2013年6月3日 星期一


Central retinal artery occlusion treated with oxygen: A literature review and treatment algorithm

H. Murphy-Lavoie , F. Butler , C. Hagan

UHM 2012, Vol. 39, No. 5:943-953

ABSTRACT

Central retinal artery occlusion (CRAO) is an uncommon eye disorder, but one that typically produces severe and irreversible vision loss in the affected eye. The retina has a dual blood supply, with the retinal circulation supplying the inner layers and the choroidal circulation supplying the outer layers. In CRAO, vision loss results from cell death in the inner retinal layers despite relative sparing of the outer layers.

If supplemental oxygen is provided, however, oxygen from the choroidal circulation may diffuse in adequate quantity to the inner layers of the retina to maintain retinal function and restore vision. In some patients this can be achieved with normobaric hyperoxia; in others, hyperbaric oxygen (HBO2) may be required.

The challenge is to provide the supplemental oxygen early enough after the onset of vision loss to prevent irreversible damage to the retina. In experimental models of complete CRAO, the ischemic time window before permanent retinal damage occurs is just over 90 minutes; in the clinical setting where occlusion may be incomplete, return of vision may be achieved even after delays of eight to 24 hours.

In patients with a clinical picture of CRAO who present within 24 hours of vision loss, supplemental oxygen should be started immediately at the highest possible fraction of inspired oxygen (FiO2). If vision is not quickly restored, emergent HBO2 should be undertaken if feasible. If the patient responds to HBO2, follow-up treatment with supplemental oxygen should be customized to maintain retinal viability until the obstructed retinal artery recanalizes, which typically occurs within the first 72 hours. This paper reviews the pertinent literature on CRAO and HBO2 and provides a treatment algorithm.

 

Based on the American Heart Association classification of evidence, treatment of CRAO with hyperbaric oxygen therapy is Level IIb . There is fair to good evidence to support its use with retrospective case series but no prospective randomized controlled trials. It is acceptable, safe, considered efficacious but lacks confirmation of efficacy by Level 1 studies. There is no evidence of harm, and consistently positive results, when HBO2 is started shortly after onset on vision loss. In addition, there are no alternative therapies with similar outcomes, that would present ethical considerations for a proposed randomized trial. The relatively rare incidence of this condition does not lend itself to randomized controlled trials, as evidenced by the paucity of trials for other therapies in treating this condition. As of 2012, a Medline search revealed only four small randomized controlled trials for all of the proposed therapies, none of which revealed clinically positive results. The hopeless and recalcitrant nature of this condition when left untreated mandates we utilize all potentially helpful treatments, including hyperbaric oxygen therapy.

Comparison of therapeutic results in sudden sensorineural hearing loss with/without additional hyperbaric oxygen therapy: a retrospective review of 465 audiologically controlled cases

Liu, S.-C., Kang, B.-H., Lee, J.-C., Lin, Y.-S., Huang, K.-L., Liu, D.-W., Su, W.-F.,
Kao, C.-H., Chu, Y.-H., Chen, H.-C. & Wang, C.-H.
 
Clin. Otolaryngol. 2011, 36, 121–128
 

Objective: To investigate the necessity of routine application of hyperbaric oxygen therapy for sudden sensorineural hearing loss.

Design setting and participants: A retrospective chart review looked at 465 patients, with 353 of them receiving pharmacologic treatments alone. Among these patients, 76 underwent systemic steroid treatment only (steroid group) and 277 received systemic steroids and dextran (steroid–dextran group). The remaining 112 patients were treated with hyperbaric oxygen in addition to pharmacologic agents (steroid–dextran–hyperbaric oxygen group).

 

Main outcome measures: The outcome was determined by comparing the difference of pure-tone thresholds and absolute hearing gains after treatment calculated at each audiometric octave frequency or grouped frequencies of audiograms. On the basis of the severity of initial hearing loss, patients were classified at three scales of hearing impairments measured in decibels hearing level (dBHL): 70 dBHL, less severe; 71–90 dBHL, severe; and 91 dBHL, profound. The outcomes of their hearing recovery were classified into three recovery grades: good, fair and poor.

 

Results:  In those patients with initial hearing loss >90 dBHL, the addition of hyperbaric oxygen to steroid–dextran gave a significant hearing gain difference (P = 0.030) by showing a greater hearing gain of 24.5 ± 2.7 dB compared with steroid only (12.9 ± 3.7 dB) or steroid–dextran (15.6 ± 2.7 dB). This outcome was confirmed when we compared the outcome using the recovery grading; steroid–dextran–hyperbaric oxygen group showed that more patients with initial profound (91 dBHL) hearing loss responded to hyperbaric oxygen treatment by exhibiting good and fair recoveries (2% and 70%) as compared with steroid only (0% and 42%) or steroid–dextran (8% and 46%) groups (P = 0.043), while the patients with initial severe (71–90 dBHL) and less severe (70 dBHL) hearing loss responded to the addition of hyperbaric oxygen treatment with less favourable recoveries. Furthermore, the addition of dextran in steroid–dextran group showed no significant benefit compared with the steroid group (P =0.435).

 

Conclusions: When applied as an adjuvant to pharmacologic agents, hyperbaric oxygen benefits patients with initial profound sudden sensorineural hearing loss. Therefore, we recommend the routine application of hyperbaric oxygen in conjunction with pharmacologic agents for those patients. The addition of dextran to steroid has no benefit and cannot be recommended.

Hyperbaric oxygen for idiopathic sudden sensorineural hearing loss and tinnitus

Michael H Bennett1, Tom Kertesz2, Matthias Perleth3, Philip Yeung2, Jan P Lehm4

Cochrane Database of Systematic Reviews 2012, Issue 10.

Copyright © 2012 The Cochrane Collaboration. Published by JohnWiley & Sons, Ltd.

A B S T R A C T

Background

This is an update of a Cochrane Review first published in The Cochrane Library in Issue 1, 2005 and previously updated in 2007 and 2009. Idiopathic sudden sensorineural hearing loss (ISSHL) is common and has a significant effect on quality of life. Hyperbaric oxygen therapy (HBOT) may improve oxygen supply to the inner ear and result in an improvement in hearing.

Objectives

To assess the benefits and harms of HBOT for treating ISSHL and/or tinnitus.

Search methods

We searched the Cochrane Ear, Nose and Throat Disorders Group Trials Register; the Cochrane Central Register of Controlled Trials (CENTRAL); PubMed; EMBASE; Database of Randomised Trials in HyperbaricMedicine (DORCTHIM); CINAHL; Web of Science; BIOSIS Previews; Cambridge Scientific Abstracts; ICTRP and additional sources for published and unpublished trials. The date of the most recent search was 2 May 2012, following previous searches in 2009, 2007 and 2004.

Selection criteria

Randomised studies comparing the effect on ISSHL and tinnitus of HBOT and alternative therapies.

Data collection and analysis

Three authors evaluated the quality of trials using the ’Risk of bias’ tool and extracted data from the included trials.

Main results

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 (sixmonths) of ISSHL and/or tinnitus.

Authors’ conclusions

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 we do not recommend the use of HBOT for this purpose.