Archived Policies - Therapy


Hyperbaric Oxygen (HBO2) Therapy

Number:THE801.003

Effective Date:07-15-2017

End Date:09-30-2018

Coverage:

*CAREFULLY CHECK STATE REGULATIONS AND/OR THE MEMBER CONTRACT*

Medical policies are a set of written guidelines that support current standards of practice. They are based on current peer-reviewed scientific literature. A requested therapy must be proven effective for the relevant diagnosis or procedure. For drug therapy, the proposed dose, frequency and duration of therapy must be consistent with recommendations in at least one authoritative source. This medical policy is supported by FDA-approved labeling and nationally recognized authoritative references. These references include, but are not limited to: MCG care guidelines, Hayes, DrugDex (IIb level of evidence or higher), NCCN Guidelines (IIb level of evidence or higher), NCCN Compendia (IIb level of evidence or higher), professional society guidelines, and CMS coverage policy.

ALERT: Health Care Services Corporation (HCSC) has created a form to facilitate review of requests for coverage of HBO2 therapy, located on the “Provider / Forms” page of each HCSC web site, i.e., BCBSIL.com, BCBSMT.com, BCBSNM.com, BCBSOK.com, or BCBSTX.com.

Therapy with topical hyperbaric oxygen (THBO2) pressurization for any indication or clinical condition is considered experimental, investigational and/or unproven.

Therapy with systemic hyperbaric oxygen (HBO2) pressurization may be considered medically necessary for the medical conditions and circumstances listed below. ALL requests and claims must include documentation of medical necessity.

ALL the following documentation requirements for systemic HBO2 pressurization therapy MUST accompany requests and claims for treatment:

When services are in excess of 1-month duration, AND/OR when services are in excess of the number of treatments listed in the grid below or listed as individual consideration; AND

Documentation must include AT LEAST TWO of the following:

1. Photo record(s), or

2. Consultation reports, or

3. Operative or treatment reports and/or other applicable hospital records (e.g., pathology report, history and physical), or

4. Office records; AND/OR

Documentation of wounds only, should include the following:

1. Primary diagnosis,

2. Secondary diagnosis,

3. Contributing factors to the primary diagnosis,

4. Co-morbid factors,

5. Prior therapy,

6. Wound description (cause, location, measurements [size, depth, undermining, granulation]),

7. Wagner classification system grade level (see NOTE 1 below in grid), AND

8. Whether this is initial treatment or extension of treatment.

ALERT: The prior approval process may be a useful method of establishing medical necessity.

The medical conditions and circumstances that may be considered medical necessary are listed in the grid below. This includes the number of treatments initially allowed for each approved condition. Approval of treatment or services beyond the number initially authorized requires review of pertinent medical record documentation. Additional information about these requirements is contained within the policy document.

IF THE MEDICALLY NECESSARY DIAGNOSIS IS:

THEN REVIEW (1) :

Diabetic wounds, which include foot wounds or marginally perfused wounds, are considered non-healing of the lower extremities in diabetic patients who meet ALL the following three criteria:

Patient has type I or type II diabetes and has a lower extremity wound that is due to diabetes, AND

Patient has a wound classified as Wagner grade-3 or higher (see NOTE 1), AND

Patient has no measurable signs of healing after 30 days of an adequate course of standard wound therapy.

Acute postoperative foot surgical treatment for patients with Wagner grade-3 or higher diabetic foot ulcers.

NOTE 1: The Wagner classification system of wounds is defined as follows:

Grade-0 = no open lesion;

Grade-1 = superficial ulcer without penetration to deeper layers;

Grade-2 = ulcer penetrates to tendon, bone, or joint;

Grade-3 = lesion has penetrated deeper than grade-2 and there is abscess, osteomyelitis, pyarthrosis, plantar space abscess, or infection of the tendon and tendon sheaths;

Grade-4 = wet or dry gangrene in the toes or forefoot; and,

Grade-5 = gangrene involves the whole foot or such a percentage that no local procedures are possible and amputation (at least at the below the knee level) is indicated.

NOTE 2: Treatments are usually given daily for 90- to 120-minutes. The initial treatment depends on severity of disease. More serious diabetic wounds may require twice daily treatments; and once stabilized treatments may be done once daily.

After 30 treatments.

(see NOTE 1 and NOTE 2 to the left)

Chronic refractory osteomyelitis.

After 30 treatments.

Soft-tissue radiation necrosis (i.e., radiation enteritis, cystitis, proctitis) and osteoradionecrosis (ORN).

NOTE 3: For soft-tissue radiation necrosis, review is required after each 20 treatments. Treatments are usually given daily for 90 to 120 minutes. Beyond 60 treatments, individual consideration is applied.

NOTE 4: For ORN, the initial course of treatment for patients with Stage I osteoradionecrosis include HBO2 followed by débridement. Stage II, if the patients are not responding, more extensive débridement, followed by additional HBO2. For patients presenting at Stage III, HBO2 is started followed by mandibular segmental resection with additional HBO2 therapy. Beyond the initial therapy course, individual consideration is applied.

After 20 treatments.

(see NOTE 3 and NOTE 4 to the left)

Crush injury, reperfusion injury, compartment syndrome, and other acute traumatic ischemias.

NOTE 5: Three treatments per day for 48-hours followed by two treatments per day over the second 48-hours and one treatment per day over the third period of 48-hours. Beyond this time period, individual consideration is applied.

After 12 treatments.

(see NOTE 5 to the left)

Venous stasis ulcer, only if venous surgery, local wound care, leg elevation, counterpressure support, and skin grafting fails for patients who have a wound classified as Wagner grade-3 or higher (see NOTE 1).

NOTE 1: The Wagner classification system of wounds is defined as follows:

Grade-0 = no open lesion;

Grade-1 = superficial ulcer without penetration to deeper layers;

Grade-2 = ulcer penetrates to tendon, bone, or joint;

Grade-3 = lesion has penetrated deeper than grade-2 and there is abscess, osteomyelitis, pyarthrosis, plantar space abscess, or infection of the tendon and tendon sheaths;

Grade-4 = wet or dry gangrene in the toes or forefoot; and,

Grade-5 = gangrene involves the whole foot or such a percentage that no local procedures are possible and amputation (at least at the below the knee level) is indicated.

After 12 treatments.

(see NOTE 1 to the left)

Compromised skin graft or flap, or for enhancement of healing in a selected problem wound.

After 12 treatments.

Gas gangrene (i.e., clostridial myonecrosis) and includes Meleney's postoperative gangrene ulcer.

NOTE 6: Treatments may be as often as three during the first 24-hours for 90-minutes, then 2-sessions per day for the next 2- to 5-days, depending on the patient’s initial response.

After 10 treatments.

(see NOTE 6 to the left)

Soft tissue infections due to mixed aerobic and anaerobic organisms with tissue necrosis and refractory bacteroides infections.

After 10 treatments.

Decompression sickness.

NOTE 7: Treatment times vary; depending on length of time elapsed between symptoms and initiation of treatment and between residual symptoms after initial treatment. The majority of cases respond to a single treatment. Usual time between treatments ranges from 90-minutes to 14-hours. Repetitive treatments may be necessary, depending on the patient’s response.

After 10 treatments.

(see NOTE 7 to the left)

Acute air or gas embolism.

After 10 treatments.

Brown recluse spider bite.

After 5 treatments.

Acute carbon monoxide poisoning (intoxication) and smoke inhalation (not chronic) and may be complicated by cyanide poisoning.

NOTE 8: Treatments will vary based on persistent neurologic dysfunction after the initial treatment and may be as frequent as once or twice daily, until there is no additional improvement in cognitive function.

After 5 treatments.

(see NOTE 8 to the left)

Thermal burns, second or third degree burns involving 15% to 90% of total body surface and initiated within 24 hours of the burn injury.

After 5 treatments.

Idiopathic sudden sensorineural hearing loss (ISSNHL).

After 5 treatments.

Acute cyanide poisoning, and may be complicated by carbon monoxide poisoning.

NOTE 8: Treatments will vary based on persistent neurologic dysfunction after the initial treatment and may be as frequent as once or twice daily, until there is no additional improvement in cognitive function.

For individual consideration of number of treatments.

(see NOTE 8 to the left)

Exceptional blood loss anemia (profound/severe), as the result of class IV hemorrhage, HBO2 is indicated when the patient will not accept blood replacement for medical or religious reasons and the following symptoms are present:

  • Shock, systolic blood pressure below 90 mm Hg, or pressure maintained by vasopressors; and
  • Disorientation to coma; and
  • Ischemic changes of the myocardium as demonstrated on the electrocardiogram (EKG); and
  • Ischemic gut.

NOTE 9: HBO2 therapy is continued as needed and discontinued when the red blood cells have been replaced in numbers to alleviate the precipitating signs and symptoms.

For individual consideration of number of treatments.

(see NOTE 9 to the left)

Selected refractory mycoses (mucormycosis, actinomycosis, or canibolus coronato).

For individual consideration of number of treatments.

Intracranial abscess.

For individual consideration of number of treatments.

Acute cerebral edema.

For individual consideration of number of treatments.

Arterial insufficiency ulcer (not acute) which persists after reconstructive surgery has restored large vessel perfusion (includes peripheral vessels).

For individual consideration of number of treatments.

Decubitus ulcers.

For individual consideration of number of treatments.

Pre- and post-treatment for patients undergoing dental surgery (non-implant-related) of an irradiated jaw.

For individual consideration of number of treatments.

Special Comment: A course of treatment may range from less than one week to several months’ duration, depending on the severity of the patient's condition and response to therapy. The average length of treatment is two to four weeks.

