Anatomical sites of SSTIs
impetigo - epidermis
ecthyma/ erysipelas - dermis
furuncle/ carbuncles - hair follicles
cellulitis - subcutaneous fat
necrotizing fasciitis - fascia
myositis - muscle
Pathophysiology of SSTIs
*best defense against SSTI is INTACT SKIN
- continuous renewal of epidermal layer
- sebaceous secretions (inhibit bacteria & fungi growth)
- normal commensal skin microbiome (prevent colonisation & overgrowth of more pathogenic strains)
disruption of normal host defeses -> overgrowth & invasion of skin & soft tissues by pathogenic micro-organisms
Risk factors for SSTI
Disruption of skin barrier
-> TRAUMATIC: lacerations/ recent surgery/ burns/ abrasion/ crush injuries/ open fractures /injection drug use / human & animal bites/ insect bites
-> NONTRAUMATIC: ulcer, tinea pedis, dermatitis, toe web intertrigo, chemical irritants
-> IMPAIRED VENOUS & LYMPHATIC DRAINAGE (saphenous venectomy/ obesity/ chronic venous insufficiency)
-> peripheral artery disease
Conditions that predispose to infection: diabetes, cirrhosis, neutropenia, HIV, transplantation & immunosuppressive medications
History of cellulitis
Prevention of SSTIs
*managing predisposing conditions (Risk factors)
Good care to maintain skin integrity: good wound care / treatment of tinea pedis / preventing dry, cracked skin / good foot care for DM pts (prevent wound & ulcers)
Predisposing factors: to be identified & treated at the time of initial diagnosis to decrease risk of recurrence
ACUTE TRAUMATIC WOUNDS to be copiously irrigated, foreign objects removed, devitalised tissues debrided
Diagnosis of SSTI (confirm presence of infection)
*HISTORY & PHYSICAL EXAMINATION
Underlying disease
Recent trauma, bites, burns, water exposure
Animal exposure
Travel history
*risk factors (history of cellulitis)
- if mild/ superficial infections: cultures may not be required
*Taking cultures of pus/ exudates/ tissue from wound:
-> open, draining wounds can often be contaminated with potentially pathogenic organisms -> wound swab should be AVOIDED -> difficult to obtain representative sample
–> TAKE SAMPLE:
1. from deep in the wound after surface cleansed
2. from base of a closed abscess, where bacteria grow
3. by curettage, rather than wound swab/ irrigation
*BLOOD CULTURE only for severe cases with marked systemic symptoms of infection/ immunocompromised pts
Likely pathogen for SSTIs
impetigo *epidermis: staphylococci, streptococci
*bullous form: caused by TOXIN-producing strains of S. aureus
Ecthyma *dermis: GAS
nonpurulent (cellulitis, erysipelas): beta-hemolytic strep, usually GAS
(s. aureus much less frequently)
** aeromonas, vibrio, pseudomonas risk factor w WATER EXPOSURE
purulent (furuncle, carbuncles, skin abscesses, purulent cellulitis): S. aureus (MAIN), beta-hemolytic strep
*isolation of multiple organisms (gram -ves & anaerobes) MORE COMMON in pts w skin abscesses involving perioral/perirectal/ vulvovaginal areas
**CA-MRSA common in US, NOT IN SG
when is systemic antibiotics indicated for purulent SSTIs?
*mainstay treatment: incision & drainage (I&D)
Adjunctive systemic antibiotics WHEN:
- unable to drain completely
- lack of response to I&D
- extensive disease involving several sites
- extremes of age
- immunosuppressed (chemotherapy, transplant)
- signs of systemic illness (*4x SIRS criteria: temp, HR, RR, WBC)
monitoring therapeutic response of SSTIs
- resolution of signs & symptoms
-> IMPROVEMENT by 48-72h AFTER initiation of EFFECTIVE abx
-> NO PROGRESSION of lesion/ development of complication
-> switch to oral abx when pt is better
-> if pt fails to respond clinically within 2-3d: reassess indication &/ choice of abx - reculture (bacteriological clearance)
-> NOT REQUIRED for pts who respond - ADR/ allergies
Use of topical abx in SSTI indicated?
