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Pediatric rashes
 

Pediatric rashes

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  • 4-12%
  • Often misdiagnosed in infants.Permethrin (Elimite cream, Acticin cream) is a synthetic pyrethrin that demonstrates extremely low mammalian toxicity. It is the drug of choice for the treatment of scabies in children and adults of all ages. Several studies show that it is more effective than lindane. A diminished sensitivity to permethrin has been documented. One application is said to be effective but a second treatment 1 week after the first application is now standard practice. The over-the-counter permethrin preparation (Nix) is lower in strength (1%) and ineffective against scabies. Unlike lindane, permethrin undergoes insignificant absorption (2%), after which it is rapidly degraded. Wash off the infant 8-12 hours later… Don’t bathe right before= increased absorption.
  • Figure 4-4  Repeated cycles of wetting and drying by lip licking resulted in irritant dermatitis.
  • Intense puritis
  • Intact skin is resistant to colonization or infection with group A beta-hemolytic streptococci, but skin injury by insect bites, abrasions, lacerations, and burns allows the streptococci to invade. A pure culture of group A beta-hemolytic streptococci may sometimes be isolated from early lesions, but most lesions promptly become contaminated with staphylococci.[2] Regional lymphadenopathy is common. The reservoirs for streptococcus infection include the unimpaired normal skin or the lesions of other individuals rather than the respiratory tract.[3] Children ages 2 to 5 years commonly have streptococcal impetigo. Warm, moist climates and poor hygiene are predisposing factors. The antistreptolysin O (ASO) titer does not increase to a significant level following impetigo. Anti-DNAase B increases to high levels and is a much more sensitive indicator of streptococcal impetigo.
  • Nonbullous impetigoNonbullous impetigo originates as a small vesicle or pustule that ruptures to expose a red, moist base. A honey-yellow to white-brown, firmly adherent crust accumulates as the lesion extends radially (Figures 9-6 to 9-9 [6] [7] [8] [9]). There is little surrounding erythema. Satellite lesions appear beyond the periphery. The lesions are generally asymptomatic. The skin around the nose and mouth and the limbs are the sites most commonly affected. The palms and soles are not affected. Untreated cases last for weeks and may extend in a continuous manner to involve a wide area (see Figure 9-7 ). Most lesions heal without scarring. The sequence of events leading to nonbullous impetigo is exposure to the infectious agent, carriage on exposed normal skin, and finally skin infection after a minor trauma that is aggravated by scratching. The infecting strain has been found on normal skin surfaces 2 or more weeks before the appearance of lesions.
  • Bullous impetigoBullous impetigo (staphylococcal impetigo) is caused by an epidermolytic toxin produced at the site of infection, most commonly by staphylococci of phage group II, and usually is not secondarily contaminated by streptococci. The toxin causes intraepidermal cleavage below or within the stratum granulosum.CLINICAL MANIFESTATIONS.Bullous impetigo is most common in infants and children but may occur in adults. It typically occurs on the face, but it may infect any body surface. There may be a few lesions localized in one area, or the lesions may be so numerous and widely scattered that they resemble poison ivy. One or more vesicles enlarge rapidly to form bullae in which the contents turn from clear to cloudy. The center of the thin-roofed bulla collapses, but the peripheral area may retain fluid for many days in an inner tube-shaped rim. A thin, flat, honey-colored, “varnishlike” crust may appear in the center and, if removed, discloses a bright red, inflamed, moist base that oozes serum. The center may dry without forming a crust, leaving a red base with a rim of scale. In most cases, a tinea-like scaling border replaces the fluid-filled rim as the round lesions enlarge and become contiguous with the others (Figures 9-1 to 9-5 [1] [2] [3] [4] [5]). The border dries and forms a crust. The lesions have little or no surrounding erythema. In some untreated cases, lesions may extend radially and retain a narrow, bullous, inner tube rim. These individual lesions reach 2 to 8 cm and then cease to enlarge, but they may remain for months ( Figure 9-5 ). Thick crust accumulates in these longer lasting lesions. Lesions heal with hyperpigmentation in black patients. Regional lymphadenitis is uncommon with pure staphylococcal impetigo. There is some evidence that the responsible staphylococci colonize in the nose and then spread to normal skin before infection.
  • Hyphae grow into the hair follicles rendering them fragile.