Systemic HBO2 pressurization therapy is considered experimental, investigational and/or unproven, including but not limited to the following indications or clinical conditions and any diagnosis not previously listed as covered:

Actinic keratosis (AK) or actinic skin damage;

Amyotrophic lateral sclerosis;

Arterial peripheral insufficiency, acute;

Asthma;

Autistic spectrum disorders;

Avascular necrosis;

Bell’s palsy;

Bone grafts;

Carbon tetrachloride poisoning, acute;

Cardiogenic shock;

Cerebral palsy;

Cerebrovascular accident (CVA), acute thrombotic or embolic, or chronic;

Coronary syndromes, acute, and as an adjunct to coronary interventions, including but not limited to percutaneous coronary interventions (PCI) and cardiopulmonary bypass;

Depression;

Fibromyalgia;

Fracture healing;

Spinal cord injury, traumatic;

Hepatic necrosis;

Hepatitis;

Herpes zoster;

Human immunodeficiency virus infection or acquired immune deficiency syndrome (HIV/AIDS);

Hydrogen sulfide poisoning;

Idiopathic femoral neck necrosis;

Ileus, postoperative;

Inflammatory bowel disease, including Crohn’s disease (CD), severe or refractory or ulcerative colitis;

Intra-abdominal abscesses;

In vitro fertilization;

Ischemic stroke, acute;

Lepromatous leprosy;

Lyme disease;

Lymphedema of arm, chronic, following radiotherapy for cancer;

Meningitis;

Mental illness, generalized anxiety disorder or depression;

Migraine or cluster headaches;

Motor dysfunction associated with stroke;

Multiple sclerosis;

Muscle soreness, delayed onset or sport’s injury;

Myocardial infarction (MI), acute;

Organ transplantation or storage;

Osteoarthritis;

Osteomyelitis, acute;

Osteonecrosis of the jaw, bisphosphonate-related;

Pancreatitis, acute;

Parkinson’s disease;

Post-traumatic stress disorder (PTSD), traumatic brain (head) injury (TBI) or other stress disorders;

Pseudomembranous colitis, antimicrobial agent-induced colitis;

Pulmonary emphysema;

Pyoderma gangrenosum;

Radiation-induced injury to head, neck, anus, or rectum (except proctitis);

Radiation necrosis of non-neurologic tissue;

Radiation-myelitis;

Radiation therapy, adverse effects, at any point of therapy, including early onset effects and delayed effects (i.e., extremity lymphedema associated with cancer radiation);

Retinal artery insufficiency, acute within the first 24 hours of diagnosis;

Retinopathy, as an adjunct to scleral buckling procedure in patients with sickle cell peripheral retinopathy and retinal detachment;

Rheumatoid arthritis;

Sickle cell crisis (SCC) and/or hematuria;

Senility;

Septicemia, anaerobic (unrelated to clostridial), or systemic aerobic infection;

Surgical and traumatic wounds, acute;

Sudden deafness (unrelated to ISSNHL);

Tetanus;

Tumor sensitization for cancer treatments includes but not limited to, radiotherapy or chemotherapy; AND

Vascular dementia or chronic brain syndromes, neovascular causes (such as Pick’s disease, Alzheimer’s disease, and Korsakoff’s disease).

Description:

Hyperbaric oxygen (HBO2) pressurization therapy is a technique of delivering higher pressures of oxygen (O2) to the tissues. Two methods of delivery are available, systemic and topical.

Background

In systemic or large HBO2 chamber, the patient is entirely enclosed in a pressure chamber and breathes pure 100% O2 at a pressure greater than 1 atmosphere (atm) (the pressure of O2 at sea level). Thus, this technique relies on systemic circulation to deliver highly oxygenated blood to the target site, typically a wound. In addition, systemic HBO2 therapy can be used to treat systemic illness such as air or gas embolism, carbon monoxide poisoning, clostridial gas gangrene, etc. Treatment may be carried out either in a monoplace (single patient unit) chamber pressurized with pure O2 or in a larger, multiplace (multiple patient unit) chamber pressurized with compressed air, in which case the patient receives pure O2 by mask, head tent, or endotracheal tube. A cycle of pressurization, with or without air breaks, inside an HBO2 chamber may be called “a dive”, which may last for 90 minutes or more. (NOTE: Breathing 100% O2 at one atmosphere without the use of a pressurized chamber is not considered to be HBO2 pressurization.)

Systemic HBO2 is a generally accepted medical treatment. HBO2 services include both consultative and therapeutic services. The HBO2 physician, certified by the American College of Hyperbaric Medicine (ACHM) and American College of Preventive Medicine (ACPM), must be actively present during all treatments.

Topical HBO2 (THBO2) therapy is a technique of delivering 100% O2 directly to an open, moist wound at a pressure slightly higher than atmospheric pressure. It is hypothesized that high concentrations of O2 diffused directly into the wound, increases the local cellular O2 tension, which in turn promotes wound healing. THBO2 devices consist of an appliance to enclose the wound area (frequently an extremity) and a source of O2. The appliances may be disposable and have been used without supervision in the home. THBO2 therapy has been investigated as a treatment of skin ulcerations due to diabetes, venous stasis, postsurgical infection, gangrene, decubitus, compromised amputations or skin grafts, burns, and frostbite. THBO2 may be performed in the provider office, clinic, or may be self-administered by the patient at home. Typically, the therapy is offered for 90 minutes per day for 4 consecutive days. After a 3-day break, the cycle is repeated. This regimen may last for 8- to 10-weeks.

Regulatory Status

In February 1999, the Numobag™ Kit (Numotech Inc., Woodland Hills, CA) for application of topical hyperbaric therapy was cleared for marketing by the U.S. Food and Drug Administration (FDA) through the 510(k) process. The FDA determined that this device was substantially equivalent to existing devices. The most recent topical oxygen therapy delivery devices to be approved are the Natrox™ Topical Oxygen Delivery System (Inotec Amd Ltd.) and Epiflo® (Neogenix LLC). Both of these devices were approved in 2012. FDA Product Code: KPJ.

In May 2005, the ATA Monoplace Hyperbaric System (ATA Hyperbaric Chamber Manufacturing Inc.) was cleared for marketing by the FDA through the 510(k) process. The FDA determined that this device was substantially equivalent to existing hyperbaric devices. FDA Product Code: CBF.

In 2013, the FDA published a statement warning that non-FDA approved uses of HBO2 therapy may endanger the health of patients. (1) If patients mistakenly believe that HBO2 therapy devices have been proven safe for uses not cleared by the FDA, they may delay or forgo proven medical therapies.

Rationale:

Created in May 1990, the original policy on systemic hyperbaric oxygenation or hyperbaric oxygen (HBO2) pressurization was based upon a search of the MedLine database and subsequently on the 1996 guidelines published by the Undersea and Hyperbaric Medical Society (UHMS). Subsequently, the UHMS has updated their guidelines periodically, with the last publication released in 2015. (1) The most recent literature search of MedLine was performed through July 2016. The following is a summary of the key literature reviewed to date.

Assessment of efficacy for therapeutic interventions involves a determination of whether the intervention improves health outcomes. The optimal study design for a therapeutic intervention is a randomized controlled trial (RCT) that includes clinically relevant measures of health outcomes. Intermediate outcome measures, also known as surrogate outcome measures, may be adequate if there is an established link between the intermediate outcome and true health outcomes. When the primary outcomes are subjective (e.g., pain, depression), sham-controlled RCTs are needed to assess the effect of the intervention beyond that of a placebo effect.

Topical Hyperbaric Oxygen (THBO2)

Due to the different methods of delivery, topical and systemic HBO2 are distinct technologies such that they must be examined separately. At the time of initial policy development, there was minimal published literature on THBO2 therapy. The literature on THBO2 primarily includes case reports or small uncontrolled case series. (2, 3) There is 1 small RCT that included 18 patients with diabetic foot ulcers who were assigned to receive either topical hyperbaric therapy plus standard wound care or standard wound care alone. (4) Changes in ulcer size and depth did not differ between the 2 groups.

Systemic Hyperbaric Oxygen (HBO2)

Since the original policy on THBO2 was created, the policy on systemic HBO2 therapy was based entirely on the 1996 guidelines published by the UHMS and was subsequently revised in 1999 based on 3 Blue Cross Blue Shield Association (BCBSA) Technology Evaluation Center (TEC) TEC Assessments. (5-7) The BCBSA TEC Assessments had conclusions similar to UHMS, except, in contrast to the UHMS guidelines, they stated that there was insufficient evidence to conclude that HBO2 therapy improved the net health outcome for the following indications:

Compromised skin grafts,

Acute thermal burns,

Chronic refractory osteomyelitis,

Necrotizing soft tissue infections,

Brown recluse spider bites.

The BCBSA TEC Assessments also stated that there was insufficient evidence to permit conclusions on the use of HBO2 therapy for treatment of brain injury, spinal cord injury, and Crohn’s disease, indications not addressed by the 1996 UHMS Guidelines. Literature updates have focused on identifying new RCTs and meta-analyses of RCTs, particularly on indications considered experimental, investigational and/or unproven at the time of the update.

Chronic Wounds

Several systematic reviews of RCTs have been published. A Cochrane review of RCTs on HBO2 treatment for chronic wounds was published by Kranke et al. in 2012. (8) The authors identified 9 RCTs, with a total of 471 participants that compared the effect of HBO2 therapy on chronic wound healing with an alternative treatment approach that did not use HBO2 therapy. Eight of the 9 trials included in the review evaluated HBO2 therapy in patients with diabetes. The remaining trial addressed HBO2 for patients with venous ulcers; that study had only 16 participants and the comparator treatment was not specified. In a pooled analysis of data from 3 trials, a significantly higher proportion of ulcers had healed at 6 weeks in the group receiving HBO2 than the group not receiving HBO2 therapy (risk ratio [RR], 5.20; 95% confidence interval [CI], 1.25 to 21.7). Pooled analyses, however, did not find statistically significant differences between groups in the proportion of ulcers healed at 6 months (2 trials) or 12 months (3 trials). There were insufficient data to conduct pooled analyses of studies evaluating HBO2 therapy for treating patients with chronic wounds who did not have diabetes.

In 2013, O’Reilly et al. published a systematic review of studies on HBO2 therapy for treatment of diabetic ulcers. (9) The authors identified 6 RCTs and 6 non-RCTs that compared HBO2 therapy with standard wound care or sham therapy in patients with diabetes who had nonhealing lower-limb ulcers. Pooled analyses of observational studies found statistically significant benefits of HBO2 therapy on rates of major amputation, minor amputation, and the proportion of wounds healed at the end of the study period. However, in pooled analyses of RCT data, the stronger study design, there were no statistically significant differences between groups on key outcomes. This included the rate of major amputation (RR=0.40; 95% CI, 0.07 to 2.23; p=0.29), minor amputation (RR=0.79; 95% CI, 0.19 to 3.30, p=0.75), and the proportion of unhealed wounds at the end of the study period (RR=0.54, 95% CI, 0.26 to 1.13, p=0.1).

