Gas Gangrene
DEFINITION

A infection commonly associated with clostridium species that causes soft-tissue destruction and localized gas production within the tissues
see also nec fasc.

D E A B M I M

EPIDEMIOLOGY

25% of necrotizing soft tissue infections relate to clostridium
(Though other bacteria implicated)

Risk Fx
Diabetes
IV Drug use
Age >50
Malnutrition or obesity
Hypertension
D E A B M I M
 
AETIOLOGY

Clostridium species
- particularly perfringens
- but virtually all species have been isolated from gas gangrene

These are gram +ve anaerobic bacilli
Ubiquitious in soil and environment
- also reside in normal GI flora
Capable of producing heat-resisting spores that can reside almost indefinitely and threaten when introduced into hosts
Typical incubation period 8d; range 3-21d, however infection <6h reported.

However, other agents commonly involved or primary, including:
- Pseudomonas areuginosa, E. coli, Klebsiella, Proteus

Infx may be post-traumatic, post-operative, or spontaneous
- commonly crush injuries that damage nutrients, contaminated wives, foreign bodies,
- contamination with GI, biliary fluids in context of ischaemic wound closure
- occasionally therapeutic administration of vasoconstricting agents
- back-alley abortions.
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BIOLOGICAL BEHAVIOUR

Pathophysiology
Spread in muscle and subcutaneous fat
Promoted by thrombosis of microvasculature and generation of an anaerobic environment.
May thrive in diabetic conditions
Anaerobic growth associated with production of gas in tissue planes
--> classic radiological features
Gas production largely due to fermentation of glucose
- is nitrogen, hydrogen and CO2

C. perfringens
Particularly likes muscle tissues; microvascular thrombosis causes necrosis
Virulence associated with production of an impressive array of toxins, both exotoxins and endotoxins
Both tissue-destructive enzymes and suppression of host immune defenses
- impairs host defense by interfering with diapedesis, and suppression neutrophil sequestration.
--> see margination of multiple neutrophils but few in infection site; can be little pus.
- this is ,ediated by an alpha-toxin that upregulates endothelial adhesion molecules
Endotoxins elicit systemic effects
Exotoxins include necrotizing, hemolysin, protease, hyaluronidase, collagenase, more.

C. septicum
Associated with advanced malignancy, diabetes and immunosuppression, particularly chemo-neutropenia.
Very high mortality (60%)
Alpha toxin haemolysin

Sepsis
Systemic exotoxin burden and mediators drive SIRS / sepsis
Systemic microvascular extravasation, progressive acidosis, intravascular volume depletion, and escalating hypoxaemia
Early death within 24-36h if not treated

IV Drug Use
Strong association, with deposition of bacteria in deep tissue spaces around buttocks and hip
Delayed presentation
Associated 'cut' additives cause more serious infections
Opiate addiction / seeking / response can confuse presentation

D E A B M I M
 
MANIFESTATIONS

Often follows contaminated puncture wounds

Typical pattern is of localized tissue destruction followed by systemic derangement due to exotoxins, leading to septic shock, organ failure, and if untreated, death.

Localized pain, often severe and out of propotion to clincial findings
As zone of infection widens, patients experience systemic symptoms and spread of exotoxins

Systemic
Fever, tachycardia
Chills and rigors are uncommon (only 5% show +ve BCs)

Signs
Skin appears dusky, can go blue-black and haemorrhagic
Rapid progression of localized oedema
Sweet mousy smell in some open wounds; some odorless
Crepitus is classic feature as gas develops
- may be difficult to feel due to oedema
Range of motion can be severely restricted

Late features of sepsis include dehydration, hypotension, oliguria


D E A B M I M

INVESTIGATIONS

Gram Stain
Large gram +ve bacteria without neutrophils

Blood work
WCC>14, sodium <135 and blood nitrogen > 15 mg/mL identifies pts more likely to have necrotizing infections
Consider lactate, DIC in cases of septic shock

XR
Gas in tissue planes is diagnostic and should prompt rapid action
CT and MRI, if performed (should not delay therapy) show oedema, gas, site and extent
Delay to surgical treatment should never occur for the sake of imaging
D E A B M I M

MANAGEMENT

1. HDU / ICU review and admission
- while resuscitating in preparation for theatre
- perform ABG, coag profile,
- estimate and replace volume, with arterial and central venous monitoring if required.
- treat acidosis and coagulation deficits
- avoid use of vasoconstrictors to maintain pressure

2. Antibiotics
- early gram stain can help focus options
- high-dose penicillin is drug of choice: penicillin G 10-24 million Units / day
--> B-lactam; interferes with cell wall mucopeptides during multiplication; bactericidal against susceptible bacteria.
- adding clindamycin is also required; (15mg/kg IV every 8h in adults)
--> inhibits protein synthesis, blocking dissociation of peptidyl t-RNA from ribosomes; blocks production of exotoxins beside targeting anaerobic Strep species.
Adjuvant Therapy?
e.g. recombinant activated Protein C = experimental; not yet recommended.
Hyperbaric oxygen?
Argued that it may improve hypoxaemia, improved phagocytosis, eradication of anaerobes, reduction of tissue oedema, simulates fibroblasts, increased collagen formation.
May be bacteriocidal against clostridial and may block alpha-toxin.
But evidence-based studies are lacking and complications can occur e.g. barotrauma and O2 toxicity (myopia and seizures)

3. Surgery
Cornerstone of effective therapy and must be done without delay except for pre-op rapid resuscitation
- tissue necrosis = poorly responsive to antibiotics; low penetrance
Diagnostic (and shows extent) as well as therapeutic
- necrosis identified by lack of bleeding, fascial planes separate easily without resistance
- muscles display overt oedema, do not respond to electrocautery (note if relaxant on board)
Complete removal of necrotic tissue mandatory
- avoid blunt digital dissection in suspected drug users
Wide open wounds to avoid anaerobic pockets that might encourage return of infection.
Tissue fluids and pieces sent for gram stain, MCS.
Repeat exploration and further debridement should be considered in next 24h

4. Reconstruction
Secondary consideration to acute phase management
VAC dressings facilitate granulation and healing in interim
Most can then be split-skin grafted, occasionally flaps are necessary.

Prognosis
High mortality; 25% in general
- diabetes, IVDU, obesity, hypertension, IHD = high risk.
- leuks > 30 or renal failure at presentation = associated with mortality
Delay to debridement = bad.


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REFERENCES

Cameron 10th