Definition and Causes

Osteomyelitis is a bone infection. Infection may spread to bone from surrounding soft tissue, from elsewhere in the body via the blood, or directly from a bone injury or bone surgery.

Osteomyelitis is a serious complication of chronic wounds and necrotizing infections and is a distinctive feature of Wagner Grade 3 diabetic ulcers.

Bone infections may be caused by any number of bacteria or fungi. The most common cause of osteomyelitis is MRSA, or methicillin-resistant Staphylococcus aureus, which has become a particularly troublesome hospital- and healthcare-acquired infection (HAI).

In children, osteomyelitis most commonly affects the long bones of the legs and upper arms.
Adults are more likely to develop osteomyelitis in the bones that make up the spine (vertebrae).
People who have diabetes may develop osteomyelitis in their feet if they have foot ulcers.

Blocked vessels (ischemia) or poor circulation of oxygenated blood in and around infected bone may lead to inflammation (osteitis), abscess (pus), swelling (edema), pressure, and death (necrosis) of soft and bony tissue.

The UHMS approval for treatment of osteomyelitis with hyperbaric oxygen therapy applies specifically to refractory osteomyelitis.

Refractory means “resistant to treatment”. Clinicians may utilize other treatments, such as antibiotics, for a period of time before assessing an infection as refractory. Hyperbaric oxygen is administered as an adjunct to antibiotics and other therapies. A qualified physician should make the recommendation to treat a bone infection with HBOT.

Treatment with Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy (HBOT) is an effective adjunct to antibiotics and surgery, the traditional treatments for osteomyelitis. When the bacteria involved are anaerobic, meaning they thrive in low-oxygen environments, hyperbaric oxygen kills them and stops them from replicating, spreading, and releasing damaging toxins.

HBOT may also improve circulation, boost the effect of antibiotics, deliver infection-fighting blood components to the infection site, and accelerate bone growth and healing.

UHMS guidelines recommend daily treatments of 90-120 minutes at 2.0-3.0 atmospheres of absolute pressure (ATA), starting soon after surgical debridement and continuing 4 to 6 weeks.

Undersea and Hyperbaric Medical Society

Mechanisms of HBO2

Common to each of these mechanisms is the restoration of normal to elevated oxygen tensions in the infected bone. The decreased oxygen tensions typically associated with bony infections can be returned to normal or above normal levels while breathing 100% oxygen in a hyperbaric chamber. Achieving such elevations has important consequences for the hypoxic milieu of osteomyelitic tissues.

Neutrophils require tissue oxygen tensions of 30-40 mmHg to destroy bacteria by oxidative killing mechanisms.Leukocyte mediated killing of aerobic Gram-negative and Gram-positive organisms, including Staphylococcus aureus, is restored when the low oxygen tensions intrinsic to osteomyelitic bone are increased to physiologic or supra-physiologic levels. This effect can be clinically important, as anaerobes make up approximately 15% of the isolates in chronic, non-hematogenous osteomyelitis.

In addition to enhanced leukocyte activity, HBO2 helps to augment the transport of certain antibiotics across bacterial cell walls. Aminoglycoside transport across the bacterial cell wall is both oxygen-dependent and impaired in a hypoxic environment. More specifically, active transport of antibiotics (e.g. gentamicin, tobramycin, amikacin) across bacterial cell walls does not occur if tissue oxygen tensions are below 20 to 30 mmHg.
Therefore, HBO2 exposures can enhance the transport and augment the efficacy of antibiotic action.(

There is evidence that HBO2 enhances osteogenesis. Animal data suggests that bone mineralization and healing can be accelerated by intermittent exposure to HBO2.(24,25) Remodeling of bone by osteoclasts is an oxygen-dependent function. Consequently, inadequate oxygen tensions inhibit microscopic debridement of dead, infected bone by osteoclasts. As previously noted, HBO2 can restore physiologic or provide supra-physiologic oxygen tension in hypoxic bone environments, thus osteoclast function in infected bone can be improved. HBO2 therapy's stimulatory effect on osteoclasts has been confirmed in animal models. Furthermore, as demarcation between healthy and necrotic bone is not always clear at the time of surgery, osteoclast enhancement may improve the overall quality of bony debridement and reduce the chances that local infections will recur.

The pathophysiology of chronic osteomyelitis is characterized by both acute and chronic sources of ischemia. HBO2 therapy has been shown to be effective in acutely reducing tissue edema, lowering intra-compartmental pressures and ameliorating the detrimental effects of inflammatory reactions.
Over the longer term, HBO2 can be used to promote new collagen formation and capillary angiogenesis in both hypoxic bone and surrounding tissues. This neovascularization works to counter the less easily reversible consequences of osteomyelitis, such as surgical trauma, tissue scarring and nutrient blood vessel occlusion.
By creating a sustained increase in the arterial perfusion of previously hypoxic bone and soft tissues, HBO2 can reduce the susceptibility of these tissues to recurrent infection and necrosis.


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