Pediatric Primary Care: Practice Guidelines for Nurses, 2nd Ed.


Dermatologic Problems

Peggy Vernon

Acne, 706.1

Papule, 709.8

Blackhead, 706.1

Pustules, 686.9

Comedone, 706.1

Skin nodule, 782.2

Hyperpigmentation, 709

Whitehead, 706.2


A. Etiology.

1. Acne vulgaris is a disorder of the pilosebaceous follicles.

2. Hormonal stimulation increases the growth of the sebaceous follicles.

3. Excess sebum, keratinocytes, and bacteria accumulate, causing follicular plugging and inflammation.

B. Occurrence.

1. 40% of children 8 to 10 years of age will develop early lesions.

2. The highest incidence of acne is during the adolescent years, with 85% of all adolescents experiencing some form of acne.

3. 10% of adults in their 30s, 40s, and 50s continue to experience acne.

4. There is a familial tendency to the disorder.

C. Clinical manifestations.

1. The primary lesions are the open and closed comedones.

a. The open comedone, or blackhead, is an obstruction of the follicle that is filled with stratum corneum cells. The black color is due to compacted melanocytes.

b. The closed comedone, or whitehead, is the result of swelling of the follicular duct below the epidermis.

2. The accumulation of sebum and keratin cause the follicle wall to rupture into the dermis, causing inflammatory acne, or papules and pustules–the inflammatory reaction to sebum, fatty acids, and the bacteria.

a. Propionibacterium acnes distend the follicle, causing leakage around the comedone.

b. Lesions developing in the lower portion of the follicle create warm, tender nodules and cysts. These lesions may result in scars, which in turn can develop into keloids.

c. Inflammatory acne lesions may resolve with postinflammatory hyperpigmentation, which usually clears after several months.

D. Physical findings. The highest concentration of sebaceous glands occurs on the face, chest, back, and shoulders. A variety of lesions appear simultaneously, presenting with a variety of comedones, papules, pustules, and nodules. Acne appears to be more severe in winter months, and females report a premenstrual hormonal correlation. The severity of acne is determined by the quantity, type, and distribution of lesions.

E. Diagnostic tests. Acne is a visual diagnosis. History should include family history, other medical disorders, duration of acne, products used, and previous treatments–over-the-counter as well as prescription medications. Physical examination should include grade of acne according to type and location of lesions. See Table 20-1. Laboratory testing is indicated only if adrenal or gonadal function are in question.

F. Differential diagnosis.

1. Tuberous sclerosis.

2. Nevus comedonicus.

3. Miliaria of the newborn.

4. Flat warts.

5. Molluscum contagiosum.

Table 20-1 Grading Scale for Acne Severity





None: skin is clear



Few comedones



Mild comedones, few papules, minimal erythema



Comedones, papules, pustules, erythema



Moderate comedones, greater number of papules, pustules extending over wider area of face, chest, shoulders, back, increasing erythema



Comedones, increasing number of papules, pustules, nodules with erythema



Comedones, papules, pustules, nodules, cysts; scarring may or may not be present with hyperpigmentation


Table 20-2 Treatment of Acne


G. Treatment. Goals of treatment include altering keratinization, counteract excess sebum production, decrease the production of P. acnes, and minimize scarring. Treatment choices depend on the severity of acne. See Table 20-2.

H. Follow up. Acne patients should be evaluated every 3 to 6 months for compliance, treatment progress, and worsening of the disorder. Dermatology referral should be considered for patients who are not 50% improved on topical medications and oral antibiotics after 6 months, or those who are developing scarring from acne lesions. Patients treated with isotretinoin are monitored monthly. The development of the iPLEDGE Program requires providers, patients, and pharmacists to access the program monthly to monitor for pregnancy, blood donation, and contraceptive counseling, as isotretinoin is teratogenic.

I. Complications. Lack of patient motivation, inappropriate treatments, and inappropriate expectations complicate acne treatment. Psychologic effects of acne include poor self-esteem, depression, and problems with interpersonal relationships. Resistance to treatment, especially oral antibiotics, also complicate treatment.

