Hyperbaric oxygen therapy (HBOT) is a mode of medical treatment that allows a patient to breathe 100% oxygen while sitting comfortably in a chamber at pressures greater than normal atmospheric (sea level).
Oxygen is the key substrate for metabolism. The average adult on a daily basis consumes about three pounds of food, three pounds of fluids, and almost six pounds of oxygen (about 2 pounds gets into the blood for transport to tissue cells). Oxygen is required to complete the energy cycle that sustains life. Many serious health problems (e.g. diabetic foot ulcers) stem from, or are complicated by, tissue hypoxia. Oxygen under increased pressure can correct this deficiency. Breathing oxygen while in a hyperbaric environment (chamber) dramatically increases the amount of oxygen dissolved in the blood plasma. This, in turn, allows more oxygen to get into tissues. It is noteworthy that, while medical education teaches that increased oxygen causes oxidative damage, it is the contrary (a lack of oxygen) which is damaging to cells. Hypoxia creates oxygen free radicals, while oxygen protects tissues from free radical damage. An inadequate oxygen supply to tissues results in the catabolism of ATP, resulting in the production of adenosine and xanthine (an electron donor). Thus, hypoxia causes a cascade of interactions that generates hydroxyl ions, which damage membranes and draw calcium into the cells. Lactic acidosis from hypoxia points to hypoxic tissue damage. Correcting hypoxia will limit this free radical formation. Reperfusion injury occurs after an episode of poor circulation is corrected, but poorly oxygenated blood flow ensues. If the patient gets hyperbaric oxygenation, a dramatic reduction in reperfusion injury occurs.
Hemoglobin can only carry a limited amount of oxygen. Red blood cells can only deliver a limited level of oxygen to tissue cells in times of crisis. This level, referred to as oxygen tension (or oxygen partial pressure, "pO2"), is measured in mmHg. Healthy blood circulation provides a tissue pO2 of 39 mmHg or less. Injuries, infections, and diseases can drop this vital tissue oxygen level down to almost zero. With aging, we can loose vital lung capacity and the ability to meet our oxygen requirements. Some diseases impair oxygen utilization. Injuries (or other conditions with associated tissue swelling) can result in decreased circulation. This reduction in blood flow, or ischemia, diminishes oxygen circulation (delivery) to the affected areas. Consequently, pO2 drops dangerously low, resulting in tissue destruction and slowed healing. The body's normal response to tissue damage includes the mobilization of scavenger cells (or histocytes), which requires adequate oxygen availability. Optimal tissue healing, after such an injury, occurs when pO2 rises to between 50 and 80 mmHg. Sustained periods of these levels can only be attained through use of hyperbaric oxygen therapy.
At 1ATA (760mmHg) at 21% O2 - Normal Conditions
PaO2 = ((760-47) X .21) - (40/0.8)
= (713 X .21) - 50
= 100 mmHg
At 2.0 ATA (1520mmHg) at 100% O2 - Under Hyperbaric Conditions
PaO2 = ((1520-47) X 1.00) - (40/0.8)
= (1473 X 1.0) -50
= 1423 mmHg
Over time (usually 4 to 6 hours), these elevated levels return to baseline. It is during these periods of elevated tissue oxygen levels that enhanced healing occurs. Therefore, to continue the healing process, daily treatments are advised.
Beneficial Mechanisms of Hyperbaric Oxygen Therapy
1. 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 produces a four fold increase in the distance capillary oxygen can diffuse into the tissue.
2. NEOVASCULARIZATION represents an indirect response to hyperbaric oxygen exposure. Therapeutic effects include enhanced fibroblast division, formation of collagen and capillary angiogenesis in tissues with sluggish neovascularization such as late radiation damaged tissue, refractory osteomyelitis, and chronic ulcers.
3. ANTIMICROBIAL ACTIVITY has been demonstrated to improve with hyperbaric oxygen therapy. Hyperbaric oxygen causes toxin inhibition and inactivation in Clostridia porringers infections (gas gangrene). Hyperoxia enhances phagocyte and white cell oxidative killing, and has been shown to enhance amino glycoside activity. Recent research has demonstrated a prolonged post-antibiotic effect when hyperbaric oxygen is combined with tobramycin against Pseudomonas aeroginosa. HBOT stimulates an increase in superoxide dismutase, thus producing antioxidants and free radical scavengers. This greatly aids in the treatment of infections by enhancing white blood cell action and potentiating germ-killing antibiotics.
4. DIRECT PRESSURE follows Boyles Law. This mechanism is the basis for the efficacy of hyperbaric oxygen therapy in the treatment of decompression sickness and cerebral arterial gas embolism (CAGE).
5. VASOCONSTRICTION (Hyperoxia-induced) is another important mechanism. It occurs without hypoxia, and is helpful in managing compartment syndrome and other conditions associated with local edema. Examples include interstitial edema surrounding graft sites and non-healing ulcers. Studies have shown significant decreases in fluid resuscitation requirements when HBOT is added to standard burn wound management protocols.
Medical Indications for Hyperbaric Oxygen Therapy
The Undersea and Hyperbaric Medical Society (UHMS) has recognized 15 medical indications for hyperbaric oxygen therapy (HBOT). These are covered by Medicare, Medicaid, and commercial insurances.
1. Acute Carbon Monoxide Poisoning
2. Decompression Sickness
3. Gas Embolism
4. Gas Gangrene
5. Acute Traumatic Peripheral Ischemia
6. Progressive Necrotizing Infections
7. Crush Injuries of Severed Limbs
8. Acute Peripheral Arterial Insufficiency
9. Cyanide Poisoning
11. Diabetic Wounds of the Lower Extremity with Inclusion Criteria:
1. Failed Standard Care for 30 days
2. Wagner Grade III or Higher
12. Chronic Refractory Osteomyelitis
13. Soft Tissue Radionecrosis
15. Preservation/Preparation of Failed Skin Graft
*Highlighted diagnoses comprise the majority of indications treated by Mobile Hyperbaric Centers.
Current protocol for treatment of mandibular ORN according to Marx
Stage I: Perform 30 HBO dives (1 dive per day, Monday-Friday) to 2.4 atmospheres for 90 minutes. Reassess the patient to evaluate decreased bone exposure, granulation tissue covering exposed bone, resorption of nonviable bone, and absence of inflammation. For patients who respond favorably, continue treatment to a total of 40 dives. For patients who are not responsive, advance to stage II.
Stage II: Perform transoral sequestrectomy with primary wound closure followed by continued HBO to a total of 40 dives. If wound dehiscence occurs, advance patients to stage III. Patients who present with orocutaneous fistula, pathologic fracture, or resorption to the inferior border of the mandible advance to stage III immediately after the initial 30 dives.
Stage III: Perform transcutaneous mandibular resection, wound closure, and mandibular fixation with an external fixator or maxillomandibular fixation, followed by an additional 10 postoperative HBO dives.
Stage IIIR: Perform mandibular reconstruction 10 weeks after successful resolution of mandibular ORN. Marx advocates the use of autogenous cancellous bone within a freeze-dried allogeneic bone carrier. Complete 10 additional postoperative HBO dives.