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4. HDS Multisystem > Skin and Soft Tissue Infections > Flashcards

Skin and Soft Tissue Infections Flashcards

1
Q

Non-Bullous Impetigo

Overview

A
  • Superficial, involves only the epidermis
  • Major pathogens:
    • Group A Streptococcus
    • Staphylococcus aureus
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2
Q

Non-Bullous Impetigo

Pathogenesis

A
  • Skin colonized following minor abrasion or insect bite → infection
  • Stays within the epidermis → vesicles and pustules
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3
Q

Non-Bullous Impetigo

Epidemiology

A
  • Children >> adults
  • Predisposing factors
    • Hot, humid weather
    • Poor personal hygiene
    • Crowded living
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4
Q

Non-Bullous Impetigo

Clinical Presentation

A

Vesicle → pustule → rupture → thick golden crust

Pruritis (itching)

Systemic symptoms are rare

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5
Q

Bullous Impetigo

Overview

A
  • Superficial infection involving the epidermis
  • Major pathogen: S. Aureus phage group II
  • Pathogenesis: skin manifestations are due to the cutaneous response to the toxin
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6
Q

Bullous Impetigo

Clinical Presentation

A

Vesicle → bullae → rupture → light brown crust

Systemic symptoms are rare

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7
Q

Folliculitis

Overview

A
  • Infection of the hair follicle
  • Most common pathogen: S. Aureus
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8
Q

Folliculitis

Clinical Presentation

A

Erythematous papule with central pustule around an individual hair

Systemic symptoms are absent

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9
Q

Folliculitis

Treatment

A

Topical anti-bacterials

Occasionally need systemic antibiotic

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10
Q

Furuncles and Carbuncles

Overview

A
  • Deeper infections of the hair follicles
  • Furuncle: abscess deep within the hair follicle
  • Carbuncle: more extensive involvement with multiple abscesses
  • Most common pathogen – S. Aureus
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11
Q

Furuncles and Carbuncles

Clinical Presentation

A
  • Furuncle: abscess deep within the hair follicle
  • Carbuncle: more extensive involvement with multiple abscesses
  • Systemic symptoms are common
  • Complications: Cellulitis, bacteremia, sepsis
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12
Q

Furuncles and Carbuncles

Treatment

A
  • Drainage (warm compresses will often accomplish this)
  • ± Abx (especially if systemic signs)
  • ± Surgery (if cannot achieve drainage)
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13
Q

Erysipelas

Overview

A
  • Infection of the dermis
  • Pathogen: Group A streptococci
  • Pathogenesis:
    • Organism enter via a break in the skin
      • E.g. abrasions, tinea infection, skin ulceration
  • Predisposing factors include:
    • Poor venous drainage
    • Chronic edema of other etiologies
    • Obstruction
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14
Q

Erysipelas

Clinical Presentation

A

Skin: Painful erythema, warmth, well-demarcated borders

Systemic symptoms and signs common

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15
Q

Erysipelas

Management

A
  • Diagnosis:
    • Classic clinical findings
  • Treatment:
    • Systemic antibiotic active against streptococci but also staphylococci
      • Practically, we cannot distinguish this from cellulitis where staphylococcus may be involved so we cover staph too
    • Sample antibiotic choices: nafcillin, oxacillin, cefazolin
    • In the penicillin allergic pt you can use vancomycin, clindamycin or erythromycin
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16
Q

Cellulitis

Overview

A
  • Deeper infection beginning in the dermis and extending into the subcutaneous fat
  • Pathogens include:
    • Group A Streptococci
    • Staphylococcus aureus
    • Clostridium
    • Other pathogens less common
  • Predisposing factors:
    • Poor venous drainage
    • Chronic edema of other etiologies
    • Lymphatic obstruction
17
Q

Cellulitis

Clinical Presentation/Management

A
  • Skin: erythema, warmth
  • Systemic symptoms and signs
  • Diagnosis: typical clinical findings
  • Treatment: systemic abx active against strep and staph
  • Sample abx as outlined above under erysipelas
18
Q

