usually obtained. Cephalosporins, clindamycin, or Tintinalli_Sec12_p0669-0996.indd 935 8/2/19 7:57 PM 936 SECTION 12: Pediatrics FIGURE 142-21. A. Abscess as visualized on US. Essentially anechoic area within the surrounding soft tissue. B. Cellulitis. Relatively hypoechoic fluid between hyperechoic soft tissue structures. This classic appearance is referred to as “cobblestones.” In some cases, the abscess contents may appear hyperechoic and mimic cellulitis. [Photos contributed by Gary Bonfante, DO, FACOEP, FACEP.] FIGURE 142-22. Petechial rash seen in meningococcemia. [Reproduced with permission from McKean S, Ross JJ, Dressler DD, Brotman DJ, Ginsber JS (eds): Principles and Practice of Hospital Medicine. The McGraw-Hill Companies, Inc., 2012, Fig. 147-22.] trimethoprim-sulfamethoxazole may be used in patients unable to take penicillin; macrolides may be considered but are limited by increasing resistance. Other forms of cellulitis are treated in a similar fashion with parenteral or oral antibiotics as listed in Table 142-2. Cellulitis is most commonly caused by S. aureus . 22 The affected area is usually erythematous, warm to palpation, and tender. Lymphangitis or regional lymphadenopathy may be seen. Once a mostly institutional issue, methicillin-resistant S. aureus has become increasingly prevalent as a community-acquired skin infection. Maintain a high suspicion for community-acquired methicillin-resistant S. aureus and be aware of local antibiotic sensitivities. If abscesses are present, they should be drained and cultures obtained. Small (<5 cm) pus collections can typically be treated with incision and drainage alone. 22,23 Bedside US can localize the abscess and differentiate cellulitis from abscess when the clinical presentation is less clear (Figure 142-21).  MENINGOCOCCEMIA A petechial rash may be the presenting symptom of many viral infections or bleeding disorders or an indication of a very serious life-threatening disease due to bacterial infections such as Neisseria meningitidis (Figure 142-22). N. meningitidis is a gram-negative diplococcus and the causative agent of invasive meningococcal disease. Since the introduction in the United States of Haemophilus influenzae type b and pneumococcal polysaccharide-protein conjugate vaccines for infants, N. meningitidis has become the leading cause of bacterial meningitis in children and remains an important cause of septicemia. Disease most often occurs in children 2 years of age or younger; the peak incidence occurs in children younger than 1 year of age. Another peak occurs in adolescents and young adults age 16 to 21 years. Outbreaks continue to occur in communities and institutions, including child care centers, schools, colleges, and military recruit camps. However, most cases of meningococcal disease are endemic, with fewer than 5% associated with outbreaks. The incubation period is 1 to 10 days but usually less than 4 days. Because of the rapid progression from initial symptoms to death, it is important to recognize the first specific clinical symptoms, which can be early indicators of sepsis such as leg pain, cold hands and feet, and abnormal skin color (pallor, mottling). In approximately half of children, the first classic symptom of meningococcal disease is rash, which sometimes evolves from nonspecific to petechial to hemorrhagic over several hours. The petechial rash appears as discrete lesions 1 to 2 mm in diameter, most frequently on the trunk and lower portions of the body.

