hyperbaric oxygen therapy

Hyperbaric Oxygen Therapy Apr 14 1

National Medical Policy Subject: Hyperbaric Oxygen Therapy Policy Number: NMP220

Effective Date*: Update of NMDAG Policy, June 2005

Updated: April 2014

This National Medical Policy is subject to the terms in the

IMPORTANT NOTICE

at the end of this document

For Medicaid Plans: Please refer to the appropriate Medicaid Manuals for

coverage guidelines prior to applying Health Net Medical Policies

The Centers for Medicare & Medicaid Services (CMS)

For Medicare Advantage members please refer to the following for coverage

guidelines first:

Use Source Reference/Website Link

X National Coverage Determination

(NCD)

Hyperbaric Oxygen Therapy:

http://www.cms.gov/medicare-coverage-

database/search/advanced-search.aspx

National Coverage Manual Citation

Local Coverage Determination

(LCD)*

X Article (Local)* Hyperbaric Oxygen Therapy: http://www.cms.gov/medicare-coverage-

database/search/advanced-search.aspx

X Other Technology assessments:

Hyperbaric Oxygen Therapy in Treatment of

Hypoxic Wounds:

http://www.cms.gov/medicare-coverage-

database/details/technology-assessments-

details.aspx?TAId=12&SearchType=Advanced&

CoverageSelection=Both&NCSelection=NCA%7c

CAL%7cNCD%7cMEDCAC%7cTA%7cMCD&Articl

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erapy&KeyWordLookUp=Doc&KeyWordSearchTy

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A Horizon Scan: Uses of Hyperbaric Oxygen

Therapy. Technology Assessment Report, Oct

2006:

http://www.cms.gov/determinationprocess/dow

nloads/id42TA.pdf

None Use Health Net Policy

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Current Policy Statement Health Net Inc. considers hyperbaric oxygen therapy medically necessary for the

following medical conditions:

1. Actinomycosis, only as an adjunct to conventional therapy when the disease

process is refractory to antibiotics and surgical treatments

2. Acute carbon monoxide intoxication

3. Acute peripheral arterial insufficiency

4. Acute traumatic peripheral ischemia

5. Chronic refractory osteomyelitis, unresponsive to conventional medical and

surgical management

6. Crush injuries and suturing of severed limbs

7. Cyanide poisoning

8. Decompression illness

9. Diabetic wounds of the lower extremities and all of the following:

Type I or type II diabetes and a lower extremity wound that is due to

diabetes

Wound classified as Wagner grade III or higher, characterized by deep

ulcer with abscess or osteomylitis

Failed course (at least 30 days) of standard wound therapy, including

all of the following:

Assessment of a patients vascular status


Correction of any vascular problems in the affected limb, if possible

optimization of nutritional status, optimization of glucose control, debridement by any means to remove devitalized tissue, maintenance of a clean, moist bed of granulation tissue, treatment to resolve any infection that might be present

Note: Wounds must be evaluated at least every 30 days during administration of HBO

therapy. Continued treatment with HBO therapy is not considered medically

necessary if measurable signs of healing have not been demonstrated within any

30-day period of treatment.

10. Gas embolism

11. Gas gangrene

12. Osteoradionecrosis as an adjunct to conventional treatment

13. Preparation and preservation of compromised skin grafts (not for primary

management of wounds)

14. Progressive necrotizing infections (necrotizing fasciitis)

15. Soft tissue radionecrosis as an adjunct to conventional treatment

16. Chronic radiation enteritis in an effort to avoid surgical intervention, when

conservative management has failed

Note: Improvement of symptoms (e.g. bleeding, pain, diarrhea, etc.)

have been noted following a series of 30 daily treatments, however, in

some patients with partial symptom response, additional treatment

sessions may be necessary.

17. Radiation cystitis that is resistant or has failed conservative intervention

Note: Soft tissue radionecrosis of the bladder has a higher response

rate if at least 30 treatments of HBO treatments are administered;

If significant fibrosis and ischemia have already occurred, HBO therapy

does not reverse the changes and only prevents further injury.

Exclusions Health Net, Inc. considers Hyperbaric oxygen therapy not medically necessary for the

any of the following conditions:

1. Acute cerebral edema

2. Acute thermal and chemical pulmonary damage (for example, smoke

inhalation with pulmonary insufficiency

3. Aerobic septicemia

4. Anaerobic septicemia and infection other than clostridial

5. Arthritic diseases

6. Autism

7. Cardiogenic shock

8. Chronic peripheral vascular insufficiency

9. Cutaneous, decubitus, and stasis ulcers

10. Exceptional blood loss anemia

11. Hepatic necrosis

12. Lyme Disease

13. Multiple sclerosis

14. Myocardial infarction

15. Nonvascular causes of chronic brain syndrome (Pick's disease, Alzheimer's

disease, Korsakoff's disease)


16. Organ storage

17. Pulmonary emphysema

18. Senility

19. Sickle cell anemia

20. Systemic aerobic infection

21. Tetanus

Health Net, Inc. considers Hyperbaric oxygen therapy investigational for any of

the following conditions because although there are ongoing studies and clinical

trials, there continues to be inadequate scientific evidence in the peer-reviewed

medical literature to support its efficacy:

1. Acute or chronic cerebral vascular insufficiency 2. Organ transplantation

3. Skin burns (thermal)

4. Topical application of oxygen (including topical HBOT administered to the

open wound in small limb-encasing devices)

5. Idiopathic Sudden Deafness, Acoustic Trauma or idiopathic sudden

sensorineural hearing loss (ISSNHL)*

Note* - HBOT is not FDA approved for any hearing loss, including but not limited to

ISSNHL.

Contraindications to Hyperbaric oxygen therapy include: Untreated pneumothorax

Treatment with doxorubicin, cisplatin (Cisplatinum), bleomycin

(Blenoxane), disulfiram (Antabuse), and mafenide acetate

(Sulfamylon), because of potentially toxic effects when combined with

HBO therapy.

Upper respiratory infections, otitis media, and acute or chronic

sinusitis are relative contraindications.

Severe obstructive pulmonary disease (COPD), as HBOT may cause

apnea with an increased risk of seizures in individuals with decreased

oxygen tolerance.

Codes Related To This Policy NOTE:

The codes listed in this policy are for reference purposes only. Listing of a code in

this policy does not imply that the service described by this code is a covered or non-

covered health service. Coverage is determined by the benefit documents and

medical necessity criteria. This list of codes may not be all inclusive.

On October 1, 2014, the ICD-9 code sets used to report medical diagnoses and

inpatient procedures will be replaced by ICD-10 code sets. Health Net National

Medical Policies will now include the preliminary ICD-10 codes in preparation for this

transition. Please note that these may not be the final versions of the codes and

that will not be accepted for billing or payment purposes until the October 1, 2014

implementation date.

ICD-9 Codes 039.0-039.9 Actinomycotic infections

040.0 Gas Gangrene


250.00 250.82 Diabetes with other specified manifestations/complications 388.2 Sudden hearing loss

444.21 Arterial Embolism and thrombosis of the upper extremity

444.22 Arterial Embolism and thrombosis of the lower extremity

444.81 Arterial embolism and thrombosis of iliac artery

526.89 Osteonecrosis, other than mandible

558.1 Gastroenteritis and colitis due to radiation

707.10 707.19 Ulcer of the lower limb, unspecified 728.86 Necrotizing fasciitis

730.10-730.19 Chronic Osteomyelitis

902.53 Injury to the iliac artery

903.1 Injury to the brachial blood vessels

903.01 Injury to the axillary artery

904.0 Injury to the common femoral artery

904.41 Injury to the popliteal artery

925.1 929.9 Crush Injuries 958.0 Air embolism

986 Toxic Effect of Carbon monoxide

987.7 Toxic effect of hydrocyanic acid gas

989.0 Toxic effect of hydrocyanic acid and cyanides

990 Radionecrosis, soft tissue

993.2 - 993.3 Decompression Sickness

996.52 Skin graft failure or rejection

996.90-996.99 Complication of reattached extremity or body part

999.1 Air embolism

ICD-10 Codes A42.0-A42.9 Actinomycosis

A48.0 Gas gangrene

E10.621 Type I diabetes mellitus with foot ulcer

E10.622 Type I diabetes mellitus with other skin ulcer

E11.621 Type 2 diabetes mellitus with foot ulcer

E11.622 Type 2 diabetes mellitus with other skin ulcer

H91.20-H91.23 Sudden Idiopathic hearing loss

I74.2 Embolism and thrombosis of arteries of the upper extremities

I74.3 Embolism and thrombosis of arteries of the lower extremities

I74.5 Embolism and thrombosis of iliac artery

L97.10-L97.929 Non-pressure chronic ulcer of lower limb, not elsewhere

classified

M27.8 Other specified diseases of jaws

M72.6 Necrotizing fasciitis

M86.31-M86.39 Chronic multifocal osteomyelitis

M84.40-M846.49 Chronic osteomyelitis with draining sinus

M86.50-M86.59 Other chronic hematogenous osteomyelitis

M86.60-M86.69 Other chronic osteomyelitis

M86.8-m86.8X9 Other osteomyelitis

S07.0-S07.9 Crushing injury of head

S35.51-S35.516 Injury of iliac artery or vein

S38.1-S38.232 Crushing injury of abdomen, lower back, and pelvis

S45.00-S45.099 Injury of axillary artery

S45.101-S45.199 Injury of brachial artery

S47.1-S47.9 Crushing injury of shoulder and upper arm

S77.00-S77.22 Crushing injury of hip and thigh


S75.00-S75.099 Injury of femoral artery

S85.00-S85.099 Injury of popliteal artery

T57.3X1-T57.3X4 Toxic effect of hydrogen cyanide

T58.01-T58.94 Toxic effect of carbon monoxide

T65.0X1-T65.0X4 Toxic effects of cyanides

T66 Radiation sickness, unspecified

T70.0-T70.9 Effects of air pressure and water pressure

T79.0 Air embolism (traumatic)

