Hyperbaric oxygen therapy in orthopedics
Hyperbaric oxygen treatment involves intermittent inhalation of 100% oxygen at greater than atmospheric pressure. This treatment is administered in a hyperbaric chamber, which is compressed with air, while the patient breathes oxygen at ambient pressure through a mask. Inspiration of oxygen at high pressure increases the amount of oxygen dissolved in the plasma in direct proportion to the rise in ambient pressure. Thus, when oxygen is inhaled at 2 to 2.4 atmospheres absolute, the plasma oxygen content increases from 0.32 volume percent to 4.8 to 5.76 volume percent. This high dissolved oxygen concentration improves oxygen delivery to bone tissue, reduces marrow edema, and thereby reduces intraosseous pressure, improving venous drainage and microcirculation. By flooding the extracellular fluid with diffused oxygen, the oxygen becomes available to the ischemic bone cells without the need for circulating hemoglobin.
- Sports Injuries
- Fracture repair, delayed and non-healing
Post surgical instability
In Osteomyelitis The oxygen tension in osteomyelitic bone is low, rarely exceeding 25mmHg of oxygen. Fibroblasts cannot synthesize collagen or migrate to the affected area when oxygen tensions are less than 20mmHg. Elevating oxygen tensions to levels greater than 200mmHg allows a return to normal function. Increasing oxygen tensions with HBO2 therapy is a means of returning fibroblastic activity to normal. Following differentiation from fibroblast-like mesenchymal cells, osteoblasts deposit a layer of coarse immature fibrillar bone. This immature bone is then replaced by mature lamellar bone, which is functionally reconstructed by resorption and deposition by osteoclasts and osteoblasts. In some cases, in both bones and wounds, HBOT draws a clear line by which the surgeon can aid in the removal of dead or diseased bones.
Benefits From Hyperbaric Oxygen Treatment
- HBOT increases oxygen tension in infected tissue including bone, to normal or above normal levels. Can increase oxygen saturations of plasma around infected areas that have some remaining degree of diffusion, encouraging healing.
- Provides adequate oxygen for fibroblasts-cells that make connected tissues/ and so promote healing and hypoxic tissue. Cells that remove dead bone (osteoclasts) need oxygen to function, and intermittent oxygen tensions of 30-40mmHg are needed to grow new blood vessels.
- Hyperbaric oxygen is bacteriostatic (bacteria stopping). Neutrophils require PO2 30-40mmHg to do their work against bacteria.
- Augments in effect of antibiotics such as Aminoglycosides, vancomycin, quinolones, and some sulfonamides.
- Prevents polymorphonuclar (PMN) leukocytes (a kind of white cell) from adhering to damaged blood vessel linings, increasing the inflammation that often accompanies surgical treatment for refractory osteomyelitis.
” Chronic osteomyelitis is the only orthopedic indication for which Hyperbaric oxygen therapy has received FDA approval and completely covered by insurance”
Hyperbaric Oxygen Therapy (HBOT) can help to heal bone disorders by stimulating the osteoclasts and osteoblasts. This helps and leads to the re-absorption of dead bone and the creation of new bone. In addition, HBOT stimulates the production of new blood vessels, so that the growing bone receives a steady supply of nutrients, including oxygen. This blood vessel network does two other things: it helps support the function of the osteoclasts, and brings infection fighting white blood cells to the area.
Infected, non-healing fractures of the leg are difficult management problems. They often result in extended hospitalizations, permanent disability and amputations. Over a six year period 21 patients with infected, non-healing fractures were referred for HBOT in addition to their injury management. After some months of treatment, Seventy five percent healed in six months or less. In addition, the infection arrested in 95% of these patients.
