Characteristics
Fulminant infection & necrosis of soft tissue
Systemic Toxicity
High Mortality
History
Hospital Gangrene1
Fournier’s Gangrene2
Meleney’s Ulcer3
Hemolytic Streptococcal Gangrene3
Gas Gangrene
Necrotizing Fasciitis4
~1500 cases/year in USA
Mortality: 20-35%
Leading cause of Inf Dz-related Malpractice Cases
Often difficult to diagnose
Easy to underestimate
Requires emergent & aggressive surg. management
Etiology
Trauma
Surgical site infections
Perinanal &/or urogenital abscesses
Neoplasm
Decubitis Ulcers
Idiopathic
Etiology of NSTI.Elliott, Ann Surg, 1996
- Pressure ulcer 2%, IV drugs 6%, Surgical site 7%, skin 11%, trauma 11%, diabetic foot 12%, anal/GU 42%
Etiology of NSTI.Anaya, Arch Surg, 2004
- Bite 1%< ulcer 7%, skin 11%, sugrical site 11%, trauma 16%, idiopathic 18%, Anal/GU 1%, drugs 30%
IV Drug Use- Related NSTI
- Clostridial contamination of black tar heroin: case clusters
- HMC data: clostridial infection 38% mortality 45% amputation rate
Predisposing Conditions
Advanced age
DM
Alcoholism
Immunosuppresion
Chronic Dz (Renal Failure, Heart Dz, PVD)
Drug Abuse
NSAID use
Epidemiology
Male 59%, female 40%
Comorbidities: DM 70%, peripheral vascular disease 22.5%, chronic liver disease 3.4%, cancer 2.2%, no comorbidities 13.5%
Location: peripheral 79% (lower limb 69%, upper limb 10%), central 20.2%
Microbiology
Type I NSTI – Polymicrobial (60-70%)
- Synergistic infection of aerobic and anaerobic bacteria (avg/case = 4)
- See with SSIs, DM, and PVD
- Common isolates: staph, strep, e-coli, enterococcus, peptostreptococcus, bacteroides fragilis, clostridium
- Associated with immunocompromised patients
Type II NSTI – Single Species (20-30%)
- Less associated with predisposing factors
- Most common isolates: Group A strep (aka strep pyogenes) - 50%, staph aureus - 30%, clostridium perfringens, clostridium septicum, vibrio vulnificus
- Seen in otherwise healthy individuals
15-18% of cases do not grow any organsims
Classification
Type I or II
Depth of involvement: necrotizing cellulitis, fasciitis or myositis
Pathophysiology
Toxin-induced, platelet/neutrophil aggregate- mediated vascular occlusion --> Tissue Necrosis --> Impairs Immune Response/Abx effect*
Similar to immune complexes in TTP
Presentation
Initially: Cellulitis or SQ Abscess
Progression over hours to days to severe skin changes of: ecchymosis, edema, necrosis, blisters/bullae, crepitus, pain out of proportion, septic picture
Admission Dx: cellulitis 58%, abscess 18%, NSTI 14.6%, other 9%
Usually: out of control diabetes
Diagnosis
Clinical – any suspicion - take patient to OR
Plain XR -
CT -
Stage 1 (early) - tenderness to palpation (extending beyond the apparent area of skin involvement), erythema, swelling, warm to palpation
Stage 2 (intermediate) - blister or bullae formation (serous fluid), skin fluctuance, induration
Stage 3 (late) - hemorrhagic bullae, skin anesthesia, crepitus, skin necrosis with dusky discoloration progressing to frank gangrene
LRINEC Score - Lab risk indicator for necrotizing fasciitis score
CRP < 150 scores 0, >=150 scores 4
WBC <15 scores 0, 15-25 scores 1, >25 scores 2
Hemoglobin > 13.5 scores 0, 11-13.5 scores 1, < 11 scores 2
Sodium >=135 scores 0, <135 scores 2
Creatinine <141 scores 0, > 141 scores 2
Glucose <=10 mmol/L scores 0, >10 mmol/L scores 1
Total score --> probablility of NSTI
< 6 --> < 50%
6-7 --> 50-75%