T86.820-T86.829 Complications of skin graft (allograft0 (autograft)

T87.0X1-T87.0X9 Complications of reattached (part of) upper extremity

T87.1X1-T87.1X9 Complications of reattached (part of) lower extremity

T87.2 Complications of other reattached body part

T80.0 Air embolism following infusion, transfusion and therapeutic

injection

CPT Codes 99183 Physician or other qualified health care professional attendance

and supervision of hyperbaric oxygen therapy, per session

HCPCS Codes N/A

Scientific Rationale Update April 2014 Cvorovic et al (2013) compared the effects of hyperbaric oxygen (HBO) and

intratympanic (IT) steroid injection on hearing after the failure of primary treatment

in patients with idiopathic sudden sensorineural hearing loss (ISSHL) in a prospective

randomized trial. Fifty patients with failure of primary therapy for ISSHL were

included in the study. After primary treatment with systemic steroids and failure of

therapy, defined as less than 10-dB hearing gain, 50 patients were enrolled in the

study and received either hyperbaric oxygen or intratympanic steroid treatment. The

patients were not matched and not similar. Main outcomes measures include

hearing gain at 0.25, 0.5, 1, 2, and 4 kHz after treatment. There were significant

differences between hearing thresholds at all frequencies before and after the HBO

treatment. Similarly, there were significant differences between hearing thresholds

at most frequencies (except 2 kHz) before and after the treatment in the IT group.

The subgroups of patients with pure tone average less than 81 dB and were younger

than 60 years had better response to HBO treatment than those with profound

deafness and in the elderly. Investigators concluded HBO and IT steroid therapy

could be successfully used as salvage therapies in patients with sudden deafness.

Further study is needed to demonstrate superiority of one of the treatments.

Yldrm et al (2013) sought to investigate whether the hyperbaric oxygen therapy starting time affects the management of sudden sensorineural hearing loss. Fifty-

nine patients with sudden sensorineural hearing loss admitted to our clinic between

2008 and 2012 were retrospectively included in this study. All patients received

hyperbaric oxygen therapy. In addition, each patient received intravenous piracetam

and 37 patients received steroid therapy. Hyperbaric oxygen therapy was initiated

between 1 and 7 days with 20 patients determined as Group A, between 8 and 14

days with 25 patients determined as Group B and between 15 and 28 days with 14

patients determined as Group C. Hearing gains of these three groups were

statistically evaluated. Each of them showed statistically significant improvement.

Lowest hearing gain was observed in Group C and the gain of this group was


statistically less than the other two groups. There was no significant difference

between the hearing gains of the Group A and Group B. Starting hyperbaric oxygen

therapy in patients with sudden sensorineural hearing loss within the first 14 days

has positive effect on the prognosis of the disease.

Ouassi et al (2014) reported that pelvic radiation disease (PRD) occurs in 2-11% of

patients undergoing pelvic radiation for urologic and gynecologic malignancies. HBOT

has previously been described as a noninvasive therapeutic option for the treatment

of PRD. The authors analyzed prospectively the results of HBOT in 44 consecutive

patients with PRD who were resistant to conventional oral or topical treatments. The

median age of the cohort was 65.7years (39-85). Twenty-seven percent of patients

required blood transfusion (n = 12). The median of delay between radiotherapy and

HBOT was 26 months (3-175). The authors evaluated the results of HBOT, using

SOMA-LENT Scale. Results. SOMA-LENT score was decreased in 59% of patient. The

median of SOMA-LENT score before HBOT was significantly higher, being equal to 14

(0-36), than after HBOT with the SOMA-LENT score of 12 (0-38) (P = 0.003).

Tenesmus (P = 0.02), bleeding (P = 0.0001), and ulceration (P = 0.001) significantly

decreased after HBOT. Regarding patients with colostomy, 33% (n = 4) benefited

from colostomies closure. HBOT was generally well tolerated. Only one patient

stopped precociously due to transient myopia. The authors concluded this study is in

favor of the interest of HBOT in pelvic radiation disease treatment (PRD).

Walker et al (2013) reported that HBOT is a proposed treatment for mild traumatic

brain injury (mTBI) and residual postconcussion syndrome (PCS) but that it has not

been rigorously studied for this condition. Investigators examined for possible

effects on psychomotor (balance and fine motor) and cognitive performance 1 week

after an HBOT intervention in service members with PCS after mTBI in a a

randomized, double-blind, sham control, feasibility trial comparing pretreatment and

posttreatment in 60 male active-duty marines with combat-related mTBI and PCS

persisting for 3 to 36 months. Participants were randomized to 1 of 3 preassigned

oxygen fractions (10.5%, 75%, or 100%) at 2.0 atmospheres absolute (ATA),

resulting in respective groups with an oxygen exposure equivalent to (1) breathing

surface air (Sham Air), (2) 100% oxygen at 1.5 ATA (1.5 ATAO2), and (3) 100%

oxygen at 2.0 ATA (2.0 ATAO2). Over a 10-week period, participants received 40

hyperbaric chamber sessions of 60 minutes each. Outcome measures, including

computerized posturography (balance), grooved pegboard (fine motor

speed/dexterity), and multiple neuropsychological tests of cognitive performance,

were collected preintervention and 1-week postintervention. Despite the multiple

sensitive cognitive and psychomotor measures analyzed at an unadjusted 5%

significance level, this study demonstrated no immediate postintervention beneficial

effect of exposure to either 1.5 ATAO2 or 2.0 ATAO2 compared with the Sham Air

intervention. Investigators concluded these results do not support the use of HBOT

to treat cognitive, balance, or fine motor deficits associated with mTBI and PCS.

Boussi-Gross et al (2013) tested the effectiveness of HBOT in improving brain

function and quality of life in mTBI patients suffering chronic neurocognitive

impairments. The trial population included 56 mTBI patients 1-5 years after injury

with prolonged post-concussion syndrome (PCS). The HBOT effect was evaluated by

means of prospective, randomized, crossover controlled trial: the patients were

randomly assigned to treated or crossover groups. Patients in the treated group were

evaluated at baseline and following 40 HBOT sessions; patients in the crossover

group were evaluated three times: at baseline, following a 2-month control period of

no treatment, and following subsequent 2-months of 40 HBOT sessions. The HBOT


protocol included 40 treatment sessions (5 days/week), 60 minutes each, with 100%

oxygen at 1.5 ATA. "Mindstreams" was used for cognitive evaluations, quality of life

(QOL) was evaluated by the EQ-5D, and changes in brain activity were assessed by

SPECT imaging. Significant improvements were demonstrated in cognitive function

and QOL in both groups following HBOT but no significant improvement was

observed following the control period. SPECT imaging revealed elevated brain activity

in good agreement with the cognitive improvements. Investigators concluded HBOT

can induce neuroplasticity leading to repair of chronically impaired brain functions

and improved quality of life in mTBI patients with prolonged PCS at late chronic

stage.

A Cochrane review reported by Eskes et al (2013) sought to determine the effects of

HBOT on the healing of acute surgical and traumatic wounds. Randomised controlled

trials (RCTs) comparing HBOT with other interventions such as dressings, steroids, or

sham HOBT or comparisons between alternative HBOT regimens were reviewed.

Two review authors conducted selection of trials, risk of bias assessment, data

extraction and data synthesis independently. Any disagreements were referred to a

third review author. Four trials involving 229 participants were included. The studies

were clinically heterogeneous, which precluded a meta-analysis. One trial (48

participants with burn wounds undergoing split skin grafts) compared HBOT with

usual care and reported a significantly higher complete graft survival associated with

HBOT (95% healthy graft area risk ratio (RR) 3.50; 95% confidence interval (CI)

1.35 to 9.11). A second trial (10 participants in free flap surgery) reported no

significant difference between graft survival (no data available). A third trial (36

participants with crush injuries) reported significantly more wounds healed (RR 1.70;

95% CI 1.11 to 2.61), and significantly less tissue necrosis (RR 0.13; 95% CI 0.02 to

0.90) with HBOT compared to sham HBOT. The fourth trial (135 people undergoing

flap grafting) reported no significant differences in complete graft survival with HBOT

compared with dexamethasone (RR 1.14; 95% CI 0.95 to 1.38) or heparin (RR 1.21;

95% CI 0.99 to 1.49). Many of the predefined secondary outcomes of the review

were not reported. All four trials were at unclear or high risk of bias. Reviewers

concluded there is a lack of high quality, valid research evidence regarding the

effects of HBOT on wound healing. Whilst two small trials suggested that HBOT may

improve the outcomes of skin grafting and trauma, these trials were at risk of bias.

Further evaluation by means of high quality RCTs is needed.