ing). In approximately half of children, the first classic symptom of meningococcal disease is rash, which sometimes evolves from nonspecific to petechial to hemorrhagic over several hours. The petechial rash appears as discrete lesions 1 to 2 mm in diameter, most frequently on the trunk and lower portions of the body. The mucous membranes of the soft palate, ocular, and palpebral conjunc tiva should also be examined for signs of hemorrhage. Petechiae may coalesce into larger purpuric and ecchymotic lesions (Figure 142-23). The petechiae correlate with the degree of thrombocytopenia and clinically are important as an indicator of the potential for bleeding complications secondary to disseminated intravascular coagulopathy. Early identification of a petechial rash is essential to allow for rapid intervention to prevent further progression to fulminant disseminated intravascular coagulopathy, meningitis, and sepsis. It is very important to perform a thorough physical exam as well as a close review of a full set of vital signs to look for early indicators of sepsis such as tachycardia or hypotension. The overall case fatality rate for meningococcal disease is 10% and is higher in adolescents. Children with a transient petechial rash who are well appearing do not need extensive testing. But the presence of petechiae in a febrile and ill-appearing child requires testing, especially a CBC to detect throm bocytopenia and leukocytosis. Cultures of blood and cerebrospinal fluid are indicated for patients with suspected invasive meningococcal disease. Cultures of a petechial or purpuric lesion scraping, synovial fluid, and other usually sterile body fluid specimens yield the organism in some patients. Treatment The priority in management of meningococcal disease is treatment of shock in meningococcemia and of raised intracranial pressure in severe cases of meningitis. Empiric therapy for suspected Tintinalli_Sec12_p0669-0996.indd 936 8/2/19 7:58 PM

ly sterile body fluid specimens yield the organism in some patients. Treatment The priority in management of meningococcal disease is treatment of shock in meningococcemia and of raised intracranial pressure in severe cases of meningitis. Empiric therapy for suspected Tintinalli_Sec12_p0669-0996.indd 936 8/2/19 7:58 PM CHAPTER 142: Rashes in Infants and Children 937 meningococcal disease is an extended-spectrum cephalosporin, such as cefotaxime or ceftriaxone. Once the microbiologic diagnosis is established, definitive treatment with penicillin G (300,000 units/kg/d; maximum, 12 million units/d, divided every 4 to 6 hours), ampicillin, or an extended-spectrum cephalosporin (cefotaxime or ceftriaxone) is recommended. Chemoprophylaxis is warranted for people who have been exposed directly to a patient’s oral secretions through close social contact, such as kissing or sharing of toothbrushes or eating utensils, as well as for child care and preschool contacts during the 7 days before onset of disease in the index case. Rifampin and ceftriaxone are the drugs of choice in children, and ciprofloxacin can be used for adult contacts. INFESTATIONS Infestations with mites are common in children and readily spread through families, day care, and school settings where close contact with index cases can occur. Both scabies and lice are common causes of pru ritic skin rash that can affect children, and scabies, in particular, may present atypically in young infants.  SCABIES Scabies is caused by infestation with the Sarcoptes scabiei mite. The female burrows into the skin, where eggs are deposited and larvae hatch, resulting in the severe pruritus that characterizes the disease. There is typically a 4- to 6-week incubation period after exposure, which may occur at day care, school, or within the home, and infestation occurs across all socioeconomic levels and is not a reflection of poor hygiene. The classic skin findings in older children and adults include a general ized eruption with linear burrows, papules, pustules, and even vesicles. Lesions show a proclivity for the hands, feet, and groin (Figure 142-24). In infants, lesions may be widespread, with involvement of the palms FIGURE 142-23. A–C. Petechial rash can progress to purpuric lesions. [Reproduced with permission from Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K (eds): Fitzpatrick’s Dermatology in General Medicine, 8th ed. McGraw-Hill, Inc., 2012, Fig. 180-1 A-C, p. 2180.] and soles, and hyperpigmented nodules may be noted in the axilla and diaper areas (Figure 142-25). Excoriations are common from scratch ing. The differential diagnosis includes impetigo, atopic dermatitis, insect bites, and drug reactions. A careful history evaluating for other family members or close contacts with similar symptoms should be sought and may provide a clue to the diagnosis, although, occasion ally, even co-sleeping parents will deny symptoms. Testing is usually not necessary, because the diagnosis is made on history and physical alone, although scrapings of pustules may reveal mites on microscopy. Treatment consists of topical permethrin cream applied from the neck down (infants may require application to the scalp and face, avoiding the mucous membranes) and left on for 8 to 12 hours before washing off. Lindane is contraindicated in young children due to neurotoxicity. For severe infestations, oral treatment with a single dose of ivermectin, 200 micrograms/kg, may be necessary. All linens and clothes should be washed in hot water. Treatment should include all family members to prevent recurrence of infestation. Antipruritics such as diphenhydr amine may be useful. Families should be counseled that pruritus may continue for weeks despite successful elimination of infestation.

