Hyperbaric Oxygen Therapy

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
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Hyperbaric Oxygen Therapy Apr 14
Reference/Website Link
Hyperbaric Oxygen Therapy:
http://www.cms.gov/medicare-coveragedatabase/search/advanced-search.aspx
Hyperbaric Oxygen Therapy:

http://www.cms.gov/medicare-coveragedatabase/search/advanced-search.aspx
Technology assessments:
Hyperbaric Oxygen Therapy in Treatment of
Hypoxic Wounds:
http://www.cms.gov/medicare-coveragedatabase/details/technology-assessmentsdetails.aspx?TAId=12&SearchType=Advanced&
CoverageSelection=Both&NCSelection=NCA%7c
CAL%7cNCD%7cMEDCAC%7cTA%7cMCD&Articl
eType=Ed%7cKey%7cSAD%7cFAQ&PolicyType
=Final&s=44&KeyWord=hyperbaric+oxygen+th
erapy&KeyWordLookUp=Doc&KeyWordSearchTy
pe=Exact&kq=true&bc=IAAAABAAAAAAAA%3d
%3d&
A Horizon Scan: Uses of Hyperbaric Oxygen
Therapy. Technology Assessment Report, Oct
2006:
http://www.cms.gov/determinationprocess/dow
nloads/id42TA.pdf
None
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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.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
Acute cerebral edema

Acute thermal and chemical pulmonary damage (for example, smoke
inhalation with pulmonary insufficiency
Aerobic septicemia
Anaerobic septicemia and infection other than clostridial
Arthritic diseases
Autism
Cardiogenic shock
Chronic peripheral vascular insufficiency
Cutaneous, decubitus, and stasis ulcers
Exceptional blood loss anemia
Hepatic necrosis
Lyme Disease
Multiple sclerosis
Myocardial infarction
Nonvascular causes of chronic brain syndrome (Pick's disease, Alzheimer's
disease, Korsakoff's disease)
16.
17.
18.
19.
20.
21.
Organ storage
Pulmonary emphysema
Senility
Sickle cell anemia
Systemic aerobic infection
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.
2.
3.
4.
5.
Acute or chronic cerebral vascular insufficiency

Organ transplantation
Skin burns (thermal)
Topical application of oxygen (including topical HBOT administered to the
open wound in small limb-encasing devices)
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 noncovered 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
040.0
Actinomycotic infections
Gas Gangrene
250.00 250.82
388.2
444.21
444.22
444.81
526.89
558.1
707.10 707.19
728.86
730.10-730.19
902.53
903.1
903.01
904.0
904.41
925.1 929.9
958.0
986
987.7
989.0
990
993.2 - 993.3
996.52
996.90-996.99
999.1
Diabetes with other specified manifestations/complications