Scientific Rationale Update April 2013 The 'Clinical Practice Guideline on Sudden Hearing Loss' (January 3, 2012) is noted

on the 'Otolaryngology, Head and Neck Surgery' site. This purpose of this guideline is

to provide clinicians with evidence-based recommendations in evaluating patients

with sudden hearing loss (SHL), with particular emphasis on managing sudden

sensorineural hearing loss (SSNHL).

The panel made strong recommendations that clinicians should:

1. Distinguish sensorineural hearing loss from conductive hearing loss in a

patient presenting with SHL;

2. Educate patients with idiopathic sudden sensorineural hearing loss (ISSNHL)

about the natural history of the condition, the benefits and risks of medical

interventions, and the limitations of existing evidence regarding efficacy;

3. Counsel patients with incomplete recovery of hearing about the possible

benefits of amplification and hearing-assistive technology and other

supportive measures; and


4. Not order computerized tomography of the head/brain in the initial evaluation

of a patient with presumptive SSNHL, nor obtain routine laboratory tests in

patients with ISSNHL.

The panel also made recommendations that clinicians should:

1. Assess patients with presumptive SSNHL for bilateral SHL, recurrent episodes

of SHL, or focal neurologic findings;

2. Diagnose presumptive ISSNHL if audiometry confirms a 30-dB hearing loss at

consecutive frequencies and an underlying condition cannot be identified by

history and physical examination;

3. Evaluate patients with ISSNHL for retrocochlear pathology by obtaining

magnetic resonance imaging, auditory brainstem response, or audiometric

follow-up;

4. Offer intratympanic steroid perfusion when patients have incomplete recovery

from ISSNHL after failure of initial management;

5. Obtain follow-up audiometric evaluation within 6 months of diagnosis for

patients with ISSNHL; and

6. Not routinely prescribe antivirals, thrombolytics, vasodilators, vasoactive

substances, or antioxidants to patients with ISSNHL.

The panel offered as options that clinicians may offer:

1. Corticosteroids as initial therapy to patients with ISSNHL; and

2. Hyperbaric oxygen therapy* within 3 months of diagnosis of ISSNHL.

Note* This recommendation is based on aggregate evidence quality Grade B,

systematic review of RCTs with methodological limitations, and with a balance

between benefit and harm.

Per the above guidelines:

Sudden hearing loss is defined as a rapid onset, occurring over a 72-hour period, of a subjective sensation of hearing impairment in one or both ears.

Sudden sensorineural hearing loss (SNHL) is a subset of SHL that is sensorineural in nature and meets certain audiometric criteria.

(a) Sensorineural hearing loss indicates an abnormality of the cochlea,

auditory nerve, or higher aspects of central auditory perception or processing.

(b) The most frequently used audiometric criterion is a decrease in hearing of

30 decibels (dB), affecting at least 3 consecutive frequencies.

Idiopathic sudden sensorineural hearing loss (ISSNHL) is defined as SSNHL with no identifiable cause despite adequate investigation.

The SSNHL definition used throughout this guideline is based on its consistent use in

the literature and National Institute on Deafness and Other Communication Disorders

(NIDCD) criteria; however, the panel recognizes that in clinical practice, expanding

the definition to cases with less than 30 dB of hearing loss may be considered. The

distinction between SSNHL and other causes of SHL is one that should be made by

the initial treating health care provider, so that early diagnosis and management can

be instituted. Nonidiopathic causes of SSNHL must be identified and addressed

during the course of management; the most pressing of these are vestibular

schwannoma (acoustic neuroma), stroke, and malignancy. Up to 90% of SSNHL,


however, is idiopathic at presentation and is presumptively attributed to vascular,

viral, or multiple etiologies.

Long-term follow-up is recommended as some patients will have an underlying cause

identified that may not be evident at initial presentation. In addition, the patient with

partial or no hearing recovery, or persistent tinnitus, will require ongoing

management from otolaryngological, audiological, and psychological perspectives.

This guideline is intended for all clinicians who diagnose or manage adult patients

(age 18 years and older) who present with SHL. After addressing causes, diagnosis,

and treatments of non- SSNHL briefly, this guideline will address SSNHL in detail.

Important points to keep in mind include the following:

A cause for SSNHL is identified in only 10% to 15% of patients at the time of

presentation. Emergency intervention may be needed for rare, life-threatening

conditions of which SSNHL is a part. In up to a third of cases, the cause may be

identified only after long-term follow-up evaluations.

In 85% to 90% of cases, despite thorough evaluation, the underlying cause is

unknown or uncertain at the time of presentation, and treatment decisions are

generally made without knowledge of the etiology. It is appropriate, therefore,

to approach these idiopathic cases in a common way, understanding that the

underlying etiologies may be very dissimilar.

The primary presenting symptom of SHL is a full or blocked ear. Because this is

such a common and nonspecific symptom, both patients and physicians are not

sufficiently frightened or worried by it. Thus, evaluation and treatment are often

delayed. New onset of ear blockage or fullness can be a symptom of potentially

serious conditions and warrants prompt evaluation.

Conversely, the patient with SHL may be very frightened; the nearly universal

accompanying tinnitus seen in SSNHL will frequently contribute intensely to his

or her anxiety and depression. All members of the hearing health care team

should be cognizant of the psychological response to the sudden loss of a

primary sense.

Familiarity with hearing aids, hearing-assistive technology (HAT), tinnitus

management, and implantable hearing solutions is required in the ongoing

management of these patients.

A team approach to the overall management of these patients is encouraged.

In summary, although the use of HBOT was noted in the 2012 Guidelines as a Grade

B recommendation by the American Academy of Otolaryngology-Head and Neck

Surgery, for treatment within 3 months of the diagnosis of idiopathic sudden

sensorineural hearing loss (ISSNHL), HBOT is not currently approved by the U.S.

Food Administration (FDA) for the treatment of any hearing loss, including but not

limited to ISSNHL. Therefore, Health Net, Inc. would continue to consider this

investigational at this time. In addition, the studies noted above in the Scientific

Rationale update for March 2013, note that there is no evidence of a beneficial effect

of HBOT on chronic ISSHL or tinnitus and the authors do not recommend the use of

HBOT for this purpose. The studies also note that the use of HBOT was not

statistically significant in the success rate with ISSHL, and that systemic plus


intratympanic steroid administration is more effective than systemic steroids plus

HBO therapy, and can be a useful first-choice treatment for ISSNHL.

Scientific Rationale Update March 2013 In a Cochrane review, Bennett et al (2012) assessed the benefits and harms of

hyperbaric oxygen therapy (HBOT) for treating Idiopathic sudden sensorineural

hearing loss (ISSHL) and/or tinnitus. Randomized studies comparing the effect on

ISSHL and tinnitus of HBOT and alternative therapies. Three authors evaluated the

quality of trials using the 'Risk of bias' tool and extracted data from the included

trials. Seven trials contributed to this review (392 participants). The studies were

small and of generally poor quality. Pooled data from two trials did not show any

significant improvement in the chance of a 50% increase in hearing threshold on

pure-tone average with HBOT (risk ratio (RR) with HBOT 1.53, 95% confidence

interval (CI) 0.85 to 2.78, P = 0.16), but did show a significantly increased chance of

a 25% increase in pure-tone average (RR 1.39, 95% CI 1.05 to 1.84, P = 0.02).

There was a 22% greater chance of improvement with HBOT, and the number

needed to treat (NNT) to achieve one extra good outcome was 5 (95% CI 3 to 20).

There was also an absolute improvement in average pure-tone audiometric threshold

following HBOT (mean difference (MD) 15.6 dB greater with HBOT, 95% CI 1.5 to

29.8, P = 0.03). The significance of any improvement in tinnitus could not be

assessed. There were no significant improvements in hearing or tinnitus reported for

chronic presentation (six months) of ISSHL and/or tinnitus. Reviewers concluded for

people with acute ISSHL, the application of HBOT significantly improved hearing, but

the clinical significance remains unclear. We could not assess the effect of HBOT on

tinnitus by pooled analysis. In view of the modest number of patients,

methodological shortcomings and poor reporting, this result should be interpreted

cautiously. An appropriately powered trial is justified to define those patients (if any)

who can be expected to derive most benefit from HBOT. There is no evidence of a

beneficial effect of HBOT on chronic ISSHL or tinnitus and the reviewers do not

recommend the use of HBOT for this purpose.

Filipo et al (2012) assessed for the first time the efficacy of the association of

intratympanic (IT) steroid and HBO therapy in patients presenting ISSNHL,

comparing this protocol with another consisting of IV steroid administration and HBO

therapy. A total of 48 patients presenting ISSNHL were recruited. Patients were

divided into two categories: the severe ISSNHL group with a pure-tone average

(PTA) between 70 and 90 dB, and the profound ISSNHL group with a PTA >90 dB.

The first protocol consisted of 10 days of HBO therapy together with IV

methylprednisolone 1 mg/kg body weight for 7 days; the second protocol consisted

of HBO therapy for 10 days, associated with an IT injection of prednisolone at a dose

of 62.5 mg/ml, once a day for 3 consecutive days, performed 2 h before the HBO

therapy. The overall success rate was superior in the group submitted to IT steroid

and HBO therapy. Nevertheless, these clinical results were not statistically

significant.