  • A kerion is a dermatophytic infection, usually of the scalp, that appears as an indurated, boggy inflammatory plaque studded with pustules.[3] It is commonly confused with bacterial infections.
  • Selenium sulfide to prevent shedding of spores.
  • The correct answer is E. SJS, often referred to as a more severe version of erythema multiforme, is a hypersensitivity reaction that occurs in response to various triggers, including infections, medications, and malignancy. Infectious agents include viruses, bacteria, fungi, and protozoa. Many medications, such as NSAIDs, antiepileptics, penicillins, sulfa drugs, TNF alpha antagonists, and some antidepressants, have also been implicated. More than a quarter of cases may be idiopathic. Image courtesy of Allen W. Mathies, MD, and the US Centers for Disease Control and Prevention.
  • SJS may involve the mucous membranes, including the eyes and gastrointestinal tract. When more than 30% of the body surface area is involved, cases are generally referred to as toxic epidermal necrolysis. Treatment is symptomatic, including treatment of superinfection and pain control. Patients with severe cases should immediately be fluid-resuscitated and treated as burn victims. Offending agents should be removed or treated. Use of steroids is controversial. Involvement of specialists, including ophthalmologists, immunologists, and burn specialists, may be indicated. Morbidity and mortality are correlated with the percentage of body surface area involved. Image courtesy of John Noble, Jr., MD, and the US Centers for Disease Control and Prevention.
  • Patients must be closely monitored for hypotension, shock, pericarditis, organ failure, and coagulopathy, usually in an intensive care unit setting. In patients with both septicemia and meningitis, a depressed level of consciousness may be from elevated intracranial pressure or hypotension. The mortality rate, even with prompt treatment, is 5%-10%. If meningococcemia is suspected, antibiotic treatment should be initiated without waiting for confirmatory culture testing. Patients with coagulopathy and gangrene may be candidates for anticoagulation therapy.
  • A 4-month-old girl presents to the ED in extremis with rapidly developing gangrene of the extremities. All of the following are true of meningococcemia EXCEPT:A. The mortality rate is 5%-10%B. Meningitis is present in all cases of septicemiaC. Empiric antibiotic treatment should be initiated immediatelyD. Transmission is person-to-person by direct contact via respiratory dropletsE. Gangrene is caused by arterial occlusionImage courtesy of the US Centers for Disease Control and Prevention.The correct answer is B. Meningococcemia is caused by the gram-negative diplococcusNeisseria meningitides. Transmission is person-to-person via respiratory droplets, often from an asymptomatic carrier. Up to 30% of teenagers and 10% of adults carry meningococci in the upper respiratory tract. The clinical presentation is variable, with 50% of patients developing meningitis only, 10% developing septicemia only, and 40% developing both. Children with meningitis are usually febrile and ill-appearing, with symptoms of lethargy, vomiting, or nuchal rigidity. Septicemia leads to capillary leak, coagulopathy, profound acidosis, and myocardial failure. Septic emboli cause arterial occlusion in the distal extremities, as shown in this infant. Image courtesy of the US Centers for Disease Control and Prevention.
  • The correct answer is D. Measles is one of the most contagious infectious diseases, with a secondary infection rate of 90% in susceptible individuals. A vaccine was introduced in 1963 which has resulted in a reduction in annual incidence in the United States of greater than 99%. However, it remains one of the leading causes of death in young children worldwide, with an estimated 197,000 deaths yearly. After exposure, the incubation period lasts for 7-14 days. Patients then develop a prodrome of high fevers, often > 104° F, with the classic triad of cough, coryza, and conjunctivitis. A couple of days later, Koplik spots develop on the buccal mucosa, appearing as white spots on an erythematous base, as shown.
  • Within a couple of days after the Koplik spots appear, an exanthem develops which consists of blanching, erythematous macules and papules, as shown. It begins on the face at the hairline and coalesces into patches and plaques that spread cephalocaudally to the trunk and extremities. This lasts for a week before fading to hyperpigmented patches which desquamate. Vitamin A deficiency has been associated with a worse prognosis, including blindness, so all children diagnosed with measles receive supplementation. Care is otherwise supportive with adequate hydration. Subacutesclerosingpanencephalitis is a late, long-term complication caused by persistent infection of immune resistant measles.
