The editors and current author would like to thank and acknowledge the significant contribution of the previous author of this chapter from the 2003 first edition, Dr. Annemarie Uliasz. This current third edition chapter is a revision and update of the original author’s work.
A 6-month-old female is brought to the office with her mother with a chief complaint of a diaper rash for one week. The mother has been using baby powder to keep the area dry, but the rash is worsening.
Upon examination, the buttocks, perianal region, and tops of the thighs appear erythematous with no ulcerations or erosions. Areas of flexure are involved and there are some beefy red areas with a few satellite lesions. The rest of the exam is normal.
Her mother is given instructions to change her infant's diapers frequently. Special attention should be made to keep the skin under the diaper dry. Baby powder does not keep the area dry once the child urinates, so its value is minimal. Hydrocortisone ointment or cream can be used to suppress the inflammation. Petroleum or zinc oxide applied to the diaper region is suggested as prophylaxis against irritation. Anticandidal agents are also recommended to eliminate any yeast infection that may be present.
The skin is composed of three different layers. The outer most layer, the epidermis, is made predominantly of keratinocytes. The most superficial layer of the epidermis, the stratum corneum, serves as a protective barrier against the environment, and prevents desiccation. The epidermis also plays a role in immune surveillance. Damage to the epidermis increases skin permeability, thereby increasing the risk of infection. The epidermis also contains melanocytes (which give the skin its color), Merkel cells (which are pressure receptors), and Langerhans cells (which participate in the skin's immune response) (1).
The dermis lies beneath the basement membrane of the epidermis. The dermis consists of collagen, elastin, and proteoglycans, which lend support and durability to the skin. Blood vessels, lymphatics, sweat glands, hair follicles, smooth muscle, and neuroreceptors are all found in the dermis. Fibroblasts in the dermis are responsible for collagen production and are the predominant cell in this layer of the skin. Other cells common in the dermis include mast cells, leukocytes, and histiocytes (1).
Subcutaneous tissue resides beneath the dermis. This layer serves as insulation, a fat depot, and a cushion against trauma. Blood vessels and lymphatics are found in the subcutaneous tissue as well as the base of hair follicles and sweat glands (1).
In order to describe a skin lesion, one must have a basic understanding of the language of dermatology. A primary lesion is a lesion that has not been altered by trauma, infection, scratching, therapy, or regression over time. Primary lesions are described as macules, patches, papules, pustules, plaques, nodules, tumors, vesicles, bullae, cysts, and wheals. A macule is a flat, circumscribed skin discoloration that is less than 1 cm in diameter. It is neither raised nor depressed and cannot be felt. Once it reaches 1 cm or greater in diameter, it is termed a patch. A papule is an elevated, solid lesion that is less than 1 cm in diameter. A papule that contains purulent material is termed a pustule. A papule that reaches 1 cm or greater in diameter is termed a plaque if it is flat or a nodule if it is rounded. Tumors are usually larger in diameter than nodules and tend to be variable in consistency and mobility. Vesicles (blisters) are raised, fluid-filled lesions less than 1 cm in diameter. Once it reaches 1 cm or greater in diameter, it is termed a bulla. A cyst is a lesion that contains fluid or semi-solid material. Its walls are circumscribed and thick, and it is located deep in the skin. Wheals are palpable, firm, edematous lesions that may vary in configuration and size. They tend to be pruritic and evanescent (existing briefly before disappearing) (2).
Primary lesions may develop or turn into secondary lesions. Secondary lesions include crusts, scales, excoriations, fissures, erosions, ulcers, and scars. Crusts (scabs) are dried collections of blood, serum, or pus. They usually arise from a primary lesion such as a pustule, vesicle, or bulla. Scales consist of compressed layers of keratinocytes on the skin surface. An excoriation is a linear erosion caused by scratching. A fissure is a crack in the skin. An erosion is a focal loss of epidermis that heals without scarring. An ulcer is a focal loss of epidermis extending into the dermis that heals with scarring. A scar is an end-stage lesion composed of connective tissue, which may be atrophic or hypertrophic (2).
Once the definitions of primary and secondary lesions are learned, a skin lesion may be described. The description should include the lesion's size, color, shape, arrangement, distribution, and whether it is a primary or secondary lesion (2). The following chapter discusses common dermatologic conditions in the pediatric patient.