may be necessary. All linens and clothes should be washed in hot water. Treatment should include all family members to prevent recurrence of infestation. Antipruritics such as diphenhydr amine may be useful. Families should be counseled that pruritus may continue for weeks despite successful elimination of infestation.  LICE As with scabies, infestations with the common head louse, Pediculus humanus capitis, are common among children in school and day care. Parents may bring children to the ED because of a diagnosis made at school or reports of an outbreak at day care. Spread is by close contact, and hats and combs may act as fomites for transmission. The mites are more commonly found in long, straight hair and, therefore, are more common among girls than boys and less common among children with dark skin tones. Infestations may be asymptomatic and noticed by a caretaker or may present with scratching from pruritus. The diagnosis is confirmed by direct observation of live mites, although the presence of nits (egg sacks) may be considered a presumptive diagnosis. Nits are Tintinalli_Sec12_p0669-0996.indd 937 8/2/19 7:58 PM

nes. Infestations may be asymptomatic and noticed by a caretaker or may present with scratching from pruritus. The diagnosis is confirmed by direct observation of live mites, although the presence of nits (egg sacks) may be considered a presumptive diagnosis. Nits are Tintinalli_Sec12_p0669-0996.indd 937 8/2/19 7:58 PM 938 SECTION 12: Pediatrics The organophosphate malathion is available by prescription as a 0.5% lotion. Malathion is approved for children >6 years of age and is applied to the hair and scalp (dry hair), left on for 8 to 12 hours, and washed out. Re-treat in 7 to 9 days. Lindane shampoo is contraindicated in young children and pregnant women due to neurotoxicity. Re-treatment after 7 to 10 days may be necessary with all of these agents, because none is completely effective. Careful removal of the nits with a fine comb (often supplied in over-the-counter products) is an important aspect of successful treatment. Shaving of the head is not necessary. COMMON NEONATAL RASHES A number of common rashes affecting neonates and infants are worth noting due to their commonality or unique presentation in this age group and because they are of frequent concern to parents, who often FIGURE 142-24. A and B. Scabies on the foot and hand of an infant. [Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine , © 2006, McGraw-Hill, Inc., New York.] FIGURE 142-25. Infantile scabies. [Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006, McGraw-Hill, Inc., New York.] FIGURE 142-26. Head lice. small (0.3 to 0.8 mm), oval, white or yellow sacks that are found on hair shafts close to the scalp and often concentrated around the ears or nape of the neck (Figure 142-26). Treatment involves the use of pediculicides, careful grooming, hot water washing of linens and clothing, and co-treatment of close contacts. Several over-the-counter and prescription pediculicides are available. Permethrin, 1% lotion, is the most commonly used (Nix ® , available without a prescription), although pyrethrins are also avail able over the counter (e.g., Rid ® ). Topical benzyl alcohol (5% lotion) is also effective and safe for children as young as 6 months of age. 26 Tintinalli_Sec12_p0669-0996.indd 938 8/2/19 7:58 PM

ethrin, 1% lotion, is the most commonly used (Nix ® , available without a prescription), although pyrethrins are also avail able over the counter (e.g., Rid ® ). Topical benzyl alcohol (5% lotion) is also effective and safe for children as young as 6 months of age. 26 Tintinalli_Sec12_p0669-0996.indd 938 8/2/19 7:58 PM CHAPTER 142: Rashes in Infants and Children 939 present with their child to the ED for evaluation. These include ery thema toxicum neonatorum, neonatal acne, seborrheic dermatitis, atopic dermatitis, and diaper rash.  ERYTHEMA TOXICUM Despite the name, erythema toxicum is a benign, self-limited rash that occurs in up to 50% of all newborns, typically in the first week of life. The etiology is unknown, and the rash spontaneously resolves over approximately 1 week, although new lesions may develop in the second week of life as well. Characteristic erythematous macules, 2 to 3 cm, develop on the face, trunk, and extremities, and may have central 1- to 3-mm pustules (Figure 142-27). The diagnosis is clinical, although Wright-stained scrapings of the pustules will reveal eosinophils if per formed to differentiate erythema toxicum from impetigo or HSV . No treatment other than reassurance is necessary.  TRANSIENT NEONATAL PUSTULAR MELANOSIS Transient neonatal pustular melanosis is less common than erythema toxicum. It is most common in black infants. Transient neonatal pustular melanosis consists of three types of lesions: small pustules on a nonerythematous base that may be present at birth, erythematous macules with a surrounding scale that develop as the pustules rupture and may persist for weeks to months, and hyperpigmented brown macules that gradually fade over several weeks to months (Figure 142-28). The diagnosis of transient neonatal pustular melanosis is usually based on the clinical appearance. Microscopic examination of a Wrightstained smear of the contents of a pustule may demonstrate numerous neutrophils and rare eosinophils. This can help differentiate it from the lesions of erythema toxicum, which contain mostly eosinophils. However, this is usually not necessary. Treatment is supportive, and full resolution is expected.  NEONATAL ACNE Neonatal or baby acne affects up to 20% of infants and typically appears around the third week of life. It results from stimulation of sebaceous glands by maternal hormones, and males are more commonly affected than females. Erythematous papules and pustules are commonly found on the face, although they may also occur on the trunk (Figure 142-29). The diagnosis is clinical, and no testing is necessary. Lesions spontane ously resolve, usually by the third month of life, and reassurance is all that is needed. FIGURE 142-27. Erythema toxicum neonatorum. [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, Inc., New York.] FIGURE 142-28. A and B. Transient neonatal pustular melanosis. [Reproduced with permission from Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K: Fitzpatrick’s Dermatology in General Medicine, 8th ed. McGraw-Hill, Inc., 2012, Fig. 107-4A&B, p. 1189.]  SEBORRHEIC DERMATITIS Seborrheic dermatitis affects neonates and infants as well as adoles cents and is an inflammatory condition of unknown etiology, although genetic and environmental factors are thought to play a role. In newborns, the rash typically starts between 2 and 6 weeks of life and improves by 6 months of life. Lesions are greasy yellow or red scales and have a proclivity for the scalp (cradle cap; Figure 142-30 ), but may appear around the eyebrows, ears, cheeks, or neck and intertriginous areas of the body and diaper area.