  • The petechial rash typically begins on the wrists and ankles but may be found anywhere, including the oral mucosa, as in this child. Spotless RMSF occurs in 10%-15% of cases. A high index of suspicion must be maintained, as the mortality rate is 20%-30% for untreated patients and 1%-5% for treated ones. Empiric antibiotic therapy is usually initiated based on the history and physical examination, without waiting for confirmatory serologic testing. There is typically a delay between presentation and diagnosis of RMSF. Up to three quarters of patients may require hospitalization. Outpatients must be closely monitored, as rapid deterioration is not uncommon and requires subsequent admission. Image courtesy of the US Centers for Disease Control and Prevention
  • The use of doxycycline to treat suspected RMSF in children is standard practice recommended by both CDC and the AAP Committee on Infectious Diseases. Use of antibiotics other than doxycycline increases the risk of patient death. Unlike older tetracyclines, the recommended dose and duration of medication needed to treat RMSF has not been shown to cause staining of permanent teeth, even when five courses are given before the age of eight. Healthcare providers should use doxycycline as the first-line treatment for suspected Rocky Mountain spotted fever in patients of all ages. Chloramphenicol
  • Folliculitis is inflammation within the wall and ostia of a hair follicle creating a pustule. Many different causes have been identified, including infection, trauma, perspiration, and occlusion. The most common infectious organism is S aureus. However, gram-negative organisms are found in patients on chronic antibiotic therapy, and Pseudomonas may be found in patients using hot tubs or wet suits. Acne represents a noninfectious form of folliculitis caused by follicular obstruction from abnormal keratinization. In superficial folliculitis, multiple small papules and pustules on an erythematous base pierced by a central hair are found (shown). Deep folliculitis may present with erythematous, fluctuant nodules. Patients typically report mild pruritus or discomfort. Folliculitis is usually self-limited and does not require treatment, but the use of antibacterial soaps is recommended for recurrent folliculitis. For patients with deep lesions or suspected infectious etiology, empirical treatment with oral or topical antibiotics may be appropriate, such as dicloxacillin, a cephalosporin, or mupirocin.
  • Group A strep infection of upper dermis. Treatment for 10-20 days is recommended with penicillin, a first-generation cephalosporin, or macrolide in penicillin-allergic patients. Elevation and rest of the affected area may help reduce swelling, and saline wet dressing should be applied to ulcerated and necrotic lesions.
  • An 11-year-old girl presents with raised violaceous plaques on her legs and arms that developed over the last few days. She has had a temperature of 100-101° F at home but no other complaints. Her current temperature is 100.2° F. The rest of her exam is normal. You conclude that she has Henoch-Schonleinpurpura (HSP). Which of the following tests are most appropriate to perform at this point?A. CBC, lumbar punctureB. CBC, electrolytes, stool for occult blood, urinalysisC. CBC, electrolytes, stool for occult blood, renal ultrasoundD. CBC, head CT, lumbar puncture, abdominal ultrasound
  • Impetigo is a gram-positive bacterial infection of the superficial layers of the epidermis. The most common organisms identified are S aureus and group A beta-hemolytic streptococci. Infection typically occurs via skin breakage from excoriation or other skin diseases. Patients are either colonized in the anterior nares, or organisms pass from one individual to another through direct hand contact. Impetigo may be bullous or nonbullous. Nonbullous impetigo is the more common variety, characterized first by a red macule or papule (2-5 mm in size) that turns into a fragile vesicle that ruptures to become a honey-yellow crusted papule or plaque. In bullous impetigo, bacterial exotoxins cause a loss of cell adhesion in the superficial dermis. An initial vesicle develops into a superficial flaccid bullae (1 cm in size) with minimal surrounding erythema that eventually ruptures, leaving behind a crusty scale (shown). Lesions are usually asymptomatic with occasional pain or pruritus. Treatment is typically with topical antibiotics, such as mupirocin. Oral antibiotics, usually cephalosporins, penicillins, or beta-lactam/beta-lactamase inhibitors, are reserved for more extensive disease. Without treatment, lesions may spread via autoinoculation. Image courtesy of Wikimedia Commons.
  • Pastia lines
  • Platelet count is generally normal in HSP, helping to differentiate it from idiopathic thrombocytopenic purpura (ITP), which has low platelets. ITP presents with petechiae, bruising (as shown), or bleeding, often in areas of trauma. If counts are sufficiently low, there is a risk for intracranial bleed. A consult with hematology can help determine appropriate management in case of uncertainty.