Contact dermatitis can result from a delayed type IV hypersensitivity response, as in allergic dermatitis, or from injury to the skin, as in irritant dermatitis. The distribution of the rash is determined by the points of contact (3). Common pediatric allergic dermatitis allergens include nickel (jewelry, toys, clothing), neomycin (topical antibiotic), fragrances (perfume, cosmetics), preservatives (personal care products, cleaning supplies), emollients (creams, ointments), rubber (latex), and leather (4,5). If a particular substance is suspected, a patch test may be used to confirm hypersensitivity (5). However, in the pediatric population, irritant dermatitis is more commonly seen than allergic dermatitis. Common pediatric irritant dermatitis irritants include saliva, urine, feces, detergents, sanitizers, soaps, and excessive washing (3,4). Treatment may be as simple as removing the irritant, but topical corticosteroid may also provide additional relief (3).
Diaper dermatitis (diaper rash) is common in infants. The main sources of irritation are urine and feces on the skin. Urinary and fecal enzymes, along with the elevated pH in the diaper area, promote inflammation that can disrupt the normal skin barrier. Diaper dermatitis may occur if diapers are not changed frequently enough, or if the infant has diarrhea. However, diaper dermatitis may also occur even if diapers are changed regularly. This is due to the contribution of other factors, such as the use of diaper wipes and topical preparations. Diaper dermatitis often appears erythematous, and the skin may look scalded. Erosions in a patchy or confluent pattern may be seen in severe cases. Concave areas are relatively spared, including the genitocrural folds. Diaper dermatitis may be treated with frequent diaper changes and close attention to keeping the skin dry. The area may be cleansed with a soft cloth and lukewarm water and later patted dry. However, excess washing should be avoided, as it can sometimes worsen the rash. First-line therapy for diaper dermatitis includes petroleum or zinc oxide, which may be used as a protective barrier. Severe cases may be treated with low-potency topical corticosteroids. A secondary Candida (sometimes called monilial) infection may complicate diaper dermatitis. In these cases, the rash is more likely to involve areas of flexure and is characterized by beefy red skin with satellite lesions. These rashes may be treated with anticandidal agents such as miconazole, clotrimazole, and nystatin creams (3).
Erythema toxicum is a skin eruption that occurs in roughly half of all newborns, usually within the first 2 days of life. The etiology is unknown, and the condition is self-limited, lasting approximately 3 to 7 days. The lesions appear as papules or tiny pustules surrounded by an irregular halo of erythema. They are often distributed on the arms, legs, and trunk with sparing of the palms and soles. A Wright stain of a smear (by pricking the skin and doing a touch prep on a slide) may reveal eosinophils with no organisms present (6).
Nevi (moles) are clusters of melanocytes that appear at the epidermal-dermal junction. The number of acquired nevi increases with age, reaching a plateau in the 30s or 40s. The average number of nevi in an adult varies and is dependent on multiple factors, including genetics, skin color, and sun exposure. Although most nevi are benign, a small percentage may undergo malignant transformation into melanoma. Risk of melanoma increases as the number of nevi increases and as the amount of sun exposure increases. Malignant change may be suspected if the nevi displays irregular borders, large size (5 to 15 mm), multiple colors, or become ulcerated, scaled, or indurated. If any of these suspicious characteristics are observed, the nevus can be easily excised. A complete skin examination every 6 to 12 months is recommended for children with atypical nevi. Photographic mole mapping may provide additional information in tracking nevus change. The children and their parents should also be counseled regarding limiting sun exposure and checking for early signs of melanoma every 3 to 4 months (7).
Paronychia is inflammation of the nail folds of the fingers and may be acute or chronic. Acute paronychia is characterized by erythema, swelling, and tenderness of the proximal nail fold. Staphylococcal (S. aureus) or streptococcal (group A streptococci) infections are often responsible for acute paronychia. Treatment includes warm soaks (to soften the skin), oral antibiotics, and abscess drainage (if one is present). Chronic paronychia is often caused by finger sucking, which creates a desirable environment for yeast, such as Candida, and bacteria to thrive. In chronic paronychia, the nail fold will swell and separate from the underlying nail plate. Foreign material present under the nail leads to inflammation and infection. Treatment includes reducing predisposing factors, careful attention to hand drying, and long-term topical antifungal agents and topical corticosteroids (8,9).