J. Education. Proper use of medications as well as cleansers, moisturizers, and make-up are important to encourage compliance. Although no evidence indicate dietary restrictions are helpful, a well-balanced diet including adequate intake of water is important in treatment. It takes weeks to months to treat acne, and occasionally the disorder will worsen with treatment. Compliance is crucial.


A. Animal bites.

1. Etiology and occurrence. Cat and dog bites, as well as other animal bites, are common injuries.

2. Clinical manifestations. Bite wounds may be infested with S. aureus, streptococci, and other oral flora bacteria. Approximately one-third of animal bites contain anaerobic bacteria. It is difficult to predict which wounds will become infected.

3. Physical findings and complications. Injuries include lacerations, crushing injuries, deep puncture wounds, as well as bone, tendon, muscle, and neurovascular tissue damage from deep bites. Secondary infection can lead to cellulitis.

4. Diagnostic tests. Wound cultures identify infectious agents. X-ray and MRI studies reveal bone, vascular, and nerve damage.

5. Differential diagnosis. Identify laceration and puncture wounds from other sources.

6. Treatment. Culture wounds before cleansing and debridement. Antibiotics for infected wounds, management of bone, tendon, nerve, and vascular wounds by appropriate specialists. If suturing is necessary, observe closely for infection. Hospitalization and reconstructive surgery as indicated. Tetanus booster if indicated. Rabies prophylaxis if indicated. Psychological management.

7. Education. Teach children not to provoke any animal. Provide adequate adult supervision of children. Report stray animals to animal control officials.

B. Human bites.

1. Clinical manifestations. Human bite wounds harbor both anaerobic and aerobic bacteria, as well as S. aureus and Haemophilus, with a higher incidence of infections and complications than other bites. Human bites include occlusional wounds when teeth are sunk into the skin, and clenched-fist injuries when a tooth penetrates a joint or bone.

2. Diagnostic tests. Radiographic and surgical evaluation if a joint or bone is penetrated. Bacterial cultures for anaerobic and aerobic bacteria.

3. Treatment. Irrigation decreases risk of infection. Debridement of wound edges, appropriate antibiotic treatment (Augmentin, Erythromycin) and immunization if indicated.

4. Complications. Residual disability are frequent after clenched-fist injuries, including abscess, osteomyelitis, tendonitis, tendon rupture, and stiffness of the joint.

C. Atopic dermatitis/eczema.

1. Etiology. Eczema is a chronic disorder characterized by exacerbations and remissions. There is a strong family history of allergies and asthma.

2. Occurrence. Atopic dermatitis, or eczema, is the most common skin disorder seen in children, affecting 10-15% of all children; 30-80% percent of atopic patients continue to experience flares during their lifetime.

3. Physical findings. Atopic dermatitis is characterized by intense pruritus, erythema, scale, and excoriations. The borders are diffuse. Crusting and oozing are common in infants. Thickened skin (lichenification) from persistent scratching and rubbing may be present. Distribution is on the scalp, face, and extensors in infants, on the neck and flexor folds in children, and on the hands and feet in adolescents and adults.

3. Diagnostic tests. Atopic dermatitis is a clinical diagnosis based on careful history and clinical examination. A potassium hydroxide (KOH) scraping will exclude fungal infections.

4. Differential diagnosis. Tinea, seborrheic dermatitis, psoriasis, scabies, and molluscum contagiosum.

5. Treatment. Goals of treatment include controlling itching with antihistamines, hydrating the skin with lukewarm tub soaks followed by application of emollient moisturizers, (Eucerin, Aquaphor) alleviating inflammation with topical corticosteroids, maintaining remission with immunomodulators such as Elidel and Protopic, and treating secondary bacterial infections with appropriate topical and systemic antibiotics. Bleach baths kill microbes that cause infection in children with atopic dermatitis. Add ¼ cup of bleach to a bath tub of lukewarm water and allow the child to soak for 10 minutes, followed by adequate moisturizers. Identifying and treating allergens helps control flares.

5. Follow up. Failure to respond to treatment requires referral to a dermatology specialist. Referral to an allergist may be necessary for evaluation and management of allergies.