Suzuki et al (2012) examined the efficacy of intratympanic steroid administration in

comparison with HBOT in patients with ISSNHL in a retrospective study. Two

hundred seventy-six consecutive patients with ISSNHL (average hearing levels at

250, 500, 1,000, 2,000, and 4,000 Hz 40 dB; time from onset to treatment 30 days) were enrolled. All the patients were given intravenous hydrocortisone (400

mg/day) followed by tapered doses. In addition, 174 patients underwent HBO

therapy (HBO group), and 102 patients received intratympanic dexamethasone

injection (IT group). The hearing outcomes were evaluated by six indices; the cure


rate, marked-recovery rate (percent of patients with hearing gains 30 dB), recovery rate (percent of patients with hearing gains 10 dB), hearing gain, hearing level after treatment, and hearing improvement rate compared to the unaffected

contralateral ear. There was no significant difference in the cure rate, marked-

recovery rate, hearing gain, hearing level after treatment, or hearing improvement

rate between the two groups; however, the recovery rate was significantly higher in

the IT group than in the HBO group (79.4% vs. 68.4%; P = .048). Multiple logistic

regression analysis also showed that patients in the IT group were significantly more

likely to recover than those in the HBO group (odds ratio: 2.045; 95% confidence

interval: 1.097-3.812; P = .024). Investgators concluded systemic plus

intratympanic steroid administration is more effective than systemic steroids plus

HBO therapy, and can be a useful first-choice treatment for ISSNHL.

Sampanthavivat et al (2012) evaluated the efficacy of HBOT in sixty Thai children

with autism, aged three to nine years, were randomly assigned to receive 20 one-

hour sessions of either HBOT at 153 kPa (1.5 ATA) or sham air at 116 kPa (1.15

ATA). Effects on behavior were measured using the Autism Treatment Evaluation

Checklist score (ATEC) and clinical improvement was measured with the Clinical

Global Impression (CGI) system; in particular the clinical change (CGIC) and severity

(CGIS) sub-scores. These were evaluated by parents and clinicians, both of whom

were blinded to the actual exposure. The mean total ATEC scores by both parents

and clinicians were significantly improved after intervention in both arms of the study

compared to the score before intervention (P < 0.001 in both groups by parents, P =

0.015 in HBOT group and P = 0.004 in sham group by clinician). There were no

statistically significant differences in average percentage changes of total ATEC score

and all subscales scores when comparing the HBOT and sham air groups, either by

parents or clinicians. Changes in the CGI scores following intervention were

inconsistent between parents and clinicians. For severity scores (CGIS), parents

rated their children as more improved following HBOT (P = 0.005), while the

clinicians found no significant differences (P = 0.10). On the other hand, for change

scores (CGIC) the clinicians indicated greater improvement following HBOT (P =

0.03), but the parents found no such difference (P = 0.28). Investigators concluded

children with autism who received 20 sessions of either HBOT or a sham air exposure

had significant improvements in overall behavior but there were no significant

differences in improvement between groups. The inconsistent changes on CGI sub-

scores between parents and clinicians are difficult to interpret, but no overall

clinically significant benefit from HBOT could be shown. Both interventions were safe

and well tolerated with minimal side effect from middle ear barotraumas.

Peng et al (2012) observed the effect of HBOT on patients with herpes zoster. A

total of 68 cases with herpes zoster were randomly divided into HBOT and control

groups. The patients in the control group were treated with drugs, while the patients

in the HBOT group were treated with both drugs and HBOT. Parameters of

therapeutic efficacy including period of blister resolution, scar formation time and

percentage of patients developing post-herpetic neuralgia (PHN) were determined for

the patients in both groups. Numeric Pain Rating Scale (NPRS) and Hamilton

Depression Rating Scale (HAMD) were also scored for the patients before and after

treatment. The therapeutic efficacy in the control group was 81.25%, which was

significantly lower than that (97.22%) in the HBO2 group (p < 0.05). The percentage

of patients developing PHN, scar formation time and NPRS score in the HBO2 groups

were significantly lower than those in the control group (p < 0.05). HAMD score in

the HBO2 group was significantly lower than that in the control group (p < 0.05).

Investigators concluded HBOT can significantly enhance therapeutic efficacy, relieve


pain, accelerate herpes blister healing and lesion resolution, reduce the percentage

of patients developing PHN and improve depression in patients with herpes zoster.

Efrati et al (2012) evaluated whether increasing the level of dissolved oxygen by

Hyperbaric Oxygen Therapy (HBOT) could activate neuroplasticity in patients with

chronic neurologic deficiencies due to stroke in a prospective, randomized, controlled

trial including 74 patients (15 were excluded). All participants suffered a stroke 6-36

months prior to inclusion and had at least one motor dysfunction. After inclusion,

patients were randomly assigned to "treated" or "cross" groups. Brain activity was

assessed by SPECT imaging; neurologic functions were evaluated by NIHSS, ADL,

and life quality. Patients in the treated group were evaluated twice: at baseline and

after 40 HBOT sessions. Patients in the cross group were evaluated three times: at

baseline, after a 2-month control period of no treatment, and after subsequent 2-

months of 40 HBOT sessions. HBOT protocol: Two months of 40 sessions (5

days/week), 90 minutes each, 100% oxygen at 2 ATA. We found that the

neurological functions and life quality of all patients in both groups were significantly

improved following the HBOT sessions while no improvement was found during the

control period of the patients in the cross group. Results of SPECT imaging were well

correlated with clinical improvement. Elevated brain activity was detected mostly in

regions of live cells (as confirmed by CT) with low activity (based on SPECT) -

regions of noticeable discrepancy between anatomy and physiology. Investigators

concluded the results indicate that HBOT can lead to significant neurological

improvements in post stroke patients even at chronic late stages. The observed

clinical improvements imply that neuroplasticity can still be activated long after

damage onset in regions where there is a brain SPECT/CT (anatomy/physiology)

mismatch.

Prakash et al (2012) studied a total 56 patients of head injury. Out of them 28

received HBOT. Only cases with severe head injury [Glasgow Coma Scale (GCS) < 8]

with no other associated injury were included in the study group. After an initial

period of resuscitation and conservative management (10-12 days), all were

subjected to three sessions of HBOT at 1-week interval. This study group was

compared with a control group of similar severity of head injury (GCS < 8). The

study and control groups were compared in terms of duration of hospitalization, GCS,

disability reduction and social behavior. Patients who received HBOT were

significantly better than the control group on all the parameters with decreased

hospital stay, better GCS, and drastic reduction in disability. Investigators concluded

children with traumatic brain injury, the addition of HBOT significantly improved

outcome and quality of life and reduced the risk of complications

Nakada et al (2012) sought to assess the safety and efficacy of HBOT for treating

radiation cystitis a long-term follow-up study was done in patients with prostate

cancer. A total of 38 patients at an age of 68 8 years with radiation cystitis

following irradiation of prostate cancer were treated with HBOT at 2 absolute

atmospheric pressures for 90 min daily. The average number of HBOT treatment

sessions in each patient was 62 12. The follow-up period was 11.6 3.7 years.

We evaluated objective and subjective symptoms periodically with special reference

to the initiation timing of HBOT. High efficacy ratios of objective and subjective

findings were obtained at 2 and 4 (79-95%) years, respectively. After 7 years'

follow-up, these ratios decreased slightly (72-83%) but still remained stable

thereafter (75-88%) without any serious accident. Comparison of late morbidity

scores before and 11.6 years after HBOT showed significant improvement (p <

0.0005). Twenty-eight patients (74%) obtained nonrecurrent outcome. They had


received 18% lower (p < 0.001) radiation dosage than recurrent patients. The

interval between the onset of hematuria and start of HBO treatment in nonrecurrent

patients was 30% shorter (p < 0.001) than that of recurrent patients. Investigators

concluded they elucidated the long-term safety and beneficial effect of HBO therapy

of radiation cystitis in patients with prostate cancer. Early application of HBO

treatment after the onset of hematuria appears to produce favorable outcome.

Scientific Rationale Update March 2012 Tang et al (2011) investigated the effects of hyperbaric oxygen (HBO2) in

postoperative patients with intracranial aneurysm. A total of 120 patients who

underwent clipping of intracranial aneurysm of the anterior circulation were

randomized into the HBO2 group (n = 60) or the Control group (n = 60). Compared

with the Control group, patients in the HBO2 group received additional HBO2

therapy, which was initiated within one to three days as soon as they were deemed

clinically stable, for at least 20 sessions (one session per day). Mean flow velocities

of the middle cerebral artery (MCA) on the operative approach side were measured

on Days 1, 3, 7, 14 and 21 after operation. CT scans were performed on Days 1, 7,

14 and 21 after surgery to determine the abnormal density volume in the operative

area. Cases associated with symptomatic cerebral vasospasm (CVS) were assessed

on Days 3, 7 as well as 14, and the functional state determined by Karnofsky

Performance Scale (KPS) score was evaluated on Days 3 and 21 after operation.

Finally, Glasgow Outcome Scale (GOS) scores were obtained at six months after

surgery. There were no differences between groups in terms of the mean flow

velocities of MCA on the operative approach side, the cases with symptomatic CVS,

and the KPS scores within three days after surgery (P > 0.05). Compared with those

of the Control group, the mean flow velocities of MCA on the operative approach side

were significantly lower in the HBO2 group on Days 7 and 14 (P < 0.05 or P < 0.01).