Systematic reviews have had mixed findings on the impact of HBO2 therapy on diabetic ulcers. A Cochrane review found short-term, but not long-term benefit on wound healing, and a 2013 meta-analysis did not find significant benefits of HBO2 therapy on outcomes in RCTs, but did find an effect in non-RCTs. There is insufficient evidence on HBO2 therapy for treatment of chronic wounds (excluding venous stasis ulcers) in patients without diabetes.

Acute Surgical and Traumatic Wounds

In 2013, an updated Cochrane review of RCTs on HBO2 therapy for acute surgical and traumatic wounds was published by Eskes et al. (10) HBO2 therapy was defined as use of 100% oxygen at pressures above 1 atm (atmosphere). To be included, studies needed to compare HBO2 therapy with a different intervention or compare 2 HBO2 therapy regimens; in addition, studies needed to objectively measure wound healing. A total of 4 met the review’s inclusion criteria. The studies ranged in size from 10 to 135 participants. Due to differences among studies in terms of patient population, comparison intervention, outcome measurement, etc., study results could not be pooled. The primary outcome examined by Cochrane reviewers, wound healing, was not reported in either of the 2 trials comparing HBO2 therapy with usual care and was not reported in the 1 trial comparing HBO2 therapy with dexamethasone or heparin. Complete wound healing was reported in the 1 RCT comparing active HBO2 therapy with sham HBO2 therapy. In this small study (n=36), there was a statistically higher rate of wound healing in the group; the time point for outcome measurement in this study was unclear. In the sham-controlled study, there was no statistically significant difference between groups in the mean-time to wound healing.

Another 2014 systematic review of studies on HBO2 therapy for acute wounds, published by Dauwe et al., included RCTs and non-RCTs. (11) The review included 8 studies, with sample sizes ranging from 5 to 125 patients. Four studies were randomized, 3 were prospective non-RCTs, and 1 was a retrospective non-RCT. As in the Eskes systematic review, data were not pooled. The authors noted that 7 of the 8 studies reported achieving statistical significance in their primary end points, but the end points differed among studies (e.g., graft survival, length of hospital stay, wound size). Moreover, the studies were heterogeneous in terms of treatment regimens, patient indications (e.g., burns, face lifts), and study designs, making it difficult to draw conclusions about the effect of HBO2 therapy on acute wound treatment.

There is insufficient evidence supporting HBO2 therapy for treatment of acute wounds; additional evidence from high-quality RCTs is needed.

Carbon Monoxide Poisoning

A 2011 Cochrane review of 7 RCTs concluded that the available evidence is insufficient to determine whether adverse neurologic outcomes in patients with carbon monoxide poisoning are reduced with HBO2 therapy. (12) In 2008, the American College of Emergency Physicians (ACEP) published a clinical policy on critical issues in carbon monoxide poisoning. (13) Their literature review indicated there was only Level C evidence (preliminary, inconclusive, or conflicting evidence) for treatment of acute carbon monoxide poisoning. The 2008 UHMS guidelines, however, list carbon monoxide poisoning as an indication for HBO2 therapy.

Two blinded randomized trials were discussed in both the Cochrane and ACEP reviews. One is a study by Scheinkestel et al., a double-blind, RCT comparing HBO2 therapy with normobaric oxygen in patients with carbon monoxide poisoning. (14) The authors reported that HBO2 therapy did not benefit patient outcomes of neuropsychologic performance when HBO2 therapy was completed and at 1-month follow-up. This study was limited, however, by a high rate (46%) of patients who were lost to follow-up. Moreover, the trial has been criticized for administrating 100% normobaric oxygen for at least 72 hours between treatments, which has been called a toxic dose of oxygen. (17) The critiques also mention that there was an unusually high rate of neurologic sequelae after the treatment period, which could be due in part to the high dose of oxygen and/or the high rate of cognitive dysfunction in the study population (69% were poisoned by carbon monoxide through suicide attempts).

The other blinded trial, by Weaver et al., also compared hyperbaric and normobaric oxygen. (16) Patients received either 3 sessions of HBO2 therapy or 1 session of normobaric oxygen plus 2 sessions of exposure to normobaric room air. The primary outcome was the rate of cognitive sequelae at 6 weeks. Cognitive function was assessed using a battery of neuropsychological tests. At the 6-week follow-up, the intention-to-treat analysis found that 19 of 76 (25.0%) in the HBO2 therapy group and 35 of 7 6 (46.1%) in the control group had cognitive sequelae; the difference was statistically significant (p=0.007). There was a high rate of follow-up at 6 weeks, 147 of 152 (97%) of randomized patients. Enrollment in the study was stopped early because an interim analysis found HBO2 therapy to be effective. A follow-up study, which included 147 patients from the randomized trial and 75 who had been eligible for the trial but had not enrolled, was published in 2007. (19) Of the group treated with HBO2 therapy (n=75), cognitive sequelae were identified in 10 of 58 (17%) at 6 months and 9 of 62 (14%) at 12 months. Of the group not treated with HBO2 therapy (n=163), 44 of 146 (30%) at 6 months and 27 of 149 (18%) at 12 months had cognitive sequelae. (The follow-up rate was higher at 12 months because the investigators received additional funding for data collection.) Thus, in light of the clinical studies, including the limitations of trials noted earlier, the use of HBO2 for acute carbon monoxide poisoning may be medically necessary.

Radionecrosis and Osteoradionecrosis

A 2008 Cochrane review by Esposito et al. reviewed the use of HBO2 therapy in patients requiring dental implants. (18) The authors identified 1 randomized trial involving 26 patients. The authors concluded that despite the limited amount of clinical research available, it appears that HBO2 therapy in irradiated patients requiring dental implants may not offer any appreciable clinical benefits. They indicated that there is a need for more RCTs to ascertain the effectiveness of HBO2 therapy in irradiated patients requiring dental implants.

In 2012, Bennett et al. published a Cochrane review on HBO2 therapy for late radiation tissue injury. (19) The authors identified 11 RCTs; there was variability among trials, and study findings were not pooled for the primary outcomes of survival, complete resolution of necrosis or tissue damage, and improvement in a late effects symptom scale. In a pooled analysis of 3 studies, a significantly higher proportion of patients with osteoradionecrosis achieved complete mucosal cover after HBO2 therapy compared with controls (RR=1.30; 95% CI, 1.09 to 1.55). From their review of the literature, the authors concluded that data from small trials “suggest that for people with LRTI [late radiation tissue injury] affecting the head, neck, anus, and rectum, [HBO2] is associated with improved outcome. HBO2 therapy also appears to reduce the chance of ORN [osteoradionecrosis] following tooth extraction in an irradiated field. There was no such evidence of any important clinical effect on neurological tissues. The application of HBO2 therapy to selected patients and tissues may be justified.”

HBO2 has long been used to treat soft tissue and bone radiation necrosis and for pre- and post-treatment of dental surgery (non-implant-related) in an irradiated jaw.

In summary, given the longstanding use of this technology, the existing literature base, and the Cochrane reviews previously noted, the use of HBO2 for treatment of soft tissue and bone radiation necrosis and for pre- and posttreatment of dental surgery (non-implant-related) in an irradiated jaw may be considered medically necessary.

Bisphosphonate-Related Osteonecrosis of the Jaw

An unblinded RCT was published by Freiberger et al. in 2012 on use of HBO2 therapy as an adjunct therapy for patients with bisphosphonate-related osteonecrosis of the jaw. (20) Forty-nine patients were randomly assigned to HBO2 therapy in addition to standard care (n=22) or standard care alone (n=27). Five patients in the standard care group received and 1 patient assigned to the HBO2 therapy group declined HBO2 therapy. The investigators decided to do a per protocol analysis (actual treatment received) because of the relatively large degree of crossover. Participants were evaluated at 3, 6, 12, and 18 months. Data were available on 46 patients; 25 received HBO2 therapy in addition to standard care and 21 received standard care alone. The primary outcome measure was change in oral lesion size or number. When change from baseline to last available follow-up was examined, 17 of 25 (68%) of HBO2-treated patients had improvement in oral lesion size or number compared with 8 of 21 (38%) in the standard care group (p=0.043). When change from baseline to 6, 12, or 18 months was examined, there was no statistically significant difference between groups in the proportion of patients with improvement. In addition, the proportion of patients who healed completely did not differ significantly between groups at any time point. This single trial does not report consistent findings of benefit across outcome measures. It also has a number of methodologic limitations, e.g., unblinded, crossover, and analysis performed on a per-protocol basis rather than intention to treat. A disadvantage of the per-protocol analysis is that randomization is not preserved, and the 2 groups may differ on characteristics that affect outcomes. As a result, this trial is insufficient to conclude that HBO2 therapy improves health outcomes for patients with bisphosphonate-related osteonecrosis of the jaw.

Osteomyelitis

No prospective clinical trials on chronic refractory osteomyelitis or acute refractory osteomyelitis were identified in updated searches. The justification for the use of HBO2 therapy in chronic osteomyelitis has been primarily based on case series. Among the larger case series, Maynor et al. reviewed the records of all patients with chronic osteomyelitis of the tibia seen at 1 institution. (21) Follow-up data were available on 34 patients who had received a mean of 35 adjunctive HBO2 treatments (range, 6-99). Of the 26 patients with at least 2 years of follow-up after treatment, 21 (81%) remained drainage-free. Twelve of 15 (80%) with follow-up data at 60 months had remained drainage-free. A study by Davis et al. reviewed outcomes for 38 patients with chronic refractory osteomyelitis treated at another U.S. institution. (22) Patients received HBO2 therapy until the bone was fully recovered with healthy vascular tissue; this resulted in a mean of 48 daily treatments (range, 8-103). After a mean posttreatment follow-up of 34 months, 34 of 38 (89%) patients remained clinically free of infection (i.e., drainage-free and no tenderness, pain, or cellulitis). Success rates from several smaller case series, all conducted in Taiwan, are 12 of 13 (92%) patients, 11 of 14 (79%) patients, and 13 of 15 (86%) patients. (23-25) Given the high percentage of refractory patients in these series that had successful outcomes, the use of HBO2 therapy for chronic refractory osteomyelitis may be considered medically necessary. HBO2 therapy for acute osteomyelitis refractory to medical treatment may be considered experimental, investigational and/or unproven.