Sudden hearing loss
Arterial Embolism and thrombosis of the upper extremity
Arterial Embolism and thrombosis of the lower extremity
Arterial embolism and thrombosis of iliac artery
Osteonecrosis, other than mandible
Gastroenteritis and colitis due to radiation
Ulcer of the lower limb, unspecified
Necrotizing fasciitis
Chronic Osteomyelitis
Injury to the iliac artery
Injury to the brachial blood vessels
Injury to the axillary artery
Injury to the common femoral artery
Injury to the popliteal artery
Crush Injuries
Air embolism
Toxic Effect of Carbon monoxide
Toxic effect of hydrocyanic acid gas
Toxic effect of hydrocyanic acid and cyanides
Radionecrosis, soft tissue
Decompression Sickness
Skin graft failure or rejection
Complication of reattached extremity or body part
Air embolism
ICD-10 Codes
A42.0-A42.9
A48.0
E10.621
E10.622
E11.621
E11.622
H91.20-H91.23
I74.2
I74.3
I74.5
L97.10-L97.929
M27.8
M72.6
M86.31-M86.39
M84.40-M846.49
M86.50-M86.59
M86.60-M86.69
M86.8-m86.8X9
S07.0-S07.9
S35.51-S35.516
S38.1-S38.232
S45.00-S45.099
S45.101-S45.199
S47.1-S47.9
S77.00-S77.22
Actinomycosis
Gas gangrene
Type I diabetes mellitus with foot ulcer
Type I diabetes mellitus with other skin ulcer
Type 2 diabetes mellitus with foot ulcer
Type 2 diabetes mellitus with other skin ulcer
Sudden Idiopathic hearing loss
Embolism and thrombosis of arteries of the upper extremities
Embolism and thrombosis of arteries of the lower extremities
Embolism and thrombosis of iliac artery
Non-pressure chronic ulcer of lower limb, not elsewhere
classified
Other specified diseases of jaws
Necrotizing fasciitis
Chronic multifocal osteomyelitis
Chronic osteomyelitis with draining sinus
Other chronic hematogenous osteomyelitis
Other chronic osteomyelitis
Other osteomyelitis
Crushing injury of head
Injury of iliac artery or vein
Crushing injury of abdomen, lower back, and pelvis
Injury of axillary artery
Injury of brachial artery
Crushing injury of shoulder and upper arm
Crushing injury of hip and thigh
S75.00-S75.099
S85.00-S85.099
T57.3X1-T57.3X4
T58.01-T58.94
T65.0X1-T65.0X4
T66
T70.0-T70.9
T79.0
T86.820-T86.829
T87.0X1-T87.0X9
T87.1X1-T87.1X9
T87.2
T80.0
Injury of femoral artery

Injury of popliteal artery
Toxic effect of hydrogen cyanide
Toxic effect of carbon monoxide
Toxic effects of cyanides
Radiation sickness, unspecified
Effects of air pressure and water pressure
Air embolism (traumatic)
Complications of skin graft (allograft0 (autograft)
Complications of reattached (part of) upper extremity
Complications of reattached (part of) lower extremity
Complications of other reattached body part
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. Fiftynine 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
10
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
11
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, markedrecovery 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 onehour 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 subscores 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
12
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 2months 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
13
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 boardcertified 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
14
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
15
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 peerreviewed 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
16
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
17
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 </=30 days). Sixty-seven patients underwent HBO plus steroid therapy
(HBO group), and 63 were given steroids alone (steroid group). Hearing recovery
was evaluated by grade assessment and by the improvement in hearing compared to
that in the unaffected contralateral ear. The cure rate and hearing improvement rate
were not statistically different between the two groups; however, the recovery rate
was significantly higher in the HBO group than in the steroid group (59.7% vs.
39.7%; P < 0.05). With regard to patients with initial hearing levels of >/=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 <80 dB, hearing outcomes were not statistically different
between the two groups. In both the HBO and steroid groups, patients with initial
hearing levels of <80 dB showed a better hearing improvement rate than those with
initial hearing levels of >/=80 dB. In conclusion HBO therapy shows a significant
additional effect in combination with steroid therapy for ISSNHL, particularly in
patients with severe hearing loss. (Although this study seems to show positive
results, it was a retrospective review and it was not randomized).
It is important to note, that most studies regarding HBO for sudden deafness were
retrospective reviews, with limited, peer-reviewed published data. None of the
studies regarding the use of HBO for idiopathic sudden deafness or acoustic trauma,
were randomized, and there was a lack of long-term efficacy and safety. There were
no comparative studies to compare this treatment with the current treatment used
for idiopathic sudden deafness.
Scientific Rationale Update June 2007

Chronic radiation enteritis is a complication of radiation therapy for cancers of the
abdomen, pelvis or rectum that may develop, especially after large doses of radiation
therapy have been delivered. Factors that influence the occurrence and severity of
radiation enteritis include dose and fractionation, tumor size and extent, volume of
normal bowel treated, concomitant chemotherapy and radiation intracavitary
implants. Only 5% to 15% of persons treated with radiation to the abdomen will
develop chronic problems.
Unlike acute radiation enteritis, which occurs during or shortly after radiation therapy
and resolves within two to six weeks, chronic radiation enteritis usually develops six
or more months after radiation therapy. Chronic radiation enteritis may begin as
acute enteritis and persist after the cessation of treatment. It can affect both the
large and small intestine and is often progressive. Symptoms of chronic radiation
enteritis include colicky abdominal pain, bloody diarrhea, tenesmus, steatorrhea,
18
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 wellstudied. 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
19
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
20
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
21
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
April 1999
July 2000
June 2002
March 2003
May 2004
June 28, 2005
March 2006
June 2006
December 2006
June 2007
October 2007
October 2008
December 2008
April 2011
March 2012
March 2013
April 2013
First review date