On Days 7, 14 and 21, patients in the HBO2 group had smaller HBO2 density volume

in the operative region than those in the Control group (P < 0.05). The HBO2 group

developed less cases of symptomatic CVS than the Control group did on Days 7 (chi2

= 4.04, P < 0.05) and 14 (chi2 = 4.18, P < 0.05). The KPS scores were higher on

Day 21 after surgery in the HBO2 group (P < 0.05). More patients in the HBO2 group

achieved GOS scores of 4 and 5 at six months after surgery (chi2 = 6.032, P <

0.05). Investigators concluded early HBO2 appears to be beneficial as an adjunctive

treatment of postoperative intracranial aneurysm. Attenuating postoperative CVS,

brain edema, and cerebral ischemia contributes to the effectiveness of HBO2.

Hampson et al (2011) prospectively collected patient outcomes from a single center's

large experience using hyperbaric oxygen to treat chronic radiation injury. Since

2002, patient outcomes at the conclusion of a course of hyperbaric oxygen treatment

for chronic radiation tissue injury at a single center have been graded by a board-

certified hyperbaric physician and prospectively recorded. From 2002 to 2010, a total

of 525 patients received treatment for 1 of 6 forms of radionecrosis analyzed. After

excluding 114 patients for incomplete records or treatment courses or for previous

receipt of hyperbaric oxygen therapy, records of 411 patients were retrospectively

reviewed in 2010, and outcomes were regraded by a second board-certified

physician. A positive clinical response was defined as an outcome graded as either

"resolved" (90%-100% improved) or "significantly improved" (50%-89% improved).

A positive outcome from hyperbaric treatment occurred in 94% of patients with

osteoradionecrosis of the jaw (n = 43), 76% of patients with cutaneous radionecrosis

that caused open wounds (n = 58), 82% of patients with laryngeal radionecrosis (n

= 27), 89% of patients with radiation cystitis (n = 44), 63% of patients with

gastrointestinal radionecrosis (n = 73), and 100% of patients who were treated in


conjunction with oral surgery in a previously irradiated jaw (n = 166). The authors

concluded the outcomes of 411 patients collected prospectively over 8 years strongly

supported the efficacy of hyperbaric oxygen treatment for the 6 conditions

evaluated. The response rates previously reported in numerous small series were

supported by the responses achieved in this large, single-center experience

Scientific Rationale Update December 2008 Radiation tissue damage includes soft tissue radionecrosis, osteoradionecrosis,

radiation mucositis, dermatitis, enteritis, laryngeal radionecrosis, cystitis, and

surgical wounding in radiation-damaged tissues. Soft tissue radionecrosis results

from damage done to non-osseous tissues by ionizing radiation during the course of

radiotherapy. The introduction of super voltage radiation therapy made the cure of

solid tumors of the head, neck, and pelvis a reality. But the radiation also exacts a

toll on the body, with tissues in the path of the radiation beam suffering damage.

Radiation cystitis is one complication of radiation therapy to pelvic tumors and

manifests primarily as an alteration of the voiding pattern. The urinary bladder can

be irradiated intentionally for the treatment of bladder cancer or incidentally for the

treatment of other pelvic malignancies. The sequelae of radiation injury to the

bladder can range from minor temporary irritative voiding symptoms and

asymptomatic hematuria to more severe complications such as gross hematuria,

contracted nonfunctional bladder, persistent incontinence, fistula formation, necrosis,

and death. The reported frequency of radiation cystitis varies. This is because of

difficulties in data collection (usually performed as a questionnaire), differences in

dosimetry and field size used, and the fact that various tumors are treated with

different fields and include varying amounts of bladder exposure. If the symptoms

of radiation cystitis are not severe but significant enough for a patient to seek help,

sodium pentosanpolysulphate with or without pentoxifylline for pain is a reasonable

first step. If symptoms become more severe or oral therapy is not satisfactory, HBO

therapy, based on the available literature, appears to have the most consistent

results.

Therapy is primarily aimed at relief of symptoms. The exception is hyperbaric oxygen

(HBO) therapy. Treatment with HBO can potentially reverse the changes caused by

radiation. HBO therapy stimulates angiogenesis, which reverses the vascular changes

induced by ionizing radiation. Preservation of bladder function and the noninvasive

nature of treatment (30 sessions total) favor its use. Some reports claim 70%

response with HBO. However, if significant fibrosis and ischemia have already

occurred, HBO therapy does not reverse the changes and only prevents further

injury.

Hemorrhagic cystitis is a more serious complication of radiation cystitis. Prophylaxis

against the development of radiation cystitis has been reported with the use of the

antioxidant orgotein prior to receiving radiation.

Hamson et al. (2007) Details of hyperbaric treatment courses of patients treated for

radiation enteritis/proctitis (n = 65) and cystitis (n = 94) at a single institution were

reviewed. Outcomes were compared with the total number of HBO treatments

administered and also rate of treatment administration. Responses were similar for

both forms of STRN whether the patient averaged fewer or greater than 5

treatments per week, or even < or = 3 versus > or = 7 treatments weekly. Outcome

did differ, however, dependant on the total number of treatments administered.

Response was better in patients receiving 30 or more total treatments, as compared


with fewer. Soft tissue radionecrosis of the gastrointestinal tract or bladder is (1)

effectively treated with hyperbaric oxygen, (2) has a higher response rate if at least

30 treatments are administered, and (3) is equally responsive to rates of hyperbaric

treatment ranging from 3 or fewer to 7 or more treatments per week.

Pasquier et al. (2004) performed a systematic search on literature from 1960 to

2004, by only taking into account the articles that appeared in peer review journals.

Hyperbaric oxygen treatment involving complications to the head and neck, pelvis

and nervous system, and the prevention of complications after surgery in irradiated

tissues have been studied. Despite the small number of controlled trials, it may be

indicated for the treatment of mandibular osteoradionecrosis in combination with

surgery, hemorrhagic cystitis resistant to conventional treatments and the

prevention of osteoradionecrosis after dental extraction, whose level of evidence

seems to be the most significant though randomised trials are still necessary.

Results for use of HBO therapy (HBOT) for radionecrosis and osteoradionecrosis

continue to be published. Given the limited number of options available to patients

with these late effects of radiation therapy, results of cohort studies as well as

randomized trials can be used in evaluating the clinical evidence. report a positive

result when HBO was delivered as treatment for or prevention of delayed radiation

injury. The authors also noted that these results were impressive in the context of

alternative interventions such as surgery of irradiated tissue. Based on the peer-

reviewed literature, the authors concluded that HBO is recommended for delayed

radiation injuries for soft tissue and bony injuries of most sites.

Scientific Rationale Update October 2008 Sudden sensorineural hearing loss (SSNHL) involves an acute sensorineural hearing

loss, which, in the majority of cases, is unilateral. The U.S. National Institute for

Deafness and Communication Disorders (NICDC) specifies that SSNHL be diagnosed

when there is idiopathic hearing loss of at least 30 dB over at least three test

frequencies occurring within three days. However, many studies differ on their

criteria for defining SSNHL, including loss of 10-20 dB in two or three frequencies;

some require hearing loss within 12 hours including hearing loss noted on

awakening. A number of conditions are associated with SSNHL, and while with some

the etiologic link is clear (eg, acoustic neuroma, trauma), in most cases the exact

etiology is uncertain. Further, the NIDCD indicates that sudden sensorineural hearing

loss should be considered a medical emergency, although other investigators openly

dispute this. The incidence of sudden hearing loss in the United States is often

reported at between 5 and 20 cases per 100,000 people annually.

The prognosis for sudden sensorineural hearing loss is reasonably good, especially if

it is a high or low frequency hearing loss pattern and not flat across all frequencies.

The prognosis is poor in patients with profound hearing loss across all frequencies:

approximately three-quarters of such patients have no recovery of hearing. Of

patients who have idiopathic SSNHL, around two-thirds will experience recovery,

although this recovery is often not complete. Prognosis is worse in patients who are

older, and may be worse in those with vertigo, though this is not a consistent

finding. Recovery may take up to four months; patients who have not improved

within three months will generally not recover significantly.

While oral corticosteroids have been considered standard therapy for sudden

sensorineural hearing loss (SSNHL), the benefit of these drugs is unclear. Results of

the meta-analysis which pooled data from the two RCTs showed no difference

between treatment groups (OR 2.47; 95% CI 0.89-6.84). Randomized trials have


not demonstrated effectiveness for the addition of antiviral therapy to steroid

protocols. However, a subset of patients with SSNHL may have HSV-1 infection, and

could benefit from antiviral drugs. A trial of intratympanic corticosteroids for patients

who do not show improvement after 10 days of oral corticosteroids is suggested.

Hyperbaric oxygen (HBO) therapy is the administration of oxygen at a pressure

greater than the atmospheric pressure. Increasing the atmospheric pressure in the

hyperbaric environment increases partial pressure of oxygen in the tissues. The use

of hyperbaric oxygen therapy in the treatment of sudden hearing loss (SHL) dates

back to at least 1979. Although little appears in the literature for much of the 1980s

and early 1990s, there seems to be renewed interest in this treatment modality, with

several reports in the past 10 years. Most of this literature comes from centers in

Europe, with fewer studies from the United States, suggesting a geographic

difference in the application of this treatment.

Rauch (New England Journal of Medicine 2008) Randomized trials comparing

corticosteroids alone to corticosteroids plus antiviral agents for sudden sensorineural

hearing loss have failed to show an added benefit for antiviral therapy; none of these

studies included a placebo group. Other treatments, including volume expanders,

anticoagulants, inhalational vasodilators, herbal remedies, and hyperbaric oxygen,

have been suggested, but adequately powered randomized trials are lacking to

support clinical benefit with their use. A retrospective observational study of 112

patients with sudden sensorineural hearing loss who were treated with tapered

corticosteroids after a high-dose intravenous bolus of either 600 mg or 1200 mg of

hydrocortisone showed a significantly greater incidence of complete recoveries in the

higher-dose group, but randomized trials of treatment with high doses of intravenous

corticosteroids are lacking.