  • Cellulitis is a nonnecrotizing infection of the dermis and hypodermis. The most common organisms involved are Streptococcus pyogenes and Staphylococcus aureus. Small breaks in the skin allow for organisms to gain entrance to the dermis and multiply. In rare cases, hematogenous or metastatic seeding may occur. Patients typically report fevers, chills, pain, swelling, tenderness, erythema, and warmth. The borders of cellulitis are not elevated or sharply demarcated. Lymphangitis or regional lymphadenopathy may develop. Mild cases may be treated in an outpatient setting with oral antibiotics, with activity against staphylococci and streptococci (eg, dicloxacillin, cephalexin, clindamycin, amoxicillin/clavulanate). Intravenous antibiotics are reserved for patients who are severely ill, with facial cellulitis, who are refractory to oral therapy, or who are immunosupressed. There is a growing presence of community-acquired methicillin-resistant S aureus (MRSA), requiring treatment with more potent antibiotics.
  • Erythema infectiosum, or fifth disease, is a common childhood exanthem caused by human parvovirus B19. Transmission is via aerosolized respiratory droplets with an incubation period of 4-14 days. The illness has 3 distinct phases with a very mild prodrome. In the first phase, which lasts for 2-4 days, bright red erythema develops over the cheeks in a classic slapped-cheek appearance, with sparing of the nasal, periorbital, and perioral regions (shown). In the second phase, which lasts for 1-4 days, an erythematous macular-to-morbilliform eruption occurs predominantly on the extensor surfaces of the extremities. In the final stage, which lasts for several days to weeks, the eruption fades leaving behind a reticulated, lacy pattern. The disease is typically self-limited and resolves without complications or sequelae in children, whereas adults may suffer significant morbidity. Some patients may develop arthralgias or pruritus that can be treated with oral analgesics, antihistamines, or topical antipruritic lotions on a case-by-case basis.
  • Hand-foot-and-mouth disease is a viral illness with oral and distal extremity lesions. It is most commonly caused by a coxsackievirus infection. Infections are highly contagious, leading to epidemics from direct contact with nasal and oral secretions or fecal material. Incubation typically averages 3-6 days. Following implantation, regional spread to lymph nodes occurs within 24 hours, and then viremia rapidly ensues. Typically by day 7, neutralizing antibody levels have sufficiently increased and the virus is eliminated. Patients may report a viral prodrome, but the lesions themselves are typically asymptomatic. Children typically have a more severe course and may develop high fevers. The oral lesions are usually 2-3 mm vesicles on an erythematous base. The cutaneous lesions on the hands, feet, and buttocks are 2-mm to 10-mm erythematous macules on which a central, gray, oval vesicle develops. Lesions are typically elliptical with the long axis parallel to skin lines (shown). Care is supportive with antipyretics and anesthetics for symptomatic relief on a case-by-case basis.
  • Molluscumcontagiosum is a cutaneous infection caused by a large DNA poxvirus. Transmission occurs via direct skin contact or by sharing towels, sports equipment, or benches. Most patients are asymptomatic, but others report pruritus, tenderness, and pain. The lesions appear as firm, smooth, umbilicated papules typically 2-6 mm in diameter either clustered or widely distributed (shown). Lesions can be variable in color ranging from flesh, white, translucent, or yellow; range in number from 1 to several hundred; and may persist for several years. Diagnosis is typically made on clinical grounds. Although typically self-limited, therapy may be appropriate for lesions that do not resolve after several months to prevent autoinoculation. Treatment options are not approved by the US Food and Drug Administration (FDA), including topical applications (eg, cantharidin, tretinoin cream), systemic agents (eg, griseofulvin, cimetidine, methisazone), and photodynamic therapy. The overall prognosis is typically excellent.
