Clostridial Myonecrosis: A (HBOT) Deep Dive

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Mike Tom

EM trained at Cooper and Undersea and Hyperbaric Medicine trained at UPenn. Still manning the ED and chamber with Penn in west Philly. Dog dad and fisherman.

The Pre-brief

Although clostridial myonecrosis often gets lumped into the broader category of ‘necrotizing infection’, it is most certainly its own animal.  Clostridial myonecrosis is the true “gas gangrene”, historically cited as a battlefield wound commonly through the first World War.  It is caused by gram positive, anaerobic, spore forming Clostridium species and most commonly Clostridium perfringens.  Left untreated it is nearly uniformly fatal, and even with optimal surgical and medical therapy, rates of mortality and limb loss remain high. 

Diagnosis:

Two requisites exist for clostridial myonecrosis:

  1. Spore introduction: as can happen through a dirty soft tissue wound (i.e. battlefield wound, farming injury, motor vehicle collision), a contaminated surgical wound, or a non-traumatic inoculation in an immunocompromised host.  
  2. Locally decreased oxidation reduction potential: as can occur from circulatory deficit from extensive soft tissue or vascular injury.

Red flags to raise suspicion for clostridial myonecrosis on presentation include pain out of proportion to exam and shiny, tense skin changes which progress to dusky and eventually bronze colors.  The affected margin of tissue can impressively spread as rapidly as 6” per hour, and patients typically have sudden, severe onset of pain whereas other types of necrotizing infections can be more insidious.  Plain radiographs classically reveal feather-like projections between muscle fibers.  Gram staining will demonstrate gram-positive bacteria in the absence of leukocytes.

The Toxins:

The fulminant nature of this disease process stems from the production of over 20 identified exotoxins, with alpha-toxin and theta toxin being the most clinically relevant, and alpha being far and away the more damaging of the duo.

Standard Therapy:

Control of alpha-toxin is paramount in the treatment of this disease. In addition to fluid resuscitation and vasopressor support as indicated, standard therapy is early and aggressive surgical debridement in conjunction with broad-spectrum antibiotics including clindamycin.   

Hyperbaric Oxygen Therapy (HBOT):

If control of disease progression is inadequate with surgery and antibiotics alone, HBOT should be considered as an adjunctive therapy.  In most cases, this requires transfer to a facility with a multiplace hyperbaric chamber, and in a patient stable enough to survive transport, this should at least be discussed with the nearest critical care capable hyperbaric facility.

Mechanisms behind the benefits of HBOT:

  • Achievement of a tissue PO2 >250mmHg, as is achieved during HBOT, can stop alpha-toxin production. This alteration in alpha-toxin production is essential to attenuating disease progression and can lead to the pronounced demarcation between necrotic and viable tissue, allowing for smaller, less heroic surgical debridements.  
  • The exaggerated neutrophil aggregation as is promoted by theta toxin is directly inhibited in a hyperbaric environment.
  • The formation of oxygen free radicals yields an unfavorable environment for the anaerobic Clostridia sp.  Though C. perfringens is not a strict anaerobe, a bacteriostatic effect is demonstrated in hyperbaric conditions.
  • Compression of air in affected tissues can transiently reduce tissue pressure, improve perfusion, and reduce pain.
  • Oxygen-dependent bacterial killing by host neutrophils is enhanced in hyperbaric conditions.  

Case series and retrospective studies report an average mortality of 38% without HBOT and 19% when HBOT is added to surgical and antimicrobial therapies.  These studies also demonstrate a reduction in amputation rates with HBOT.   If utilized, therapy should be pursued and started as early as possible in the disease course as delay in HBOT initiation yields mortality rates similar to those seen with standard therapy alone.

The Debrief

  • Standard treatment of clostridial myonecrosis or “gas gangrene” is aggressive surgical debridement with concurrent broad spectrum antibiotics.  
  • With inadequate source control from surgery alone and where logistically possible, adjunctive HBOT should be strongly considered. 
  • There are well demonstrated physiologic mechanisms by which HBOT can counteract the injurious effects of alpha and theta toxins.
  • Retrospective evidence suggests improved mortality and amputation rates when HBOT is added as an adjunctive therapy for Clostridial myonecrosis.   

References: 

  1. Stevens DL. The pathogenesis of clostridial myonecrosis. Int J Med Microbiol. 2000 Oct;290(4-5):497-502. doi: 10.1016/S1438-4221(00)80074-0. PMID: 11111933.
  2. Stevens DL, Bryant AE. The role of clostridial toxins in the pathogenesis of gas gangrene. Clin Infect Dis. 2002 Sep 1;35(Suppl 1):S93-S100. doi: 10.1086/341928. PMID: 12173116.
  3. Van Unnik A. Inhibition of toxin production in clostridium perfringens in vitro by hyperbaric oxygen. Antonie Van Leeuwenhoek. 1965;31:181-6. doi: 10.1007/BF02045889. PMID: 14315638.
  4. Thom S. R. Hyperbaric oxygen: its mechanisms and efficacy. Plastic and reconstructive surgery.  2011; 127 Suppl 1(Suppl 1), 131S–141S. https://doi.org/10.1097/PRS.0b013e3181fbe2bf
  5. Hill GB, Osterhout S. Experimental effects of hyperbaric oxygen on selected clostridial species. II. In-vitro studies in mice. J Infect Dis. 1972 Jan;125(1):26-35. doi: 10.1093/infdis/125.1.26. PMID: 4332848.
  6. Clark LA, Moon RE. Hyperbaric oxygen in the treatment of life-threatening soft-tissue infections. Respir Care Clin N Am. 1999 Jun;5(2):203-19. PMID: 10333449.

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