Fracture Healing

In 2012, Bennett et al. published a Cochrane review on HBO2 therapy to promote fracture healing and treat nonunion fractures. (26) The investigators did not identify any published RCTs on this topic that compared HBO2 therapy with no treatment, sham or another intervention and reported bony union as an outcome. Due to the lack of RCTs, it is not possible to conclude whether the use HBO2 therapy to promote fracture healing improves outcomes; therefore, the use of HBO2 therapy for this indication is considered experimental, investigational and/or unproven.

Compromised Skin Grafts and Flaps

In 2006, Friedman et al. published a systematic review of literature on use of HBO2 therapy for treating skin flaps and grafts. (27) No RCTs were found. The authors identified 2 retrospective case series on use of HBO2 therapy for clinically compromised skin grafts and flaps. The series had sample sizes of 65 and 26, respectively; both were published in the 1980s based on treatment provided in the 1970s and 1980s. Given the limited published data and lack of recent data, this indication remains experimental, investigational and/or unproven.

Necrotizing Soft Tissue Infections

A 2015 Cochrane review by Levett et al. evaluated the literature on HBO2 therapy as adjunctive therapy for necrotizing fasciitis. (28) No RCTs were identified. Previously in 2005, a systematic review by Jallali et al. evaluated the literature on HBO2 therapy as adjunctive therapy for necrotizing fasciitis. (29) They did not identify any RCTs. There were only a few retrospective studies with small sample sizes and findings were inconsistent. The authors concluded that more robust evidence is needed before widespread use of HBO2 therapy is recommended. A 2009 retrospective cohort study compared outcomes in 48 patients at 1 center who received adjunctive HBO2 therapy for necrotizing soft issue infections with those in 30 patients at a different center who did not receive HBO2 therapy. (30) There was no significant difference in the mortality rate between the 2 groups; this was 4 of 48 (8%) in the HBO2 therapy group and 4 of 30 (13%) in the non-HBO2 therapy group (p=0.48). The median number of days in the intensive care unit and the median number of days in the hospital also did not differ significantly. There was a higher median number of débridement procedures per person in the HBO2 therapy group, 3.0 versus 2.0 in the non- HBO2 therapy group (p=0.03). Despite the available evidence just cited, HBO2 therapy for necrotizing soft tissue infections remains medically necessary as cited earlier from reviews by the Alberta Heritage Foundation for Medical Research’s (AHFMR) March 2003 Information Paper. (75)

Refractory Mycoses

No recent clinical trials on refractory mycoses (mucormycosis, actinomycosis, conidiobolus coronato) and cerebral edema were found. However, these indications remain as medically necessary based upon evidence in the Cimsit et al. report, in which HBO2 therapy acts as an O2 radical to treat fungal infections by increasing tissue O2 tensions. (76)

Acute Peripheral Arterial Insufficiency

No clinical trial publications were identified that demonstrated benefit in HBO2 therapy for acute peripheral arterial insufficiency, and thus the evidence basis for coverage (31) by Medicare is unclear as Medicare has long listed acute peripheral arterial insufficiency as a medically necessary indication. Due to the lack of published literature, acute peripheral arterial insufficiency is listed as an experimental, investigational and/or unproven indication.

Acute Coronary Syndromes

A 2011 Cochrane review by Bennett et al. identified 6 trials with a total of 665 patients evaluating HBO2 therapy for acute coronary syndrome. (32) All studies included patients with acute myocardial infarction (MI); 1 study also included individuals presenting with unstable angina. Additionally, all trials used HBO2 therapy as an adjunct to standard care. Control interventions varied; only 1 trial described using a sham therapy to blind participants to treatment group allocation. In a pooled analysis of data from 5 trials, there was a significantly lower rate of death in patients who received HBO2 therapy compared with a control intervention (RR=0.58; 95% CI, 0.36 to 0.92). Due to variability of outcome reporting in the studies, few other pooled analyses could be conducted. A pooled analysis of data from 3 trials on improvements in left ventricular function did not find a statistically significant benefit of HBO2 therapy (RR=0.09; 95% CI, 0.01 to 1.4). The authors noted that, although there is some evidence from small trials that HBO2 therapy is associated with a lower risk of death, larger trials with high-quality methods are needed to determine which patients, if any, can be expected to derive benefit from HBO2 therapy.

One of the trials was by Sharifi et al. who randomly assigned 69 patients with unstable angina or MI to receive or not receive HBO2 therapy after a percutaneous coronary intervention (PCI). (33) The 24 patients randomly assigned to the HBO2 therapy group reported only 1 adverse event (death, MI, coronary artery bypass, or revascularization of target lesion), compared with 13 in the 37 control patients. However, this study lacked adequate detail (e.g., on the type of PCI performed) to permit scientific conclusions. In another RCT of 64 patients, Alex et al. concluded both neuropsychometric dysfunction and inflammatory response can be reduced postcardiopulmonary bypass when hyperbaric pretreatment is given. (34) Based on this evidence, the treatment of acute coronary syndromes with HBO2 therapy is considered experimental, investigational and/or unproven.

Acute Ischemic Stroke

In a 2014 update of a Cochrane systematic review, Bennett et al. evaluated HBO2 for acute ischemic stroke. (35) The investigators identified 11 RCTs, with a total of 705 participants, that compared HBO2 with sham HBO2 or no treatment. The authors were only able to pool study findings for 1 outcome (mortality at 3-6 months). A pooled analysis of data from 4 trials with a total of 106 participants did not find a significant benefit of HBO2 compared with a control condition for this outcome (RR=0.97; 95% CI, 0.34 to 2.75). Based on the available evidence, acute ischemic stroke is considered experimental, investigational and/or unproven.

Motor Dysfunction Associated with Stroke

In 2013, Efrati et al. published an RCT evaluating HBO2 therapy for treatment of neurologic deficiencies associated with a history of stroke. (36) The study included 74 patients with at least 1 motor dysfunction who had an ischemic or hemorrhagic stroke 6 to 36 months prior to study participation. Participants were randomly assigned to receive 2 months of HBO2 therapy (40 daily sessions, 5 d/wk, n=30) or delayed treatment (n=32). Patients were evaluated at baseline and 2 months. For patients in the delayed treatment control group, outcomes were evaluated at 4 months after crossing over and receiving HBO2 therapy. Twenty-nine of 32 patients (91%) in the delayed treatment group crossed over to the active intervention. Outcome measures included the National Institutes of Health Stroke Scale (NIHSS), which was measured by physicians blinded to treatment group, and several patient-reported quality-of-life and functional status measures.

At 2-month follow-up, there was statistically significantly greater improvement in function in the HBO2 therapy group than in the control group as measured by NIHSS, quality-of-life scales and the ability to perform activities of daily living (ADLs). These differences in outcome measures were accompanied by improvements in single photon emission computed tomography imaging in the regions affected by stroke. For the delayed treatment control group, there was a statistically significant improvement in function after HBO2 therapy compared with before treatment. This RCT raises the possibility that HBO2 therapy may induce improvements in function and quality of life for poststroke patients with motor deficits. However, the results are not definitive for a number of reasons. This RCT is small and enrolled a heterogeneous group of poststroke patients. The study was not double-blind and most outcome measures, except for NIHSS, were patient reported and thus prone to the placebo effect. Also, there was a high total dropout rate of 20% at the 2-month follow-up point. Therefore, larger, double-blind studies with longer follow-up are needed to corroborate these results. Because of these limitations in the evidence, HBO2 therapy is considered experimental, investigational and/or unproven for treating motor dysfunction associated with stroke.

Bell’s Palsy

In 2012, Holland et al. published a Cochrane systematic review evaluating HBO2 therapy in adults with Bell’s palsy. (37) The authors identified 1 RCT with 79 participants, and this study did not meet the Cochrane review’s methodologic standards because the outcome assessor was not blinded to treatment allocation. Due to the publication of the Cochrane review and the finding of insufficient evidence, Bell’s palsy was added to the experimental, investigational and/or unproven coverage listing.

Traumatic Brain Injury

A 2012 Cochrane systematic review addressed HBO2 therapy as adjunctive therapy for traumatic brain injury. (38) The investigators identified 7 RCTs with a total of 571 participants comparing a standard intensive treatment regimen with the same treatment regimen plus HBO2 therapy. The review did not include studies in which interventions occurred in a specialized acute care setting. The HBO2 therapy regimens varied among studies; for example, the total number of individual sessions varied from 3 to between 30 and 40. No trial used sham treatment or blinded the staff members who were treating the patients, and only 1 had blinding of outcome assessment. Allocation concealment was inadequate in all of the studies. The primary outcomes of the review were mortality and functional outcomes. A pooled analysis of data from 4 trials that reported this outcome found a statistically significantly greater reduction in mortality when HBO2 therapy was added to a standard treatment regimen (RR=0.69; 95% CI, 0.54 to 0.88). However, when data from the 4 trials were pooled, the difference in the proportion of patients with an unfavorable functional outcome at final follow-up was not statistically significant (RR=0.71; 95% CI, 0.50 to 1.01). Unfavorable outcome was commonly defined as a Glasgow Outcome Scale score of 1, 2, or 3, which are described as ‘dead,’ ‘vegetative state,’ or ‘severely disabled.’ Studies were generally small and were judged to have substantial risk of bias.

Several trials on mild traumatic brain injury in military populations have been published and they did not find significant benefits of HBO2 compared with sham treatment. (39-41) The first trial, published by Wolf et al. in 2012, included 50 military service members, 48 of whom were male, with combat-related mild traumatic brain injury. (39) Participants were randomized to 30 sessions of HBO2 over 8 weeks (n=25) or a sham intervention (room air at 1.3 atmosphere, absolute [ata]) (n=25). The primary outcome measures were scores on the Immediate Post-Concussive Assessment and Cognitive Testing (ImPACT) and Post- Traumatic Disorder Check List?Military Version (PCL-M) instruments. Patients were evaluated after every 5 treatment sessions and at 6 weeks postexposure. Forty-eight of 50 participants (96%) completed the study. There were no statistically significant differences on the ImPACT total mean score or the PCL-M composite score at any time point. For example, at the 6-week follow-up, mean composite PCL-M scores were 41.6 in the HBO2 group and 40.6 in the sham-control group (p=0.28). While the sample size was relatively small, the study was powered to detect clinically significant differences among groups on the cognitive tests.