In newborns, the rash typically starts between 2 and 6 weeks of life and improves by 6 months of life. Lesions are greasy yellow or red scales and have a proclivity for the scalp (cradle cap; Figure 142-30 ), but may appear around the eyebrows, ears, cheeks, or neck and intertriginous areas of the body and diaper area. Rarely seborrheic dermatitis can have more widespread plaques on the trunk and extremities and can be eas ily confused for atopic dermatitis. Unlike atopic dermatitis (see “ Atopic Dermatitis”), seborrhea is not usually pruritic and does not involve the extensor surfaces. The differential diagnosis includes atopic dermatitis (which should be considered when the onset occurs in the second or third month of life, when lesions are found to be weeping and pruritic, or with a strong family history of atopy), tinea capitis, and psoriasis. The diagnosis is clinical, and testing is usually not necessary. It is important to emphasize to parents that seborrheic dermatitis is typically selflimited. Treatment for cradle cap includes selenium sulfide–containing Tintinalli_Sec12_p0669-0996.indd 939 8/2/19 7:58 PM

history of atopy), tinea capitis, and psoriasis. The diagnosis is clinical, and testing is usually not necessary. It is important to emphasize to parents that seborrheic dermatitis is typically selflimited. Treatment for cradle cap includes selenium sulfide–containing Tintinalli_Sec12_p0669-0996.indd 939 8/2/19 7:58 PM 940 SECTION 12: Pediatrics shampoos or the application of mineral oil followed by washing and removal of scales with a fine-tooth comb.27  ATOPIC DERMATITIS Infantile atopic dermatitis or infantile eczema is a chronic, recurrent inflammatory disorder of the dermis and epidermis of unclear etiol ogy but with a strong genetic component. A complete discussion of the FIGURE 142-29. Neonatal acne. [Reproduced with permission from Wolff K, Goldsmith LA, Katz SI, et al: Fitzpatrick’s Dermatology in General Medicine, 7th ed. © 2008, McGraw-Hill, Inc., New York.] FIGURE 142-30. Cradle cap or infantile seborrheic dermatitis. [Photo contributed by University of North Carolina Department of Dermatology.] FIGURE 142-31. Atopic dermatitis. [Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006, McGraw-Hill, Inc., New York.] disorder is beyond the scope of this chapter, but atopic dermatitis is common throughout childhood and often presents in the first months of life. Triggers include excessive bathing or desiccation, heat, contact irritants, and allergens (foods and environmental). The disorder is associated with food allergies, asthma, and allergic rhinitis later in life. The infantile form typically manifests between 2 and 6 months of life, somewhat later than seborrheic dermatitis, from which it must be distinguished. Character istic findings include xerosis (dry skin) and erythematous papular or papulovesicular lesions and plaques that may become excoriated or weep. The classic flexural distribution seen in older children ( Figure 142-31) is less common in infants in whom the face is most commonly involved, although diffuse involvement is possible (Figure 142-32). The nose and diaper areas are typically spared. Lesions are usually pruritic, which, in infants, may manifest as fussiness. The differential diagnosis includes scabies and seborrheic dermatitis. A careful history, including affected caretakers and a family history of atopy, and the clinical appearance are usually all that are needed to make the diagnosis. Treatment involves counseling of parents to establish realistic expectations of probable recurrences. Therapy is aimed at identifying and eliminating triggers, reducing drying of skin (including limiting exposure to water with brief and infrequent bathing and minimal use of drying soaps), liberal application of emollients (e.g., Vaseline ® ), symptomatic treatment of pruritus (e.g., diphenhydramine), and topical steroids for active inflammation. In general, ointments are more effective than creams, and lowpotency steroids (see Chapter 248, “Initial Evaluation and Management of Skin Disorders”) should be used on the face and urogenital area, with medium-potency agents reserved for the trunk and extremities. Immunomodulators, such as tacrolimus ointment, are approved for children >2 years of age, but should not be used in infants unless prescribed by a dermatologist. Occasionally, oral antibiotics or antivirals may be indicated for superinfected areas (e.g., impetigo, eczema, herpeticum).  DIAPER DERMATITIS Diaper rash is a common ED complaint that is specific to neonates and infants. Although rare disorders such as psoriasis, immunodeficiencies, and dietary insufficiencies (e.g., zinc, biotin) may present with diaper Tintinalli_Sec12_p0669-0996.indd 940 8/2/19 7:58 PM

