Skin and Soft Tissue Infections Flashcards

1
Q

Impetigo

A

pathology:
* intraepidermal vesicopustule
etiology:

  • Group A Strep
  • Staph aureus

epidemiology:

  • all ages, most often kids (very communicable)
  • hot, humid weather

O:

  • face and extremities
  • golden “stuck-on” crusts, not painful
  • highly communicable

P/TX:

  • PCNase resistant PCN ie dicloxacillin (this covers both staph and strep infection)
  • PCN G, V
  • Erythromycin
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2
Q

Folliculitis

A

pathology:

  • w/n hair follicules and apocrine sweat glands
  • pruritic papule often w/ pustule

etiology:

  • most common = Staph aureus
  • can be Strep A (Strep pyogenes)

epidemiology:
* predisposing underlying conditions, ie DM, exposures (hot tub)

O:

  • buttocks, axillae
  • hair bearing areas
  • tender
  • surrounding erythema
  • acute and/or chronic (recurrent)

P:

  • problem for recurrence, one spreads to another
  • get rid of all razors, perpetuating factors
  • warm compresses
  • topical abx
  • in general just drain it out
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3
Q

Furuncles

A

pathology:

  • deep inflamm nodules developing from preceding folliculitis

etiology:

  • Staph aureus

epidemiology:

  • skin w/ hair follicles subject to friction and perspiration
  • obesity, DM, use of corticosteroids (if on anti-inflamm, dont see as much redness and dont notice it)

O:

  • firm, tender nodule which progresses to painful fluctuant lesion
  • often drains spontaneously
  • often look from a distance too
  • warm
  • firm
  • surrounding, extending erythema

P/TX:

  • proper I&D of abscess or other focal infections is mainstay of therapy and may be sufficient for cutaneous abscess
  • for uncomplicated infections oral antimicrobial therapy is satisfactory
  • can move to IV abx for more complicated infections
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4
Q

Carbuncle

A

pathology:

  • more extensive furuncle, extending to subQ fat
  • multiple abscesses drain along hair follicles

etiology:

  • Staph aureus

epidemiology:

  • occur more often in nape of neck, back, back of thighs (thick, elastic skin)
  • otherwise similar to furuncle

O:

  • pt often acutely ill (fever/malaise)
  • can be complicated by bacteremia or cellulitis
  • can see lesions at different stages

P/TX:

  • proper I&D of abscess or other focal infections is mainstay of therapy and may be sufficient for cutaneous abscess
  • for uncomplicated infections oral antimicrobial therapy is satisfactory
  • can move to IV abx for more complicated infections
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5
Q

Ecthyma

A

pathology:

  • starts intraepidermal, penetrates into epidermis and dermis

etiology:

  • Group A Strep (primary or secondary due to trauma)

epidemiology:

  • elderly and children, usually on LE

O

  • punched out” ulcers
  • violaceous heaped borders w/ or w/o exudate
  • clinically similar to lesions which occur in neutropenic pts w/ Pseudomonas bacteremia (ecthyma gangrenosa)
  • surrounding erythema
  • flaky skin (common in Strep infections)
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6
Q

Erysipelas

A

pathology

  • superficial cellulitis w/ lymphatic involvement

etiology

  • Group A strep (Strep pyogenes)

epidemiology

  • infants, kids, and elderly
  • LE mostly and face
  • occur at sites of trauma, ulcers, abrasions
  • predisposing factors:
    • venous stasis/lymph obstruction
    • lymphedema secondary to radical mastectomy
    • DM, nephrotic syndrome and alcoholism

O:

  • distinct, raised border (can feel drop off to normal skin
  • painful, bright red lesion
  • **advancing, raised border which is sharply demarcated from NL skin **
  • fever is common
  • up to 5% may have strep bacteremia
  • potential to spread to **deeper **dermis
    • subQ abscesses
    • cellullitis
    • necrotizing fasciitis

P/TX:

  • parenteral abx indicated for pts with facial erysipelas or evidence of systemic infection
  • PCN is drug of choice
  • initial therapy for pts w/ risk factors for Staph aureus should cover this strep
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7
Q

Cellulitis

A

pathology

  • spreading infection of skin involving the subQ tissues

etiology

  • MOST COMMON
    • ​Group A strep
    • Staph aureus
  • RARE
    • bacteremic seeding
  • **OTHER **- epidemiologic clues…
    • Vibrio spp. (expsoure to warm sea water
    • Aeromonas sp. (exposure to fresh water)
    • Erysipelothrix sp. (handling of saltwater fish, shellfish, meats/hides)
    • Acinetobacter sp. (war wounds in Iraq and Afghanistan)

epidemiology

  • occurs frequently at site of previous trauma (lac, puncture) or skin lesion (furuncle, ulcer)
  • look for portal of entry e.g. Tinea pedis
  • post-op wound infections
  • IV drug use (skin “popping”)
  • ass w/ sites of **abnormal lymph drainage **(SV grafts, radiation therapy, peripheral vascular disease)
  • often RECURRENT

