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An Introduction to Hyperbaric Oxygen Therapy

An Introduction to Hyperbaric Oxygen Therapy


An Introduction to Hyperbaric Oxygen Therapy


The Undersea and Hyperbaric Medical Society has approved indications for treatment that will be listed below. These may be classified as emergent, urgent or elective.  Providers must consider the beneficial effects of HBOT and weigh them against the risks of therapy for each patient. It is imperative that the patient receives a thorough history and physical, and has the risks and benefits explained, and understands expectations of this type of therapy. Clinicians have the added obligation of familiarizing themselves with the Coding and Reimbursement guidelines for HBOT to ensure compliance with the Centers for Medicare and Medicaid Services.  



This following is an introduction to hyperbaric oxygen therapy. For more detailed information and actionable tools, please refer to specific topics within the Hyperbaric Oxygen Therapy Knowledge Base. 


The UHMS defines hyperbaric oxygen therapy as an intervention in which an individual breathes 100% oxygen intermittently while inside a hyperbaric chamber that is pressurized to greater than sea level pressure (1 atmosphere absolute, or ATA). For clinical purposes, the pressure must equal or exceed 1.4 ATA while breathing 100% oxygen. 

How the intervention works  change title and re-write

The air we breathe has approximately 21% oxygen at 14.7 pounds of pressure per square inch (psi) when measured at sea level. In the hyperbaric chamber, the atmospheric pressure can be increased to as much as 3 times normal (about 44.1 psi), with the patient breathing 100% oxygen. This increases the amount of oxygen in the blood plasma to approximately 3 times its normal levels at 1 atmosphere pressure. As a results, higher oxygen levels are delivered to end organ tissues throughout the body. This can result in many beneficial effects in a variety of disease processes that will be discussed in the paragraphs below. [1]


An Emergent indication would be defined as any medical condition in which hyperbaric oxygen therapy is the primary standard of care. The following are considered to be emergent conditions for the use of HBOT:

  Medicare Covers the above indications

An Urgent condition is a medical condition in which hyperbaric oxygen therapy is an adjunctive modality. The following are considered to be urgent conditions for the use of HBOT:

  Medicare Covers the above indications with the exception of Idiopathic Sudden Sensorineural Hearing Loss and Severe Anemia

An elective condition is a medical condition in which HBOT is utilized in a supportive care modality. The following are considered to be elective indications for the use of HBOT:

  Medicare Covers the above indications

Emergent Indications

Acute Carbon Monoxide Poisoning

The toxicity of carbon monoxide is based on a number of pathophysiological mechanisms. Carbon monoxide can cause hypoxic stress to tissues (e.g., heart or brain) leading to injury. A second mechanism of injury is thought to be through an inflammatory response to the toxic chemical. This inflammation primarily attacks brain tissue. The blood level of carbon monoxide has not correlated well with resultant neurological injuries. Administration of supplemental oxygen has long been the cornerstone of therapy for patients suffering carbon monoxide poisoning. Oxygen inhalation hastens the dissociation of CO from the hemoglobin molecule, as well as providing enhanced tissue oxygenation. Hyperbaric oxygen causes this dissociation to occur at a much greater rate than that achievable by breathing pure oxygen at ambient atmospheric pressure. In addition, HBOT has shown to be anti-inflammatory and reduces tissue injury.

Air or gas embolism

Gas embolism occurs when gas bubbles (regardless of source) enter arteries or veins. Arterial gas embolism (AGE) was classically described during submarine escape training, caused by pulmonary barotraumas during free ascent after breathing compressed gas at depth. AGE commonly occurs when a pulmonary bleb ruptures during normal SCUBA ascent, asthma with air trapping, a concussive blast injury (in or out of the water), mechanical ventilation, penetrating chest trauma, chest tube placement, or bronchoscopy. Venous gas embolism (VGE) is more rare and can occur after compressed gas diving. A large amount of venous bubbles overcome the pulmonary arterial capillary network and are passed to the left side of the heart. There are numerous causes for gas embolism outside of diving, some of which are iatrogenic accidents during invasive procedures. Hyperbaric oxygen remains the definitive treatment for gas embolism. Indications for treatment include neurological or cardiac manifestations of gas embolism in any procedure at risk. Gas bubbles can persist for many days, so a trial of hyperbaric oxygen treatments should be started on any patient with symptoms, even days after the event. Recompression and hyperbaric oxygen administration has 3 main effects: 1) decreasing bubble size, 2) oxygenation of compromised tissues, and 3) an anti-inflammatory effect. 

