Necrotizing Soft Tissue Infections
These infections may be single aerobic or anaerobic but are more often mixed infections that often occur as a result of trauma, surgical wounds, or foreign bodies, including subcutaneous and muscular injection of contaminated street drugs. They are often seen in compromised hosts who have diabetes or a vasculopathy of another type. These infections are named based on their clinical presentation and include necrotizing fasciitis, clostridial and nonclostridial myonecrosis, and Fournier gangrene.
Regardless of the depth of the tissue invasion, these infections have similar pathophysiology that includes local tissue hypoxia, which is exacerbated by a secondary occlusive endarteritis. Intravascular sequestration of leukocytes is common in these types of infections, mediated by toxins from specific organisms. Clostridial theta toxin appears to be one such mediator. All of these factors together foster an environment for facultative organisms to continue to consume remaining oxygen, and this promotes growth of anaerobes.
The cornerstones of therapy are wide surgical debridement and aggressive antibiotic therapy. Hyperbaric oxygen therapy (HBOT) is used adjunctively with these measures, as it offers several mechanisms of action to control the infection and reduce tissue loss. First, HBOT is toxic to anaerobic bacteria. Next, HBOT improves polymorphonuclear function and bacterial clearance. Based on results of work related to CO poisoning, HBOT may decrease neutrophil adherence based on inhibition of beta-2 integrin function. Further investigation is needed to see if this mechanism is at work in necrotizing infections as well. In the case of clostridial myonecrosis, HBOT can stop the production of the alpha toxin. Finally, limited evidence indicates that HBOT may facilitate antibiotic penetration or action in several classes of antibiotics, including aminoglycosides, cephalosporins, sulfonamides and amphotericin.
Multiple clinical studies suggest that HBOT is efficacious in the treatment of necrotizing soft tissue infections. These include case series, retrospective and prospective studies, and non-randomized clinical trials. They suggest significant reductions in mortality and morbidity. The reduction in mortality was remarkably similar in two studies: 34% (untreated) vs. 11.9% (treated) in one study; 38% (untreated) vs. 12.5% (treated) in the other. In another study, the treated group had more patients with diabetes and more patients in shock and still had significantly less mortality (23%) than the untreated group (66%). Clinical studies involving patients with Fournier gangrene treated with HBOT bear similar results.
Initial HBOT is aggressively performed at least twice per day in coordination with surgical debridement. Typically, a treatment pressure ranging from 2.0-2.5 ATA is adequate. However, in the specific case of clostridial myonecrosis, 3 ATA is often used to ensure adequate tissue oxygen tensions to stop alpha toxin production. For the same reason, HBOT should be initiated as quickly as possible in this circumstance and performed 3 times in the first 24 h if at all feasible.
The disorders considered in treatment of intracranial abscesses (ICA) include subdural and epidural empyema as well as cerebral abscess. Studies from around the world have reviewed mortality from ICA with a resulting mortality of about 20%. HBOT has multiple mechanisms that make it useful as an adjunctive therapy for ICA.
HBOT induces high oxygen tensions in tissue, which helps to prevent anaerobic bacterial growth, including organisms commonly found in ICA. HBOT can also help reduce increased intracranial pressure (ICP) and its effects are proposed to be more pronounced with perifocal brain swelling. As discussed earlier, HBOT can enhance host immune systems and the treatment of osteomyelitis. [
Candidates for adjunctive HBOT are patients who have multiple abscesses, who have an abscess that is in a deep or dominant location, whose immune systems are compromised, in whom surgery is contraindicated, who are poor candidates for surgery, and who exhibit inadequate response despite standard surgical and antibiotic treatment.
HBOT is administered at 2.0-2.5 ATA for 60-90 minutes per treatment. HBOT may be 1-2 sessions per day. The optimized number of treatments has not been determined.