In 2014, Cifu et al. published findings of an RCT with 61 male Marines who had a history of mild traumatic brain injury and postconcussive syndrome. (40) The study was sham-controlled and double-blinded. Patients were randomized to receive 1 of 3 treatments: 75% oxygen at 1.5 ata (n=21); 100% oxygen at 2.0 ata (n=19); and 3) sham treatment with normal air (n=21). Outcomes were assessed 3 months after the last exposure. The primary outcome was a clinically meaningful improvement, defined as a 10% difference between groups in the score on the Rivermead Post-Concussion Questionnaire (RPQ)-16 (scale ranges from 50 to 84, with higher values indicating more severe symptoms). At follow-up, there was no statistically significant difference among groups on RPQ-16 score (p=0.41). A variety of secondary outcomes were also assessed. None of these, including measures of attention, cognition, or depression, differed significantly among groups at follow-up.

In 2015, Miller et al. evaluated HBO2 therapy in 72 military service members with continuing symptoms at least 4 months after mild traumatic brain injury. (41) Patients were randomized to receive 40 daily HBO2 therapy sessions at 1.5 ata, 40 sham sessions consisting of room air at 1.2 ata, or standard care with no hyperbaric chamber sessions. The primary outcome was change in RPQ score. A cutoff of 15% improvement was deemed clinically important, which translates to a change score of at least 2 points on the RPQ-3 subscale. The proportion of patients who met the prespecified change of at least 2 points on the RPQ-3 was 52% in the HBO2 therapy group, 33% in the sham group, and 25% in the standard care-only group. The difference between rates in the HBO2 therapy and sham groups was not statistically significant (p=0.24). None of the secondary outcomes significantly favored the HBO2 therapy group. A criticism of this study, as well as the other military population studies, was that the response in the sham group was not due to a placebo effect but to an intervention effect of slightly increased atmospheric pressure (1.2 ata). (42) Other researchers have noted that room air delivered at 1.2 ata would not be considered an acceptable therapeutic dose for any indication, and especially for a condition with persistent symptoms like postconcussive syndrome.

In summary, systematic review of small trials with limitations found a mortality reduction with HBO2 therapy but no significant improvement in patient function among survivors of traumatic brain injury. Additional trials, conducted with military personnel, did not find significant benefits of HBO2 therapy in patients with mild traumatic brain injury. Thus, the evidence is insufficient that HBO2 therapy improves health outcomes in patients with traumatic brain injury, and this indication is considered experimental, investigational and/or unproven.

Inflammatory Bowel Disease

A 2014 systematic review by Dulai et al. examined the evidence on HBO2 therapy for inflammatory bowel disease (Crohn’s disease and ulcerative colitis). (43) The review was not limited by study design. The authors included 17 studies: 1 RCT, 2 case-control studies, 3 case series, and 11 case reports. The studies reported on a total of 613 patients, 286 with Crohn’s disease and 327 with ulcerative colitis. The only RCT identified was published in 2013; it was open-label and included 18 patients with ulcerative colitis. (44) Patients were randomized to treatment with standard medical therapy only (n=8) or medical therapy plus HBO2 therapy (n=10). The hyperbaric oxygen intervention consisted of 90 minutes of treatment at 2.4 atm, 5 days a week for 6 weeks (total of 30 sessions). The primary outcome was the Mayo score, which has a potential range of 0 to 12. (45) Patients with a score of 6 or more are considered to have moderate to severe active disease. At follow-up, there was no significant difference between groups in the Mayo score; the median score at 6 months was 0.5 in the HBO2 therapy group and 3 in the control group (exact p value not reported). In addition, there were no significant differences in any of the secondary outcomes, including laboratory tests and fecal weight. This is a small study that may have been underpowered. Overall, the authors found that the studies had a high risk of bias, particularly in the areas of attrition and reporting bias.

In summary, there is insufficient evidence that HBO2 therapy is effective for treating inflammatory bowel disease. Only 1 small RCT has been published, and this study did not find a significant improvement in health outcomes when HBO2 therapy was added to standard medical therapy.

Idiopathic Sudden Sensorineural Hearing Loss (ISSNHL)

In 2011, UHMS added ISSNHL within the past 14 days as an approved indication for HBO2 therapy. (46)

A 2012 Cochrane review on HBO2 therapy for ISSNHL and tinnitus identified 7 RCTs with a total of 392 participants. (47) All trials included patients with ISSNHL with and/or without tinnitus; 2 trials also included patients with tinnitus in the absence of ISSNHL. Randomization procedures were only described in 1 study, and only 1 study stated they blinded participants to treatment group assignment using sham therapy. Six of the studies included time-based entry criteria for hearing loss and/or tinnitus; this was 48 hours in 3 studies, 2 weeks in 2 studies (for acute presentation), and 6 months in 1 study. The dose of oxygen per treatment session and the treatment protocols varied among studies, e.g., the total number of treatment sessions varied from 10 to 25.

All trials reported on change in hearing following treatment; but specific outcomes varied. Two trials reported the proportion of participants with greater than 50% return of hearing at the end of therapy. A pooled analysis of these studies did not find a statistically significant difference in outcomes between the HBO2 therapy and the control groups (RR=1.53; 95% CI, 0.86 to 2.78). In contrast, a pooled analysis of 2 trials reporting the proportion of participants with greater than 25% return of hearing at the end of therapy found a significantly higher rate of improvement after HBO2 therapy than a control intervention (RR=1.39; 95% CI, 1.05 to 1.84). Moreover, a pooled analysis of 4 trials found a significantly greater mean improvement in hearing over all frequencies with HBO2 therapy compared with control (mean difference, 15.6 dB; 95% CI, 1.5 to 29.8). The authors stated that, due to methodologic shortcomings of the trials and the modest number of patients, results of the meta-analysis should be interpreted cautiously; they did not recommend use of HBO2 therapy for treating ISSNHL.

In 2013, Cvorovic et al. published an RCT that included 50 patients with ISSNHL who had failed primary therapy with intravenous steroids. (48) Patients were randomized to receive HBO2 therapy (20 sessions, 5 daily sessions per week) or intratympanic steroid injection (4 injections in 13 days). The HBO2 therapy sessions consisted of 10 minutes of compression on air, 60 minutes of 100% oxygen at 2 ata, and 10 minutes of decompression on air. Outcomes were change in the mean hearing thresholds at each of 5 frequencies (0.25, 0.5, 1, 2, and 4 kHz). After treatment, there were no statistically significant differences in mean hearing thresholds at 4 of the 5 frequencies. The exception was 2 kHz, and at this frequency, the improvement was significantly greater in the HBO2 therapy group.

Based on the UHMS adding ISSNHL as an approved indication and the report within the literature that hearing has improved, and some studies showing a significant greater mean improvement of hearing in all frequencies, HBO2 would be appropriate for the treatment of ISSNHL.

Cancer Treatment

In an RCT of 32 patients, Heys et al. found no increase in 5-year survival in patients treated with HBO2 therapy prior to chemotherapy for locally advanced breast carcinoma to increase tumor vascularity. (49) This approach is being studied because studies in animal models have suggested that HBO2 therapy increases tumor vascularity and thus may make chemotherapy more effective. In a Cochrane review, Bennett et al. concluded that HBO2 therapy given with radiotherapy may be useful in tumor control; however, the authors expressed caution because significant adverse effects were common with HBO2 therapy and indicated further study would be useful. (50) Therefore, a coverage statement was added to indicate HBO2 therapy for tumor sensitization for cancer treatments, including but not limited to radiotherapy or chemotherapy, is considered experimental, investigational and/or unproven.

In Vitro Fertilization (IVF)

Van Voorhis et al. reported that HBO2 therapy was well-tolerated in women undergoing ovarian follicular stimulation for IVF; however, no outcomes were reported, and further study is needed. (51) IVF was added to the coverage listing of experimental, investigational and/or unproven indications for HBO2 therapy.

Delayed-Onset Muscle Soreness

In a Cochrane review, Bennett et al. concluded that available evidence is insufficient to demonstrate beneficial outcomes with HBO2 therapy for delayed-onset muscle soreness and closed soft tissue injury. (52) It was noted that HBO2 therapy possibly increases pain initially and further studies are needed. Therefore, a policy statement was added to indicate HBO2 therapy for delayed-onset muscle soreness is considered experimental, investigational and/or unproven.

Autism Spectrum Disorders

A 2012 systematic review of evidence on HBO2 therapy for treatment of children with autism identified 2 RCTs with a total of 89 participants. (53) One of the 2 RCTs found better outcomes after HBO2 therapy compared with placebo treatment, and the other did not find significant differences in outcomes. The author concluded that additional sham-controlled trials with rigorous methodology are needed to draw conclusions about the efficacy of HBO2 therapy for treating autism. A 2012 review article also concluded that, although studies to date suggest that HBO2 therapy is safe and potentially effective, additional studies are warranted. (54) In particular, it was recommended that future studies use standardized behavioral measurement tools and also assess physiologic biomarkers.

One of the RCTs was by Rossignol et al. (54) This double-blind trial included 62 children, ages 2 to 7 years, who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for autistic disorder. The active treatment was hyperbaric treatment at 1.3 atm and 24% oxygen in a hyperbaric chamber. (This regimen differs from standard HBO2 therapy, which uses 100% oxygen and a pressure of at least 1.4 atm.) The other group received a sham treatment consisting of 1.03 atm and ambient air (21% oxygen). Both groups received 40 sessions of active or sham treatment lasting 60 minutes each over 4 weeks. The equipment, procedures, etc. in the 2 groups were as similar as possible to maintain blinding. The investigators, participants, parents, and clinic staff were blinded to treatment group. Only the hyperbaric technician, who had no role in outcome assessment, was aware of group assignment. After completion of the 4-week study, families with children in the control group were offered the active intervention. When asked at the end of the study, there was no significant difference in the ability of parents to correctly guess the group assignment of their child.