Decompression illness

Decompression illness (DCI) arises from the generation of bubbles of inert gas in tissue and/or blood in volumes sufficient to interfere with organ function. This state can be caused by rapid decompression during ascent from diving, flying after diving, or a hyperbaric/ hypobaric chamber exposure. Bubble formation occurs when the rate of decompression exceeds the rate at which diffusion and perfusion reduce the tissue inert gas partial pressure. There are a variety of clinical expressions of DCI, the most serious of which causes neurologic deficits as evidenced on the physical examination. The diagnosis of DCI is a diagnosis of exclusion and depends greatly upon the history and physical examination of the diver.  

A wide variety of hyperbaric regimens have been described in the medical literature. These vary in treatment pressure, time at pressure, partial pressure of oxygen, and use of other mixed gases. There have been no broad scientific studies in a prospective, randomized controlled fashion. However, the following points are generally accepted: 1) Complete resolution occurs when patients are treated early in the disease process, and 2) the US Navy oxygen treatment tables (TT6) with initial recompression to 60 fsw have been the most widely used treatments and have a high degree of success. Recompression and hyperbaric oxygen administration has 3 main effects: 1) decreasing bubble size, 2) oxygenation of compromised tissues, and 3) an anti-inflammatory effect. 

Urgent Indications

Acute peripheral arterial insufficiency

Acute peripheral arterial insufficiency covers a spectrum of diseases that includes acute traumatic and non-traumatic events sharing the common feature of sudden occlusion of the arterial blood supply. The resultant tissue hypoxia and ischemia leads to increased local concentrations of cellular byproducts, compromised microcirculation, advancing hypoxia, decreased nutrient delivery to the end tissues, vascular membrane breakdown, and edema formation. These factors threaten wound healing and contribute to advancing infectious processes.   
Hyperbaric oxygen can be beneficial in managing acute peripheral arterial insufficiency by several mechanisms: 1) Increasing tissue oxygen concentrations, thus preventing cellular death, 2) stimulating fibroblasts and macrophages to secrete collagen and enhance neovascularization, 3) reducing edema formation by reducing capillary leakage and tissue swelling, thus increasing tissue perfusion, and 4) maintaining the bacterial killing ability of leukocytes after phagocytosis. 

Acute traumatic ischemia (Trauma, Crush Injuries, Compartment Syndrome)

Acute traumatic ischemia occurs when there is a severe injury to a limb that results in compromise of the arterial blood supply or perfusion differential pressure to that limb. The immediate, emergent threat is determined by whether perfusion of the limb is sufficient to maintain viability of the tissues. Crush injuries are directly associated with trauma while skeletal muscle compartment syndromes arise from ischemia, venous outflow obstruction, exertion, external compression, or trauma. There are 3 common features: 1) ischemia and hypoxia at the injury site, 2) a gradient of injury, and 3) the potential for self-perpetuation of the injury.  

While hyperbaric oxygen is a useful adjunct to healing, surgery and aggressive medical interventions will often be required in order to manage the condition. Conditions with related pathophysiology, which are also amenable to hyperbaric oxygen therapy, include threatened flaps, grafts, re-implantations, and frostbite. 

The pathophysiology is a picture of vasogenic edema as a consequence of physical injury that is exacerbated by cytogenic edema because the injured tissues are no longer able to maintain intracellular water. When tissue oxygen tensions fall below 30 mmHg, the host responses to infection and ischemia are compromised. White blood cell phagocytic killing becomes ineffective, fibroblasts are no longer able to secrete collagen, and neovascularization cannot occur in hypoxic tissue.

