Pustules, Vesicles, Bullae, and Erosions












CHAPTER 16
PUSTULES, VESICLES, BULLAE, AND EROSIONS

 


Acne




































Synonym Acne vulgaris.
Inheritance Patients with a history of a first-degree relative with severe acne have an increased risk of developing moderate-to-severe inflammatory acne.
Prenatal Diagnosis n/a
Incidence About 80% of Americans will have acne to some degree at some point in their lives.
Age at Presentation Adolescence with some appearing transiently after birth (neonatal acne). Infants and young children may rarely develop acne.
Pathogenesis Subclinical inflammation is common in early acne lesions, not just those that are clinically inflamed. The formation of a Propionibacterium acnes biofilm, increased sebum formation, and hyperkeratinization of the follicle lead to obstruction and produces the spectrum of clinical findings. Varying degrees of inflammation occur based on a person’s reaction to comedonal contents.
Key Features

  • Comedones:

    • Open (whiteheads)
    • Closed (blackheads)


  • Inflammatory lesions:

    • Erythematous papules and pustules
    • Cysts
    • Nodules
    • Scarring
Differential Diagnosis Folliculitis (bacterial and fungal), Gram-negative folliculitis, steroid-induced folliculitis, and occlusion folliculitis.
Laboratory Data

  • In the majority of acne patients, lab testing is not necessary. If isotretinoin therapy is required, then monitoring with lipid and hepatic testing and pregnancy monitoring if the patient is of child-bearing potential will be necessary.
  • Young children with persistent acne should be screened for signs of precocious puberty and hyperandrogenism.
Management Topical salicylic acid and benzoyl peroxide preparations:

  • Bar and liquid soaps, gels or other formulations.

Topical retinoids (mainstay of therapy, very effective for comedones and some early inflammatory lesions, often take 6-8 weeks to see full effectiveness): creams are very effective with less side effects than gels (ie, less dryness and irritation)



  • Tretinoin

    • Various brands, concentrations, and vehicles:0.025%, 0.05%, and 0.1% cream or micronized gel formulations are most common.

  • Adapalene:

    • 0.1% cream (now over the counter [OTC]).0.1% and 0.3% gel, 0.1% lotion.

  • Tazarotene:

    • 0.1% cream or gel.

  • Trifarotene, fourth-generation topical retinoid

    • 0.005% cream.

Topical antibiotics (effective for inflammation and P. acnes, can often see rapid improvement):



  • Clindamycin.
  • Erythromycin.

Combination medications (may be more effective than monotherapy with topical antibiotics):



  • Benzoyl peroxide and clindamycin.
  • Benzoyl peroxide and erythromycin.
  • Tretinoin and clindamycin.
  • Benzoyl peroxide and adapalene.

Other topical alternatives (excellent antiinflammatory benefit):



  • Azaleic acid.
  • Dapsone 5% and 7.5% gel.

Systemic antibiotics (1-3 month courses may be necessary, repeating as necessary):



  • Tetracycline

    • 250 to 500 mg twice per day 1 hour before or 2 hours after meals and not with dairy products.

  • Doxycycline

    • 100 mg twice per day with food and not before lying down (to avoid esophagitis).

  • Minocycline

    • 50 to 100 mg twice per day

  • Trimethoprim-sulfamethoxazole (TMP-SMX)

    • One double-strength capsule twice per day

  • Clindamycin

    • 300 mg bid (increased risk of Clostridium difficile colitis)

Systemic retinoids:



Oral contraceptives



  • Antiandrogenic estrogens

    • Ortho-Tri-Cyclen, Yaz
Prognosis Most patients can be managed well with OTC products (benzoyl peroxide and salicylic acid). Treatment failure or progression of lesions while being treated with OTC products is an indication for prescription treatment.