CONTROVERSIAL
- most mild cases are SELF-LIMITING
- local wound care CENTRAL in treatment
- NOT recommended in SEVERE cases
- adds cost to treatment
*mupirocin
-> HIGHLY effective against aerobic gram +ve cocci esp. S. aureus (bactericidal @ 2% ointment)
-> NOT effective against enterococci & gram -ves
-> useful for eradication of NASAL staphylococcal carriage
**resistance in MRSA MAJOR concern (11-65% reported in widespread use, even 13% in absence)
Definition of diabetic foot infection (DFI)
soft tissue OR bone infections below the malleolus
*areas of DFI:
- skin ulceration (peripheral neuropathy)
- wound (trauma)
**bacterial colonisation of ulcers/ wound COMMON -> NOT ALWAYS INFECTED!
definition of INFECTION:
- purulent discharge OR
- >/= 2 signs/ symptoms of inflammation: Erythema, Warmth, Tenderness, Pain, Induration
Complications of DFI
hospitalisation
osteomyelitis -> amputation *in SG: one of the world’s highest rate of lower extremity amputation in diabetes pts
Pathophysiology of DFI
- Neuropathy: peripheral (lowered pain sensation & altered pain response) // motor (muscle imbalance) // autonomic (increased dryness, cracks & fissures)
- Vasculopathy: early atherosclerosis, peripheral vascular disease; WORSENED by hyperglycemia & hyperlipidemia
- Immunopathy: impaired immune response // increased susceptibility to infections // worsened by hyperglycemia
-> ulcer formation/ wounds -> bacterial colonisation, penetration & proliferation -> DFIs
Clinical presentation of DFI
Superficial ulcer (mild erythema) -> deep tissue infection (extensive erythema) -> infection of bone & fascia, purulent discharge -> localised gangrene
Possible pathogens involved in DFI
*OFTEN POLYMICROBIAL
- S. aureus & strep MOST COMMON
- Gram -ve bacilli *chronic wounds/ prev treated w abx: E.coli, Klebsiella, Proteus (P. aeruginosa less common)
- Anaerobes *ischemic/ necrotic wounds: peptostreptococcus, veillonella, bacteriodes
Culture indication for DFIs
mild DFIs - optional
Moderate to severe DFIs: DEEP tissue culture AFTER cleansing & before starting abx (if possible); AVOID SKIN SWABS
** DO NOT CULTURE UNINFECTED WOUNDS
Adjunctive measures for DFI management
- wound care: debridement, “off-loading”, apply dressings that promote healing environment & control excess exudation
- Foot care: daily inspection, prevent wounds & ulcers
- OPTIMAL GLYCEMIC CONTROL
how do pressure ulcers form
pressure ulcers = decubitus ulcers = bed sores
**synergistic interaction between 4 factors:
1. moisture
2. PRESSURE (amount & duration)
3. shearing force
4. friction
risk factors for pressure ulcers
- reduced mobility eg. spinal cord injuries, paraplegic
- debilitated by SEVERE chronic diseases eg. multiple sclerosis, stroke, cancer
- reduced consciousness
- Sensory & autonomic impairment eg. incontinence
- extreme of ages
- malnutrition
clinical presentation of pressure ulcers (various stages)
stage 1: epidermis abrasion, irregular area of tissue swelling *no open wound
stage 2: extends through dermis, open wound
stage 3: extends deep into subcutaneous fat, open sore/ ulcer
stage 4: involves muscle & bone; deep sore/ ulcer
**criteria for INFECTED pressure ulcer SAME AS DFI
- purulent discharge, OR
- >/=2 signs & symptoms of inflammation (erythema, pain, tenderness, warmth, induration)
pathogen involved in pressure ulcers
*similar to DFIs: polymicrobial
- S. aureus & strep MOST COMMON
- Gram -ve bacilli *chronic wounds/ prev treated w abx: E.coli, Klebsiella, Proteus (P. aeruginosa less common)
- Anaerobes *ischemic/ necrotic wounds: peptostreptococcus, veillonella, bacteriodes
culture for pressure ulcers
*deep tissue cultures/ biopsy specimens
AVOID skin swabs
Adjunctive measures for pressure ulcer treatment
- debridement of infected/ necrotic tissue
- local wound care: normal saline (avoid harsh chemicals)
- relief of pressure (turn/ reposition q2h) *IMPT FOR PREVENTION