., impetigo, eczema, herpeticum).  DIAPER DERMATITIS Diaper rash is a common ED complaint that is specific to neonates and infants. Although rare disorders such as psoriasis, immunodeficiencies, and dietary insufficiencies (e.g., zinc, biotin) may present with diaper Tintinalli_Sec12_p0669-0996.indd 940 8/2/19 7:58 PM CHAPTER 142: Rashes in Infants and Children 941 anti-inflammatory and antiepileptic medications. One study found that 45% of drug reactions were manifested in the skin.23 Most commonly, the rash appears as red macules with papules and can occur any time after drug therapy is initiated (often 7 to 10 days). The rash can take longer to appear, especially with antiepileptic medications, and last 1 to 2 weeks. The reaction usually starts on the upper trunk or head and neck and then spreads symmetrically downward to the limbs ( Figure 142-34). The eruptions may become confluent in a symmetric, generalized distribution that spares the face. Mild desquamation is normal as the rash resolves. These rashes can sometimes be more morbilliform or even appear as the targetoid lesions of erythema multiforme. Occa sionally these rashes can progress to Stevens-Johnson syndrome, toxic epidermal necrolysis ( Table 142-3), serum sickness, or drug-induced hypersensitivity syndrome. Drug-induced hypersensitivity syndrome involves a distinct triad of fever, rash, and systemic involvement of any internal organ. This should always be discussed with caregivers of chil dren being discharged to home with a diagnosis of cutaneous drug rash as warning signs of worsening illness. Often management just includes discontinuation of the offending drug. Children with more severe skin FIGURE 142-32. Infantile atopic dermatitis. [Reproduced with permission from Wolff KL, Johnson R, Suurmond R: Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 5th ed. © 2005, McGraw-Hill, Inc., New York.] FIGURE 142-33. Diaper rash (Candida). [Reproduced with permission from Wolff KL, Johnson R, Suurmond R: Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology, 6th ed. © 2009, McGraw-Hill, Inc., New York.] rash, for all practical purposes, two forms of diaper rash compose the vast majority: contact (irritant) dermatitis and candidal dermatitis. Reducing substances in stool and irritants in the urine can cause a contact dermatitis when left in contact with the skin for prolonged periods of time or during diarrheal illness. The characteristic rash is erythematous, macular, or papular and has well-demarcated borders. The differential diagnosis includes perianal streptococcal infection, which is usually warm and macular and may be associated with desquamation. Treatment of contact diaper dermatitis includes good hygiene, air drying, and the use of bar rier creams or ointments such as zinc oxide. Candidal diaper dermatitis results from superficial infection with Candida species that are ubiquitous in the infant GI tract. Typical lesions are erythematous with papular and pustular lesions and scaling around margins (Figure 142-33). The classic finding is “satellite lesions, ” which are small pustules beyond the margins of the main rash. The differential diagnosis includes atopic dermatitis, psoriasis, and contact dermatitis, although the diagnosis is usually made by clinical examination alone based on the characteristic scale and satellite lesions. Treatment is with topical application of anti fungal agents, most commonly nystatin cream (100,000 units/gram as a cream, powder, or ointment applied three times a day for 10 to 14 days), which may be applied in combination with barrier ointments (zinc oxide applied after nystatin) and topical steroids (1% to 2% hydrocortisone cream or ointment applied after nystatin, but before zinc oxide if used) for severely inflamed lesions.