It is our opinion that the primary problem in the infected non-healing fracture is that of ischemia at the fracture site. This is due to revitalized bone and poorly vascularized scar tissue. HBOT is believed to compliment the debridement process by improving oxygenation at the fracture site. This promotes revascularization and improves other host factors such as white blood cell oxidative killing, fibroblastic proliferation and osteoclastic activity. The osteoclast is known to be very oxygen dependent cell. HBOT appears to stimulate osteoclast function. The osteoclasts then become effective in clearing residual infected, non-viable bone whereas they were unable to do so in the hypoxic environment.
” Hyperbaric oxygen therapy can be used as an adjuvant therapy in fracture non unions as it can decrease infection, increase oxygenation within scar tissue and stimulate new bone formation”
AVN Femoral Head
Since AVN of the femoral head occurs most often in younger individuals, the therapeutic goal is to prevent collapse of the femoral head and to preserve the joint rather than to replace it. Unfortunately, there is currently no completely satisfactory treatment which can accomplish this. Numerous therapeutic measures have been studied including core decompression, free, pedicle and microvascular fibular bone grafting and electrical stimulation. There is no consensus of opinion on the efficacy of these methods.
In AVN of the femoral head, damage to the microcirculation is an early event. It is thus clearly desirable to restore the oxygenation of the affected bone. The osteoclast has a high rate of metabolic activity and its function in removing necrotic bone is oxygen-dependent. Moreover, increasing the oxygen tension in hypoxic areas promotes synthesis of collagen, proliferation of fibroblasts and capillary angiogenesis.
“Results have shown 80-90% prevention of progression of disease and return to normal MRI findings.The treatment comprised six daily sessions each week up to a total of 100. A session involved breathing 100% oxygen at 2 to 2.4 atmospheres absolute in a multiplace pressure chamber for 90 minutes and using a mask breathing system.”
Crush Injuries and compartment syndrome
Crush injuries are traumatic ischemia that cause such severe damage to tissues from the energy transfer that tissue survival is in question . Usually, two or more tissues are injured severely enough that their survival is unsure. Edema due to tissue hypoxia has detrimental effects on wound healing and infection control. It interferes with oxygen availability for cells that already have increased oxygen needs. A second harmful effect of edema is the collapse of capillaries. The edema fluid increases the interstitial pressure around the capillaries. Once the interstitial fluid pressure exceeds the capillary perfusion pressure in a closed space, the capillary bed collapses, and flow in the microcirculation ceases. Bacteria grow almost without restraint if circulation is disrupted at the site of injury. With the disruptions of the blood supply, antibiotics can no longer reach the injury or infection site. In the hypoxic environment, neutrophils lose the ability to generate the reactive oxygen species that kill bacteria. As tissue oxygen is much reduced in acute traumatic peripheral ischemia and decreases a local site’s ability to handle infection, impaired wound healing, and wound contracture are additional secondary problems. A wound will not heal unless there are sufficient oxygen tensions for fibroblasts to function . A tissue oxygen tension of 30mmHg is required for fibroblasts to mobilize and produce the collagen matrix needed for neovascularisation and wound repair. Vasoconstriction is a secondary effect of HBO2. This leads to edema reduction. Hyperbaric oxygen exposure causes a 20% reduction in blood flow. With decreased blood flow, extravasation of fluid in the area of injury is decreased. Since capillary resorption of extracellular fluid continues, the net effect is edema reduction. Edema reduction of 20% or more has been observed in laboratory studies . Increased oxygen content in the blood from HBO2 compensates for the decreased flow. Moreover, flow in the microcirculation is improved as edema decreases and reduces external pressure around the microcirculation. HBO2 reduces the amount of skeletal muscle necrosis. It also reduces post-injury muscle necrosis and edema. HBO2 for crush injuries should be started as soon as feasible. It is also used as an adjunct for the management of compartment syndromes and other acute traumatic peripheral ischemias. We have treated many crush injuries with severe swelling, edema and infections, and the wounds completely healed.
” HBOT is an good adjuvant in Trauma and compartment syndrome after initial surgical intervention as it reduces tissue edema, increases tissue oxygenation, decreasing infection thus minimizing tissue necrosis”