Hyperbaric oxygen (at 2.4 atmospheres absolute) increases blood oxygen content and raises plasma and tissue oxygen tensions by several times over surface oxygen breathing. Hyperbaric oxygen also induces vasoconstriction (decreasing blood flow by 10-20%) in normal tissues, thus reducing edema in the injured tissues. In this indication, hyperbaric oxygen enhances oxygen concentration at the tissue level, increases oxygen delivery per unit of blood flow, and reduces edema.

gas gangrene

Gas gangrene (Also known as clostridial myositis, myonecrosis, or spreading clostridial cellulitis with systemic toxicity) is an acute, rapidly progressive, non-pyogenic, invasive clostridial infection of the muscles, characterized by profound toxemia, extensive edema, massive death of tissue, and a variable degree of gas production. The infection is caused by anaerobic, spore-forming, Gram-positive, encapsulated bacilli. The most common organism in Clostridium Perfringens, however, there are more than 150 clostridial species which can cause the disease. While there are many toxins produced in this infection, the alpha toxin (Lecithinase and Phospholipase-C) cause most of the tissue destruction.

Hyperbaric oxygen therapy increases tissue oxygen levels to more than 250 mmHg, thus reaching levels that stop alpha-toxin activity. Hyperbaric oxygen has been shown to be bacteriocidal/bacteriostatic to the Clostridium organisms. Hyperbaric oxygen should not be used alone but is adjunctive to aggressive surgical and medical management. Early hyperbaric oxygen treatment is 1) lifesaving because less heroic surgery needs to be performed, and 2) it is limb- and tissue-saving because no major amputations are performed prematurely. Hyperbaric oxygen treatments clarify the demarcation between viable and dead tissue, thus the total amount of tissue lost is greatly reduced.

Compromised Grafts & Flaps

Hyperbaric oxygen therapy is not needed for routine, uncompromised skin grafts or flaps. However, in cases where there is decreased perfusion or frank hypoxia, hyperbaric oxygen can help maximize the viability of the compromised tissue thus reducing the need for re-grafting or repeat flap procedures. There are multiple clinical studies showing the benefit of hyperbaric oxygen for failed or failing flaps and skin grafts. Types of grafts and flaps studied include pedicle flaps, random flaps, irradiated wounds and flaps, composite grafts and axial pattern flaps. Although the types of flaps and grafts are different, the common denominator to flap necrosis is tissue hypoxia. 

Hyperbaric oxygen can be beneficial in managing failing flaps and skin grafts by several mechanisms: 1) Increasing tissue oxygen concentrations, thus preventing cellular death, 2) stimulating fibroblasts and macrophages to secrete collagen and enhance neovascularization, 3) reducing edema formation by reducing capillary leakage and tissue swelling, thus increasing tissue perfusion, and 4) maintaining the bacterial killing ability of leukocytes after phagocytosis. 

Necrotizing Soft Tissue Infections

Hyperbaric oxygen therapy is an accepted adjunct to surgical and antibiotic treatment for necrotizing soft tissue infections. Such conditions may result from a combination of anaerobic and aerobic bacteria. Necrotizing infections appear in a wide variety of clinical settings, including trauma, surgical wounding, and/or foreign bodies. The patient is frequently compromised with diabetes, vasculopathy, or other immune-affecting diseases. Infections frequently cause local hypoxia and an infection-induced occlusive endarteritis. This hypoxic condition profoundly impairs white blood cell bacterial killing actions. Clinical signs of mixed soft tissue infection include tissue necrosis, a putrid discharge, gas production (often visible on x-ray), and infection burrowing through soft tissue and fascial planes. This is often seen without the typical inflammatory response in severe infections. 

Hyperbaric oxygen works by increasing local tissue oxygen levels, thus helping white cell-mediated bacterial killing and by stopping synergistic interaction present in mixed bacterial infections. Aggressive hyperbaric oxygen treatment is clearly recommended for necrotizing fasciitis, Fournier’s gangrene, crepitant anaerobic cellulitis, progressive bacterial gangrene, and non-clostridial myonecrosis (synergistic necrotizing cellulitis). 


