A2. Pyodermas

Revision as of 11:42, 18 June 2024 by Nikolas (talk | contribs) (Created page with "= Impetigo = {{#lst:Impetigo|dermatology}} = Cellulitis = {{#lst:Cellulitis|dermatology}} = Erysipelas = {{#lst:Erysipelas|dermatology}} = Necrotising soft tissue infection = {{#lst:Necrotising soft tissue infection|dermatology}} = Folliculitis = {{#lst:Folliculitis|dermatology}} = Furuncle and carbuncle = {{#lst:Furuncle and carbuncle|dermatology}} = Skin abscess = * Large nodule")
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Impetigo

  • Superficial skin infection
  • Highly infectious
  • Children
    • Most common bacterial skin infection in children
  • Etiology
    • Staph aureus – 80%
    • Strep pyogenes
    • Risk factors
      • Diabetes
      • Immunosuppression
    • Secondary – superinfection of atopic dermatitis, etc
  • Clinical features
    • Honey-crusted lesions
      • The result of ruptured pustules
    • Central face
    • Itching
    • Can be bullous
  • Types
    • Ecthyma
      • A form of impetigo that extends into the dermis and ulcerates
      • Risk factors
        • Diabetes
        • Immunosuppression
      • Round superficial ulcers
  • Treatment
    • Antibacterial wash
    • Mild – topical antibiotics
      • Mupirocin
    • Severe – oral antibiotics
      • Amoxicillin
  • Complications
    • Post-streptococcal GN

Cellulitis

  • Deeper than impetigo
  • Infection of deep dermis and subcutaneous tissue
  • Etiology
    • Staph aureus -> purulent cellulitis
    • Strep pyogenes -> nonpurulent cellulitis
  • Primary – entry through minor skin injury
  • Secondary – to systemic infection
  • Clinical features
    • Erythematous lesion with poorly defined margins
    • Purulent cellulitis -> purulent exudate
  • Treatment
    • Cloxacillin

Erysipelas

  • Special type of cellulitis caused by strep pyogenes
  • Epidemiology
    • Children
    • Poor circulation
      • Stasis
    • Diabetics
    • Chronic oedema
  • Spreads by superficial lymph vessels
  • Clinical features
    • On lower limbs – 80%
    • On face – rarely
    • Large erythema, irregular borders
    • Tender
    • Rapidly advancing borders
    • Oedema
    • Warm
    • Fever
  • Site of entry needs to be located
    • Ulcers
    • Interdigital lesion
    • Fungal infections
  • Treatment
    • Antibiotics
      • Primary: Amoxicillin and clavulanic acid (in Norway: penicillin G)
      • Secondary: Ciprofloxacin and clindamycin
      • Tertiary: Ceftriaxone and metronidazole
    • Bed rest
    • Icing
    • Compression
    • Elevation
  • Complications
    • Necrotizing fasciitis
    • Sepsis
    • Residual erysipelas

Necrotising soft tissue infection

Necrotising soft tissue infections (NSTI) are necrotising bacterial infections of the soft tissues, which are life-threatening and must be treated surgically immediately. Depending on the affected soft tissue, this may be necrotising fasciitis, necrotising myositis, or necrotising cellulitis. It can progress rapidly and so early recognition is important. Treatment involves early broad-spectrum antibiotics and surgical debridement. Despite optimal therapy, the mortality is high.

Etiology

Necrotising fasciitis may be polymicrobial (type I necrotising fasciitis), or monomicrobial (type II). Monomicrobial necrotising fasciitis is usually caused by group A streptococci (GAS).

Type III necrotising fasciitis is also called gas gangrene or clostridial myonecrosis. It’s caused by clostridium perfringens.

There is usually a history of trauma to the overlying skin, which provides an entry point for bacteria. Immunosuppression, including diabetes, further increases the risk.

Clinical features

The infection usually progresses over hours or days. The clinical features include erythema, oedema, severe pain, and fever. The patient may be septic. In some cases, the infection is caused by gas-producing bacteria, in which case crepitus may be a finding. Crepitation is highly specific for NSTI but not always present. In the later stages, necrosis will occur.

When the perineum is affected, the condition is known as Fournier gangrene.

Diagnosis and evaluation

The diagnosis is clinical, and must be made urgently to prevent delay in management. Labs show elevated inflammatory parametres. Elevated AST or CK may be a sign of muscle or fascia affection. Blood cultures should be obtained.

Imaging may help in the diagnosis, but if the diagnosis can be made clinically, imaging should not be performed as it delays the treatment. CT is the most helpful in showing soft tissue necrosis.

Management

Surgical debridement is essential in the management; antibiotic treatment without surgery results in a 100% mortality rate. However, even with optimal management, the mortality rate may be 20% or higher. The goal of surgery is to remove all necrotic tissue, often requiring limb amputation. Inspection and debridement (if necrotic tissue is still present) should be repeated daily until no necrotic tissue is present.

Antibiotic therapy must be broad-spectrum and cover gram-positives, gram-negatives, and anaerobes. Several antibiotics are needed, one of which should be clindamycin, for its anti-toxin properties.

In case of confirmed or suspected streptococcal infection, administration of IVIG is indicated as it reduces mortality.

Folliculitis

  • Inflammation of follicle
  • Any age group
  • Terminal or vellus hairs
  • Usually bacterial
    • Mainly staph aureus
  • Clinical features
    • Tender papule/pustule of hair follicle
  • Treatment
    • Dicloxacillin
    • Incision and drainage for large lesions

Furuncle and carbuncle

  • Furuncle
    • Well-demarcated, firm, painful, purulent nodule
    • Large red base
    • Subcutaneous abscess
  • Carbuncle
    • Coalescence of furuncles

Skin abscess

  • Large nodule