6. Complications. Secondary bacterial infections from excoriations include Group A beta-hemolytic streptococci and staphylococcus. Patients with atopic dermatitis have a higher incidence of viral infections, including herpes simplex, molluscum contagiousum, and warts.

7. Education. There is no cure for atopic dermatitis. It is characterized by exacerbations and remissions. Teach proper use of antihistamines, topical corticosteroids, and immunomodulators, as well as bathing followed by application of moisturizers. Identify aggravating factors such as stress, allergies, weather change, and infections.


A. Etiology and occurrence. Burns can be caused by thermal, chemical, or electrical agents. The majority of burns are thermal, and the minority of burns are chemical. Most burns are minor and can be managed on an outpatient basis.

B. Clinical manifestations. Burns are classified by depth of injury. Superficial or first-degree burns involve only the epidermis. Partial thickness or second-degree burns involve damage to the epidermis and varying depths of the dermis. Full thickness or third-degree burns involve the epidermis, the dermis, and the subcutaneous fat. Third-degree burns are painless. The size of the burn is measured by the percent of total body surface area (TBSA) involved. The rule of nines estimates the TBSA. see Figure 20-1.

C. Physical findings. Physical examination includes the TBSA, distribution, and depth of involvement.

D. Diagnostic tests. Bacterial cultures for suspected infection. Laboratory evaluation for serious burns includes complete blood count (CBC), serum electrolytes, serum glucose, blood urea nitrogen (BUN), creatinine, and urinalysis.

Figure 20-1 Rule of nines.


E. Differential diagnosis. Careful history will determine the type of injury and degree of burn. Other diseases include scalded skin syndrome and Ritter's disease.

F. Treatment. Management depends on the classification of the burn. Electrical and chemical burns usually require hospital observation. Injuries with associated upper airway injury, fractures, abuse, or severe pain also should be hospitalized. Outpatient treatment includes maintenance of proper nutrition. Superficial burns are treated with cool compresses and pain management. Partial thickness burns are treated with daily cleansing, debridement of devitalized tissue, application of silver sulfadiazine cream, bacitracin, or gentamycin ointment, and a thin guaze dressing, as well as appropriate pain management.

G. Follow up. Treatment should continue for 1 to 2 weeks, or until wounds are healed. Assessment for infection should continue.

H. Complications. Local infection and inflammation, as well as neurologic and vascular compromise.

I. Education. Home and environmental safety issues should be addressed, firstaid measures, proper use of sunscreen to prevent sunburn of the affected areas. The extent of scarring is difficult to predict, depending on the severity and extent of the burn, whether grafting was needed, and skin color.


A. Etiology. Diaper dermatitis is an inflammation of the skin in the diaper area due to breakdown of the skin's natural barrier.

B. Occurrence. Diaper dermatitis is perhaps the most common skin disorder seen under 2 years of age. If not properly controlled, diaper dermatitis can recur regularly until toilet training is complete.

C. Clinical manifestations. Causes of diaper dermatitis include irritant secondary to prolonged contact with urine and feces, Candida albicans, bacterial infections including impetigo secondary to staphylococcus or streptococcus, and psoriasis.

D. Physical findings.

1. The most prevalent form of diaper dermatitis is irritant dermatitis. Usually confined to the buttocks, perineal area, and medial thighs, sparing the interiginous areas. Contributing factors are prolonged time between diaper changes, harsh soaps, improper moisturization, use of barrier ointments, and excessive heat in warm climates.

2. Candidal diaper dermatitis should be suspected when a diaper rash does not respond to topical treatments. It is a common occurrence with the use of oral antibiotics.

3. Characterized by erythema on the buttocks, suprapubic area, and medial thighs with raised edges with sharply demarcated margins with pinpoint satellite lesions surrounding the borders.

4. Impetigo is characterized by flaccid vesicles and bullae on the lower abdomen, medial thighs, and buttocks.

5. Psoriasis is a violaceous plaque with adherent silvery-white scale. Borders are sharply demarcated.

E. Diagnostic tests. Microscopic examination with KOH will reveal budding yeasts with hyphae in Candidal infections. Bacterial culture of a vesicle or crust will diagnose bacterial infection. See Table 20-3.