Idiopathic Sudden Sensorineural Hearing Loss (ISSHL) is clinically defined as a hearing loss of at least 30 dB occurring within 3 days over at least 3 contiguous frequency ranges. The common presentation is unilateral hearing loss, tinnitus, a sensation of aural fullness, and dizziness or vertigo. The ear, nose, and throat surgeon will have ruled out mass lesions of the eighth cranial nerve. The specific etiologies of this syndrome remain unclear and multiple drug regimens have been used with moderate success.

Addition of hyperbaric oxygen therapy in addition to drug regimens has been shown to impart a 37.7 dB improvement in hearing in those with severe hearing loss and a 19.3 dB gain in those with a moderate hearing loss. Nine of 11 studies in the literature demonstrate positive results with the addition of HBOT to the treatment regimen. There is Class IIa evidence to support its use.

Patient selection criteria include patients with the collection of signs and symptoms above who present during the first two weeks after symptom onset. The patient should be evaluated carefully by an otolaryngologist and audiologist with appropriate imaging and hearing tests performed. In addition to appropriate medical management, hyperbaric oxygen should be administered. 


An intracranial abscess involving the brain or its membranes. It is seldom primary but usually occurs secondary to infections of the middle ear, nasal sinuses, face, or skull or from contamination from penetrating wounds or skull fractures. It may also have a metastatic origin arising from septic foci in the lungs (bronchiectasis, empyema, lung abscess), in bone (osteomyelitis), or in the heart (endocarditis). Infection of nerve tissue by the invading organism results in necrosis and liquefaction of the tissue, with edema of surrounding tissues. Brain abscesses may be acute, subacute, or chronic. Their clinical manifestations depend on the part of the brain involved, the size of the abscess, the virulence of the infecting organism, and other factors. 

The beneficial influence of HBO on increased intracranial pressure has been documented for more than 50 years. HBOT provides sufficient oxygen delivery to potentially hypoxic brain areas potentiating the effects of antibiotics. HBOT acts against specific anaerobic microorganisms as the predominant cause of intracranial abscess. [2]  


Patients who have marked blood loss of red blood cell mass by hemorrhage, hemolysis, or aplasia run the risk of lacking adequate oxygen-carrying capacity by blood. The more quickly the patient develops the anemia, the less tolerant the body is of that insult. Patients may not be able to be transfused for a variety of reasons. Common reasons include refusal of transfusion on religious grounds or inability to crossmatch blood for transfusion. 

Blood substitutes are still undergoing randomized clinical trials. No blood substitute is currently recommended for safe clinical use. Pulsed hyperbaric oxygen therapy provides a way to rectify accumulating oxygen debt in exceptional blood loss anemia when transfusion is not possible. Hyperbaric oxygen is considered adjunctive to pursuing adequate crossmatching, transfusion of red blood cells, and/or use of hematinic agents. 

Elective Indications


Patients with diabetes are at high risk for developing foot ulcers due to neuropathy and peripheral arterial occlusive disease. The pathophysiology of diabetic foot ulcers include progressive development of a sensory, motor, and autonomic neuropathy leading to loss of protective sensation, deformity causing increased plantar foot pressure, and alterations in autoregulation of dermal blood flow. Diabetes causes advanced peripheral vascular disease generally at the trifurcation level just below the knee. 

Neuropathy, vascular disease, impaired white blood cell response to infection, and cellular dysfunction all contribute to the poor clinical outcomes of diabetic foot ulcers. Despite standard wound care, these foot ulcerations can progress and are associated with cellulitis, deep tissue necrosis, abscess formation, and the development of osteomyelitis. This type of ulcer is a Wagner grade III ulcer, an equivalent of the University of Texas IIB, IID, IIIB, or IIID ulcers. Progression to frank distal foot gangrene (Wagner grade IV) or gangrene involving the whole foot (Wagner grade V) can occur. 

Hyperbaric oxygen therapy has been proven to be a beneficial adjunct to advanced wound care in diabetic foot ulcers meeting the following criteria: 1) the patient has type 1 or 2 diabetes and a lower extremity ulcer due to diabetes, 2) the ulcer is a Wagner grade III or higher, and 3) the patient has failed a 30-day standard wound therapy regimen that included assessment and attempts to correct vascular abnormalities, optimizing diabetes control, nutrition, debridement, moist wound dressing, off-loading, and treatment of underlying infection. 


