Diseases & Treatments
Diseases & Treatments
This list includes conditions covered by most insurance plans. Additional conditions not listed below may be treatable and/or covered. Click a condition below to jump to that section.
Arterial gas embolism
Carbon monoxide poisoning
Chronic refractory osteomyelitis
Radiation necrosis, soft tissue radiation injury, and osteoradionecrosis
Diabetic foot wounds
Ideopathic Sudden Sensorineural Hearing Loss (ISSHL)
Central retinal artery occlusion
Decompression sickness arises from the generation of bubbles of inert gas in the tissues and/or blood caused by rapid decompression during ascent from diving, flying, or a hyperbaric/hypobaric chamber. The bubbles exert deleterious effects by several mechanisms. These include occlusion of blood flow, activation of platelets resulting in endothelial dysfunction, clot formation, capillary leakage, and white blood cell activation. Hyperbaric oxygen attacks these problems directly by compressing the bubble, oxygenating hypoxic tissue, and modulating white blood cell interaction.
Arterial gas embolism can be caused by diving accidents or medical procedures (e.g., lung biopsy or invasive vascular procedures) – hyperbaric oxygen therapy compresses the air bubbles and allows return of perfusion to compromised tissue.
Carbon monoxide poisoning is the result of binding of carbon monoxide(CO) to hemoglobin, myoglobin, and to the cytochrome system in mitochondria. Hyperbaric oxygen therapy displaces CO from the heme proteins (hemoglobin, myoglobin, cytochrome system),reverses hypoxia, prevents WBC adherence to endothelium, and reduces lipid peroxidation in the central nervous system. Candidates for therapy include those with cardiac ischemia, hypotension, altered mental status or a history of unconsciousness and coma. The thresholds for treatment are lower for pregnant women. Treatment within 6 hours of exposure has yielded the best results. Prompt treatment not only reverses the immediate effects of hypoxia but also reduces the long-term mental disability often associated with CO poisoning.
Gas gangrene is caused by necrotizing toxins released by pathologic clostridium bacteria. Elevated tissue oxygen levels from HBOT can restrict clostridium growth and halt alpha-toxin production. HBOT can also have an effect on necrotizing infections caused by organisms other than clostridia. These are generally synergistic combinations of bacteria with differing oxygen requirements. In these cases HBOT can serve as a useful adjunct to definitive surgical treatment and can also synergistically enhance antibiotic effect, often preventing the need for amputation or ablative surgery.
Crush injury involves severe trauma to bones, soft tissue, nerves, and vascular structures and often results in marginal oxygenation of peripheral tissue. In this setting, HBOT should be initiated as soon as possible to enhance support of marginally viable tissue, enhance WBC killing, and promote edema reduction. A reduction in surgery and improved tissue salvage has been demonstrated, particularly in patients more than 40 years old.
In chronic refractory osteomyelitis, periodic elevation of bone oxygen levels from hypoxic to normal or above-normal levels promotes fibroblast division, collagen production, capillary angiogenesis, increased WBC killing, and osteoclast activity. HBOT can be used as an adjunct to surgical debridement, wound care, and appropriate long-term antibiotic administration with improved outcomes.
Radiation necrosis, soft tissue radiation injury, and osteoradionecrosis share a common pathophysiology of fibroatrophic tissues, obliterative endarteritis, and hypoxia. Daily HBOT can promote capillary proliferation and the restoration of a functioning capillary bed, enhance stem cell recruitment, and reverse local hypoxia. Surgery in previously irradiated tissue is associated with a high incidence of potentially fatal complications but HBOT can mitigate these risks by promoting optimal tissue oxygenation and function. HBO is also indicated postoperatively to ensure adequate oxygenation for healing.
Compromised flaps/grafts – Hyperbaric oxygen can be used for preparing a granulating base for skin grafting where viability of a graft or flap is compromised or when previous grafts have failed. Preoperative HBO therapy is effective in promoting capillary proliferation to prepare a site in poorly granulating wounds. In selected problem wounds (e.g., diabetic ulcers, chronic nonhealing wounds), HBOT therapy can be used as an adjunct in a regimen of meticulous wound care, careful attention to nutritional status, tight glucose control, and revascularization, when indicated.
Diabetic foot wounds – Hyperbaric oxygen used as an adjunct to surgical and medical management results in increased salvage of limbs. Criteria for adjunctive hyperbaric oxygen therapy include at least 30 days of prior wound care and lack of improvement of the wound by 50% in 4 weeks. Hyperbaric oxygen therapy should be part of an aggressive team approach, including tight glucose control, infectious disease and vascular assessment, and vascular repair when indicated.
The ability to preserve a functional extremity can reduce the high cost of disability resulting from amputation. These effects appear to be long-lasting. The shortened healing time for chronic wounds reduces the cost of frequent, repeated surgical procedures. Most importantly, however, is the reduction in morbidity associated with acute and chronic tissue injury. Reversal of local ischemia with HBOT appears to be a new and useful application of this treatment in selected cases.
Thermal burns - Adjunctive HBO for thermal injury is controversial. Some burn centers experienced in its use have reported reductions in length of hospital stay, need for grafting, and mortality rates.
Reperfusion injury - Recent data suggest that HBOT may have a potent effect on ischemia reperfusion injury. This effect appears to be mediated by nitric oxide (NO) providing temporary but reversible blocking of the CD11/CD18 integrins and their binding with endothelial cellular adhesion molecules. High doses of oxygen appear to have a profound effect on this reaction, ameliorating many of the effects of reperfusion injury by increasing NO synthesis.
Ideopathic Sudden Sensorineural Hearing Loss (ISSHL) represents sudden hearing loss of 30 dB in three days over at least three contiguous frequencies. Although almost 65% of patients recover spontaneously within 2 weeks, those who do not suffer permanent disability. The exact pathophysiology of ISSHL is unclear and may be multifactorial but the common thread is the high metabolism and paucity of vascularity make the cochlea vulnerable to hypoxic injury. HBO is thought to reverse this hypoxia, restoring function to the cochlea. Recent meta-analysis by the Cochrane collaboration demonstrated HBOT as the only effective therapy of all therapies assessed. On the other hand controlled trials have also shown improved outcomes with the use of HBOT and steroids concurrently. Early utilization is also shown to enhance outcomes. Most treatment protocols do not exceed 10-20 treatments.
Central retinal artery occlusion is a relatively rare emergency condition of the eye resulting in sudden, painless vision loss. Patients particularly at risk include those with giant cell arteritis, atherosclerosis, and thromboembolic disease. The visual signs and symptoms of vascular occlusive disease are dependent on the vessel occluded. It has been demonstrated that enough oxygen can be supplied via diffusion from the coroidal circulation to maintain viability utilizing elevated partial pressures of oxygen. Patients presenting within 24 hours of symptoms should be considered for hyperbaric oxygen therapy.
The importance of nitric oxide (NO) in the wound healing process is becoming increasingly appreciated. Several investigators have also demonstrated that HBO serves as a signal transducer for the production of growth factors such as platelet-derived beta and vascular endothelial growth factor, both of which are necessary for tissue repair. Many of these reactions appear to be mediated by a direct effect of HBO at the gene level. As an understanding of these processes improves, the prescription of HBO therapy may become more precise.