image PEARL/WHAT PARENTS ASK

image

16.1. Comedones and inflammatory papules.

image

16.2. Infantile acne.











Skin | Associated Findings
image

Erythema Nodosum




































Synonym n/a
Inheritance n/a, though rare cases of familial EN reported in adults.
Prenatal Diagnosis n/a
Incidence 1 to 5 per 100,000 persons worldwide; most common ages 18 to 34; uncommon before puberty and very rare under age 2 years; M = F in pediatric patients, no racial or ethnic predilection.
Age at Presentation 18 to 34 years most common.
Pathogenesis Reactive process causing panniculitis (inflammation of subcutaneous fat); the most common form of septal panniculitis (inflammation of the interlobular septae); immune complex deposition within and around venules in septae of subcutaneous fat; neutrophil activation creates the inflammatory environment that creates the clinical signs and symptoms hypersensitivity reaction to numerous triggers including antigens, and infectious agents; in children infections are the most common trigger, group A beta-hemolytic streptococcus (GABHS) the most reported association; tuberculosis, Yersinia, mycoplasma, fungal and viral infections, medications (including oral contraceptives, sulfa drugs, and penicillin), sarcoidosis, pregnancy, inflammatory bowel disease, rare reports of vaccine-associated; ~50% are idiopathic.
Key Features

  • Skin: Erythematous, tender, bruise-like subcutaneous nodules, most often on bilateral shins, no epidermal changes; possible prodrome of fever, upper respiratory infection, joint pains (up to 50% of patients), malaise 1 to 3 weeks prior to onset of skin findings but uncommon in young children; may appear less commonly on face arms, thighs, buttocks, or calves.
Differential Diagnosis Urticaria, angioedema, erysipelas, insect bites, sarcoidosis, superficial thrombophlebitis, nodular vasculitis, pancreatic panniculitis, deep fungal infections, subcutaneous bacterial and mycobacterial infections, malignant infiltrates, familial Mediterranean fever, subcutaneous fat necrosis of newborn, cold panniculitis, lupus panniculitis, subcutaneous granuloma annulare, self-induced deep soft-tissue injuries, and polyarteritis nodosa.
Laboratory Data Diagnosis is clinical though a deep biopsy to include subcutaneous fat can aid in questionable cases (punch within a punch or incisional biopsy) to evaluate for septal panniculitis; always look for a possible trigger (eg, throat culture, TB screening, and chest x ray); review medications; acute-phase reactants are usually elevated so can check sedimentation rate, C-reactive protein, complete blood cell count with leukocytosis, if GI symptoms, consultation with GI may be necessary.
Management Symptomatic treatment; cool, wet compresses, elevation of legs; nonsteroidal antiinflammatory drugs as needed for pain (eg, ibuprofen: if 6 months to 11 years, 5-10 mg/kg PO q6-8 hours as needed; if 12 years or older, then 400 mg PO q4-6 hours as needed, max dose of 2,400 mg per day, can take with food if upsets stomach; naproxen, indomethacin are other options; colchicine and supersaturated potassium iodide for severe, recurrent or refractory cases); systemic corticosteroids are not usually necessary, may lead to worsening of an infectious etiology; possible referral to pediatrician or possibly an infectious disease specialist for more in-depth evaluation for an underlying cause.
Prognosis Generally excellent, spontaneous resolution in the majority of patients in 6 to 8 weeks; may take longer in idiopathic cases; chronic or recurrent cases are rare.

image PEARL/WHAT PARENTS ASK


How do I identify the trigger? Infections are a common cause so need to discuss symptoms that might provide a clue (eg, respiratory or gastrointestinal symptoms, sore throat). When there is no history of infection, the most common identifiable cause is related to medications. In adolescent girls contraceptives are probably the most common cause followed by antibiotics in boys and girls and all age groups.