Bennet (Cochrane Database 2007) Randomised studies comparing the effect on

ISSHL and/or tinnitus of therapeutic regimens which include HBOT with those that

exclude HBOT. Three authors independently evaluated the quality of the relevant

trials using the validated Oxford-Scale (Jadad 1996) and extracted the data from the

included trials. Six trials contributed to this review (308 subjects). Pooled data from

two trials involving 114 patients did not show any significant improvement in the

chance of a 50% increase in hearing threshold on Pure Tone Average (PTA) when

HBOT was used (relative risk [RR] with HBOT 1.53, 95% CI 0.85 to 2.78, P = 0.16),

but did show a significantly increased chance of a 25% increase in PTA (RR 1.39,

95% CI 1.05 to 1.84, P = 0.02). There was a 22% greater chance of improvement

with HBOT, and the number needed to treat (NNT) to achieve one extra good

outcome was five (95% CI 3 to 20). A single trial involving 50 subjects also

suggested significantly more improvement in the mean PTA threshold with HBOT,

expressed as a percentage of baseline (WMD 37%, 95% CI 22% to 53%, P <

0.001). The significance of any improvement following HBOT in a subjective rating of

tinnitus could not be assessed due to poor reporting. There were no significant

improvements in hearing or tinnitus reported in the single study to examine chronic

presentation (six months) of ISSHL and/or tinnitus. For people with early

presentation of ISSHL, the application of HBOT significantly improved hearing loss,

but the clinical significance of the level of improvement is not clear. We could not

assess the effect of HBOT on tinnitus by pooled data analysis. The routine application

of HBOT to these patients cannot be justified from this review. In view of the modest

number of patients, methodological shortcomings and poor reporting, this result

should be interpreted cautiously, and an appropriately powered trial of high

methodological rigour is justified to define those patients (if any) who can be


expected to derive most benefit from HBOT. There is no evidence of a beneficial

effect of HBOT on chronic presentation of ISSHL and/or tinnitus and we do not

recommend use of HBOT for this purpose based on the single study available.

Cochrane Database (2005) A systematic review concluded that hyperbaric oxygen

therapy might be of some benefit when administered early in the course of SSNHL,

although the clinical significance of the benefit was unclear and the underlying

studies had methodologic shortcomings. Therapy with HBO requires further

evaluation before it can be recommended.

Fujimura et al. (2007) completed a controlled retrospective analysis of medical

records of 130 inpatients with idiopathic sudden sensorineural hearing loss [ISSNHL]

(hearing levels >/=40 dB; time from the onset of hearing loss to the start of

treatment /=80 dB,

the hearing improvement rate was significantly higher in the HBO group than in the

steroid group (51.1 +/- 7.0% vs. 27.1 +/- 7.8%; P < 0.05), while in patients whose

initial hearing levels were


weight loss, and nausea and vomiting. Less common are bowel obstruction, fistulas,

bowel perforation, and massive rectal bleeding.

Radiologic findings include submucosal thickening, single or multiple stenoses,

adhesions, and sinus or fistula formation. Recurrent tumor should be ruled out. The

management of chronic radiation enteritis remains a major challenge because of the

progressive evolution of the disease including development of obstructive endarteritis

and fibrosis. Experience with specific medical treatments has been derived largely

from small clinical trials and case series. Medical management includes treating

diarrhea, dehydration, malabsorption, and abdominal or rectal discomfort. Symptoms

usually resolve with conservative measures (e.g., antidiarrheal agents, opiods,

steroids, dietary changes, and rest). Antibiotics are indicated if there is small bowel

bacterial overgrowth syndrome. In severe cases of malnutrition, total parenteral

nutrition should be considered. Surgical intervention is generally reserved for

patients with persistent ileus, intestinal fistulization, and massive adhesions,

however, diffuse fibrosis and adhesions between bowel loops can make resection

technically challenging and it can be difficult to distinguish healthy tissue for

irradiated tissue by gross inspection alone. Despite attempts at conservative

management, approximately one-third of patients progress to the point where

surgery is required. Mortality rates are as high and many patients require more than

one laparotomy.

A recent approach to treatment of chronic radiation enteritis is the application of

hyperbaric oxygen therapy (HBOT), although its effectiveness has not been well-

studied. The rationale for the use of hyperbaric oxygen is that it may promote

healing of hypoxic tissues and aid in angiogenesis.

Marshal et al. (2007) evaluated the effectiveness of hyperbaric oxygen therapy

(HBOT) as a treatment for chronic radiation enteritis and the relative effectiveness in

treatment of the proximal and distal gastrointestinal tract. A case series of 65

patients with chronic radiation enteritis were treated with HBOT for radiation damage

to the alimentary tract. The primary indication for HBOT was bleeding (n = 54) with

16 patients requiring transfusions. Additional indications were pain, diarrhea, weight

loss, fistulas and obstruction. Follow-up ranged from 1 to 60 months. The main

outcome measures were effects on bleeding, pain, diarrhea, weight loss, fistulas and

obstruction. Endoscopic documentation of healing was used when available. The

response rate was 68%, with a complete and partial response rate of 43 and 25%,

respectively. The response rate for rectal disease was 65% and for proximal sites

was 73%. The response rate for bleeding was 70% and for other symptoms was

58%. The author concluded that findings suggest that HBOT results in healing or

clinically significant improvement in two thirds of patients with chronic radiation

enteritis.

A Cochrane review evaluated randomised controlled trials (RCTs) comparing the

effect of HBOT versus no HBOT on late radiation tissue injury (LRTI). The authors

found that small trials suggest that for people with LRTI affecting tissues of the head,

neck, anus and rectum, HBOT is associated with improved outcome. The application

of HBOT to selected patients and tissues may be justified. Further research is

required to establish the optimum patient selection and timing of any therapy.

In a technology assessment report requested by the Centers for Medicare & Medicaid

Services (CMS), Feldmeirer performed a systematic review of the literature reporting

the results of HBOT therapy in the treatment and/or prophylaxis of delayed radiation


injury. Three randomized controlled trials, two nonrandomized comparative trials,

and 69 case series to evaluate the efficacy of HBOT in treating delayed radiation

injuries. Specifically, the authors recommend HBOT for delayed radiation injuries for

soft tissue or bony injuries of most sites: necrosis of the mandible, head and neck,

chest wall and breast, abdominal wall and pelvic injuries, the nervous system, the

extremities, radiation cystitis, proctitis and enteritis.

In a retrospective study by Gouello et al. (1999) 36 patients with chronic digestive

tract necrosis that developed a mean 42 months after irradiation therapy were

treated with HBOT. The patients underwent a mean 67 hyperbaric sessions (100%

O2, 2.5 atm, 90 min). Three patients died within one month of the first session due

to radiation enteritis, a neoplastic process or another concomitant cause. Immediate

outcome after hyperbaric oxygen therapy was cure (n = 3) or improvement (n = 16)

in 19 patients (53%) and failure in 17 (47%). Long-term results evaluated in 32

subjects with a mean 52 months follow-up were: cure (n = 9) or improvement (n =

12) in 21 patients (66%) and failure in 11 (34%). Nine patients died within a mean

25 months after the end of the hyperbaric sessions. Death was related to digestive

tract radionecrosis in 1 case and neoplasia in 5. The investigator concluded that

HBOT provides clinical relief in 2 out of 3 patients and can be a useful alternative to

conventional treatment in patients with chronic radiation-induced necrosis of the

digestive tract.

Although, published peer review literature is limited, studies suggest that HBOT may

be useful in the treatment of chronic radiation enteritis. This treatment should be

reserved for the select group of patients that have failed conservative treatment, as

an alternative to surgical intervention, which has a high mortality rate in addition to

being technically challenging. Further research is required to establish optimum

patient selection and timing of any therapy.

Scientific Rationale - Initial Hyperbaric oxygen (HBO) therapy, is the administration of oxygen at a pressure

greater than the atmospheric pressure (sea level.) An individual is placed in a

hyperbaric chamber, which is then pressurized with air or oxygen under increased

atmospheric pressure (minimum of 1.4 atmospheres). Increasing the atmospheric

pressure in the hyperbaric environment increases partial pressure of oxygen in the

tissues. HBO facilitates fibroblast proliferation, angiogenesis, and wound healing. It

also augments neutrophil bactericidal activity, limits clostridial exotoxin and spore

production, kills anaerobes such as Clostridium perfringens, and inhibits the growth

of several other bacterial pathogens. Breathing 100% oxygen at 1 atm abs or

exposing isolated parts of the body to 100% oxygen does not constitute HBO

therapy.

Most hyperbaric chambers are monoplace or single person chambers. The chamber

itself is a horizontal cylinder with a clear acrylic hull that allows for continuous visual

contact. Use in some critically ill patients is limited as direct access to the patient

during treatment is inhibited, however the chamber can be configured with

mechanical ventilation as well as invasive and noninvasive monitoring.

Multiplace chambers are larger and allow treatment of more than one patient at a

given time (eg. treatment of an entire family with carbon monoxide poisoning). The

chamber is compressed with air, and face mask or a head tent delivers oxygen.