Refractory osteomyelitis is a chronic osteomyelitis that persists or recurs after appropriate interventions have been performed, or where acute osteomyelitis does not respond to accepted management techniques. Hyperbaric oxygen, when combined with appropriate antibiotics, nutritional support, surgical debridement and reconstruction, provides a useful clinical adjunct in the management of refractory bone infections. Addition of hyperbaric oxygen to appropriate clinical management produces an infection arrest rate of nearly 80%. 

Hyperbaric oxygen benefits healing by enhancing bacterial killing activity of white blood cells. Next, certain antibiotics require an oxygen-mediated pathway in order to transport the medication across bacterial walls. Third, there is evidence that osteogenesis and osteoclast remodeling is an oxygen-dependent activity. Finally, osteomyelitis is characterized by both acute and chronic forms of hypoxia. Hyperbaric oxygen raises tissue levels of oxygen, decreases edema, decreases tissue hypoxia, enhances neovascularization, and supports new collagen and bone formation. 


Delayed effects of radiation are a complication of modern radiotherapy that can be treated with hyperbaric oxygen therapy. Some examples of delayed radiation effects include soft tissue radionecrosis, osteoradionecrosis, radiation cystitis, radiation proctitis, and laryngeal chondroradionecrosis. The basic pathophysiology of delayed radiation tissue damage is endarteritis with resultant tissue hypoxia and secondary fibrosis. 

Delayed radiation complications are often manifest as non-healing wounds located in previously irradiated areas and are precipitated by an additional insult such as surgery or trauma within the field of radiation. Hyperbaric oxygen has been shown to induce neovascularization and increase cellularity in irradiated, hypoxic tissues. The success with randomized controlled studies in patients with mandibular osteoradionecrosis has led to successful use of hyperbaric oxygen in other body areas affected by radiation. Dental extractions or other surgical procedures are fraught with high complication rates and a much higher incidence of non-healing when performed in heavily irradiated tissues without the benefit of preoperative hyperbaric oxygen therapy. 

Risks versus benefits

The risks and benefits of hyperbaric oxygen therapy should be discussed with each patient. 

The benefits include: 

  • Reduction in the volume of blood’s and tissue’s gas bubble, improved tissue oxygenation and acceleration of nitrogen elimination from the tissues  
  • Raising the tissue oxygen levels in order to enhance healing of difficult wounds thru neovascularization.
  • Raising the tissue oxygen levels to reverse toxic effects of chemicals and inhaled gases. 
  • Improved post-ischemic tissue survival after reperfusion. 
  • Bacteriostatic and bacteriocidal effects
  • Prevention of bone loss from hypoxic bone lesions [2]  

Potential risks include:

  • Ear, sinus, tooth, or pulmonary barotraumas. This can result in pain and discomfort in the ears, sinuses, or teeth, and rarely to pneumothorax of the lung
  • There are several potential eye changes, most commonly slight worsening of far vision with improvement of near vision. This is reversible without intervention in most cases. Rarely, certain types of cataracts may mature more quickly than in patients not treated with hyperbaric oxygen. 
  • There is a remote risk of fire. Prohibited items that will not be allowed into the chamber at any time. 
  • There is the risk of oxygen toxicity that can be manifest as a seizure or lung changes. 
  • confinement anxiety [2] 



Due to Trapped Gas

  • Pneumothorax (unvented) 
  • Intraocular Gas (except for bubble manifestation with decompression sickness)
  • Hollow orbital prosthesis
  • Acute severe bronchospasm unresolved
  • Other rare, gas-filled structures that might develop gas trapping [2] 

Due to Oxygen Toxicity

  • Bleomycin- concurrent use with HBO should be avoided
  • Doxorubicin- concurrent use with HBO should be avoided [2] 