The outcomes were change versus baseline after 4 weeks on the following scales: Aberrant Behavior Checklist (ABC) total score and 5 subscales: Autism Treatment Evaluation Checklist (ATEC) total score and 4 subscales; and Clinical Global Impression-Improvement (CGI) overall functioning score and 18 subscales. P values of less than 0.05 were considered statistically significant; there was no adjustment for multiple comparisons. The analysis included all children who completed at least 1 complete session. Of the 33 children assigned to active treatment, 30 were included in the analysis, and 29 completed all 40 treatments. Of the 29 children assigned to the control treatment, 26 completed all 40 sessions and were included in the analysis.

There was no significant between-group improvement on the ABC total score, any of the ABC subscales, or on the ATEC total score. Compared with the control group, the treatment group had a significant improvement in 1 of 4 subscales of the ATEC, the Sensory/Cognitive Awareness subscale. The change from baseline on this subscale was a mean of 16.5 in the treatment group and a mean of 5.4 in the control group, a difference of 11.1 (p=0.037). (Note: due to an administrative error, baseline ATEC was not collected at 1 site, and thus data were not available for 23 children in the treatment group and 21 children in the control group.) On the physician-rated CGI total score, 9 of 30 (30%) children in the treatment group had a score of 1 (very much improved) or 2 (much improved) compared with 2 of 26 (8%) in the control group (p=0.047). On the parental-rated CGI total score, 9 of 30 (30%) children in the treatment group had a score of 1 or 2 compared with 4 of 26 (15%) in the control group (p=0.22, not statistically significant). (The exact numbers receiving scores of 1 versus 2 were not reported.) Change in mean CGI scores was also reported, but this may be a less appropriate way to analyze these data. Among the parental-rated CGI subscales, significantly more children were rated as improved in the treatment group compared with controls on 2 of 18 subscales, Receptive Language (p=0.017) and Eye Contact (p=0.032).

A key limitation of this study was that the authors reported only outcomes at 4 weeks, directly after completion of the intervention. It is not known whether there were any long-term effects. Additional followup data cannot be obtained because members of the control group crossed over to the intervention after 4 weeks. Other limitations include lack of adjustment for multiple comparisons and unclear clinical significance of the statistically significant outcomes. UHMS issued a position paper after publication of the Rossignol et al. study stating that it still did not recommend routine HBO2 therapy for autism. (55)

An additional 2012 RCT, published after the 2012 systematic review now complete, was conducted in Thailand and randomly assigned 60 children with autism to receive 20 one-hour sessions with HBO2 therapy or sham air (n=30 per group). (56) The primary outcome measures were change in ATEC and CGI scores, evaluated separately by clinicians and parents. There were no statistically significant differences between groups for any of the primary outcomes. For example, posttreatment clinician-assessed mean scores on ATEC were 52.4 in the HBO2 therapy group and 52.9 in the sham air group. In summary, there is insufficient evidence from rigorous RCTs that HBO2 therapy improves health outcomes for patients with autism spectrum disorder; therefore, HBO2 therapy for this indication is considered experimental, investigational and/or unproven.

Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s Disease

In the updated searches, no randomized trials were found evaluating HBO2 therapy for treatment of amyotrophic lateral sclerosis. In a small case series, Steele et al. treated 5 patients with HBO2 therapy and reported some improvements in fatigue but noted that further study is needed, and attention to placebo effects must be given. (57) Thus, ALS was added to the coverage as an experimental, investigational and/or unproven indication.

Cerebral Palsy

Two published RCTs were identified. In 2012, Lacey et al. published a double-blind RCT that included 49 children age 3 to 8 years with spastic cerebral palsy. (58) Participants were randomized to receive 40 treatments with either HBO2 therapy (n=25) or hyperbaric air to simulate 21% oxygen at room air (n=24). The primary efficacy outcome was change in the Gross Motor Function Measure (GMFM-88) global score after the 8-week treatment period. The study was stopped early due to futility, when an interim analysis indicated that there was less than a 2% likelihood that a statistically significant difference between groups would be found. At the time of the interim analysis, the posttreatment GMFM-88 global score was a mean (SD) of 40.8 (33.4) in the HBO2 therapy group and 41.2 (29.6) in the hyperbaric air group. The between-group difference was 0.9 (95% CI, -1.5 to 3.3; p=0.54).

Previously, in 2001, Collet et al. randomly assigned 111 children with cerebral palsy to 40 treatments over a 2-month period of either HBO2 therapy (n=57) or slightly pressurized room air (n=54). (59) The authors found HBO2 therapy produced similar improvements in outcomes such as gross motor function and ADLs in both groups as slightly pressurized air. The available evidence does not support HBO2 therapy for cerebral palsy; therefore, this is considered experimental, investigational and/or unproven.

Vascular Dementia

A 2012 Cochrane review identified 1 RCT evaluating HBO2 therapy for vascular dementia. (60) The 2009 study, conducted in China compared HBO2 therapy plus donepezil to donepezil-only in 64 patients. The HBO2 therapy plus donepezil group had significantly better cognitive function after 12 weeks of treatment, as assessed by the Mini-Mental State Examination. The Cochrane investigators judged the trial to be of poor quality because it was not blinded and the methods of randomization and allocation concealment were not discussed. This single trial with limitations provides insufficient evidence on the efficacy of HBO2 therapy on vascular dementia; thus, HBO2 therapy is considered experimental, investigational and/or unproven for this indication.

Radiotherapy Adverse Effects

In 2010, Spiegelberg et al. conducted a systematic review of studies on HBO2 therapy to prevent or treat radiotherapy-induced head and neck injuries associated with treatment of malignant tumors. (61) The authors identified 20 studies. Eight of the studies included control groups; their sample sizes ranged from 19 to 78 subjects. Four (50%) of the studies with a control group concluded that HBO2 therapy was effective, and the other 4 did not. The authors noted a paucity of RCTs but did not state the number of RCTs that they identified in their review.

A study by Teguh et al. published in 2009 included 17 patients with oropharyngeal or nasopharyngeal cancer who were treated with radiotherapy; the study was conducted in The Netherlands. (62) HBO2 therapy was used to prevent adverse events following radiotherapy. Eight patients were randomly assigned to receive 30 sessions of HBO2 therapy, beginning within 2 days of completing radiotherapy, and 9 patients received no additional treatment. All patients were included in the analysis. Quality-of-life outcomes were assessed, and the primary outcome was specified as xerostomia at 1 year. Quality-of-life measures did not differ significantly between groups in the acute phase (first 3 months). For example, 1 month after treatment, the mean visual analog scale (VAS) score for xerostomia (0-to-10 scale) was 5 in the HBO2 therapy group and 6 in the control group. However, at 1 year, there was a statistically significant difference between groups; the mean VAS score for xerostomia was 4 in the HBO2 therapy group and 7 in the control group (p=0.002). Also at 1 year, the mean quality-of-life score for swallowing (0-to-100 scale) was 7 in the HBO2 therapy group and 40 in the control group (p<0.001). The study is limited by the small sample size and the wide fluctuation over the follow-up period in quality-of-life ratings.

In 2010, Gothard et al. in the U.K. published findings of an RCT using HBO2 therapy for arm lymphedema occurring after radiotherapy for cancer. (63) Fifty-eight patients with arm lymphedema (at least 15% increase in arm volume) following cancer treatment were randomized in a 2:1 ratio to receive HBO2 therapy (n=38) or usual care without HBO2 therapy (n=20). Fifty-three patients had baseline assessments and 46 of 58 (79%) had 12-month assessments. At the 12-month follow-up, there was no statistically significant difference in the change from baseline in arm volume. The median change from baseline was -2.9% in the treatment group and -0.3% in the control group. The study protocol defined response as at least an 8% reduction in arm volume relative to the contralateral arm. According to this definition, 9 of 30 (30%) of patients in the HBO2 therapy group were considered responders compared with 3 of 16 (19%) in the control group; the difference between groups was not statistically significant. Other outcomes, e.g., quality-of-life scores on the 36-Item Short-Form Health Survey, were similar between groups.

Due to the limited data, use of HBO2 therapy in patients with arm lymphedema or radiation-induced injury in the head and neck after radiotherapy, as well as early use of HBO2 therapy after radiotherapy to reduce adverse effects, are considered experimental, investigational and/or unproven.

Idiopathic Femoral Neck Necrosis

A double-blind RCT that evaluated HBO2 therapy to treat femoral head necrosis was published in 2010 by Camporesi et al. (64) The study included 20 adult patients with idiopathic unilateral femoral head necrosis. Patients received 30 treatments over 6 weeks with either HBO2 therapy at 2.5 ata (n=10) or a sham treatment consisting of hyperbaric air (n=10). The mean severity of pain on a 0-to-10 scale was significantly lower in the HBO2 therapy group than the control group after 30 sessions (p<0.001) but not after 10 or 20 sessions. (The article did not report exact pain scores.) Several range-of-motion outcomes were also reported. At the end of the initial treatment period, extension, abduction, and adduction, but not flexion, were significantly greater in the HBO2 therapy group than in the control group. Longer term comparative data were not available because the control group was offered HBO2 therapy at the end of the initial 6-week treatment period. This single, small short-term RCT represents insufficient data on which to draw conclusions about the efficacy of HBO2 therapy for femoral head necrosis.

Migraine

A 2008 Cochrane review by Bennett et al. identified RCTs that evaluated the effectiveness of systemic HBO2 therapy for preventing or treating migraine headache compared with another treatment or a sham control. (65) In a search of the literature through May 2008, 5 trials with a total of 103 patients were identified that addressed treatment of acute migraine with HBO2 therapy. A pooled analysis of 3 trials (total N=43 patients) found a statistically significant increase in the proportion of patients with substantial relief of migraine within 45 minutes of HBO2 therapy (RR=5.97; 95% CI, 1.46 to 24.38; p=0.001). No other pooled analyses were conducted due to variability in the outcomes reported in the trials. The meta-analysis does not report data on treatment effectiveness beyond the immediate posttreatment period, and the quality of trials’ methodology was moderate to low, e.g., randomization was not well-described in any trial. Based on the above limitations of the meta-analysis, the use of HBO2 therapy to treat migraines remains experimental, investigational and/or unproven.