a cream, powder, or ointment applied three times a day for 10 to 14 days), which may be applied in combination with barrier ointments (zinc oxide applied after nystatin) and topical steroids (1% to 2% hydrocortisone cream or ointment applied after nystatin, but before zinc oxide if used) for severely inflamed lesions. Infants with candidal diaper dermatitis should be carefully examined for concomitant oral thrush. If oral disease is present, it should be treated with oral nystatin in mixtures of 100,000 units/ mL. Use 2 mL four times a day in infants and 4 to 6 mL four times a day in children. Administer for up to 48 hours after resolution of oral lesions. CUTANEOUS DRUG REACTIONS Many medications commonly used by children can cause a significant exanthem for which parents will seek medical care. Often, the parents suspect an allergic reaction to the medication. There are a number of medications that are known to cause rash including antibiotics and FIGURE 142-34. Coalescing papular lesions of a drug eruption. [Reproduced with permission from Strange GR, Ahrens WR, Schafermeyer RW, Wiebe RA: Pediatric Emergency Medicine, 3rd ed. © 2009. The McGraw-Hill Companies, Inc., New York, Fig. 16-1.] Tintinalli_Sec12_p0669-0996.indd 941 8/2/19 7:58 PM

luding antibiotics and FIGURE 142-34. Coalescing papular lesions of a drug eruption. [Reproduced with permission from Strange GR, Ahrens WR, Schafermeyer RW, Wiebe RA: Pediatric Emergency Medicine, 3rd ed. © 2009. The McGraw-Hill Companies, Inc., New York, Fig. 16-1.] Tintinalli_Sec12_p0669-0996.indd 941 8/2/19 7:58 PM 942 SECTION 12: Pediatrics TABLE 142-3 Clinical Distinctions Among Common and Serious Skin Infections Disease Image Reference Age Skin Findings Mucosal Involvement Nikolsky Sign Mortality (normal immune) Prognosis Bullous impetigo Figure 142-16 Newborn and young Localized bullae. Easily ruptured. None Present None Excellent. Staphylococcal scalded skin syndrome Figure 142-17 <6 y of age Bullae, easily ruptured. More extensive involvement. None Present Rare Good. Erythema multiforme Figure 142-35 >3 y of age Target lesions, atypical raised lesions. Blisters less common. Usually limited to oral mucosa when involved Usually absent Possible Good. May have recurrence. SJS Variant of TEN Usually beyond childhood Widespread blisters, purple macules. Usually <10% TBSA. Extensive and may involve more than one mucosal surface Present 5%–10% Usually good. Toxic epidermal necrolysis Figure 249-4 Usually beyond childhood Same as SJS. >30% TBSA. May involve nails. Extensive and may involve more than one mucosal surface Present 30% Variable. Cutaneous drug rashes Figure 142-34 Child through adult Diffuse maculopapular; become confluent. Minimal to no mucosal involvement Absent Rare Excellent. Abbreviations: SJS = Stevens-Johnson syndrome; TBSA = total body surface area; TEN= Toxic epidermal necrolysis. FIGURE 142-35. Symmetric distribution seen with erythema multiforme. [Reproduced with permission from Strange GR, Ahrens WR, Schafermeyer RW, Wiebe RA: Pediatric Emergency Medicine, 3rd ed. © 2009. The McGraw-Hill Companies, Inc., New York, Fig. 16-3.] findings or evidence of systemic involvement may require hospital admission. Treatment is mostly supportive with topical skin care, hydration, topical steroids if necessary, and oral antihistamines as needed.28 ERYTHEMA MULTIFORME Until the early 1990s, erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis were classified as a continuum of a spectrum of disease; it is now appreciated that erythema multiforme is distinct from the more serious or even life-threatening Stevens-Johnson syndrome and toxic epidermal necrolysis (see Chapter 249, “Generalized Skin Disorders”). 29 Although all may be induced by the use of medications, such as barbiturates, penicillins, sulfonamides, NSAIDs, and phenothiazines, erythema multiforme in children is most commonly caused by infec tion, particularly herpes viruses and Mycoplasma pneumoniae. 30 HSV-1 and HSV-2 account for 70% to 90% of all erythema multiforme cases. Erythema multiforme is rare under the age of 3 years old, affects boys more than girls, and does not favor a particular race or ethnicity. Erythema multiforme typically presents with an abrupt onset of rash, sometimes preceded by a burning sensation. Pruritus is usually absent. The characteristic lesions are described as “target” with two to three zones consisting of a dark, ruddy-appearing center and a lighter colored area surrounding the center ( Figure 142-35). A red-appearing outer ring is sometimes present. Lesions typically present as plaques and coalesce and frequently involve the palms and soles. When limited in distribution, the term erythema multiforme minor is often applied; rarely there is involvement of the oral mucosa, in which case it is termed erythema multiforme major. Lesions last 1 to 3 weeks and may recur.

