Hyperbaric Chamber

What is Hyperbaric Oxygen Therapy?

Hyperbaric oxygen is a mode of therapy in which the patient breathes 100% oxygen at pressures greater than normal atmospheric (sea level) pressure. In contrast with attempts to force oxygen into tissues by topical applications at levels only slightly higher than atmospheric pressure, hyperbaric oxygen therapy involves the systematic delivery of oxygen at levels 2-3 times greater than atmospheric pressure.

Hyperbaric medicine is an emerging specialty of medicine that delivers oxygen at greater than atmospheric pressures to treat a variety of disorders.

For years, hyperbaric oxygen therapy has been recognised as the definitive treatment for decompression sickness, air embolism (diatrogenic and diving related) and carbon monoxide poisoning.

Today, hyperbaric oxygen is used successfully as an adjunctive therapy for such indications as deep-seated acute and chronic bone and soft issue infections, hypoxic non-healing wounds, preservation of compromised soft issue flaps and grafts, and management of wounds in radiated tissue. In hyperbaric oxygen therapy, patients are treated with 100 percent oxygen at elevated atmospheric pressures.

The increased pressure (up to three atmospheres) causes a 10 to 15 fold increase in plasma oxygen concentration with a resultant increase in tissue oxygenation. This effect is delivered via the lungs to the developing capillary bed where it helps capillaries proliferate white cell kill and fibroblasts create new tissue. It cannot be duplicated with topical O2.

What are the Beneficial Mechanisms?

Several beneficial mechanisms are associated with intermittent exposure to hyperbaric doses of oxygen. Either alone, or more commonly in combination with other medical and surgical procedures, these mechanisms serve to enhance the healing process of treatable conditions.

Hyperoxygenation provides immediate support to poorly perfused tissue in areas of compromised blood flow. The elevated pressure within the hyperbaric chamber results in a 10-15 fold increase in plasma oxygen concentration. This translates to arterial oxygen values of between 1500 and 2000 mmHg, thereby producing a four-fold increase in the diffusing distance of oxygen from functioning capillaries, While this form of hyperoxygenation is only a temporary measure, it will often serve to buy time and maintain tissue viability until corrective measures can be implemented or a new blood supply established.

Neovascularization represents an indirect and delayed response to hyperbaric oxygen exposure. Therapeutic effects include enhanced fibroblast division, neoformation of collagen, and capillary angiogenesis in areas of sluggish neovascularization such as late radiation damaged tissue, refractory osteomyelitis and chronic ulcerations in soft issue.

Hyperoxia enhanced Antimicrobial Activity has been demonstrated at a number of levels. Hyperbaric oxygen causes toxin inhibition and toxin inactivation in Clostridial perfringens infections (gas gangrene). Hyperoxia enhances phagocytosis and white cell oxidative killing, and has been shown to enhance aminoglycocide activity. Recent research has demonstrated a prolonged post antibiotic effect, when hyperbaric oxygen is combined with tobramycin against Pseudomonas aeroginsoa.
Direct Pressure utilises the concept of Boyle's Law to reduce the volume of intravascular of other free gas. For more than a century this mechanism has formed the basis for hyperbaric oxygen therapy as the standard of care for decompression sickness and cerebral arterial gas embolism. Commonly associated with divers, CAGE is a frequent iatrogenic event in modern medical practice. It results is significant morbidity and mortality and remains grossly under diagnosed.

Hyperoxis-induced Vasoconstriction is another important mechanism. It occurs without component hypoxia, and it is helpful in managing intermediate compartment syndrome and other acute ischemias in injured extremities, and reducing interstitial edema in grafted tissue. Studies in burn wound applications have indicated a significant decrease in fluid resuscitation requirements when hyperbaric oxygen therapy is added to standard burn wound management protocols.

Attenuation of Reperfusion Injury is the most recent mechanism to be discovered. Much of the damage associated with reperfusion is brought about by the inappropriate activation of leukocytes. Following an ischemic interval, the total injury pattern is the result of two components: a direct irreversible injury component from hypoxia, and an indirect injury, which is largely mediated by the inappropriate activation of leukocytes. Hyperbaric oxygen reduces the indirect component of injury by preventing such activation. The net effect is the preservation of marginal tissues that may otherwise be lost to ischemia-reperfusion injury.