Second review date
Third review date
Fourth review date
Fifth review date
Sixth review date
Medical Advisory Council - no revisions
Codes Added
Code revisions
Revised added autism as not medically necessary
Added chronic radiation enteritis to the list of medically
necessary indications for a select group of patients when
conservative treatment has failed
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.
Update. Revised policy to add HBO as investigational for
idiopathic sudden deafness or acoustic trauma.
Update. Revised policy to include HBO for radiation cystitis as
medically necessary. Clarified COPD under Contraindications to
HBO.
Update no revisions
Update no revisions
Update no revisions. Code updates
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.
22
This policy is based on the following evidence-based guidelines:

1.
2.
3.
Hyperbaric Oxygen therapy for brain injury, cerebral palsy, and stroke
National Cancer Institute. Gastrointestinal Complications. Radiation Enteritis.
Last Modified: 04/19/2006.
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
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-LossClinical-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):47985.
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.
23
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.

1.
2.
3.
4.
5.
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.
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-approvedconditions
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.
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.
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.
24
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):10837.
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):S135.
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 NovDec;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):3240.
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
25

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, Katzman P, Nilsson A, Hammarlund C. Hyperbaric oxygen therapy
facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care.
2010 May;33(5):998-1003.
8. Parra C, Gmez R, Marchetti P, et al. Management of Hemorrhagic Radiation
Cystitis with Hyperbaric Oxygen Therapy. Actas Urol Esp. 2011 Mar;35(3):175179
9. Rockswold SB, Rockswold GL, Zaun DA, et al. A prospective, randomized clinical
trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral
metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain
injury. J Neurosurg. 2010 May;112(5):1080-94.
10. Rossignol DA, Rossignol LW, Smith S, et al. Hyperbaric treatment for children
with autism: a multicenter, randomized, double-blind, controlled trial. BMC
Pediatr. 2009 Mar 13;9:21.
11. Teguh DN, Levendag PC, Noever I, et al. Early hyperbaric oxygen therapy for
reducing radiotherapy side effects: early results of a randomized trial in
oropharyngeal and nasopharyngeal cancer. Int J Radiat Oncol Biol Phys. 2009
Nov 1;75(3):711-6
12. Wang CJ, Wu RW, Yang YJ. Treatment of diabetic foot ulcers: A comparative
study of extracorporeal shockwave therapy and hyperbaric oxygen therapy.
Diabetes Res Clin Pract. 2011 Feb 8
References Update December 2008

1.
2.
3.
4.
5.
Muruve NA. Radiation Cystitis. eMedicine. February 7, 2008.

Centers for Medicare & Medicaid (CMS). NCD for Hyperbaric Oxygen Therapy
(20.29)
Centers for Medicare & Medicaid (CMS). Local Medicare LCD L26598. Trailblazer.
Effective March 1, 2008.
Centers for Medicare & Medicaid Services (CMS). Local Medicare - Wisconsin
Physicians Service Insurance Corporation LCD for Hyperbaric Oxygen Therapy.
Effective 5/1/2008. L26567.
Hampson NB, Corman JM. Rate of delivery of hyperbaric oxygen treatments does
not affect response in soft tissue radionecrosis. Undersea Hyperb Med. 2007
Sep-Oct;34(5):329-34.
26
6.
Centers for Medicare & Medicaid (CMS). Local Medicare First Coast L1315
Florida. Hyperbaric Medicine Literature Update. The Year in Review. UHMS
Annual Scientific Meeting, June 15, 2007.
7. Centers for Medicare & Medicaid (CMS). Local CMS, LCD DL24772, Group Health
(New York). Hyperbaric Oxygen Therapy. 2/14/07.
8. Technology Assessment. Department of Health and Human Services (DHHS). A
Horizon Scan: Uses of Hyperbaric Oxygen Therapy. October 5, 2006. Available
at: http://www.cms.hhs.gov/determinationprocess/downloads/id42TA.pdf
9. Neumeister M. Hyperbaric Oxygen Therapy. EMedicine. July 21, 2005.
10. Pasquier D, Hoelscher T, Schmutz J, et al. Hyperbaric oxygen therapy in the
treatment of radio-induced lesions in normal tissues: a literature review.
Radiother Oncol. 2004 Jul;72(1):1-13.
References Update October 2008