>=8 --> >75%
Danger of LRINEC Score = Paralysis by Analysis
Barie, PS. Crit Care Med 2004; 32: 1618-9
“Practical” LRINEC Score
UCLA General Surgical Lab Model in ST Infections without Hard Signs of NSTI
Na+ < 135 or WBC > 15,400
Na+ corrected for any hyperglycemia (NaC = NaM +0.0016 (glucose-100))
Sensitivity = 90%, Specificity = 76%
PPV = 26%, NPV = 99%
The “Finger Test”
Gray, Necrotic Tissue
Lack of resistance of normally adherent fascia to blunt dissection
Non-bleeding tissue
Dishwater pus
OR – Diagnostic Findings
Gray, Necrotic Tissue
Lack of resistance of normally adherent fascia to blunt dissection
Non-bleeding tissue
Dishwater pus
SQ Necrosis often extends beyond Skin changes
Definitive Dx: Pathologic eval of resected tissue, frozen section can be helpful in difficult case
Summary of Dxic Approach to NSTIs
Hard Signs-->OR
- Hemodynamic instability
- Crepitance
- Gas on XR
- Skin necrosis
- Skin bullae
No Hard Signs but worries you --> OR
No Hard Signs & doesn’t worry you, but WBC is > 15,000 or Na < 135 --> OR
Others --> Observe
Prognosis
Time from admission to operation
Percent of body surface involved
Acidosis
Peripheral vascular disease
Number of comorbid illnesses
Age
Antibiotics
Beta-Lactam c Anaerobic Coverage + Clindamycin* +/- MRSA coverage
- eg: zosyn + clindamycin + vancomycin or linezolid
Continue until:
- Debridements completed/starting to granulate and systemic effects of sepsis resolve
- ? Benefit to longer duration?
Efficacy hampered by lack of blood flow due to necrosis - inhbitis some endotoxin effects
Surgical treatment
Emergent & aggressive debridement
“Re-look” within 24 hr
(Skin Coverage)
Zone 1 – Necrotic
- Mandatory excision
Zone 2 – Inflamed
- Selective excision
Zone 3 - Normal
- Avoid excision +/- counter incisions
Adjuvent Treatment
Hyperbaric Oxygen
- Goal: increase tissue oxygenation --> decreased necrosis
- Strongest benefit seen in clostridial infections
- Should not delay surgical debridement
- No consistent decrease in mortality demonstrated
Immunoglobulin
- Some benefit seen with type II GAS NSTIs associated with sepsis
- Increases survival in Strep Toxic Schock Syndrome from 34% to 67%
- Mechanism: neutralization of "superantigen activity"
- Median dose 2g/kg IVIG
Fournier’s Gangrene
Necrotizing Faciitis of Perineal/Perianal region
Described in 1883
Typically Type I NSTI
Result of penetration of GI or uretheral organisms into perineal/perianal soft tissues
Skin changes often an understatement
Fournier’s-. after debridement
Cervical Necrotizing Fasciitis
Result of bacterial penetration into fascial compartments of neck after surgery, dental procedures, or head/neck trauma
Can spread to face, lower neck, mediastinum
Type I infections in most cases
Gas Gangrene
Classically seen after penetrating trauma in dirty environment
C perfringens most common organism
Also seen in IV drug abusers & in OB complications
Result of excessive phospholipase C & sphingomyelinase stimulation by alpha & theta toxins
Group A Strep
Most common cause of Type II Infections
“Flesh eating bacteria” of 1990s (incidence of 0.085/100,000 in ’91, increased to 0.4/100,000 in '95)
Typically affects otherwise healthy patients
Can also cause toxic shock syndrome
Accounts for 5% of bacterial infections after chicken pox
M-proteins result in exotoxin production --> exhuberant T-cell response & increased cytokine production