  • Herpes simplex viruses (HSVs) are DNA viruses that cause acute skin infections that present as grouped vesicles on an erythematous base. Infection occurs from transmission of body fluids onto a mucous membrane or open skin from an actively shedding individual to a susceptible person. HSV invades and replicates in the neurons and epidermal and dermal cells. Latency is established when virions migrate to a dorsal root ganglion. Recurrent outbreaks occur at or near the same location from viral replication in the sensory ganglia as a result of stress, trauma, immunosuppression, hormonal fluctuations, extremes in temperature, or ultraviolet light. HSV-1 reactivates predominantly in the trigeminal ganglia, called herpes labialis (shown), whereas HSV-2 reactivates in the lumbosacral ganglia, called herpes genitalis. Patients typically report painful ulcerating lesions. Most infections are self-limited but antiviral therapy, such as acyclovir, will shorten the course of symptoms and may help to prevent dissemination and transmission.
  • Chickenpox is an infectious vesicular rash caused by primary infection from the double-stranded DNA VZV. Ninety percent of cases occur in children younger than 10 years. Chickenpox is highly contagious and acquired via inhalation of airborne respiratory droplets or direct vesicle contact. The virus first infects the conjunctiva or mucosa of the upper respiratory tract. Proliferation in regional lymph nodes occurs 2-4 days after inoculation with viremia developing on days 4-6. A second round of viral replication develops 14-16 days post infection in the liver and spleen causing a secondary viremia. This viremia invades the capillary endothelial cells and epidermis, producing inter- and intracellular edema, resulting in vesicle formation. The clear vesicles are surrounded by an erythematous halo with subsequent central umbilication and crusting (shown). Patients may report a mild prodrome and then intense pruritus with vesicle formation. On exam, vesicles in all stages of development are typically present. Treatment is for symptomatic relief with topical antipruritic creams or oral antihistamines. Acyclovir is not often prescribed for children. The disease typically resolves spontaneously, but adults may have significant morbidity and are often given antiviral medications.

Pediatric rashes Pediatric rashes Presentation Transcript

  • Pediatric Rashes Kersten Milligan RII Wednesday August 7, 2013
  • Before we begin • Objectives – Learn to recognize common pediatric rashes – Learn to recognize emergent rashes
  • So You’ve got patient with a rash • Step 1: Don blue gloves • Step 2: History • Onset • Evolution • Associated symptoms • Prior treatment • Step 3: Physical • Strip • Examine
  • Remember your anatomy…
  • Epidermis Rashes involving the Epidermis • Eczematous • Scaling • Vesicular • Papular • Pustular • Hypopigmented Rashes not involving the epidermis • Erythema • Purpura • Induration
  • Common Rashes • Scabies • Acne • Contact Dermatitis • Irritant • Allergic • Atopic Dermatitis
  • Scabies
  • Adult infection
  • Now what? • Permethrin • Tx household contacts • Recommend spring cleaning
  • Acne
  • Zit Pathology
  • Treatment “Permanent scarring of the skin and the psyche can result...”
  • Contact Dermatitis Irritant • Physical and chemical alteration of epidermis • High concentration required • Gradual onset • Tx: – Decrease exposure – Protective barrier Allergic • Delayed hypersensitivity reaction • Reaction to low concentration • Rapid onset • Tx: – Avoid exposure (wash skin!) – Diphenhydramine – Topical steroids
  • Irritant Dematitis
  • Irritant (Pacifier) Dermatitis
  • Allergic Contact Dermatitis http://www.webmd.com/skin-problems-and-treatments/picture-of-allergic-contact-dermatitis
  • Allergic Contact Dermatitis Brown henna with paraphenylenediamine (PPD) = “black henna”
  • Allergic Contact Dermatitis
  • Atopic Dermatitis (Eczema) Infant • 4mo-5 yo • Cheeks • Extensor surfaces • Diaper area Child • 3yo-adulthood • Antecubital and popliteal flexion area • Neck • Face • Upper chest
  • Atopic Dermatitis