1.
O'Malley MR, Haynes DS. Sudden Hearing Loss. Otolaryngolic Clinics of North
America - Volume 41, Issue 3 (June 2008)
2. Rauch S. Idiopathic Sudden Sensorineural Hearing Loss. New England Journal of
Medicine. Volume 359:833-840 August 21, 2008 Number 8. Available at:
http://content.nejm.org/cgi/content/short/359/8/833
3. Weber PC. Sudden sensorineural hearing loss. UpToDate. Available at:
4. Bennett MH, Kertesz T, Yeung P. Hyperbaric oxygen for idiopathic sudden
sensorineural hearing loss and tinnitus. Cochrane Database Syst Rev 1. 2007.
5. Fujimura T, Suzuki H, Shiomori T, et al. Hyperbaric oxygen and steroid therapy
for idiopathic sudden sensorineural hearing loss. Eur Arch Otorhinolaryngol.
2007 Aug;264(8):861-6. Epub 2007 Mar 6.
6. Satar B, Hidir Y, Yetiser S. Effectiveness of hyperbaric oxygen therapy in
idiopathic sudden hearing loss. J Laryngol Otol. 2006 Aug;120(8):665-9. Epub
2006 Jun 9.
7. Narozny W, Kuczkowski J, Mikaszewski B. HBO effectively supports SSNHL
therapy. Eur Arch Otorhinolaryngol 262. (2): 163-164.2005.
8. Horn CE, Himel HN, Selesnick SH. Hyperbaric oxygen therapy for sudden
sensorineural hearing loss: a prospective trial of patients failing steroid and
antiviral treatment. Otol Neurotol 26. (5): 882-889.2005.
9. Racic G, Maslovara S, Roje Z, et al. Hyperbaric oxygen in the treatment of
sudden hearing loss. ORL J Otorhinolaryngol Relat Spec 65. (6): 317-320.2003.
10. National Institute of Health. Sudden Deafness. Bethesda, MD. National Institutes
of Health; 2000. NIH publication 00-4757.
11. Lamm K, Lamm H, Arnold W. Effect of hyperbaric oxygen therapy in comparison
to conventional or placebo therapy or no treatment in idiopathic sudden hearing
loss, acoustic trauma, noise-induced hearing loss and tinnitus. A literature
survey. Adv Otorhinolaryngol. 1998;54:86-99.
References - Update June 2007

Marshall GT, Thirlby RC, Bredfeldt JE, Hampson NB. Treatment of gastrointestinal
radiation injury with hyperbaric oxygen. Undersea Hyperb Med. 2007 JanFeb;34(1):35-42.
2. Huddy JE, Patel P, Johnson MW, et al. Hyperbaric oxygen as a treatment for
malabsorption in a radiation-damaged short bowel. Eur J Gastroenterol Hepatol.
2006 Jun;18(6):685-8.
3. Feldmeier JJ. Hyperbaric oxygen for delayed radiation injuries. Undersea Hyperb
Med. 2004 Spring;31(1):133-45.
4. Feldmeier JJ, Hampson NB. A systematic review of the literature reporting the
application of hyperbaric oxygen prevention and treatment of delayed radiation
1.
27
injuries: an evidence based approach. Undersea Hyperb Med. 2002