Lesions typically present as plaques and coalesce and frequently involve the palms and soles. When limited in distribution, the term erythema multiforme minor is often applied; rarely there is involvement of the oral mucosa, in which case it is termed erythema multiforme major. Lesions last 1 to 3 weeks and may recur. Differential diagnosis includes urticaria, viral exanthem, hypersensi tivity reaction, cutaneous drug eruptions, Stevens-Johnson syndrome, toxic epidermal necrolysis, and vasculitis. Treatment for erythema multiforme is supportive and includes reassurance, although recurrent dis ease associated with herpes virus has been treated with oral antivirals. KAWASAKI’S DISEASE Kawasaki’s disease, or mucocutaneous lymph node syndrome, remains a vasculitis of unknown etiology. Infectious processes, toxin-mediated processes, and processes triggering a common inflammatory pathway are all postulated theories of the disease. The most devastating complication is sudden cardiac death in a child as a result of coronary artery aneurysms. However, mortality is less than 0.5% and is most common in the first year following the illness in patients with large aneurysms. Kawasaki’s disease peaks at age 18 to 24 months, with most cases occurring by age 10 years and the majority of patients being seen by age 5 years.32,33 Children younger than 6 months or older than 9 years tend to have poorer outcomes.34 Because of the potentially devastating sequelae and the potential for incomplete or atypical presentation of the disease, maintain a high index of suspicion for the diagnosis. Y ounger infants have increased risk for long-term sequelae and sudden death and are more likely to present with incomplete clinical manifestations. Kawasaki’s disease is the leading cause of acquired heart disease in children (see Chapter 129, “Congenital and Acquired Pediatric Heart Disease”). Kawasaki’s disease is recognized as either complete (classic) disease or incomplete (atypical) disease. The criteria for classic and atypical disease are listed in Table 142-4. Criteria for classic disease are fever of at least 5 days in duration and the presence of four other findings, which may include bilateral nonexudative conjunctivitis, cervical lymphadenopathy, erythema of the lips and oral mucosa, various skin changes of the extremities, and rash. The fever is usually high and abrupt. The course of illness spans from acute to subacute to convalescent and occurs over several weeks. Infants and children are typically very irritable. Cervical lymphadenopathy is the least common finding of the case definition. The type of rash is variable, although vesicles have not been described. Its appearance usually accompanies the onset of fever and has a predilection for the perineum. Desquamation in this area as well as the fingers and toes may be seen at various times during the disease, but desquamation in the extremities is more common later in the disease course. Erythema and associated edema in the extremities may cause arthralgia and fussiness. The child may refuse to bear weight. In Tintinalli_Sec12_p0669-0996.indd 942 8/2/19 7:58 PM

ngers and toes may be seen at various times during the disease, but desquamation in the extremities is more common later in the disease course. Erythema and associated edema in the extremities may cause arthralgia and fussiness. The child may refuse to bear weight. In Tintinalli_Sec12_p0669-0996.indd 942 8/2/19 7:58 PM CHAPTER 142: Rashes in Infants and Children 943 TABLE 142-4 Diagnostic Criteria for Kawasaki’s Disease29 Classic (Complete) Kawasaki’s Disease Atypical (Incomplete) Kawasaki’s Disease Fever for 5 days or more plus four of the following symptoms: Fever for 5 days and two to three clinical criteria of classic Kawasaki’s disease 1. Bilateral nonexudative conjunctivitis Plus 2. Mucous membrane changes (erythema, peeling, cracking of lips, “strawberry tongue,” or diffuse oropharyngeal mucosae) C-reactive protein ≥3.0 milligrams/L and/ or erythrocyte sedimentation rate ≥40 mm/h plus three or more of the following supplemental labs or positive echo: 3. Changes of the extremities (erythema or swelling of hands/feet, peeling of finger tips/toes in the convalescent stage) 4. Rash 1. Albumin <3 grams/dL 2. Anemia for age 3. Elevated alanine aminotransferase 4. Platelets >450,000/mm3 after 7 d of fever onset 5. Cervical adenopathy (more than one node >1.5 cm unusually unilateral anterior cervical) 5. WBC count >12,000/mm3 6. Presence of pyuria most cases, all external clinical manifestations have resolved by 6 weeks. Cardiac complications develop early in the illness, but coronary artery aneurysm development is most prevalent as the fever begins to lessen (see Chapter 129, “Congenital and Acquired Pediatric Heart Disease”). Incomplete Kawasaki’s disease is suggested by fever for at least 5 days and two of the clinical symptoms of classic disease but with supportive laboratory findings detailed in Table 142-4. Recognition and close follow-up are required in cases of incomplete Kawasaki’s disease because the risk for the development of coronary artery aneu rysms is greater in incomplete disease than in classic disease. There are no evidenced-based studies upon which to develop strict criteria for incomplete disease. 