Herpes Zoster

In 2012, Peng et al. in China published an RCT evaluating HBO2 therapy for herpes zoster. (66) Sixty-eight patients with herpes zoster diagnosed within the previous 2 weeks were randomized to 30 sessions of HBO2 therapy (n=36) or medication treatment (n=32). Pharmacotherapy included antiviral, pain, nerve nutritive, and antidepressive medication. Therapeutic efficacy was calculated at the end of the 3-week treatment period and included the proportion of patients who were healed (i.e., complete subsidence of pain and rash) or improved (i.e., significant pain relief and rash subsistence). Rates of therapeutic efficacy were 97.2% in the HBO2 therapy group and 81.3% in the medication group. The difference between groups was statistically significant (p<0.05). In the HBO2 therapy group, 22 of 36 patients (61%) were considered to be healed and 13 (36%) were improved. In the medication group, 17 of 32 (53%) patients were healed and 9 (28%) were improved. Limitations of the study included a lack of blinding and lack of long-term follow-up. The evidence from this single RCT is insufficient to draw conclusions about the effect of HBO2 therapy on health outcomes for patients with herpes zoster; therefore, HBO2 therapy is considered experimental, investigational and/or unproven for this indication.

Fibromyalgia

One quasi-randomized trial and 1 delayed-treatment RCT on HBO2 therapy for fibromyalgia were identified. In 2004, a study by Yildiz et al. included 50 patients with fibromyalgia who had ongoing symptoms despite medical and physical therapy. (67) On an alternating basis, patients were assigned to HBO2 therapy or a control group. HBO2 therapy consisted of fifteen 90-minute sessions at 2.4 ata (1 session per day, 5 d/wk). The control group breathed room air at 1 ata on the same schedule. Baseline values on the 3 outcomes were similar in the 2 groups. After the course of HBO2 therapy treatment, the mean (SD; standard deviation) number of tender points were 6.04 (1.18) in the HBO2 therapy group and 12.54 (1.10) in the control group. The mean (SD) pain threshold was 1.33 kg (0.12) and 0.84 kg (0.12), respectively, and the mean VAS was 31.54 (8.34) and 55.42 (6.58), respectively. In the study abstract, the authors stated that there were statistically significant differences between the HBO2 therapy and the control groups after 15 therapy sessions, but the table presenting outcomes lacked the notation used to indicate between-group statistical significance. It is not clear whether the control group actually received a sham intervention that would minimize any placebo effect (i.e., whether the control intervention was delivered in a hyperbaric chamber). The authors stated that the study was double-blind but did not specify any details of patient blinding.

In 2015, Efrati et al. published an RCT that included 60 female patients who had fibromyalgia for at least 2 years and were symptomatic. (68) Patients were randomized to an immediate 2-month course of HBO2 therapy or delayed HBO2 therapy after 2 months. The HBO2 therapy protocol was forty 90-minute sessions of 100% oxygen at 2 ata (1 session per day, 5 d/wk). Forty-eight of 60 patients (80%) completed the study and were included in the analysis. After the initial 2 months, outcomes including number of tender points, pain threshold, and QOL (SF-36) were significantly better in the immediate treatment group than the delayed treatment group (which received no specific intervention during this time). After the delayed treatment group had undergone HBO2 therapy, outcomes were significantly improved compared with scores prior to HBO2 therapy treatment. These findings are consistent with a clinical benefit of HBO2 therapy, but also with a placebo effect. A sham-control is needed to confirm the efficacy of HBO2 therapy in the treatment of fibromyalgia and other conditions where primary end points are pain and other subjective outcomes.

The above studies were few in number with relatively small sample sizes and they have methodological limitations (e.g., quasi-randomization and no or uncertain sham control for a condition with subjective outcomes susceptible to a placebo effect). Moreover, the HBO2 therapy protocol varied (e.g., 15 HBO2 therapy sessions versus 40 HBO2 therapy sessions). Thus, the evidence is insufficient to draw conclusions about the impact of HBO2 therapy on health outcomes for patients with fibromyalgia and is considered experimental, investigational and/or unproven.

Mental Illness

A Rapid Response Report from the Canadian Agency for Drugs and Technologies in Health searched the literature through July 2014 on the clinical effectiveness of HBO2 therapy for treatment of adults with posttraumatic stress disorder, generalized anxiety disorder, and/or depression. (69) The review’s inclusion criteria were health technology assessments, systematic reviews, meta-analyses, RCTs, or nonrandomized studies comparing HBO2 therapy with any active treatment and reporting clinical outcomes. No eligible studies were identified. Based on the lack of studies, the use of HBO2 therapy to treat mental illness is considered experimental, investigational and/or unproven.

Stroke and Cerebrovascular Disease

In a systematic review, Carson et al. concluded current available evidence does not demonstrate any benefit with the use of HBO2 therapy for the treatment of stroke. (77) The authors noted it is undetermined whether there are any benefits with HBO2 therapy that would outweigh potential harms and further study is required. In a non-randomized, controlled trial of 26 patients treated with or without HBO2 for symptomatic cerebrovascular disease, Vila et al. concluded HBO2 therapy improved neurologic outcomes for up to 6 months. (75) However, the authors noted further study in larger patient groups is needed.

Radiation Tissue Injury

In a Cochrane systematic review from Bennett et al., the authors concluded that there was “some evidence that HBO2 therapy improves the probability of healing in radiation proctitis and following hemimandibulectomy and reconstruction of the mandible; improves the probability of achieving mucosal coverage and the restoration of bony continuity with ORN (osteoradionecrosis); prevents the development of ORN following tooth extraction from a radiation field; and reduces the risk of wound dehiscence following grafts and flaps in the head and neck”. (78) They concluded that there was no benefit using HBO2 therapy in important clinical outcomes with radiation brachial plexus lesions or cerebral tissue injury. No data was reported from randomized trials for other manifestations of late radiation tissue injury. Given the small size of many of these trials, the extended time periods of reporting, and the poor methodological quality of some studies, the use of HBO2 therapy for this indication is considered experimental, investigational and/or unproven.

Actinic Skin Damage

One published article discussed use of HBO2 therapy in combination with photosensitization and iron to treat actinic skin damage or actinic keratosis (AK). Al-Walili et al. discuss the advantages photodynamic therapy as the new approach to treatment of malignant tumors in addition to the beneficial effects of HBO2 in various modalities of cancer interventions. (79) No data was reported from randomized trials for treatment of AK. The authors noted the possibility of combining HBO2, iron, light, and local photosensitizers to overcome skin tumors deserve extensive laboratory and clinical research work.

Postoperative Ileus or Acute Pancreatitis

Reports of uncontrolled studies, some from outside the United States, are reporting preliminary results for use of HBO2 therapy in other conditions such as postoperative ileus and acute pancreatitis. (80-81)

Additional Indications or Clinical Conditions

There is a lack of scientific evidence from which conclusions can be made concerning the safety and efficacy of utilizing HBO2 therapy for various other indications mentioned as clinical conditions and not a labeled indication by the FDA nor listed on the guidelines from the UHMS, or any other authoritative source, (72) such as:

Arthritic diseases;

Asthma;

Avascular necrosis;

Bone grafts;

Carbon tetrachloride poisoning;

Cardiogenic shock;

Depression;

Spinal cord injury;

Hepatic necrosis;

Hepatitis;

Human immunodeficiency virus infection or acquired immune deficiency syndrome (HIV/AIDS);

Hydrogen sulfide poisoning;

Intra-abdominal abscesses;

Lepromatous leprosy;

Lyme disease;

Lymphedema of arm;

Meningitis;

Motor dysfunction associated with stroke;

Multiple sclerosis;

Organ transplantation or storage;

Parkinson’s disease;

Post-traumatic stress disorder (PTSD) or other stress disorders;

Pseudomembranous colitis, antimicrobial agent-induced colitis;

Pulmonary emphysema;

Pyoderma gangrenosum;

Radiation-induced injury to head, neck, anus, or rectum (except proctitis);

Radiation necrosis of non-neurologic tissue;

Radiation-myelitis;

Retinal artery insufficiency;

Retinopathy, as an adjunct to scleral buckling procedure in patients with sickle cell peripheral retinopathy and retinal detachment;

Sickle cell crisis and/or hematuria;

Senility;

Septicemia, anaerobic (unrelated to clostridial), or systemic aerobic infection;

Sport’s injury;

Sudden deafness (unrelated to ISSNHL);

Tetanus; and/or

Vascular dementia or chronic brain syndromes, neovascular causes (such as Pick’s disease, Alzheimer’s disease, and Korsakoff’s disease).

Practice Guidelines and Position Statements

Undersea and Hyperbaric Medical Society (UHMS)

In 2015, the UHMS published a guideline on use of HBO2 therapy for treating diabetic foot ulcers. (71) Recommendations are:

Suggest against using HBO2 therapy in patients with “Wagner Grade 2 or lower diabetic foot ulcers….”

Suggest adding HBO2 therapy in patients with “Wagner Grade 3 or higher diabetic foot ulcers that have now shown significant improvement after 30 days of [standard of care] therapy….”

Suggest “adding acute postoperative hyperbaric oxygen therapy to the standard of care” in patients with “Wagner Grade 3 or higher diabetic foot ulcers” who have just had foot surgery related to their diabetic ulcers.

In 2011, the UHMS updated their list of indications considered appropriate for HBO2 therapy. (72-73) These indications are as follows:

Air or gas embolism;

Carbon monoxide poisoning and carbon monoxide complicated by cyanide poisoning;

Clostridial myositis and myonecrosis (gas gangrene);

Crush injury, compartment syndrome, and other acute traumatic ischemias;

Decompression sickness;

Arterial insufficiencies:

o Central retinal artery occlusion,

o Enhancement of healing in selected problem wounds;

Severe anemia;

Intracranial abscess;

Necrotizing soft tissue infections;

Osteomyelitis (refractory);

Delayed radiation injury (soft tissue and bony necrosis);

Skin grafts and flaps (compromised);

Acute thermal burn injury;

Idiopathic sudden sensorineural hearing loss (ISSNHL) (patients with moderate to profound

ISSNHL who present within 14 days of symptom onset).

American Academy of Otolaryngology-Head and Neck Surgery (AAOHNS)

In 2012, the AAOHNS published a clinical guideline on treatment of sudden hearing loss. (74) The guideline includes a statement that HBO2 may be considered a treatment option for patients who present within 3 months of a diagnosis of ISSNH. The document states, “Although HBO2 therapy is not widely available in the United States and is not recognized by many U.S. clinicians as an intervention for ISSNHL, the panel felt that the level of evidence for hearing improvement, albeit modest and imprecise, was sufficient to promote greater awareness of HBO2 therapy as an intervention for [this condition]”.