Relative Risks

 Due to trapped Gas

  • Chronic Obstructive Pulmonary Disease, specifically emphysema
  • Recent pneumothorax
  • History of spontaneous pneumothorax
  • Chest surgery/trauma
  • Dental problems: cavities, incomplete or cracked root fillings [2] 

Due to Oxygen Toxicity

  • Optic Neuritis if acute
  • Retrobulbar optic neuritis
  • Retinopathy of prematurity
  • Current Bleomycin
  • Current Doxorubicin [2]  

Due to Pressure Change

  • Acute upper Respiratory Infection
  • Otitis Media- Inability to equalize middle-ear pressure
  • Mastoidectomy- Inability to equalize middle-ear pressure
  • Cochlear implant- malfunction of internal components
  • Implanted devices- pacemakers, defibrillators, shunts-malfunction [2] 

Various other Systemic effects


How to explain an HBO intervention to your patients

Below is a brief outline:

"The treatment is painless. At the beginning and end of your treatment, you may notice a feeling of “fullness” in your ears, very much like the feeling when changing altitude in an airplane, driving in the mountains or diving underwater. As your eardrums respond to the changing pressure, you may hear “popping” or “crackling” noises. It is not usually painful, but if you do not fully clear your ears, you may develop an earache. To clear or pop your ears, you will have a water bottle with you in the chamber to help you swallow. We may also treat you with a decongestant spray before each treatment.

After entering the chamber, the door is closed and compression of the oxygen inside begins. You may feel warm for a moment until you reach the desired depth of treatment. After 10 to 15 minutes, compression is complete and the usual feeling of fullness in your ears will disappear. You will continue breathing oxygen for 90 minutes. After 90 minutes, the treatment will come to an end. You may again notice a “popping” or fullness in your ears. If you wear glasses for reading, you may have a few weeks in which you can read without your glasses. If your eyes are normal, your reading vision may temporarily worsen. This does not hurt in any way and is temporary. Do not discard your old corrective lenses.

Heart rhythm is routinely monitored on all patients for the first treatment. For patients with a preexisting heart condition, monitoring may be done with each treatment. If you are diabetic, your blood sugar will need to be taken before and after each treatment."

Hyperbaric Oxygen Therapy patient education materials



Medicare Administrative Contractor (MAC)                                National or Local Coverage Determination (NCD) (LCD)
Novitas Solutions, Inc. LCD Hyperbaric Oxygen (HBO) Therapy (L35021)[3]
CGS Administrators, LLC NCD 20.29 [4]
First Coast Service Options, Inc. (FCSO) LCD Hyperbaric Oxygen (HBO) Therapy (L36504)[5]
Noridian NCD 20.29 [4]
Wisconsin Physicians Service Insurance Corporation (WPS) NCD 20.29 [4]
National Government Services, Inc. (NGS) NCD 20.29 [4]
Cahaba NCD 20.29 [4]
Palmetto  NCD 20.29 [4]

More details on requirements, medical necessity and documentation in specific Medicare National and Local Coverage Determinations (if available). To go to NCD or LCD, click on the reference number and on the reference page, click on the green button "View Source Site".

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NOTE: This is a controlled document. This document is not a substitute for proper training, experience, and exercising of professional judgment. While every effort has been made to ensure the accuracy of the contents, neither the authors nor the Wound Reference, Inc. give any guarantee as to the accuracy of the information contained in them nor accept any liability, with respect to loss, damage, injury or expense arising from any such errors or omissions in the contents of the work.


  1. National Baromedical Services. Introduction to Hyperbaric Medicine Primary Training Manual .;.
  2. Harry T. Whelan, Eric Kindwall et al. Hyperbaric Medicine Practice 4th Edition Best Publishing Company. 2017;.
  3. Novitas Solutions, Inc et al. Local Coverage Determination for Hyperbaric Oxygen (HBO) Therapy (L35021) . 2015;.
  4. CMS. National Coverage Determination (NCD) for Hyperbaric Oxygen Therapy (20.29) . 2017;.
  5. First Coast Service Options, Inc. et al. Local Coverage Determination Hyperbaric Oxygen (HBO) Therapy (L36504) . 2016;.
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