F. Treatment.

1. Irritant diaper dermatitis is treated with frequent diaper changes, cleansing the skin with a mild cleanser, drying the skin, and applying a barrier such as petrolatum or Aquaphor. Air drying between changes is also helpful.

Table 20-3 Diagnosis and Treatment of Diaper Dermatitis (691.0)


2. Candidal rashes should be treated with topical antifungal medications. Avoid topical corticosteroid ointments, including combination antifungal and corticosteroid medications to reduce the possibility of atrophy in an occluded area. Resistant infections should be treated with appropriate oral antifungal medications.

3. Bacterial infections should be treated with appropriate antibiotics. Infections that include a large proportion of the diaper area are best treated orally. Isolated areas may be treated appropriately with topical antibiotics, such as Mupirocin.

4. Psoriasis is a chronic condition. Topical steroid ointment should be applied twice daily for 2-week periods. Ointments such as petrolatum or Aquaphor can be used at diaper changes. Watch for psoriatic plaques in other areas, as well as psoriatic arthritis.

G. Complications. Resistant infections.

H. Education. Parents should be taught proper skin cleansing, frequent diaper changes, and proper use of barriers to prevent contact of urine and stool with skin.


A. Allergic, contact: See Atopic Dermatitis.


A. Etiology and occurrence. Pediculosis or lice are spread from human to human, and epidemics are common in schoolchildren. Pediculosis corporis is often found in crowded living conditions and areas of poor personal hygiene.

B. Clinical manifestations and physical findings. Nits (louse eggs) are found in the hair on the scalp. Pediculosis corporis begins as small papules with secondary lesions developing from scratching, resulting in crusted papules and ulcerations.

C. Diagnostic tests. White nits are obvious on the hair shaft. A hair may be plucked and microscopic examination will reveal nits. Pediculosis corporis is diagnosed by examination of the seams of the clothing, which reveals the louse.

D. Differential diagnosis. Atopic dermatitis or other eczematous dermatitis, as well as scabies.

E. Treatment. Remove nits with a fine-tooth comb after soaking in vinegar or over-the-counter products such as Nix Crème Rinse, Rid, and Acticin. A second application of these agents is recommended in 7-10 days. Shaving the affected area is not necessary. Also can use dryer sheets to remove nits.

F. Complications. Atopic dermatitis secondary to pruritus and reaction to nits and eggs. Treat with appropriate topical corticosteroids and antihistamines.

G. Education. Proper use of topical medications and proper use of nit comb. Application of gasoline is not an accepted treatment and must be avoided.


A. Etiology and occurrence. An infestation caused by Sarcoptes scabiei. Usually spread by skin-to-skin contact among household members and by sexual contact. The fertilized female mite burrows in the stratum corneum, laying eggs and feces which create irritation and pruritus.

B. Physical findings. Pinpoint vesicles and erythematous papules in S-shaped pattern. Finger webs, flexor wrists, areola, umbilicus, waist-band area, groin, and axilla are common sites of lesions. Children and adults rarely have lesions above the neck. Infants can manifest lesions on the palms and soles. Incubation from infestation to onset of symptoms is usually 1 month, with nocturnal itching most intense.

C. Diagnostic tests. Mineral oil applied to the vesicle, scraped with a No. 15 blade and placed on a slide with a cover slip reveals mites, eggs, or feces on microscopy.

D. Differential diagnosis. Insect bites, atopic dermatitis, drug eruptions.

E. Treatment. Permethrin is the treatment of choice. It has not been proven safe in infants younger than 2 months, or in pregnant or lactating women, therefore precipitated sulfur ointment is used for 3 nights. All household contacts should be treated. Treat pruritus with appropriate antihistamines, and secondary dermatitis with appropriate corticosteroids.