35 In the presence of fever for 5 days and at least two clinical criteria consistent with the disease, the patient should undergo laboratory evaluation, including C-reactive protein and erythrocyte sedimentation rate. If C-reactive protein is <3.0 milligrams/dL and the erythrocyte sedimentation rate is <40 mm/h, the child is followed daily until resolution or typical peeling occurs. With desquamation, an echocardiogram should be performed. If either C-reactive protein or erythrocyte sedimentation rate is elevated, perform additional labora tory testing. Obtain the specimen tubes for these tests at the time of initial evaluation to avoid additional venipuncture. If less than three criteria are present, the patient should undergo an echocardiogram, and if positive, treatment should be started. If the fever persists after a negative echocardiogram, a repeat study is suggested. If three or more criteria are present, obtain an echocardiogram and begin treatment for the disease. Once the presence of incomplete Kawasaki’s disease is suspected or the disease is thought to be classic, admission and specialty referral are indicated. High-dose aspirin (80 to 100 milligrams/kg/d in four doses for 14 days, then 3 to 5 milligrams/kg/d for 6 to 8 weeks in the absence of coronary aneurysms, and indefinitely in those with aneurysms) with concomitant IV immunoglobulin infusion (2 grams/kg in a single infu sion over 8 to 12 hours) is recommended. Aspirin alone does not appear to lessen the appearance of coronary artery aneurysms. IV immunoglobulin should be administered within the first 7 to 10 days of illness.

indefinitely in those with aneurysms) with concomitant IV immunoglobulin infusion (2 grams/kg in a single infu sion over 8 to 12 hours) is recommended. Aspirin alone does not appear to lessen the appearance of coronary artery aneurysms. IV immunoglobulin should be administered within the first 7 to 10 days of illness. Steroids are not routinely indicated but may be useful in those who do not improve with IV immunoglobulin. There is practice variability with both the duration of aspirin and the use of steroids. Infliximab, cyclosporine, other monoclonal antibodies, and plasma exchange have been studied as possible therapies. 35 Patients who develop aneurysms or coronary sequelae are referred to a pediatric cardiologist and/or cardiothoracic surgeon. HENOCH-SCHÖNLEIN PURPURA Henoch-Schönlein purpura is the most common vasculitis in child hood and presents with the tetrad of a palpable purpura, renal disease, abdominal pain, and polyarthralgias. A majority of cases are preceded by upper respiratory tract infection. Case reports have described an FIGURE 142-36. A. Henoch-Schönlein purpura on lower extremities. B. Henoch-Schönlein purpura on buttocks. [Reproduced with permission from Strange GR, Ahrens WR, Schafermeyer RW, Wiebe RA: Pediatric Emergency Medicine , 3rd ed. © 2009. The McGraw-Hill Companies, Inc., New York, Fig. 85-3 A&B.] association with virtually all respiratory pathogens, with Streptococcus, Staphylococcus, and parainfluenza being the most commonly impli cated. Medications and vaccinations have also been associated with episodes of Henoch-Schönlein purpura. 36 Henoch-Schönlein purpura is characterized by deposition of immunoglobulin A, immunoglobulin C3, and other immune complexes in the walls of the smaller vascular supply to multiple organs throughout the body. The kidneys and the GI tract are the two most commonly affected organ systems. Renal involvement occurs in approximately half the cases. Children typically present between the age of 3 and 15 years, with a peak incidence between 5 and 7 years. 31 Males and females are affected equally. 36,37 Adult cases have been reported.38 The rash occurs in nearly all patients. It is predominantly seen on the buttocks, legs, and arms. Failure to fully undress the child for examination would lead the clinician to miss the diagnosis. The rash is a non blanching palpable purpura (Figure 142-36). It is not pruritic. Lesions Tintinalli_Sec12_p0669-0996.indd 943 8/2/19 7:58 PM