Scalded Skin Syndrome

Overview

A
  • Toxin-mediated skin disease
  • Most common pathogen: S. Aureus
  • Neonates and small children
  • Pathogenesis: local infection, then subsequent systemic effects due to exfoliative exotoxin
19
Q

Scalded Skin Syndrome

Clinical Presentation

A
  • Erythematous rash
  • Bullae
  • Exfoliation
  • Fever
20
Q

Scalded Skin Syndrome

Management

A
  • Diagnosis:
    • Clinical findings
    • You cannot find the organism in the skin (except at the site of the primary infection)
  • Treatment:
    • Antibiotic active against S. Aureus
21
Q

Scarlet Fever

A
  • Pathogen: Group A Streptococci
  • Pathogenesis:
    • Erythrogenic toxin
    • Capillary fragility
  • Clinical presentation:
    • Erythematous rash
    • Pastias lines
    • Strawberry tongue
    • Circumoral pallor
    • Exfoliation
  • Diagnosis: culture pharynx
  • Treatment: penicillin
22
Q

Toxic Shock Syndrome

Overview

A
  • Pathogens:
    • S. Aureus (TSST-1)
      • Menstrual-related (tampons)
      • Non-menstrual (surgical procedures, vaginal colonization)
    • Group A Strep (SPE A)
      • Usually associated with skin and soft tissue infection
23
Q

Toxic Shock Syndrome

Clinical Presentation

A
  • Fever
  • Hypotension
  • Diffuse erythematous rash, which eventually exfoliates
  • Multi-organ involvement
24
Q

Toxic Shock Syndrome

Management

A
  • Diagnosis:
    • Clinical syndrome
    • Vaginal or cervical cultures
    • Blood cultures
    • Skin lesion culture
  • Treatment:
    • Fluid replacement/resuscitation
    • Removal of tampon if present
    • Surgical debridement, if necessary
    • Systemic (IV) abx active against streptococci and staphylococci
25
Q

Necrotizing Fasciitis

Overview

A
  • Infection penetrates beneath subcutaneous fat, into the fascial layers
  • Two main syndromes:
    • Group A Streptococcus (“flesh-eating bacteria”)
      • Organism gains entry into skin, either spontaneously or from minor trauma, and progresses to deep infection
    • Mixed infection: facultative and anaerobic organisms
      • Source of organisms is the gut
      • Seen when there is some break in the gut barrier
        • E.g. Abdominal surgery, perirectal or periurethral infection or trauma
  • Increased incidence in diabetics
26
Q

Necrotizing Fasciitis

Clinical Manifestations

A
  • At first it may look like cellulitis but you need to look for clues to deeper infection
  • Skin - erythema, purplish hue, dusky gray, bullae
    • Skin exquisitely tender and as time passes, there are is anesthesia
  • Crepitance and foul odor in mixed infection
  • Pt extremely ill
  • Mortality 25-50%
27
Q

Fournier’s Gangrene

A

Perineal gangrene in diabetic men

28
Q

Necrotizing Fasciitis

Management

A
  • Diagnosis:
    • Must have a high index of suspicion given the high mortality
    • You can often take a probe and find that it will easily go down to the fascial layer
    • Culture the skin/tissues/wound
  • Treatment: systemic abx and surgery
29
Q

Myonecrosis

Overview

A
  • Infection penetrates to muscle
  • Common pathogens:
    • Streptococcus pyogenes
    • Mixed infection
    • Clostridium (perfringens or septicum)
  • Pathogenesis:
    • Usually infection gets to muscle by local spread
    • Occasionally can get there hematogenously
30
Q

Myonecrosis

Clinical Manifestations

A
  • Muscle pain and edema
  • Systemic symptoms
  • Crepitance, with clostridium or mixed infection
  • Pt usually also has necrotizing fasciitis
  • Draining wound with bronze skin discoloration in clostridial infection
31
Q

Myonecrosis

Management

A
  • Prognosis: mortality 60-100%
  • Diagnosis: must have a high index of suspicion given the high mortality
  • Treatment: systemic abx and surgery

4. HDS Multisystem (43 decks)

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