Necrotising Fasciitis

DEFINITION

Life threatening rapidly-spreading infection of the soft tissues.
Includes gas gangrene
Several eponyms eg Fournier (perineal) accompany subdermal necrotising infections.

D E A B M I M


EPIDEMIOLOGY

Risk Factors
Immunocompromised
Diabetics, steroids, cancer therapy.
Morbid obesity
Peripheral vascular disease
IV Drug users
     
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AETIOLOGY

Mostly polymicrobial
- 4.4 organisms per infection on average
Strep pyogenes (group A, beta-hemolytic)
Clostridial gas gangrene is less common but serious
MRSA being increasingly isolated
In bites, Pasturella, Capnocytophaga and in humans Haemophilus and Eikenella.
Water infections: Aeromonas, Vibrio sp., mycobacterium marinum.

Sites
Common sites include perineal and perianal, peri-rectal abscesses
Also foot, lower extremities, esp in diabetic / PVD feet
Post-surgical wounds, pressure ulcers, bites, GI wounds after perforations.

Polymicrobial infections
Often perineal, perianal, diabetics, bite wounds.
Both gram +ve and gram -ve, aerobic and anaerobic; GI contaminants in context of perforations

Group A Beta-haemolytic Strep
Rapid and agressive with high mortality
Virulence factors and exotoxins: allows infx to spread rapidly through otherwise healthy tissue and induce sepsis and shock.

Clostridia
See gas gangrene

MRSA
In US, 60% of community staph isolates are now in the MRSA spectrum.
Also produces toxins that lead to direct invasion and can result in nec fasc.

Type I mixed infection of aerobic and anaerobic bacteria and occurring mostly after surgical procedures and in patients with diabetes and peripheral vascular disease. 70-80%. Average of 3-4 organisms. Mixed aerobic and anaerobic infections.

 

Clostridia, Clostridium perfringens

enterococcus, E.coli,

enterobacter, pseudomonas, acinetobacter

Staphylococci, Streptococci, Klebsiella,

Bacteroides, corynebacteria,

 

Most patients have underlying illness previous surgical procedures, diabetes, PVD, cirrhosis, elderly

 

Type II Monomicrobial infection caused by group A Strep (Strep pyogenes). NF caused by community-associated MRSA can also cause type I NF. Clostridium perfingens may also produce mono-microbial NF. These patients are often healthy and infection occurs after

            blunt trauma

            chickenpox

            injecting drug use

            laceration

            surgical procedures



D E A B M I M

BIOLOGICAL BEHAVIOUR

Pathophysiology
1. Blood supply to the soft tissues and fascia is relatively poor and vulnerable to rapidly spreading infections.
2. Bacteria invade into soft tissues and spread along either the superficial or deep fascial planes.
3. Microvascular thrombosis results from toxins and polymorphonuclear leukocytes --> tissue ischaemia and necrosis.
4. Some organisms, eg. clostridium secrete toxins that cause necrosis in other populations (see gas gangrene).
5. In the immunocompromised there is often a synergistic bacterial infection, where different species help create a perfect environment for each other's growth.

What are the virulence factors for Steprococcus pyogenes (Pathogenesis of Type 2 NF)

M proteins antiphagocytic

Exotoxin: Haemolysin, Streptolysin O and S and Leukocydin: leads to cell destruction and inflammation

Exotoxin A, B or C also Act as a superantigen which able to stimulated T-Cell Respondent without antigen by binding to MHC class II protein on APC. Lead to production of IL-1. IL-6 and TNF-alpha leading to toxic shock syndrome and MODS.

            Exotoxin initiate the vascular thrombosis and inflammation. Its superantigen ability also initiate             the immune response for MOFS and SIRS

 

What is the pathogenesis of polymicrobial necrotizing soft tissue infection (Type I NF)

aerobic and anaerobic

facultative organisms lower the oxidation-reduction potential of the microenvironment and promote anaerobes

anaerobes interfere with host phagocyte function, and allow aerobes to proliferate

some (e.g. B. fragilis) produce B-lactamase to interfere with antibiotic activity

bacterial exotoxins (C. perfringens -  alpha toxin, S. pyogenes - haemolysin, Streptolysin O and S, Leucocidin) cause tissue digestion and act as superantigens

inflammatory process produces involves local blood vessels leading to obliterative endarteritis, necrosis of blood vessel walls and thrombosis of small blood vessels

bacterial heparinase contributes to thrombosis

pressure increases due to the infection, further impairing blood supply

Ischaemia leads to liqufactive necrosis of fascia with concomitant breakdown to skin, muscle and surrounding tissue.

 

Exotoxin: the toxin release from bacteria that can damage the local host cells

Endotoxin: the toxin contained within the Gram Negative bacteria that only release once the bacteria is dead




D E A B M I M

MANIFESTATIONS

Symptoms

Some pts exhibit few signs
Pain out of proportion to clinical signs is common.
Local

Superficial spreading infection and necrosis
Systemic
Systemic sepsis
- tachycardia, hypotension, low urine output, high fluid requirements.

Signs
Few early skin features
Erythema, skin blistering
Progresses to blue-black discoloration, crepitus and dishwater grey fluid discharge from wound.

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INVESTIGATIONS

Bloods
- very high white cell counts and renal impairment at presentation are prognostic.
ABG = prognostic
Surgical intervention
- do not delay surgery for imaging
Radiology, when performed, may show gas in tissue planes
- may be helpful to show deep seated tissue abscesses as primary source.
- may simply show fat stranding in the superficial fat planes
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MANAGEMENT

Life threatening and early recognition is essential
- delay to therapy of 12h+ associated with mortality.

Antibiotics
Broad spectrum ABx.
Treat up front with polymicrobial cover
e.g. tazocin (piperacillin - tazobactam), Timentin, MRSA cover with vancomycin,
Clindamycin (1200 mg IV every 6h) beneficial if high-virulence wounds; has protein-synthesis inhibiting properties that prevent toxin release.
Penicillin 24M Units / day

Operative
Surgical incision down to deep muscle fascia
- inspection of all tissue layers for necrotic tissue
Then wide debridement / tissue excision to bleeding edges
- together with antibiotics and systemic support.
--> all dead tissue must be excised
Explore tissue planes for extent.
- extensive oedema, dishwater grey fluid, and fluid collections suggestive of spreading infection zones.
More than one operation commonly needed
- ie return to OR at 24h for inspection after saline-soaked packing
- serial dressing changes
Avoid VAC / negative pressure dressings until after resolution of sepsis; may result in unrecognized progression.
Reconstruction:
- may need to involve plastics; often wise to consult early.

Adjuvant therapies?
Hyperbaric oxygen therapy, IV immunoglobulins, extracorporeal plasma exchange = experimental; no RCT evidence and not in routine use.

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REFERENCES

Cameron 10th