Alberta Heritage Foundation for Medical Research (AHFMR)

The March 2003 Information Paper, produced by AHFMR, Alberta, Canada government sponsored research programs, reviewed recent findings on evidence for the effectiveness of HBO2 therapy as a Health Technology Assessment. (75) The AHEMR conclusions are as follows.

“There is support for use of HBO2 in for the following conditions: Decompression sickness, air and gas embolism, and gas gangrene.”

“There is conditional support for use of HBO2 in: Carbon monoxide poisoning, osteoradionecrosis, diabetic wounds, necrotizing soft tissue infections.”

“There is no consensus on support for use of HBO2 in: Osteomyelitis, thermal burns, soft tissue radionecrosis, compromised skin grafts and flaps, dental implants following radiotherapy, retinal artery occlusion.”

“Use of HBO2 is not supported for: Crush injury, non-diabetic wounds, MS, CP, or for a large number of conditions, including but not limited to: decubitus ulcers, necrotizing arachnidism, actinomycosis, cardiovascular conditions, Bell’s palsy, cluster or migraine headaches, Legg-Calve-Perthes disease, sudden deafness and acoustic trauma, Crohn’s disease, osteoporosis, cancer cyanide poisoning, head trauma, cerebral edema, acquired brain injury, cognitive impairment, senile dementia, glaucoma, keratoendotheliosis, HIV infection, anemia from exceptional blood loss, insulin-dependent diabetes mellitus, facial neuritis, arthritis, spinal injuries, and non-union of fractures.”

Summary of Evidence

The evidence for the use of THBO2 therapy in individuals who might respond to increased oxygen delivery to tissues includes primarily case series and case reports. Relevant outcomes are overall survival, symptoms, change in disease status, and functional outcomes. Only 1 RCT was published on any indication. This study, in patients with diabetic foot ulcers, had a small sample size and did not find a significant benefit of topical HBO2. The evidence is insufficient to determine the effects of the technology on health outcomes. THBO2 therapy is considered experimental, investigational and/or unproven.

The evidence for the use of systemic HBO2 therapy in individuals with nonhealing diabetic wounds of the lower extremities; chronic refractory osteomyelitis; soft-tissue radiation necrosis (e.g., radiation enteritis, cystitis, proctitis); crush injury, reperfusion injury, compartment syndrome, and other acute traumatic ischemias; venous stasis ulcers; compromised skin graft or flap, or for enhancement of healing in a selected problem wound; gas gangrene; soft tissue infections due to mixed aerobic and anaerobic organisms with tissue necrosis and refractory bacteroides infections; decompression sickness; acute air or gas embolism; brown recluse spider bite; acute carbon monoxide poisoning (intoxication) and smoke inhalation (not chronic); thermal and specific second and third degree burns; idiopathic sudden sensorineural hearing loss; acute cyanide poisoning; profound anemia with exceptional blood loss when blood transfusion is impossible or must be delayed; selected refractory mycoses; intracranial abscess; acute cerebral edema; non-acute arterial insufficiency ulcer; decubitus ulcers; planned dental surgery (non-implant-related) of an irradiated jaw, and includes systematic reviews and/or recommendations from the UHMS’s guidelines. Relevant outcomes include overall survival, symptoms, change in disease status, and functional outcomes. For all of the above indications, evidence and/or UHMS guidelines support use of systemic HBO2 therapy. The evidence is sufficient to determine qualitatively that the technology results in a meaningful improvement in health outcomes and may be considered medical necessary.

The evidence for the use of systemic HBO2 therapy in individuals with any condition other than those specified in the previous paragraph includes systematic reviews, a few small RCTs or small uncontrolled studies. Relevant outcomes include overall survival, symptoms, change in disease status, and functional outcomes. The available studies do not demonstrate that HBO2 therapy improves relevant outcomes. The evidence is insufficient to determine the effects of the technology on health outcomes and is considered experimental, investigational and/or unproven.

Contract:

Each benefit plan, summary plan description or contract defines which services are covered, which services are excluded, and which services are subject to dollar caps or other limitations, conditions or exclusions. Members and their providers have the responsibility for consulting the member's benefit plan, summary plan description or contract to determine if there are any exclusions or other benefit limitations applicable to this service or supply. If there is a discrepancy between a Medical Policy and a member's benefit plan, summary plan description or contract, the benefit plan, summary plan description or contract will govern.

Coding:

HCPCS code A4575 is used to describe the disposable appliance that is positioned around the wound area for THBO2 therapy. Conventional O2 tanks, typically gas, are used to supply the O2.

CODING:

Disclaimer for coding information on Medical Policies

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive.

The presence or absence of procedure, service, supply, device or diagnosis codes in a Medical Policy document has no relevance for determination of benefit coverage for members or reimbursement for providers. Only the written coverage position in a medical policy should be used for such determinations.

Benefit coverage determinations based on written Medical Policy coverage positions must include review of the member’s benefit contract or Summary Plan Description (SPD) for defined coverage vs. non-coverage, benefit exclusions, and benefit limitations such as dollar or duration caps.

CPT/HCPCS/ICD-9/ICD-10 Codes

The following codes may be applicable to this Medical policy and may not be all inclusive.

CPT Codes

99183

HCPCS Codes

A4575, G0277

ICD-9 Diagnosis Codes

Refer to the ICD-9-CM manual

ICD-9 Procedure Codes

Refer to the ICD-9-CM manual

ICD-10 Diagnosis Codes

Refer to the ICD-10-CM manual

ICD-10 Procedure Codes

Refer to the ICD-10-CM manual


Medicare Coverage:

The information contained in this section is for informational purposes only. HCSC makes no representation as to the accuracy of this information. It is not to be used for claims adjudication for HCSC Plans.

The Centers for Medicare and Medicaid Services (CMS) does have a national Medicare coverage position.

A national coverage position for Medicare may have been changed since this medical policy document was written. See Medicare's National Coverage at <http://www.cms.hhs.gov>.

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76. Cimsit M, Uzun G, Yildiz S. Hyperbaric oxygen therapy as an anti-infective agent. Expert Rev Anti Infect Ther. Oct 2009; 7(8):1015-26. PMID 19803709

77. Carson S, McDonagh M, Rusmman B, et al. Hyperbaric oxygen therapy for stroke: A systematic review of the evidence. Clin Rehab. Dec 2005; 19(8):819-33. PMID 16323381

78. Vila JF, Barcarce PE, et al. Improvement in motor and cognitive impairment after hyperbaric oxygen therapy in a selected group of patients with cerebrovascular disease: A prospective single-blind controlled trial. Undersea and Hyperbaric Medicine (2006 September-October) 32(5):341-9.

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82. Hyperbaric Oxygen Therapy. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Reference Manual (2015 August) Medicine 2.01.04.

Policy History:

Date Reason
7/15/2017 Reviewed. No changes.
10/1/2016 Document updated with literature review. The following indication was added as medically necessary: a cute postoperative foot surgical treatment for patients with Wagner grade-3 or higher diabetic foot ulcers. The following indications were added as experimental, investigational and/or unproven: fibromyalgia and mental illness.
5/1/2015 Document updated with literature review. The following indications were added as experimental, investigational and/or unproven: Arthritic diseases, osteoarthritis or rheumatoid; Asthma; Cardiogenic shock; Depression; Inflammatory bowel disease; Hepatic necrosis; Hepatitis; Herpes zoster; Human immunodeficiency virus infection or acquired immune deficiency syndrome; Motor dysfunction associated with stroke; Organ transplantation or storage; Osteonecrosis of the jaw, bisphosphonate-related; Post-traumatic stress disorder or other stress disorders; Pulmonary emphysema; Senility; Sport’s injury; Septicemia, anaerobic (unrelated to clostridial), or systemic aerobic infection; Tetanus; Ulcerative Colitis; Vascular dementia or chronic brain syndromes, neovascular causes (such as Pick’s disease, Alzheimer’s disease, and Korsakoff’s disease). Title changed from Hyperbaric Oxygen (HBO 2 ) Pressurization.
12/1/2013 Document updated with literature review. The following was added: 1) New medically necessary indications for uses of HBO 2 therapy when criteria is met: Idiopathic sudden sensorineural hearing loss (ISSNHL); 2) New experimental, investigational and unproven indications for uses of HBO 2 therapy: Bell’s palsy; idiopathic femoral neck necrosis; lymphedema of the arm; acute osteomyelitis; radiation-induced injury to head, neck, anus, or rectum; radiation necrosis of non-neurologic tissue; reduction of adverse effects at any point of therapy, including early onset effects and delayed effects; and acute surgical and traumatic wounds. Otherwise, coverage for all other indications remains unchanged.
7/15/2011 Coverage revised only. The following changes were made: 1) Systemic HBO 2 may be considered medically necessary to treat soft-tissue radiation necrosis, including radiation enteritis, cystitis, or proctitis; 2) Review of diabetic wounds may occur after 30 systemic HBO 2 treatments.
3/1/2010 Revised/updated entire document, HBO 2 may be considered medically necessary when clinical criteria is met.
9/15/2008 Coverage revised, Rationale revised, References revised.
8/15/2007 Revised/updated entire document.
11/1/2000 Revised/updated entire document.
3/1/2000 Revised/updated entire document.
1/1/1996 Revised/updated entire document.
5/1/1996 Medical policy number changed.
5/1/1990 New medical document.

Archived Document(s):

Title:Effective Date:End Date:
Hyperbaric Oxygen (HBO2) Therapy10-01-201810-14-2019
Hyperbaric Oxygen (HBO2) Therapy07-15-201709-30-2018
Hyperbaric Oxygen (HBO2) Therapy10-01-201607-14-2017
Hyperbaric Oxygen (HBO2) Therapy05-01-201509-30-2016
Hyperbaric Oxygen (HBO2) Pressurization12-01-201304-30-2015
Hyperbaric Oxygen (HBO2) Pressurization07-15-201111-30-2013
Hyperbaric Oxygen (HBO2) Pressurization03-01-201007-14-2011
Hyperbaric Oxygen (HBO2) Pressurization09-15-200802-28-2010
Hyperbaric Oxygen (HBO2) Pressurization08-15-200709-14-2008
Hyperbaric Oxygen (HBO2) Pressurization11-01-200008-14-2007
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