SSTI Flashcards
how does the skin protect against infection
- protective barrier
- continuous renewal of epidermal layer -> shedding of keratocytes & skin microbiota
- sebaceous secretion inhibit growth of many bacteria & fungi
- normal commensal skin microbiome prevent colonisation & overgrowth of pathogenic strains
pathophysiology of SSTI
disruption of normal host defence -> allow overgrowth & invasion of skin & soft tissues by pathogenic micro-organisms & prevent enzyme/cytokine from reaching site of infectionf
actors that impair skin barrier function
1) age (both extreme ends)
2) infection
3) physical damage
4) ischaemia
5) drugs & diseases
6) pH
7) excessive soap & detergent use
8) high humidity & moisture
types of disruption of skin barrier
1) traumatic
2) nontraumatic
- ulcer, tinea pedis, dermatitis, toe web intertrigo, chemical irritant
3) impaired venous & lymphatic drainage
- saphenous venectomy
- obesity
- chronic venous insufficiency
4) peripheral artery disease
prevention of SSTI
1) manage predisposing conditions
2) good care to maintain skin integrity
3) acute traumatic wound (irrigated, remove foreign object, debride devitalised tissue)
where to obtain culture for SSTI
1) deep in wound after surface cleansed
2) base of closed abscess
3) curettage rather than wound swab/irrigation
when to not take culture for SSTI?
1) mild/superficial infection
2) culture of pus, exudates, tissues from wound (can be contaminated & hard)
when to take blood culture for SSTI?
only when systemic symptoms/immunocompromised
clinical presentation of impetigo (superficial SSTI)
- erythematous papules -> rapidly evolve into vesicles & pustules that rupture -> dry discharge
- usually on exposed areas (face & extremities)
- well localised & a lot
- bollous/non bollous
clinical presentation of ecthyma (superficial SSTI)
- ulcerative form of impetigo
- lesions extend through epidermis & deep into dermis
- pruritus -> scratch spread infection
clinical presentation of furuncles (follicular SSTI)
- infection of hair follicle
- purulent material extend through dermis into subcutaneous tissue -> form small abscess
clinical presentation of carbuncles (follicular SSTI)
- group of furuncles
- furuncle coalesce -> extend into subcutaneous tissue
clinical presentation of skin abscess (follicular SSTI)
- collection of pus within dermis & deeper skin tissue
- painful, tender, fluctuant, erythematous nodules
clinical presentation of erysipelas (SSTI)
- affect upper dermis
- fiery red, tender, painful plaque
- raised above surrounding skin w well-demarcated edges
- common on face & lower extremities
clinical presentation of cellulitis
- deeper & subcutaneous fats
- acute, diffuse, spreading, non-elevated, poorly demarcated area of erythema
- rapid onset/progression
- unilateral
- anywhere, usually lower extremities
complications for both erysipelas & cellulitis
bacteraiaemia, endocarditis, toxic shock, glomerulonephritis, lymphoedema, osteomyelitis, necrotising soft-tissue infections
conditions that are similar to cellulitis
DVT, calciphylaxis, stasis dermatitis, haematoma, erythema migrans
impetigo likely pathogen
- staphylococci or streptococci
- toxin-producing strains of staph aureus -> bullous form
mild, limited impetigo lesion treatment
topical mupirocin
ecthyma likely pathogens
Group A streptococci (pyogenes)
treatment of multiple impetigo/ecthyma lesions
1) empiric
- staph/strep: PO cephalexin/PO cloxacillin
- penicillin allergy: PO clindamycin
2) culture-directed
- S. pyogenes: PO pen V, amoxicillin
- MSSA: PO cephalexin, cloxacillin
- 7 days
likely pathogens for nonpurulent (cellulitis, erysipelas)
- beta-haemolytic streptococcus
- group A streptococci
- less common
1) S. aureus
2) aeromonas (Freshwater), vibrio vulnificus (seawater), pseudomonas w water exposure
nonpurulent (cellulitis, erysipelas) treatment categories
1) mild (wo systemic)
- cover strep pyogenes w oral Abx
- Pen V, cephalexin, cloxacillin
- penicillin allergy: clindamycin
2) moderate (w systemic, purulence)
- cover MSSA w IV Abx
- cefazolin, cloxacillin, clindamycin (Pen allergy)
3) severe systemic, fail oral/immunocompromised)
- IV Abx: pip/tazo, cefepime, meropenem
- MRSA risk factors: IV vanco, dapto, vibrio
4) water exposure
- add ciprofloxacin
duration of treatment for nonpurulent (cellulitis, erysipelas)
- 5-10days
- 14 days if immunocompromisedn
nonpharmaco for nonpurulent (cellulitis, erysipelas)
- rest
- limb elevation to drain oedema & inflam substances
monitoring for SSTI
- within 48-72 hrs of effective Abx
- X lesion progression/development of complication
- switch to oral when improve
mainstay for purulent SSTI
incision & drainage
when to use adjunctive for purulent SSTI
1) X drain completely
2) lack response to I&D
3) extensive disease involving multiple site
4) extreme ages
5) immunocompromised
6) signs of systemic infection
treatment for purulent SSTI based on severity
1) mild
- I&D or warm compress to promote drainage
2) moderate (systemic)
- I&D + oral Abx (cloxacillin/cephalexin/clindamycin)
3) severe
- I&D + IV Abx (cloxacillin, cefazolin, clindamycin [allergy], vanco [MRSA])
treatment duration for nonpurulent SSTI
5-10 days
