McCance 48 M10.4 - Acne Vulgaris in Children

• Skin diseases in children can be minor, severe, localized, or generalized, potentially differing in cause and distribution from adult skin diseases.

Acne Vulgaris

• Acne vulgaris affects 85% of individuals aged 12-25 and onset is occurring at a younger age.

• The incidence is equal in both sexes, yet males are more often affected severely.

• Genetic susceptibility can determine disease susceptibility and severity.

• Acne develops within sebaceous follicles, mainly on the face, chest, and back and include large sebaceous glands, a small vellus hair, and a dilated follicular canal.

• Noninflammatory acne involves open (blackheads) and closed (whiteheads) comedones, which obstruct and distend the follicle.

• Inflammatory (cystic) acne occurs when a closed comedone ruptures, expelling sebum, causing inflammation that can result in pustules, papules, cystic nodules, and potential scarring.

• Principal factors in acne are follicular proliferation of Propionibacterium acnes, hyperkeratinization of follicular epithelium, excessive sebum production, and follicle rupture from accumulated debris and bacteria.

• During puberty, increased androgens boost sebaceous gland size which promotes P. acnes.

• P. acnes produces porphyrins and proinflammatory molecules, and hydrolytic enzymes that convert triglycerides into free fatty acids (FFAs).

• FFAs activate toll-like receptors, T-cell-associated and Th17-associated inflammation causing edema, pus formation, and follicle wall breakdown.

• Increased sebum production feeds bacterial growth.

• Acne may be associated with polycystic ovary syndrome, congenital adrenal hyperplasia, and endocrine tumors because of elevated androgen levels.

• Treatment can be topical retinoids, benzoyl peroxide, and antimicrobial agents, or even combined oral contraceptives, oral antibiotics, sex hormones and systemic therapies.

• Acne surgery and psychological support are sometimes needed.

• Acne conglobata, a severe inflammatory form can cause scarring, with remissions tending to occur in summer.

Dermatitis

• Atopic dermatitis (AD), also known as atopic eczema, affects approximately 25% of children and 2-3% of adults and usually begins by age 5.

• Individuals with AD often develop asthma and allergies later in life, and positive skin tests to food and inhalant allergens occur in approximately 80% of individuals.

• It stems from genetic predisposition, altered skin barrier function from filaggrin gene mutations, reduced ceramide levels, altered innate immunity, and immune responses to allergens, irritants, and microbes.

• Pathophysiology involves immunologic dysregulation and epidermal barrier abnormality, and barrier repair is required.

• In AD, memory T cells expressing cutaneous lymphocyte antigen (CLA) home to the skin, and inflammation is associated with Th2 activation and switch to Th1 cells in the chronic phase.

• A deficiency in filaggrin protein causes transepidermal water loss, pathogen/allergen penetration, and a systemic hyperactive immune response.

• Keratinocytes deficient in toll-like antimicrobial peptides predispose individuals to skin colonization by pathogens which promotes pathogenic microorganism colonization.

• AD clinical features are exacerbations, pruritus, and redness, edema, and scaling.

• Itching marks atopic dermatitis, and scratching to relieve the itch is responsible for skin changes.

• In young children, rash appears on the face, scalp, trunk, and extensor surfaces of arms and legs.

• In older children/adults, rash is on the neck, antecubital/popliteal fossae, hands, and feet, potentially causing irritability and sleep interference.

• Management includes triggers and treatment response evaluation; managing confounding factors; and educating individuals and caregivers.

• Avoidance of triggers/promoting skin hydration, including emollients and nonsoap cleansers, are key.

• Bleach baths may be helpful for recurrent infection.

• Wet wrap therapy may be used for severe eczema.

• Antiinflammatory agents such as topical corticosteroids and calcineurin inhibitors, are necessary.

• Systemic steroids should generally be avoided in adults and children because the potential short- and long-term adverse effects largely outweigh the benefits.

• Diaper dermatitis is a form of irritant contact dermatitis initiated by urine ammonia and feces, maceration, and friction which involves wet diapers and plastic diaper covers.

• Lesions vary from mild erythema to erythematous papular lesions.

• Candidal (monilial) diaper dermatitis is erythematous, with sharp margination and pustulovesicular satellite lesions affecting the abdomen, genitalia, buttock, and upper thigh.

• Treatment involves frequent diaper changes, perineal area exposure to air, super-absorbent diapers, and topical protection with petrolatum or zinc oxide, or both.

• Topical antifungal medication is used to treat C. albicans when present.

Infections of the Skin

• Bacterial, viral, and fungal infectious diseases: Breaks in skin integrity can cause or exacerbate them, and these infections often occur superficially.

Bacterial Infections

• Impetigo: A common bacterial skin infection from Staphylococcus aureus (S. aureus) and Streptococcus pyogenes and transmits through contact.

• Impetigo is more common in mid to late summer in hot, humid climates and is infectious among people in crowded conditions.

• Bacterial invasion occurs through minor breaks in the cutaneous surface or as a secondary infection of a dermatosis or infestation.

• Staphylococci produce bacterial toxins called exfoliative toxins (ETs) that cause a disruption in desmosomal adhesion molecules with blister formation.

• Nonbullous and bullous (caused only by S. aureus) impetigo can develop with vesicles that rupture to form a honey-colored crust common on the face, and requires differentiation from herpes simplex lesions.

