Diabetic and certain chronic wounds, Osteoradionecrosis, and post-radiation soft tissue injury. 

Problem wounds often have an inadequate blood supply to support healing.  Over several weeks of daily hyperbaric therapy, new capillaries develop in tissues that are deficient in microvasculature and have resulting low oxygen tensions.  Hyperbaric therapy also promotes macrophage and fibroblast activity at the wound margins.  These factors (and others) in combination often result in spontaneous healing of problem wounds that have been refractory to standard wound care alone.

A recent Cochrane Review on the use of hyperbaric therapy as an adjunctive treatment for chronic ulcers of the lower limbs concluded that hyperbaric therapy significantly reduced the risk of major amputations related to diabetes compared to alternative therapy (RR 0.31, 95% CI 0.13 to 0.71).¹

A second Cochrane Review, assessing the benefits and harms of hyperbaric therapy for treating or preventing late radiation tissue injury (LRTI), found improved outcomes for people with LRTI in specific soft tissue.  More specifically, the report finds improved chance of healing following hyperbaric therapy for radiation proctitis (RR 2.7, 95% CI 1.2 to 6.0, p=0.02), surgical flaps (RR 8.7, 5% CI 2.7 to 27.5, p=0.0002), hemimandibulectomy (RR 1.4, 95% CI 1.1 to 1.8, p=0.001), and irradiated tooth sockets (RR 1.4, 95% CI 1.1 to 1.7, p=0.009). ²

Refractory Infections

HBOT acts as an adjunctive therapy in chronic osteomyelitis, necrotizing soft tissue infections, and other select problem infections.  HBOT increases the killing efficiency of WBCs (neutrophils) and macrophages as well as directly inhibiting bacterial growth.  Appropriate use of antibiotics and surgical interventions, as indicated by best practices, are continued while hyperbaric therapy is being used.  

A retrospective cohort study of 44 patients admitted to hospital with a diagnosis of necrotizing soft tissue infection over a five-year period concluded that hyperbaric therapy was associated with improved chance of survival (OR 8.9, CI 95% 1.3 to 58.0, p=0.02) and limb salvage (p=0.05).³    

Crush Injuries, Compartment Syndromes, Compromised Flaps & Grafts, Serious Burns.  

HBOT is beneficial as adjunctive therapy (in addition to standard therapies) in a variety of conditions associated with localized edema and tissue oxygen deficiency.  Besides providing dramatic increases in oxygen delivery to compromised tissues, HBOT can provide a marked reduction in localized tissue edema which is detrimental to these conditions.

A double-blind control trail of 36 patients with crush injuries randomized to either a hyperbaric or placebo group demonstrated the former group had significant improvements in wound healing and reduced rates of repeat-surgery.  Complete healing was found in 17 of 18 patients in the hyperbaric group versus 10 of 18 in the placebo group (p <0.01).  One patient in the hyperbaric group had a repeated surgical procedure compared to 6 in the placebo (p<0.05).⁴

“Bubble” Illness

Decompression syndromes as well as air or gas embolism respond to HBOT through several physiological mechanisms.  The compressive pressures of the hyperbaric chamber assist the dissolution of large and small air or gas bubbles.  High tissue and lung oxygen partial pressures also facilitate rapid clearing of inert gases from tissues, the blood stream, and lungs.  HBOT also assists with the amelieration of reperfusion injury which is a concomitant feature of these pathologies.

It is widely accepted that hyperbaric medicine is indicated for decompression syndromes and air or gas embolisms.  While there are no clinical trials into the use of hyperbaric therapy to treat decompression syndromes or air embolisms it is strongly indicated for such ailments and is the standard of care for these conditions as no effective alternative treatment exists.  Many case reports and case series have demonstrated the benefits.  The largest case series included 19 patients with iatrogenic cerebral arterial gas embolism treated with hyperbaric therapy within 30 hours of insult.  After immediate completion of therapy, 16 (84%) of the patients had resolved completely or demonstrated signs of improvement.⁵  

Carbon Monoxide Poisoning, Smoke Inhalation (including cyanide gas)  

The pathophysiology of these conditions is complex.  The therapeutic benefits of HBOT occur in circulating blood (more rapid displacement of carbon monoxide bound to haemoglobin) in body tissue (reduction of reperfusion injury, including vascular changes and edema) and at the intra-cellular level (poisoning of the cytochrome oxidation system is reversed). 

Recently published randomized trials have concluded that the administration of hyperbaric therapy significantly reduces the risk of cognitive sequelae after serious acute carbon monoxide poisoning.  One of these trials of 147 patients concluded that hyperbaric therapy is indicated for patients over 36 years of age or have exposure intervals greater than or equal to 24 hours (OR 0.3, CI 95% 1.0 to 3.8, p<0.001).⁶   Another trail of 152 patients concluded that three hyperbaric therapy treatments within a 24-hour period reduced the risk of cognitive sequelae 6 weeks and 12 months after acute carbon monoxide poisoning (OR 0.45, CI 95% 0.22 to 0.92, p =0.03).⁷