Skin and Soft Tissue Infection Flashcards

1
Q

classification of SSTI by layers of skin

A

epidermis - impetigo
dermis - ecthyma & erysipelas
hair follicles: furuncles & carbuncles
subcutaneous fat and deep dermis: cellulitis
fascia: necrotizing fascilitis
muscle: myositis

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2
Q

clinical presentation of impetigo

A

localised superficial infection characterised by pustules or vesicles which then ruptured to form crusts or bullae on an erythematous base
located at the face & extremities

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3
Q

clinical presentation of ecthyma

A

deeper variant of impetigo begins as vesicles/pustules –> evolve to become ulcers.
- pruitis is common.

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4
Q

clinical presentation of erysipelas

A

superficial infection of the upper dermis involving the lymphatics. characterised by tender erythematous plaque with well-demarcated borders
common on face & lower extremities

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5
Q

clinical presentation of furuncles & carbuncles

A

infection of hair follicles with associated small subcutaneous abscess
carbuncle: a cluster of furuncles

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6
Q

clinical presentation of cellulitis

A

acute infection involving deep dermis and subcutaneous fat
- almost unilateral
- common on lower extremities

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7
Q

mimickers of cellulitis:

A

deep venous thrombosis, calciphylaxis, stasis dermatitis, hematoma, erythema migrans

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8
Q

the function of the skin

A

act as physical, chemical and immunological barriers against infection
- chemical: maintain acidic environment to keep microbial load low & regulate desquamation to keep transient bacteria low & sebaceous secretion inhibit growth of bacteria and fungi
- immunological: part of innate immunity & produce anti-microbial peptides to kill pathogens & normal skin commensal prevents colonisation and overgrowth of more pathogenic strains

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9
Q

pathophysiology of SSTI

A

majority results from the disruption of normal host defences –> lead to overgrowth and invasion of pathogenic micro-organisms

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10
Q

risk factors of SSTI

A
  1. disruption of the skin barrier via
    - traumatic & non-traumatic
    - reduced venous & lymphatic drainage due to obesity, saphenous venectomy, chronic venous insufficiency
    - peripheral artery disease
    - age
    - physical environment (pH, soap and detergent use, humidity & moisture)
  2. medical conditions: (DM, cirrhosis, neutropenia, HIV)
    3 drugs: immunosuppressive agents & SGLT2i
  3. history of cellulitis
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11
Q

prevention of SSTI:

A
  • good care to maintain skin integrity
  • identity and treat predisposing factors at the time of initial diagnosis to decrease the risk of occurrence
  • acute traumatic wounds should be copiously irrigated & remove foreign objects & debride devitalised tissue
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12
Q

when culture is needed for SSTI?

A

mild and superficial infections no need (eg. impetigo, ecthyma)

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13
Q

What can lead to disruption of the skin barrier

A
  • traumatic injury
  • non-traumatic
  • reduced venous and lymphatic drainage
  • peripheral artery disease
  • advanced age
  • physical environment (eg. pH, soap, detergent, moisture, urine, feces, sweat, chronic wound fluid)
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14
Q

what are some conditions can lead to a reduced venous & lymphatic drainage

A

saphenous venectomy, obesity, chronic venous insufficiency

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15
Q

conditions predispose to SSTI

A

diabetes, cirrhosis, neutropenia, HIV, history of cellulitis

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16
Q

drugs predispose to SSTI

A

immunosuppressants, SGLT2i

17
Q

how should the sample be taken for culture?

A
  • from deep in the wound after the surface cleansed
    ==> bc surface may be contaminated
  • from the base of a closed abscess where bacteria grow
  • by curettage, rather than wound swab or irrigation
    ==> bc difficult to obtain representative samples from wound swabs
18
Q

what culture is needed?

A
  • cultures of pus, exudates or tissues from the wound
  • blood culture (for severe cases with marked systemic sx of infection or immunocompromised pt)
19
Q

what conditions are considered as purulent

A

furuncles, carbuncles, skin abscesses, purulent cellulitis

20
Q

clinical presentaitons of skin abscess

A

collection of pus within the dermis and deeper skin tissues. manifest as painful, tender fluctuant and erythematous nodules

21
Q

complications of cellulitis

A

more common in immunocompromised patients
- bacteremia, endocarditis, toxic shock, glomerulonephritis, lymphedema, osteomyelitis, necrotising soft-tissue infection

bc infection is usually caused by gram pos which likes to stick to heart, joint, spine & release toxins that cause accentuated response to go into sepsis & shock

22
Q

pathogens need to cover for impetigo

A

staphylococci or streptococci, MSSA
toxin producing strain of S.aureus cause bullous

23
Q

pathogens need to cover for ecthyma

A

group A streptococcus (S.pyogenes), MSSA

24
Q

coverage for non-purulent cellulitis, erysipelas

A

mainly beta-hemolytic streptococcus (S.pyogenes), MSSA cover for moderate
Water exposure: aeromonas, vibrio vulnificus, pseudomonas aeruginosa

25
Q

coverage for purulent infection

A
  • mainly S.aureus.
  • some beta-hemolytic strep
  • gram-neg & anaerobe (common in patients with skin abscess involving perioral, perirectal or vulvovaginal areas)
  • HA-MRSA (depends on the risk factors)
26
Q

definition for HA-MRSA

A

infection occurs >48 hours after hospitalisation OR outside of hospital within 12 months of exposure to healthcare

27
Q

empiric treatment for impetigo ecthyma with multiple lesions

A

PO cephalexin or cloxacillin
PO clindamycin if penicillin allergy
duration for 7 days (severe:10-14 days)

28
Q

culture-directed (S.pyogenes) treatment for impetigo & ecthyma

A

PO penicillin V and amoxicillin

29
Q

culture-directed (MSSA) treatment for impetigo & ecthyma

A

PO cephalexin or cloxacillin

30
Q

treatment for mild impetigo

A

often self-limiting.
can give topical mupirocin BD x 5d or tropical tetracycline

31
Q
A