F. Follow up. Treatment failures, usually secondary to noncompliance, improper application of scabicide, or reinfection.

G. Complications. Secondary atopic dermatitis and bacterial infection.

H. Education. Proper application of scabicide. Mites can survive for 2 to 5 days on inanimate objects such as clothing and stuffed animals. Proper laundering should be taught.


A. Etiology and occurrence. A systemic infection caused by the spirochete, Borrelia burgdorferi. Successful transmission requires 48-72 hours. It is found in the northeastern and midwestern United States, and can occur in any season, although most prevalent during the warmer months.

B. Clinical manifestations. Flulike symptoms including malaise, arthralgias, headache, fever and chills precede development of the rash.

C. Physical findings. A red macule or papule at the site of a tick bite 2-30 days after infection. The lesions expand to form annular erythematous lesions, generally with central clearing. The center of the lesion becomes darker, vesicular, hemorrhagic, or necrotic. Common sites are thigh, groin, trunk, and axilla.

D. Diagnostic tests. History, including exposure to tick bite, is important. Enzyme-linked immunosorbent assay (ELISA) and Western blot analyses for B. burgdorferi are recommended by the U.S. Centers for Disease Control and Prevention.

E. Differential diagnosis. Tinea corporis, urticaria, granuloma annulare, erythema annulare.

F. Treatment. Doxycycline 100 mg 2 times/day for 21 days, amoxicillin 500 mg 3 times/day for 21 days, ceftriaxone 500 mg 2 times/day for 21 days; azithromycin or erythromycin are second-line treatments for pregnant patients or those unable to tolerate above treatments.

G. Education. Educate patients on proper use of insect repellents, and to wear long pants, socks, and long-sleeved shirts in endemic areas.


A. Etiology and occurrence. Rocky Mountain spotted fever, a prototype for all tick-borne spotted fevers, is caused by R. rickettsii. It occurs primarily in the southeastern and south central United States. All ages are susceptible; however, it is most common in children younger than 15 years of age. The incidence is highest in mid-summer, and lowest in winter.

B. Clinical manifestation and physical findings. A history of tick bite is common in more than 80% of cases. A prodrome of low-grade fever, headache, malaise, joint or muscle pain, and anorexia may precede the illness, which is sudden, consisting of sweating, chills, severe aches, vomiting, and diarrhea. The most common clinical findings are rash, edema, and fever. The rash may appear soon after the onset of symptoms, first on the ankles and feet, and spreading to the wrists, hands, trunk, and head. Discrete, rose-colored macules, blanching on pressure, soon become popular or purpuric. The resolving rash may desquamate with resulting hyperpigmentation. Nonpitting edema is frequent, with periorbital edema common in children. Conjunctivitis, pharyngitis, photophobia, CNS symptoms including confusion, delirium, seizures, and coma are common.

C. Diagnostic tests. Generally no rise in antibody titer is detected until the second week of the disease. An enzyme linked immunosorbent assay (ELISA) assay if IgM and IgG to R. rickettsii is sensitive and specific is indicated. Tissue direct and indirect immunofluorescence may identify rickettsiae.

D. Differential diagnosis. Viral exanthems, drug eruption, varicella, disseminated gonococcal infection, and Lyme disease.

E. Treatment. Doxycycline or tetracycline are the drugs of choice. Alternative treatment for those unable to treat or with history of allergies to these drugs include chloramphenicol. Supportive treatment for fever and myalgias.

F. Follow up. Close follow up for complications persisting beyond 1 year after acute infection for neurologic and nonneurologic disabilities.

G. Complications. Death is associated with older patients, those with delay in treatment, or undiagnosed disease. Untreated disease death rate is 25%. Other complications include neurologic disorders including hearing loss, peripheral neuropathy, bladder and bowel incontinence, cerebellar dysfunction, language disorders.

H. Education. Avoidance of tick bites and prompt removal of ticks. No vaccine is available.


A. Etiology. Molluscum contagiosum is a virus caused by a poxvirus infecting the epidermis, causing white papules. The center of the lesions are filled with keratinous material.