Skin | Associated Findings
image
image

16.3. Erythema nodosum. Courtesy of Scott Norton, M.D.


Impetigo




































Synonym Impetigo contagiosa.
Inheritance n/a
Prenatal Diagnosis n/a
Incidence Most common bacterial skin infection in children; ~10% of pediatric outpatient visits; annual incidence ~3% of children <4 years and ~1.7% of children 5 to 15 years.
Age at Presentation Nonbullous impetigo is most common in children 2 to 5 years. 90% or more of cases of bullous impetigo are in children under 2 years. M = F.
Pathogenesis Primary or secondary infection with GABHS or Staphylococcus aureus (SA); intact skin is the primary preventive barrier; SA can produce toxins that are toxic to streptococci resulting in only SA being found if site is cultured; methicillin-resistant SA (MRSA) also possible;

  • Nonbullous impetigo (70%-80% of cases): >50% are SA, ~45% are SA and GABHS; GABHS more common in warmer climates; consider group B strep in newborns; occasional MRSA.
  • Bullous impetigo: Most often SA, phage type 71 (also causes staph scalded skin syndrome [SSSS]); produces exfoliative exotoxins targeting adhesion molecules in stratum corneum causing clinical blisters/bullae and sloughing of the skin; can be considered a localized form of SSSS; MRSA increasingly identified but more often seen in nonbullous impetigo.
Key Features

  • Primary impetigo: Develops on already colonized intact skin after minor trauma (eg, insect bites, scratches, or scrapes); Secondary impetigo is infection in the setting of chronic skin disease with resultant barrier dysfunction (ie, atopic dermatitis, contact dermatitis, and papular urticaria).
  • Nonbullous impetigo: Erythematous macules appear first that rapidly progress to form vesicles or pustules; face and extremities; lesions rupture and form classic “honey-crusted” exudate; can rapidly spread to other areas from scratching and autoinoculation particularly in patients with underlying dermatoses (eg, atopic dermatitis); usually asymptomatic; no systemic symptoms.
  • Bullous impetigo: Variable-sized fragile bullae appear quickly then rupture leaving only a simple collarette of scale; face, trunk and extremities; distant spread through autoinoculation is common; fever possible in some.
Differential Diagnosis Cutaneous candidiasis, dermatophyte infections bullous pemphigoid, linear IgA disease, dermatitis herpetiformis, bullous lupus erythematosus, secondary impetiginization in atopic dermatitis/eczema, chemical burns, irritant contact dermatitis, allergic contact dermatitis, viral infections (herpes simplex, varicella, and enterovirus).
Laboratory Data Culture not usually necessary, diagnosis is clinical; if unresponsive to treatment then consider culture to evaluate for MRSA; if recurrent then consider culturing for nasal carriage (anterior nares colonization with SA in about 30% of population); GABHS carriage also possible though less common.
Management Topical antibiotics have been shown to be more effective than antiseptics (eg, chlorhexidine, hydrogen peroxide) for localized infection; consider systemic antibiotics for disseminated impetigo or special settings (eg, familial or clusters within a childcare site or multiple cases in sports teams).

  • Topical mupirocin ointment: Twice per day to affected areas for 5-7 days; SA and MRSA resistance rare; treatment of nares may decrease colonization and repeat infection.
  • Retapamulin ointment: Twice per day for 5 days in children >9 months of age; avoid use in nasal mucosa because of the risk of epistaxis.
  • Oral cephalexin: 40 mg/kg/d divided into 3 to 4 doses per day for 10 days. Rare admission for inpatient care for younger patients with disseminated bullous disease.
Prognosis Even without treatment impetigo can resolve within 2 to 3 weeks in up to half of cases (~15%-50%); ~10% can develop cellulitis or lymphangitis; scarlet fever (scarlatina) and guttate psoriasis are reported in some patients with GABHS impetigo.

  • Acute poststreptococcal glomerulonephritis: Rare complication, ~1 case per 1,000,000 population; more common in tropics.
  • SSSS: Because of the absorption of exfoliative exotoxins from SA strains in infants and younger children, and older children with renal dysfunction.

Related posts:

  1. Brown Lesions (Macules, Patches, and Papules)
  2. Red and Scaly (Papulosquamous Disorders)
  3. White Lesions (Macules, Patches, and Papules)
  4. Bug Bites and Infestations

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Aug 17, 2025 | Posted by in PEDIATRICS | Comments Off on Pustules, Vesicles, Bullae, and Erosions

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