Spring;29(1):4-30.
5. Gouello JP, Bouachour G, Person B, et al. The role of hyperbaric oxygen therapy
in radiation-induced digestive disorders. 36 cases. Presse Med. 1999 Jun
5;28(20):1053-7.
6. Bennett MH, Feldmeier J, Hampson N, et al. Hyperbaric oxygen therapy for late
radiation tissue injury. Cochrane Database Syst Rev. 2005 Jul 20;(3).
7. Bui QC, Lieber M, Withers HR, et al. The efficacy of hyperbaric oxygen therapy in
the treatment of radiation-induced late side effects. Int J Radiat Oncol Biol Phys.
2004 Nov 1;60(3):871-8.
References - Update June, 2005

1. Roeckl-Wiedmann I, Bennett M, Kranke P. Systematic review of hyperbaric
oxygen in the management of chronic wounds. Br J Surg. 2005 Jan;92(1):24-32.
2. Kranke P, Bennett M, Roeckl-Wiedmann I, et al. Hyperbaric oxygen therapy for
chronic wounds. Cochrane Database Syst Rev. 2004;(2):CD004123.
3. Centers for Medicare and Medicaid Services. Medicare Coverage Issues Manual.
20-29. "NCD for Hyperbaric Oxygen Therapy." April 2003
4. Wang C, Schwaitzberg S, Berliner E, et al. Hyperbaric oxygen for treating
wounds: a systematic review of the literature. Arch Surg. 2003 Mar;138(3):2729; discussion 280.
5. Villanueva E, Bennett MH, Wasiak J, et al. Hyperbaric oxygen therapy for thermal
burns. Cochrane Database Syst Rev. 2004;(3):CD004727.
6. Hampson NB, Mathieu D, Piantadosi CA, et al. Carbon monoxide poisoning:
interpretation of randomized clinical trials and unresolved treatment issues.
Undersea Hyperb Med. 2001 Fall;28(3): 157-64.
7. Bennett M, Heard R. Treatment of multiple sclerosis with hyperbaric oxygen
therapy. Undersea Hyperb Med. 2001 Fall;28 (3):117-22.
8. Papazian O, Alfonso I. Hyperbaric oxygen treatment for children with cerebral
palsy Rev Neurol. 2003 Aug 16-31;37(4):359-64.
9. Hardy P, Collet JP, Goldberg J, et al. Neuropsychological effects of hyperbaric
oxygen therapy in cerebral palsy. Dev Med Child Neurol. 2002 Jul;44(7):436-46.
10. Collet JP, Vanasse M, Marois P, et al. Hyperbaric oxygen for children with cerebral
palsy: a randomised multicentre trial. HBO-CP Research Group. Lancet. 2001
Feb 24;357(9256):582-6.
11. Montgomery D, Goldberg J, Amar M, et al. Effects of hyperbaric oxygen therapy
on children with spastic diplegic cerebral palsy: a pilot project. Undersea Hyperb
Med. 1999 Winter;26(4):235-42.
12. Rudack C, Eikenbusch G, Stoll W, Hermann W. Therapeutic management of
necrotizing neck infections HNO. 2003 Dec; 51 (12):986-92.
13. O'Brien, C.D. and Manaker, S. "Hyperbaric Oxygen Therapy." UpTo Date. August
2002.
14. Heng MC. Topical hyperbaric therapy for problem skin wounds. J Dermatol Surg
Oncol. 1993 Aug;19(8):784-93.
15. Edsberg LE, Brogan MS, Jaynes CD, et al. Topical hyperbaric oxygen and
electrical stimulation: exploring potential synergy. Ostomy Wound Manage. 2002
Nov;48(11):42-50.
References - Initial
1. Diabetic Foot Wound Care. Diabetes Care. August 1999; 22(*):1354-1361.
28
2. Berkow, Robert, ed. The Merck American Diabetes Association. Consensus