Varicella zoster (chickenpox) is spread via respiratory secretions and direct contact with cutaneous lesions. Routine varicella immunization has drastically reduced the incidence of this infection. The incubation period is approximately 2 weeks (10 to 21 days). Subsequently, a pruritic, vesicular rash originates on the scalp, face, or trunk and spreads to the rest of the body. Macular or papular lesions appear and later develop into vesicles. The vesicles then dry up and become crusts. Typically, there are lesions in various stages of healing. Children may be contagious 1 to 2 days before the onset of the rash, and they may remain contagious for up to 3 to 7 days after. A Tzanck smear may be helpful in confirming the diagnosis of varicella zoster (reveals multinucleated giant cells), but this is usually unnecessary. Complications of chickenpox include secondary infection with staphylococci or streptococci, encephalitis, and pneumonia. Immunocompromised patients with chickenpox may experience persistent vesicular eruptions that may become hemorrhagic or they may experience disseminated varicella. It is recommended that high-risk individuals (immunocompromised) receive human varicella zoster immunoglobulin (VZIG) following exposure to chickenpox. Additionally, neonates whose mothers develop chickenpox within 5 days prior to or 2 days following delivery should receive VZIG as well as premature neonates born less than 28 weeks gestation who have been exposed to chickenpox. Acyclovir may be administered in cases of severe varicella, but the American Academy of Pediatrics urges against routine acyclovir therapy for uncomplicated varicella in the otherwise healthy child. For acyclovir-resistant varicella zoster infections, foscarnet and cidofovir may be considered. Because of the risk of Reye syndrome, aspirin and other salicylates should be avoided (10).
Once chickenpox subsides, the virus becomes latent. Latent varicella may then reactivate and cause herpes zoster (shingles). Herpes zoster is characterized by groups of vesicles distributed along a cutaneous nerve (a dermatome). However, herpes zoster is not typically common in childhood, with majority of cases occurring after age 45 (10).
Cutaneous warts may develop in roughly 5% to 10% of children. Common warts, typically found on the hands, are often caused by human papilloma virus (HPV) types 2 and 4. Common warts are well-circumscribed, rough, hyperkeratotic papules. When the superficial surface is excised, many black dots (loops of capillaries) may be visible. Plantar warts, typically found on the soles of the foot, are often caused by HPV type 1. They commonly compress against the surface of the foot due to continual weight-bearing pressure and may be painful. Flat warts, typically found on the forehead and dorsum of the hand, are often caused by HPV types 3 and 10. They are slightly raised, typically less than 3 mm in diameter, and vary in color from pink to brown. Condylomata acuminata, typically found on the anogenital region, are often caused by HPV types 6 and 11. They are moist, soft, papillomatous lesions that may occur as single or multiple lesions. They are most commonly seen in sexually active adolescents. In a young child, these warts may have been transmitted through the birth canal, through spread from cutaneous warts, or they may signify child abuse. If untreated, condylomata acuminata may grow to cauliflower-like masses. Infection with certain HPV types are also associated with an increased risk for the development of cervical cancer (11). Genital warts are further discussed in the chapter on sexually transmitted infections.
Over 65% of warts regress spontaneously within 2 years. However, untreated warts have the potential to spread and progress. When treating warts, it is imperative to protect the surrounding skin from irritation. Prior to treatment, common and plantar warts should be pared down until the capillaries are revealed. This makes the warts more responsive to treatment. It is recommended that therapy be administered every 2 to 4 weeks. Liquid nitrogen or pulsed dye laser may be used to treat common warts. Salicylic acid treatments (over-the-counter topical wart medication) may be used to treat both common and plantar warts. Podophyllin may be used to treat condylomata acuminata which is applied weekly (11).