Multiplace chambers are ideal for the treatment of critically ill patients as the


technician or nurse can remain inside therefore allowing for continuos monitoring

and emergeny treatment, if necessary.

HBO therapy is safe with relatively few complications and side effects. Middle ear

barotrauma, or ear squeeze, is the most common side effect, occurring on compression, causing pain and hemorrhage. It can lead to tympanic membrane

rupture. It is usually caused by an upper respiratory infection, Eustachian tube

dysfunction, or inadequate techniques of equalization. Prevention includes slow

compression rates with frequent stops, proper auto inflation techniques, or

myringotomies. Inner ear barotrauma is less common and results in tinnitus,

vertigo, and loss of hearing and requires evaluation by an otolaryngologist.

The second most common complication is sinus barotrauma, or sinus squeeze It is usually caused by an upper respiratory infection or allergic sinusitis or rhinitis.

Treatment with a decongestant nasal spray or antihistamine prior to HBO therapy

may modulate the problem, allowing the patient to proceed. Less common side

effects are oxygen or pulmonary toxicity, claustrophobia, visual refractive changes,

seizures and decompression sickness.

Hyperbaric oxygen therapy (HBO) should not replace other standard successful

therapeutic measures. Depending on the response of the patient and the severity of

the original problem, treatment may last from less than one week to several months.

Acute therapy may require only one or two treatments, while chronic medical

conditions may warrant up to 30 or more sessions. Typically, the average length of

treatment is two to four weeks.

Published evidence suggests that diabetic patients with foot ulcers may improve

healing with the use of hyperbaric oxygen, which in turn reduces the risk of major

amputation. A review of six randomized controlled trials involving the use of HBOT

for chronic wounds were performed. Pooled data from five trials on diabetic ulcers

(118 patients) suggested a significant reduction in the risk of major amputation in

diabetic patient. Another article reviewed fifty-seven studies obtained from

technology assessment reports and a Medline search from 1998-2001. This study,

involving more than 2000 patients concluded that HBO may be beneficial as an

adjunctive therapy for chronic nonhealing diabetic wounds, compromised skin grafts,

osteoradionecrosis, soft tissue radionecrosis, and gas gangrene compared with

standard wound care alone.

Another published study in 2003 reviewed nine patient, four with severe necrotizing

neck infections and five suffering from necrotizing fasciitis necrotizing. The patients

were all treated HBO therapy in conjunction with conservative treatment along and

surgical intervention (functional neck dissection). Eight of the nine patients

recovered completely, with one patient dying due to toxic shock as consequence of a

delayed in therapy. The study concluded that hyperbaric oxygen should be

considered as a treatment adjunct in patients with necrotizing fasciitis if early and

aggressive surgery and antibiotic treatment fail.

Further research is needed to better define the role of HBO in the treatment of

thermal burns. A 2004 review of evidence obtained from Cochrane Controlled Trials

Register (The Cochrane Library, Issue 3, 2002), MEDLINE (Ovid 1966 to November

Week 2, 2003), CINAHL (Ovid 1982 to December Week 2 2003), EMBASE (Ovid 1980

to September 2003), DORCTHIM (Database of Randomized Controlled Trials in

Hyperbaric Medicine) from inception to 2003, suggests that there is insufficient

evidence to support the effectiveness of HBO in treatment of thermal burns. Only 2


randomized studies met the inclusion criteria. One trial reported no decrease in

mortality or number of necessary surgeries while the second trial reported shorter

healing times. Based on the results of currently published data, HBO therapy for the

treatment of thermal burns is not recommended.

Despite considerable research effort there is little controlled evidence that a course

of hyperbaric oxygen therapy results in any benefit for patients with multiple

sclerosis (MS) as compared to current practice. Randomized trials involving a course

of 20 HBO vs. placebo treatments over a four-week period provided no significant

benefit from the administration of HBO.

The use of HBO therapy in the treatment of acute coronary syndrome including acute

myocardial infarction and unstable angina remains inconclusive due to insufficient

evidence in the peer-reviewed literature to support its use.

Published literature lacks scientific evidence for the use of HBO in the treatment of

Cerebral Palsy, brain injury, or stroke.

Review History April 1998 First review date

April 1999 Second review date

July 2000 Third review date

June 2002 Fourth review date

March 2003 Fifth review date

May 2004 Sixth review date

June 28, 2005 Medical Advisory Council - no revisions

March 2006 Codes Added

June 2006 Code revisions

December 2006 Revised added autism as not medically necessary June 2007 Added chronic radiation enteritis to the list of medically

necessary indications for a select group of patients when

conservative treatment has failed

October 2007 Added additional note under indication #9 - Diabetic wounds of

the lower extremities requiring wound evaluation at least every

30 days during administration of HBO therapy.

October 2008 Update. Revised policy to add HBO as investigational for

idiopathic sudden deafness or acoustic trauma.

December 2008 Update. Revised policy to include HBO for radiation cystitis as

medically necessary. Clarified COPD under Contraindications to

HBO.

April 2011 Update no revisions March 2012 Update no revisions March 2013 Update no revisions. Code updates April 2013 Added information to Scientific Rationale regarding Clinical

Practice Guidelines on Sudden Hearing Loss noted on the Otolaryngology, Head and Neck Surgery site. The panel offered clinicians options that with idiopathic sudden

sensorineural hearing loss (ISSNHL), corticosteroids may be

given as initial therapy and hyperbaric oxygen may be given

within 3 months of initial diagnosis. However, HBOT is not

currently approved by the U.S. FDA for treatment of any

hearing loss, including but not limited to ISSNHL, so this would

continue to be considered investigational.


This policy is based on the following evidence-based guidelines: 1. Hyperbaric Oxygen therapy for brain injury, cerebral palsy, and stroke

National Cancer Institute. Gastrointestinal Complications. Radiation Enteritis.

Last Modified: 04/19/2006.

2. Agency for Healthcare Research and Quality. Technology Assessment Program.

A Horizon Scan: Uses of Hyperbaric Oxygen Therapy. October 2006. Available

at: http://www.cms.hhs.gov/determinationprocess/downloads/id42TA.pdf

3. Stachler RJ, Chandrasekhar SS, Archer SM, et al; American Academy of

Otolaryngology-Head and Neck Surgery. Clinical practice guideline: sudden

hearing loss. Otolaryngol Head Neck Surg. March 1, 2012. 146(3 Suppl):S1-35.

Available at: http://www.entnet.org/Community/upload/Sudden-Hearing-Loss-

Clinical-Practice-Guideline.pdf

References Update April 2014 1. Boussi-Gross R, Golan H, Fishlev G, et al. 1. Hyperbaric oxygen therapy can

improve post concussion syndrome years after mild traumatic brain injury -

randomized prospective trial. PLoS One. 2013 Nov 15;8(11):e79995.

2. Cvorovic L, Jovanovic MB, Milutinovic Z, et al. Randomized prospective trial of

hyperbaric oxygen therapy and intratympanic steroid injection as salvage

treatment of sudden sensorineural hearing loss. Otol Neurotol. 2013

Aug;34(6):1021-6.

3. Dauwe PB, Pulikkottil BJ, Lavery L, et al. Does hyperbaric oxygen therapy work

in facilitating acute wound healing: a systematic review. Plast Reconstr Surg.

2014 Feb;133(2):208e-15e.

4. Eskes A, Vermeulen H, Lucas C, Ubbink DT. Hyperbaric oxygen therapy for

treating acute surgical and traumatic wounds. Cochrane Database Syst Rev.

2013 Dec 16.

5. Gupta P, Sahni T, Jadhav GK, et al. A retrospective study of outcomes in

subjects of head and neck cancer treated with hyperbaric oxygen therapy for

radiation induced osteoradionecrosis of mandible at a tertiary care centre: an

Indian experience. Indian J Otolaryngol Head Neck Surg. 2013 Jul;65(Suppl

1):140-3.

6. Irgens A, Vaagb G, Aanderud L. Quality of life--the effect of hyperbaric oxygen

treatment on radiation injury. Undersea Hyperb Med. 2013 Nov-Dec;40(6):479-

85.

7. Ouassi M, Tran S, Mege D, et al. Pelvic radiation disease management by

hyperbaric oxygen therapy: prospective study of 44 patients. Gastroenterol Res

Pract. 2014;2014:108073.

8. Ueno T, Omi T, Uchida E, et al. Evaluation of hyperbaric oxygen therapy for

chronic wounds. J Nippon Med Sch. 2014;81(1):4-11.

9. U.S Food and Drug Administration. Hyperbaric Oxygen Therapy: Don't Be

Misled. Aug 2013. Available at:

http://www.fda.gov/forconsumers/consumerupdates/ucm364687.htm

10. van der Veen EL, van Hulst RA, de Ru JA. Hyperbaric Oxygen Therapy in Acute

Acoustic Trauma: A Rapid Systematic Review. Otolaryngol Head Neck Surg.

2014 Mar 19

11. Walker WC, Franke LM, Cifu DX, Hart BB. Randomized, Sham-Controlled,

Feasibility Trial of Hyperbaric Oxygen for Service Members With Postconcussion

Syndrome: Cognitive and Psychomotor Outcomes 1 Week Postintervention.

Neurorehabil Neural Repair. 2013 Dec 26.


12. Yldrm E, Murat zcan K, Palal M, et al. Prognostic effect of hyperbaric oxygen therapy starting time for sudden sensorineural hearing loss. Eur Arch

Otorhinolaryngol. 2013 Nov 24.