Development Conference on Manual. Sixteenth Edition. Rahway, N. J.: Merck
Research Laboratories, 1992.
3. Centers for Medicare and Medicaid Services. Medicare Coverage Issues Manual.
35-10. "Hyperbaric Oxygen Therapy." October 2000.
4. Centers for Medicare and Medicaid Services. Decision Memorandum. "Hyperbaric
Oxygen Therapy in Treatment of Hypoxic Wounds and Diabetic Wounds of the
Lower Extremities (#CAG-00060N)." August 30, 2002.
5. Department of Health and Human Services. Health Care Financing
Administration. Program Memorandum. Delay of Hyperbaric Oxygen Therapy
Coverage Policy. Transmittal AB-O0-15. March 2000.
6. Fischback, Francis. A Manual of Laboratory & Diagnostic Tests. Fourth edition.
Philadelphia: J. B. Lippincott Company, 1992.
7. Hayes Directory. Hyperbaric Oxygen Therapy for Burns, Infections, and
Wounds. HYPE0501.19. May 2002.
8. Hayes Directory. Hyperbaric Oxygen Therapy for Carbon Monoxide Poisoning.
HYPE0501.18. May 2002.
9. Juurlink, D.N., et al. "Hyperbaric Oxygen for Carbon Monoxide Poisoning." The
Cochrane Library. February 17, 2000.
10. Jacobs, Davis S., et al. Laboratory Test Handbook. 3rd edition. Hudson, Ohio:
LexiComp, Inc., 1994.
11. O'Brien, C.D. and Manaker, S. "Hyperbaric Oxygen Therapy." UpToDate. August
2002.
12. Tibbles, Patrick M. and Edelsberg, John S. HyperbaricOxygen Therapy. The
New England Journal of Medicine. June 20, 1996; 334(25):16421647.
13. Undersea and Hyperbaric Medical Society. Committee Report. Hyperbaric
Oxygen Therapy. 1999.
14. Undersea and Hyperbaric Medical Society. Position Statement. "Hyperbaric
Oxygen Therapy for Chronic Brain Injury." June 2002.
15. Undersea and Hyperbaric Medical Society. Position Statement. "The Treatment of
Multiple Sclerosis with Hyperbaric Oxygen Therapy." Position Statement.
16. Weaver, L.K., et al. "Hyperbaric Oxygen for Acute Carbon Monoxide Poisoning."
The New England Journal of Medicine. October 3, 2002; 347(14):1057-1067.
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excluded, limited, or subject to dollar caps. The policy provides for clearly written, reasonable and current
criteria that have been approved by Health Nets National Medical Advisory Council (MAC). The clinical
criteria and medical policies provide guidelines for determining the medical necessity criteria for specific
procedures, equipment, and services. In order to be eligible, all services must be medically necessary and
otherwise defined in the member's benefits contract as described this "Important Notice" disclaimer. In all
cases, final benefit determinations are based on the applicable contract language. To the extent there are
any conflicts between medical policy guidelines and applicable contract language, the contract language
prevails. Medical policy is not intended to override the policy that defines the members benefits, nor is it
intended to dictate to providers how to practice medicine.
29
Policy Effective Date and Defined Terms.