Molluscum contagiosum is a viral infection of the skin caused by a DNA containing pox virus. It is most commonly seen in children ages 2 to 6. The lesions are pearly, skin-colored papules that are centrally umbilicated. They may appear as one or multiple lesions, and tend to be approximately 1 to 5 mm in diameter. The papules may occur anywhere on the body, but they are usually found on the face, axillae, thighs, and genital region. Molluscum contagiosum may be spread by direct contact or by autoinoculation. Infection typically resolves spontaneously within 6 to 9 months. Instructions on washing well (to prevent spread) may be all that is necessary, but other treatment options include Candida or Trichophyton antigen and liquid nitrogen cryotherapy (11).
Pediculosis (lice) affects people of all ages. There are three types of lice: Pediculus humanus corporis (body or clothing lice), Pediculus humanus capitis (head lice), and Phthirus pubis (pubic or crab lice). Pruritus is the hallmark of all types of pediculosis. The lice bite the skin and feed on the blood. Female lice lay 3 to 10 eggs daily and have a life span of approximately 1 month. The diagnosis is made by identifying lice or eggs (nits) on the patient’s hair shaft or clothing fibers. The nits appear as small, white, oval-shaped capsules (12).
Pediculus humanus corporis (body or clothing lice) is rare in children. It may be seen in conditions of poor hygiene, especially in colder environments where there is less opportunity to regularly change clothes. The lice are transmitted on contaminated clothing or bedding and are only transiently found on the skin when feeding. At other times, the nits are firmly attached to the seams of clothing. The primary lesion, found on the shoulders, trunk, or buttocks, is often a small, red macule or papule with a central hemorrhagic punctum. Treatment consists of improved hygiene and washing all infested clothing and bedding in hot water. All eggs and lice will die at 149 degrees F, wet or dry. Alternatively, clothing stored at 75 to 85 degrees F for 2 weeks will allow the eggs to hatch but will starve the lice (12).
Pediculus humanus capitis (head lice) infest the scalp hair. It is especially bothersome among school children, and patients often present with scalp itching. Transmission occurs by head-to-head contact, and shared combs, brushes, or towels. Translucent eggs are laid near the proximal portion of the hair shaft. Treatment involves application of malathion lotion to the hair for 8 to 12 hours. The hair is then washed, and the dead nits are removed from the hair shafts by a fine toothed comb. Clothes must be laundered or dry-cleaned. Other topical treatments include ivermectin, spinosad, benzyl alcohol lotion, pyrethrin, or permethrin creme rinse. These are applied and rinsed after 10 minutes, with a repeat application 7 to 10 days later. Lindane (gamma benzene hexachloride) is potentially toxic and is not recommended for infants and young children (12).
Phthirus pubis (pubic or crab lice) is transmitted by skin-to-skin or sexual contact with an infested individual. The infestation is usually encountered in adolescents, although small children may occasionally present with infestation of the eyelashes. Whereas body and head lice are 2 to 4 mm in length, pubic lice are only 1 to 2 mm in length. Thus, because they are greater in width than length, pubic lice tend to have a crab-like appearance. Treatment includes a 10 minute application of a pyrethrin preparation, with a repeat application 7 to 10 days later, if needed. Eyelash infestation may be treated by petroleum applied 3 to 5 times per day for 8 to 10 days. Clothing, bedding, and towels should be thoroughly washed or dry-cleaned (12).
Scabies is caused by the Sarcoptes scabiei mite. A papular and vesicular rash is seen as a result of the mite burrowing into the stratum corneum. Itching occurs 4 to 6 weeks after infestation, and may be more intense at night when the mites are more active (12,13). Lesions are most commonly seen between the fingers and toes, axillae, flexor surfaces of the wrists, belt line, and areas surrounding the nipples, genitals, and buttocks. A diagnosis of scabies is made based on clinical history and the characteristic burrowing lesions. A definitive diagnosis is made upon identification of the adult mite, ova, or larvae upon microscopic examination of skin scrapings from the lesions (12). Treatment includes two applications of permethrin cream, 1 week apart. The first application is intended to kill live mites, and the second application is intended to kill mites that had not yet hatched at the time of the first application. The infected patient, household members, and close contacts should all be treated, regardless of whether or not they are symptomatic. Clothing, towels, and bedding should be cleaned thoroughly (13).