B. Occurrence. Molluscum contagiosum is common in infants and toddlers, and most adults are immune.

C. Clinical manifestations and physical findings. One- to 6-mm discrete umbiliated papules are seen usually in the interiginous areas. Occasionally, larger lesions up to 15 mm may be found. Incubation period is 2-7 weeks. Children are contagious as long as lesions are present. Lesions may resolve spontaneously, but this may take years.

D. Differential diagnosis. Warts, closed comedones, epidermal cysts. Blisters may be confused with molluscum contagiosum.

E. Treatment. Papules may be removed by curette or incision and drainage, however, this procedure is painful and may result in scarring. Treatment with liquid nitrogen, cantharidin, potassium hydroxide, or podophyllin applied to the central umbilication is less traumatic. Topical treatment at home with imiquimod cream is an alternative.

F. Complications. Secondary impetigo. Atopic dermatitis. Scarring.

G. Follow up. Office visits every 2 weeks for treatment will control spread of lesions.

H. Education. Lesions are benign but highly contagious.


A. Etiology. Warts are benign virus-induced tumors caused by human papillomavirus (HPV). More than 76 subtypes have been identified and are associated with specific cutaneous and mucous membrane location.

B. Occurrence. Transmission is by direct contact, and infection can occur by autoinnoculation, especially in interiginous areas. Immunocompromised patients are at increased risk.

C. Clinical manifestations and physical findings. Verrucous papules appear as solitary lesions or may be grouped, confluent, flat, or pedunculated. They may appear anywhere on the body, but occur most often on the extremities, interrupting the dermal ridges.

D. Diagnostic tests. No testing is necessary.

E. Differential diagnosis. Plantar warts may be differentiated from calluses by the interruption of dermal ridges. Common and filiform warts present no diagnostic challenge. Flat warts are often confused with closed comedones, lichen planus, and molluscum contagiosum.

F. Treatment. Multiple therapeutic modalities are available for treatment, including liquid nitrogen, cantharidin, electrodessication, laser therapy, candida and bleomycin injection, and excision. It is unlikely the warts will resolve with a single treatment except excision, and recurrence is high. Warts frequently resolve spontaneously, and good clinical judgment should be exercised when considering various therapies versus cautious observation. Multiple salicylic acid treatments are available over the counter, as well as prescription retinoids, podophyllin, and imiquimod cream. Cimetidine 30-40 mg/kg/day in combination with other treatment modalities is effective for resistant warts. See Table 20-4.

G. Follow up. Close follow up every 2 weeks.

Table 20-4 Treatment of Viral Warts


H. Complications. Proliferation of warts resulting in pain or difficulty with daily tasks. Social anxiety and social isolation due to cosmetic embarrassment requires more aggressive treatment.

I. Education. The recalcitrant nature of warts should be emphasized, as well as the need for multiple treatments. Genital warts in infants and toddlers should be evaluated for the possibility of sexual abuse.


A. Etiology and occurrence. Erythema infectiosum (fifth disease) is caused by human parvovirus B19.

B. Clinical manifestations and physical findings. Fifth disease begins with intense red cheeks (“slapped cheeks”) and spreads to involve arms, legs, and trunk with a macular red lacy exanthem. Although initially lasting less than 1 week, with heat exposure the exanthem can recur for up to 4 months.

E. Diagnostic tests. Serum obtained within 30 days of onset of rash will confirm the presence of immunoglobulin M (IgM) B19 antibodies

F. Differential diagnosis. Drug eruptions and other morbilliform eruptions can be differentiated by the classic lacy rash of fifth disease.

G. Treatment. There is no specific treatment nor are there specific control measures, other than avoid exposure to pregnant women and those who are immunocompromised. The disease is no longer contagious once the skin eruption occurs.

H. Complications. Hydrops fetalis may result in pregnant women who have not developed antibodies. Immunocompromised children may develop persistent infection. Patients with transient anemias may develop aplastic crisis and severe anemia.

I. Education. Inform of the likelihood of recurrence with heat exposure, including exercise and sun exposure. Avoid pregnant women and immunocompromised individuals, and those with chronic anemias.