References Update April 2013 1. Carlsson PI, Hall M, Lind KJ, et al. Quality of life, psychosocial consequences,

and audiological rehabilitation after Downloaded from oto.sagepub.com at

American Academy of Otolaryngology-Head and Neck Surgery Foundation, Inc.

on March 1, 2012. Int J Audiol. 2011;50(2):139-144.

2. Hyperbaric Centers of Texas. Hyperbaric Oxygen Therapy for Non-FDA Approved

Conditions. Health Concerns that May Be Improved by HBOT Treatments.

Available at: http://www.hyperbariccentersoftexas.com/hbot-non-fda-approved-

conditions

3. Korpinar S, Alkan Z, Yigit O, et al. Factors influencing the outcome of idiopathic

sudden sensorineural hearing loss treated with hyperbaric oxygen therapy. Eur

Arch Otorhinolaryngol. 2011;268(1):41-47.

4. Rauch SD, Halpin CF, Antonelli PJ, et al. Oral vs intratympanic corticosteroid

therapy for idiopathic sudden sensorineural hearing loss: a randomized trial.

JAMA. 2011;305(20):2071-2079.

5. Suzuki H, Hashida K, Nguyen KH, et al. Efficacy of intratympanic steroid

administration on idiopathic sudden sensorineural hearing loss in comparison

with hyperbaric oxygen therapy. Laryngoscope. 2012 May;122(5):1154-7.

References Update March 2013 1. Bennett MH, Feldmeier J, Hampson N, et al. Hyperbaric oxygen therapy for late

radiation tissue injury. Cochrane Database Syst Rev. 2012 May

16;5:CD005005.

2. Bennett MH, Kertesz T, Perleth M, et al. Hyperbaric oxygen for idiopathic

sudden sensorineural hearing loss and tinnitus. Cochrane Database Syst Rev.

2012 Oct 17;10:CD004739.

3. Bennett MH, Trytko B, Jonker B. Hyperbaric oxygen therapy for the adjunctive

treatment of traumatic brain injury. Cochrane Database Syst Rev. 2012 Dec

12;12:CD004609.

4. Degener S, Strelow H, Pohle A, et al. Hyperbaric oxygen in the treatment of

hemorrhagic radiogenic cystitis after prostate cancer. Urologe A. 2012

Dec;51(12):1735-40.

5. Efrati S, Fishlev G, Bechor Y, et al. Hyperbaric oxygen induces late

neuroplasticity in post stroke patients - randomized, prospective trial. PLoS

One. 2013;8(1):e53716.

6. Filipo R, Attanasio G, Viccaro M, et al. Hyperbaric oxygen therapy with short

duration intratympanic steroid therapy for sudden hearing loss. Acta

Otolaryngol. 2012 May;132(5):475-81.

7. Ghanizadeh A. Hyperbaric oxygen therapy for treatment of children with

autism: a systematic review of randomized trials. Med Gas Res. 2012 May

11;2:13.

8. Kranke P, Bennett MH, Martyn-St James M, et al. Hyperbaric oxygen therapy for

chronic wounds. Cochrane Database Syst Rev. 2012 Apr 18;4:CD004123.

9. Lacey DJ, Stolfi A, Pilati LE. 1. Effects of hyperbaric oxygen on motor function in

children with cerebral palsy. Ann Neurol. 2012 Nov;72(5):695-703.

10. Liu R, Li L, Yang M, et al. Systematic review of the effectiveness of hyperbaric

oxygenation therapy in the management of chronic diabetic foot ulcers. Mayo

Clin Proc. 2013 Feb;88(2):166-75.


11. Massey PR, Sakran JV, Mills AM, et al. Hyperbaric oxygen therapy in necrotizing

soft tissue infections. J Surg Res. 2012 Sep;177(1):146-51.

12. Nakada T, Nakada H, Yoshida Y, et al. Hyperbaric oxygen therapy for radiation

cystitis in patients with prostate cancer: a long-term follow-up study. Urol Int.

2012;89(2):208-14.

13. Oliai C, Fisher B, Jani A, et al. Hyperbaric oxygen therapy for radiation-induced

cystitis and proctitis. Int J Radiat Oncol Biol Phys. 2012 Nov 1;84(3):733-40.

14. Peng Z, Wang S, Huang X, Xiao P. Effect of hyperbaric oxygen therapy on

patients with herpes zoster. Undersea Hyperb Med. 2012 Nov-Dec;39(6):1083-

7.

15. Prakash A, Parelkar SV, Oak SN, et al. Role of hyperbaric oxygen therapy in

severe head injury in children. J Pediatr Neurosci. 2012 Jan;7(1):4-8.

16. Sampanthavivat M, Singkhwa W, Chaiyakul Tet al. Hyperbaric oxygen in the

treatment of childhood autism: a randomised controlled trial. Diving Hyperb

Med. 2012 Sep;42(3):128-33.

17. Stachler RJ, Chandrasekhar SS, Archer SM, et al. Clinical practice guideline:

sudden hearing loss. Otolaryngol Head Neck Surg. 2012 Mar;146(3 Suppl):S1-

35.

18. Suzuki H, Hashida K, Nguyen KH, et al. Efficacy of intratympanic steroid

administration on idiopathic sudden sensorineural hearing loss in comparison

with hyperbaric oxygen therapy. Laryngoscope. 2012 May;122(5):1154-7.

19. Wolf EG, Prye J, Michaelson R, et al. . Hyperbaric side effects in a traumatic

brain injury randomized clinical trial. Undersea Hyperb Med. 2012 Nov-

Dec;39(6):1075-82.

References Update March 2012. 1. Bennett MH, Lehm JP, Jepson N. Hyperbaric oxygen therapy for acute coronary

syndrome. Cochrane Database Syst Rev. 2011 Aug 10;(8):CD004818.

2. Bennett M, Heard R. Hyperbaric oxygen therapy for multiple sclerosis. CNS

Neurosci Ther. 2010 Apr;16(2):115-24.

3. Game FL, Hinchliffe RJ, Apelqvist J, et al. A systematic review of interventions to

enhance the healing of chronic ulcers of the foot in diabetes. Diabetes Metab

Res Rev. 2012 Feb;28 Suppl 1:119-41

4. Hampson NB, Holm JR, Wreford-Brown CE, Feldmeier J. Prospective assessment

of outcomes in 411 patients treated with hyperbaric oxygen for chronic radiation

tissue injury. Cancer. 2011 Dec 2. doi: 10.1002/cncr.26637.

5. Holland NJ, Bernstein JM, Hamilton JW. Hyperbaric oxygen therapy for Bell's

palsy. Cochrane Database Syst Rev. 2012 Feb 15;2:CD007288.

6. Kleinman Y, Cahn A. Conservative management of Achilles tendon wounds:

results of a retrospective study. Ostomy Wound Manage. 2011 Apr;57(4):32-

40.

7. Lndahl M, Fagher K, Katzman P. What is the role of hyperbaric oxygen in the

management of diabetic foot disease? Curr Diab Rep. 2011 Aug;11(4):285-93

8. Peters EJ, Lipsky BA, Berendt AR, et al. A systematic review of the effectiveness

of interventions in the management of infection in the diabetic foot. Diabetes

Metab Res Rev. 2012 Feb;28 Suppl 1:142-62. doi: 10.1002/dmrr.2247

9. Tang XP, Tan M, Zhang T, et al. Effects of early hyperbaric oxygen therapy on

clinical outcome in postoperative patients with intracranial aneurysm. Undersea

Hyperb Med. 2011 Nov-Dec;38(6):493-501.

10. Vilar DG, Fadrique GG, Martn IJ, et al. Hyperbaric oxygen therapy for the

management of hemorrhagic radio-induced cystitis. Arch Esp Urol. 2011

Nov;64(9):869-74


References Update April 2011 1. Annane D, Chadda K, Gajdos P, et al. Hyperbaric oxygen therapy for acute

domestic carbon monoxide poisoning: two randomized controlled trials.

Intensive Care Med. 2011 Mar;37(3):486-92

2. Cekin E, Cincik H, Ulubil SA, Gungor A. Effectiveness of hyperbaric oxygen

therapy in management of sudden hearing loss. J Laryngol Otol. 2009

Jun;123(6):609-12. Epub 2009.

3. Eskes A, Ubbink DT, Lubbers M, et al. Hyperbaric oxygen therapy for treating

acute surgical and traumatic wounds. Cochrane Database Syst Rev. 2010 Oct

6;(10

4. Gothard L, Haviland J, Bryson P, et al. Randomised phase II trial of hyperbaric

oxygen therapy in patients with chronic arm lymphoedema after radiotherapy for

cancer. Radiother Oncol. 2010 Oct;97(1):101-7.

5. Lawson-Smith P, Jansen EC, Hilsted L, Hyldegaard O. et al. Effect of hyperbaric

oxygen therapy on whole blood cyanide concentrations in carbon monoxide

intoxicated patients from fire accidents. Scand J Trauma Resusc Emerg Med.

2010 Jun 15;18:32.

6. Liu SC, Kang BH, Lee JC, et al. Comparison of Therapeutic Results in Sudden

Sensorineural Hearing Loss with/without Additional Hyperbaric Oxygen Therapy.

Clin Otolaryngol. 2011 Mar 17

7. Lndahl M, Katzm

hyperbaric oxygen therapy

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