  • Atopic Dermatitis
  • Atopic Dermatitis
  • Atopic Dermatitis (Eczema) Treatment • Cotton clothing, avoid nonessential toiletries and detergents (bounce, downy, snuggle syndrome) • Warm baths  pat dry  topical steroids and moisturizers (Cetaphil or Vaseline) • Watch for super imposed infection
  • Rashes that need treatment • Impetigo • Tinea
  • Impetigo
  • Impetigo
  • Impetigo
  • Impetigo
  • Impetigo
  • Impetigo
  • Bullous impetigo • Epidermolytic toxin • Bullae • Crust
  • Bullous impetigo
  • Bullous Impetigo
  • Impetigo • Staphylococcus aureus • Group A streptococcus • Not usually painful • Palpate for regional lymphadenopathy • Contagious • Complications: Postpyodermal acute glomerulonephritis
  • Impetigo Treatment • Mupirocin 2% ointment – Soften crusts first with wet washcloth – TID • Erythromycin • 30 mg/kg/day x 10 days • Cephalexin • 30-40 mg/kg/day TID x 7-10 days
  • Tinea Corporis
  • Tinea Corporis Dermatophyte
  • Tinea Versicolor Malassezia globosa
  • Tinea Capitis Dermatophyte
  • Kerion
  • Treatment • Tinea Corporis – Topical antifungals • Clotrimazole (Lotrimin), tolnaftate (Tinactin), miconazole, terbinafine, haloprogin • Tinea Versicolor – Topical antifungals – Selenium Sulfide shampoo • Tinea Capitus – Systemic treatment – Griseofulvin 20 mg/kg/day x 6 wks – Selenium sulfide shampoo twice weekly • Kerion – Treat as Tinea Capitus – Add prenisone 1 mg/kg/day x 1-2 wks
  • Emergent Rashes • Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis • Neisseria meningitidis • Measles • Rocky Mountain Spotted Fever
  • Stevens-Johnson Syndrome/ Toxic Epidermal Necrolysis
  • SJS/TEN
  • SJS/TEN
  • SJS/TEN
  • SJS/TEN
  • Stevens-Jonhson Syndrome/ Toxic Epidermal Necrolysis Diagnsosis • Prodrome – HA, pharyngitis, stomatitis, conjuctivitis • Spectrum of disease from <10% to >30% epidermal detachment • Hypersensitivity reaction • Separation of the epidermis from the dermis (Nikolsky’s sign) • Death from sepsis Treatment • Admission to Burn Unit • Supportive care • Steroids controversial
  • Neisseria meningitidis
  • N. meningitidis
  • N. meningitidis
  • N. meningitidis
  • N. meningitidis Treatment Rosens. Table 173-3 -- Empirical Antibiotics for Treatment of Acute Bacterial Meningitis
  • Measles • Vaccine 1963 • 99% reduction in US • >150,000 deaths annually worldwide • 90% infection rate
  • Measles
  • Measles • Exanthem • Blanching macules and papules • Hyperpigmented patches that desquamate
  • Measles Diagnosis • Fever, malaise • Cough, coryza, conjunctivitis • Koplik’s spots • Maculopapular erythematous lesions starting on forehead and upperneck • Complications: – Otitis Media, encephalitis, pneumonitis – 1/1000 encephalitis, 15% mortality Treatment • Supportive • Isolation ? as patient contagious 2 days before symptom onset • 0.25 mL/kg IM ISG (human immune serum globulin) within 6 days • Live vaccine w/in 72 hours of exposure • Vitamin A
  • Rocky Mountain Spotted Fever
  • RMSF • Erythematous blanching macules
  • RMSF
  • RMSF
  • RMSF
  • Rocky Mountain Spotted Fever Diagnosis • Mostly SE US • HA, N/V, fever • Rash on 2nd-4th day • Erythematous blanching macules. • Wrists and ankles  trunk • May become petechial Treatment • Children <45 kg – Doxycycline 2.2 mg/kg BID x 7-14 days • 25% mortality without treatment Doxycycline is the first line treatment for adults and children of all ages and should be initiated immediately whenever RMSF is suspected. -CDC
  • 1. Cydulka RK, Garber B. Dermatologic Presentations. In Marx J, ed. Rosen’s Emergency Medicine. Philadelphia, PA: Elsevier; 2010. 2. Habif MD, Thomas P. Clinical Dermatology, 4th Edition – A Color Guide to Diagnosis and Therapy. Philadelphia, PA: Mosby; 2004. 3. Murray OMSII, Alexandra. Deadly Rashes Not to Miss in the ED. American Academy of Emergency Medicine. http://www.medscape.com/viewarticle/804255?nlid=31985_541&src=wnl_e dit_medp_emed&spon=45. Accessed August 06, 2013. 4. Rampal MD, Angelika. Pediatric Rashes to Worry About: Slideshow. http://reference.medscape.com/features/slideshow/pediatric-rashes. Accessed August 06, 2013. References