Atopic dermatitis, 691.8

Psoriasis, 696.1


Candida infection, 112.9

Scale, 782.8


Contact dermatitis, 692.9

Seborrhea dermatitis, 690.1


Infantile seborrhea dermatitis, 690.12

Tinea, 110


A. Etiology. Seborrheic dermatitis is an inflammatory disorder characterized by yellow-waxy scales in the scalp, eyebrows, auricular areas, and interiginous areas. These are areas of active sebaceous glands. Malasezia furfur is a yeast found on normal skin but highly prevalent in seborrheic dermatitis.

B. Occurrence. Usually appears in infancy and continues through adolescence and adulthood. More common in males. Affects 2-5% of the population.

C. Clinical manifestations. Greasy scales with well-defined borders, thick adherent symmetrical plaques distributed in the scalp, face, chest, and diaper area.

D. Differential diagnosis. Candidiasis, tinea, psoriasis, perioral dermatitis, as well as discoid lupus erythematosus.

E. Treatment. Removal of scalp scale with mineral oil and a fine tooth-comb provides relief. Shampoos containing selenium sulfide, pyrithione zinc, or ketaconazole can be used on the scalp as well as a face and body wash twice weekly as needed. Mild topical corticosteroids used sparingly control pruritus and erythema. In children older than 2 years of ages, topical immunomodulators may be used in place of topical steroids.

F. Education. This disorder waxes and wanes, therefore patients should be educated to restart therapy at the first sign of recurrence.


Erythema toxicum, 778.8

Pyoderma, 686

Herpes simplex, 054.9

Skin disorder, 709.9

A. Etiology. A common benign, self-limited eruption in the healthy, full-term newborn. Correlated with birth weight and gestational age, and seldom seen in preterm infants.

B. Occurrence. 30-70% full-term newborns, affecting sexes and races equally.

C. Clinical manifestations. One- to 2-mm discrete, pale yellow papules and pustules surrounded by erythematous wheal, predominantly on the face, trunk, and proximal extremities.

D. Diagnostic tests. Clinical appearance. Microscopic examination with Gram stain or Wright stain of pustular contents shows predominance of eosinophils.

E. Differential diagnosis.

Congenital cutaneous candidiasis, 112.9

Miliaria rubra, 705.1


Cytomegalovirus, 771.1

Scabies, 133


Group A streptococcal infection, 041.01

Superfi cial staphylococcal


Herpes simplex, 054.9

  infection, 041.11


F. Treatment. No treatment necessary.

G. Education. Reassure parents that this is transient and benign. Postinflammatory hyperpigmentation may follow but resolves within weeks to months.


Pityriasis rosea, 696.3 

  Psoriasis, 696.1


A. Etiology. Common, benign, self-limited rash characterized by solitary salmoncolored “herald patch” which precedes exanthema by 1 to several weeks. Lesions usually asymptomatic. Human herpes virus types 6 and 7 have been implicated but not proven in etiology.

B. Occurrence. 10-35 years. Rare under 2 years of age. Most common in fall and spring of the year.

C. Clinical manifestations. Herald patch 1-10 cm followed by smaller, salmon-colored plaques with a fine collarette of scale, follows skin lines in a “Christmas tree configuration.” Headache, malaise, and pharyngitis precedes rash in <5% of cases.

D. Physical findings. Lesions on the trunk most common, in the axillae, posterior trunk, inguinal areas. Less common on the arms and legs. The face and head typically spared.

E. Diagnostic tests. Usually a clinical diagnosis based on history and clinical appearance. A KOH may be performed to rule out tinea.

F. Differential diagnosis.

Inea versicolor, 111   

   Tinea corporis, 100.5


Psoriasis, 696


G. Treatment. No treatment is necessary, as this condition is self-limited. If lesions are pruritic, mild topical corticosteroids applied sparingly to affected areas as well as antihistamines control itching.

H. Education. Stress the benign nature of the exanthema. Post-inflammatory hyperpigmentation in pigmented skin can occur, and should be protected from sun exposure. Hyperpigmentation will resolve with time. It is uncommon for pityriasis rosea to recur.


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Please see the end of the book for color images of dermatological conditions.

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