Mosquito bites and flea bites are common sources of skin irritation in children. Fleas tend to bite multiple times in one area, whereas mosquitoes usually bite in random, widely dispersed areas that are not covered by clothes. The irritation that stems from an insect bite is due to a localized hypersensitivity reaction. Treatment of mosquito and flea bites consists of cool compresses and oral antihistamines to alleviate pruritus. Topical corticosteroids may also be used. Insect repellants may be used on exposed skin as prophylaxis. N,N-diethyl-3-methylbenzamide (DEET) containing mosquito repellents are effective, but DEET is potentially toxic and should be applied judiciously. A safer alternative is the use of clothes to completely cover the skin. Fleas may be eradicated by treating pets and decontaminating the house (12).
Questions
1. Name the three layers of skin. Name three functions of skin.
2. What organism is responsible for the development of warts?
3. What are the two organisms responsible for infection in acute paronychia?
4. What is the treatment for head lice?
5. Describe some differences between body lice and scabies.
6. What characteristics of a mole are suspicious for malignant melanoma?
References
1. Bender NR, Chiu YE. Chapter 663. Morphology of the Skin. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3439-3441.
2. Bender NR, Chiu YE. Chapter 664. Dermatologic Evaluation of the Patient. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3441-3451.
3. Bender NR, Chiu YE. Chapter 674. Eczematous Disorders. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3491-3496.
4. Neale H, Garza-Mayers AC, Tam I, et al. Pediatric allergic contact dermatitis. Part I: Clinical features and common contact allergens in children. J Am Acad Dermatol. 2021;84(2):235-244. doi:10.1016/j.jaad.2020.11.002
5. Brown C, Yu J. Pediatric Allergic Contact Dermatitis. Immunol Allergy Clin North Am. 2021;41(3):393-408. doi:10.1016/j.iac.2021.04.004
6. Long KA, Martin KL. Chapter 666. Dermatologic Diseases of the Neonate. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3453-3456.
7. McClean ME, Martin KL. Chapter 670. Cutaneous Nevi. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3469-3474.
8. Ken KM, Martin KL. Chapter 683. Disorders of the Nails. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3543-3547.
9. Paller AS, Mancini AJ. Chapter 7. Disorders of hair and nails. In: Paller, Mancini, and Hurwitz Clinical Pediatric Dermatology, 6th edition. 2022. Elsevier, St. Louis. pp:160-204.
10. LaRussa PS, Marin M, Gershon AA. Chapter 280. Varicella-Zoster Virus. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:1708-1715.
11. Diiorio DA, Humphrey SR. Chapter 687. Cutaneous Viral Infections. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3566-3568.
12. Kliegman RM, St. Geme JW, Blum NJ, et al. Chapter 688. Arthropod Bites and Infestations. In: Kliegman RM, St. Geme JW, Blum NJ, et al (eds). Nelson Textbook of Pediatrics, 21st edition. 2020. Elsevier, Philadelphia. pp:3568-3576.
13. Moon M, Guerrero AM, Li X, et al. Chapter 8. Dermatology. In: Zitelli BJ, McIntire SC, Nowalk AJ, Garrison J (eds). Zitelli and Davis’ Atlas of Pediatric Physical Diagnosis. 8th edition. 2023. Elsevier, Philadelphia. pp:276-341.
Answers to questions
1. The three layers of skin are the epidermis, dermis, and subcutaneous tissue. The skin serves as a barrier against the environment, protection against desiccation, and plays a role in immune surveillance.
2. Human papilloma virus is the organism responsible for the development of warts.
3. Staphylococci or streptococci infections are often responsible for acute paronychia.
4. Pediculosis capitis is treated with application of malathion to the hair for 12 hours. After the shampoo is rinsed, the hair is combed with a fine toothed comb to remove dead nits. Clothes and bedding must be washed in hot water.
5. Body lice is caused by the organism Pediculus humanus corporis (which is classified as a louse or lice), while scabies is caused by the organism Sarcoptes scabiei (which is classified as a mite). Body lice is generally treated with body hygiene measures in most instances, while scabies requires treatment with permethrin cream or other insectical treatment.
6. Suspicion of malignant transformation of nevi should arise upon observation of irregular borders, size greater than 5 to 15 mm, variegated color (multiple colors), and any change in texture including ulceration, scale, or induration.