• Staphylococcal Scalded-Skin Syndrome (SSSS): Serious infection in children under 5 years that is caused by group II staphylococci producing an exfoliative toxin and leading to circulation to the epidermis.

• Symptoms begin with fever, malaise, rhinorrhea, and irritability followed by generalized erythema with skin tenderness which can spread across the face and trunk.

• Blisters and bullae may develop, and fluid loss from ruptured blisters and water evaporation may cause dehydration and heat loss, and skin healing occurs within 10-14 days usually without scarring.

• Culture, histologic and exfoliative cytology must be performed to differentiate SSSS from Stevens-Johnson syndrome and toxic epidermal necrolysis and confirmed infection requires systemic antibiotics and maintenance of the fluid balance.

Fungal Infections

• Fungal disorders are known as mycoses and when caused by dermatophytes (fungi that thrive on keratin), the mycoses are termed tinea.

• Different types of tinea are classified according to their location on the body.

• Dermatophytes of the genus Epidermophyton are the major cause of superficial fungal infections in children and invade the stratum corneum triggering a cell-mediated immune response.

• Tinea capitis (scalp ringworm) is the most common fungal infection of childhood and is caused by Trichophyton tonsurans which can directly transmit or Microsporum canis on cats, dogs, and rodents, to humans.

• The lesions has broken hairs 1-3 mm above the scalp, leaving alopecia from 1 to 5 cm in diameter and a potassium hydroxide (KOH) examination and fungal culture confirms best diagnosis.

• Systemic treatment is always required because topical antifungal agents do not penetrate the hair follicle.

• Tinea corporis (ringworm) is a dermatophyte infection in children caused by M. canis and Trichophyton mentagrophytes and contact with kittens and puppies is a common source.

• Tinea corporis affects nonhairy parts of the face, trunk, and limbs with erythematous scaling patches that spread peripherally with clearing in the center.

• Most lesions respond well to topical antifungal medications.

• Thrush is caused by Candida albicans (C. albicans) in the mucous membranes of the mouth of infants are attracts neutrophils to skin sites of invasion but evades neutrophil killing releasing keratolytic proteases that form white plaques or spots in the mouth that lead to shallow ulcers.

• Infection can spread to the groin, buttocks, and other parts of the body.

Viral Infections

• Molluscum contagiosum: Contagious poxvirus infection of the skin epidermis affecting school-aged children that is transmitted by skin-to-skin contact, autoinoculation, and fomites causing epidermal proliferation that blocks immune responses.

• Lesions are discrete, slightly umbilicated, dome-shaped, waxy or pearl-like papules 1 to 5 mm in diameter that appear anywhere on the skin or conjunctiva and in children is mainly on the trunk, face, and extremities.

• Rubella (German or 3-Day Measles): Caused by entering a ribonucleic acid (RNA) virus the bloodstream through the respiratory route.

• It is mild in most children with prodromal symptos of enlarged cervical and postauricular lymph nodes, low-grade fever, headache, sore throat, runny nose, and cough and a faint pink-to-red rash develops on the face which spreads.

• Rubeola (Red Measles) is a highly contagious disease of children from an RNA-containing paramyxovirus which transmits directly across droplets and enters the respiratory tract.

• Prodromal symptoms include high fever, malaise, enlarged lymph nodes, runny nose, conjunctivitis, and coughing with lesions and a red rash on the head which spreads but can have complications either from the infection or a secondary bacterial infection can be prevented by vaccination.

• Roseola: Caused by human herpesviruses 6 or 7 which is followed by a sudden onset of fever followed by an erythematous rash with light clothing, cool baths, and air conditioning assists.

• Chickenpox and Herpes Zoster are caused by the varicella-zoster virus (VZV), a complex deoxyribonucleic acid (DNA) virus of the herpes group.

• The vesicular lesions occur in the epidermis as infection occurs within keratinocytes and ruptures leading to various transient ulcers.

• Hand, Foot, and Mouth Disease. A contagious viral disease primarily of infants and young children, caused by the coxsackievirus A16 (CV-A16) and the enterovirus 71 (EV-A71), that manifests fever, lesions and rashes.

Insect Bites and Parasites

• Scabies: caused by the itch mite, Sarcoptes scabiei colonizing in the epidermis which is transmittrd by contact.

• Immunocompromised individuals has an increased risk.

• The primary lesions are burrows of 2-15 mm in length, papules, and vesicular lesions with severe itching that worsens, and pruritus comes from a type IV sensitivity reaction to the mite and all waste.

• First symptoms from both adult and first infestation appears after weeks but can be diagnosed by tunnels and scraping the skin to reveal microscopic feces.

• Pediculosis Louse: The three known types of lice in humans are the head, body, and pubic louse.

• They are contagious parasites that survive by sucking blood and produces 7-10 eggs(nits) through out a months life.

• Fleas: Bite producing an wheal that occurs through tight clothing.

• Bedbugs: Live on blood by attaching to the skin causing pruritic papules.

Cutaneous Hemangiomas and Vascular Malformations

• Cutaneous hemangiomas: benign tumors which form from rapid growth of vascular endothelial cells by vascular endothelial cells and placenta.
• Cutaneous vascular malformations: occur during birth with lesions which can occur by hormonal changes.
• Salmon patches: are common anomalies in the skin.