The date of posting is not the effective date of the Policy. The Policy is effective as of the date determined
by Health Net. All policies are subject to applicable legal and regulatory mandates and requirements for
prior notification. If there is a discrepancy between the policy effective date and legal mandates and
regulatory requirements, the requirements of law and regulation shall govern. * In some states, new or
revised policies require prior notice or posting on the website before a policy is deemed effective. For
information regarding the effective dates of Policies, contact your provider representative. The Policies do
not include definitions. All terms are defined by Health Net. For information regarding the definitions of
terms used in the Policies, contact your provider representative.
Policy Amendment without Notice.
Health Net reserves the right to amend the Policies without notice to providers or Members. In some
states, new or revised policies require prior notice or website posting before an amendment is deemed
effective.
No Medical Advice.
The Policies do not constitute medical advice. Health Net does not provide or recommend treatment to
members. Members should consult with their treating physician in connection with diagnosis and
treatment decisions.
No Authorization or Guarantee of Coverage.
The Policies do not constitute authorization or guarantee of coverage of particular procedure, drug, service
or supply. Members and providers should refer to the Member contract to determine if exclusions,
limitations, and dollar caps apply to a particular procedure, drug, service or supply.
Policy Limitation: Members Contract Controls Coverage Determinations.
The determination of coverage for a particular procedure, drug, service or supply is not based upon the
Policies, but rather is subject to the facts of the individual clinical case, terms and conditions of the
members contract, and requirements of applicable laws and regulations. The contract language contains
specific terms and conditions, including pre-existing conditions, limitations, exclusions, benefit maximums,
eligibility, and other relevant terms and conditions of coverage. In the event the Members contract (also
known as the benefit contract, coverage document, or evidence of coverage) conflicts with the Policies,
the Members contract shall govern. Coverage decisions are the result of the terms and conditions of the
Members benefit contract. The Policies do not replace or amend the Members contract. If there is a
discrepancy between the Policies and the Members contract, the Members contract shall govern.
Policy Limitation: Legal and Regulatory Mandates and Requirements.
The determinations of coverage for a particular procedure, drug, service or supply is subject to applicable
legal and regulatory mandates and requirements. If there is a discrepancy between the Policies and legal
mandates and regulatory requirements, the requirements of law and regulation shall govern.
Policy Limitations: Medicare and Medicaid.
Policies specifically developed to assist Health Net in administering Medicare or Medicaid plan benefits and
determining coverage for a particular procedure, drug, service or supply for Medicare or Medicaid
members shall not be construed to apply to any other Health Net plans and members. The Policies shall
not be interpreted to limit the benefits afforded Medicare and Medicaid members by law and regulation.
30

Hyperbaric Oxygen Therapy

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National Medical Policy

Hyperbaric Oxygen Therapy

Update of NMDAG Policy, June 2005

This National Medical Policy is subject to the terms in the

National Coverage Manual Citation

Hyperbaric Oxygen Therapy Apr 14

Hyperbaric Oxygen Therapy:

Use Health Net Policy

Current Policy Statement

Hyperbaric Oxygen Therapy Apr 14

Correction of any vascular problems in the affected limb,

Acute cerebral edema

Hyperbaric Oxygen Therapy Apr 14

Acute or chronic cerebral vascular insufficiency

Contraindications to Hyperbaric oxygen therapy include:

Codes Related To This Policy

Hyperbaric Oxygen Therapy Apr 14

Diabetes with other specified manifestations/complications

Hyperbaric Oxygen Therapy Apr 14

Injury of femoral artery

Physician or other qualified health care professional attendance

Scientific Rationale Update April 2014

Hyperbaric Oxygen Therapy Apr 14

Hyperbaric Oxygen Therapy Apr 14

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

Scientific Rationale Update April 2013

Hyperbaric Oxygen Therapy Apr 14

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

Sudden sensorineural hearing loss (SNHL) is a subset of SHL that is sensorineural

Idiopathic sudden sensorineural hearing loss (ISSNHL) is defined as SSNHL with

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

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

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

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

Hyperbaric Oxygen Therapy Apr 14

intratympanic steroid administration is more effective than systemic steroids plus

Scientific Rationale Update March 2013

Hyperbaric Oxygen Therapy Apr 14

rate, marked-recovery rate (percent of patients with hearing gains 30 dB),

Hyperbaric Oxygen Therapy Apr 14

Hyperbaric Oxygen Therapy Apr 14

Scientific Rationale Update March 2012

Hyperbaric Oxygen Therapy Apr 14

Scientific Rationale Update December 2008

Hyperbaric Oxygen Therapy Apr 14

Scientific Rationale Update October 2008

Hyperbaric Oxygen Therapy Apr 14

not demonstrated effectiveness for the addition of antiviral therapy to steroid

Hyperbaric Oxygen Therapy Apr 14

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

Scientific Rationale Update June 2007

Hyperbaric Oxygen Therapy Apr 14

Hyperbaric Oxygen Therapy Apr 14

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

Scientific Rationale - Initial

Hyperbaric Oxygen Therapy Apr 14

Hyperbaric Oxygen Therapy Apr 14

First review date

Hyperbaric Oxygen Therapy Apr 14