O:

  • acute
  • **rapid development of local tenderness **
  • **site is erythematous, swollen and warm to touch **
  • often ass w/ fever, chills and malaise
  • border NOT well demarcated
  • commonly ass w/ lymphangitis
    • **​look for lymphangetic streaking **(can see streaking up leg)
  • **local abscess may develop **(should be drained)
  • overlying necrosis may develop

A:

  • DX by hx and PE
  • cx of skin/wound useful when:
    • suspect unusual/abx-resistant pathogens
    • failed course of empiric therapy
    • fluctuant areas present or there are bullae

P/TX:

  • most therapy is EMPIRIC as it is rare to id a causative organism
  • THERAPY - supportive (elevation) and abx (IV vs oral)
    • PCN G, V
    • erythromycin
    • PCNase resistant PCN
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8
Q

Necrotizing Fascitis

A

pathology:

  • involves subQ soft tissues including the superficial and deep fascia

etiology:

  • TYPE I
    • polymicrobial infection
    • anaerobes - commonly Bacteroides or Peptostrep spp
    • w/ one or more facultative anaerobes
      • E coli, Enterobacter, Klebsiella
      • Strep non Group A
      • Vibrio sp (exposure to warm sea water)
      • Pseudomonas (immunocompromised, IVDU)
      • Acinetobacter sp (OEF/OIF war wounds)
  • TYPE II
    • Group A Strep
    • Alone or polymicrobial (often Staph aureus)

epidemiology:

  • usually at site of trauma (lac, burn, abrasion, bite), also post-op
  • any part of body, over half in LE
  • DM (30%), PVD, alcoholism and IV drug use, skin “popping”
  • Scrotum/perineum - Fournier’s gangrene

O:

  • acute and/or subacute presentation (NSAIDS)
  • starts - diffuse redness, warm, and is very tender
  • progresses rapidly (hours to days)
    • fluid filled bullae (purplish-blue)
    • cutaneous necrosis
    • crepitus (subQ gas - polymicrobial)
    • pain out of proportion to physical findings
  • loss of pain may be due to deeper injury
    • due to loss of superficial nerves secondary to thrombosis of small blood vessels in skin

Complications:

  • compartment syndrome due to swelling and edema, may require fasciotomy
  • systemic toxicity w/ hihg fever/leukocytosis
  • blood cx often positive
  • hypocalcemia w/ necrosis of subQ fat

P/TX:

  • early recognition and TX
    • prompt surgical intervention
    • high overall mortality (worst in DM)
    • early DX leads to decreased mortality
  • PCN G,V, erythromycin, PCNase resistant PCN
  • add Clindamycin
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9
Q

Clostridial Myonecrosis

“Gas Gangrene”

A

pathology:

  • skeletal muscle necrosis due to histotoxic Clostridia spp.
  • muscle disintegrates (coagulation necrosis)
  • pale edematous on inspection, when cut does not bleed

etiology:

  • C. perfringens in 80-90%
    • alpha Toxin
    • often find as contaminant in wounds, low incidence of infection
    • lower inoculum needed for devitalized tissues/FBs

epidemiology:

  • contamination w/ SOIL or material 2/ Clostridial spores
  • trauma (compound fx)
  • war wounds
  • post-surgical (bowel, biliary tract surgery)
  • spontaneous, non-traumatic (bacteremia)

S/O:

  • LIFE THREATENING
  • incubate 1-2 days and rapidly progressive - hours
  • PAIN is often severe, important early sign (sudden onset rapidly increasing pain in affected area)
  • XR may see subQ air
  • toxic appearance - shock and renal failure follow
  • sudden onset hypotension, tachycardia
  • fever, delirium/stupor (esp in last stages)
  • local tenderness, tense edema, crepitus
  • skin bronzed w/ dark green-black area of necrosis and fluid-filled blebs
  • d/c serosanguinous, dark color (“coca-cola”); foul odor +/- gas bubbles

A:

  • radiographic studies may show gas w/n soft tissues
  • anaerobic cx confirms DX
  • DDX: other bacteria can produce gas infected tissues

P/TX:

  • prompt surgical evaluation and abx
  • adequate surgical debridement and exposure of infected areas are essential w/ radical surgery often necessary
  • IV PCN is effective
  • Clindamycin may decrease production of bacterial toxin
  • hyperbaric O2 therapy has been used empirically
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