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| CASE REPORT |
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| Year : 2022 | Volume
: 24
| Issue : 3 | Page : 117-119 |
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Hyperbaric Oxygen Therapy for Recalcitrant Macular Edema Following Branch Retinal Vein Occlusion
Avadhesh Oli1, Rupali Bhirud2, Kartikey P Solanki3, Dattakiran Joshi4
1 Department of Ophthalmology, INHS Asvini, Colaba Mumbai, Maharashtra, India
2 Department of Ophthalmology, INHS Asvini, Colaba, Mumbai, Maharashtra, India
3 Department of Hyperbaric Medicine, INHS Asvini, Colaba Mumbai, Maharashtra, India
4 Dy PMO, HQ Western Air Command (IAF), New Delhi, India
| Date of Submission | 07-May-2021 |
| Date of Acceptance | 29-May-2021 |
| Date of Web Publication | 01-Apr-2022 |
Correspondence Address:
Wg Cdr (Dr) Avadhesh Oli
INHS Asvini, Near RC Church, Colaba Mumbai - 400 005, Maharashtra
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jmms.jmms_65_21
Cystoid macular edema (CME) is the most common cause of reduced vision in branch retinal vein occlusion (BRVO). The treatment protocols for macular edema in BRVO have changed considerably in the previous decade because of the increased popularity of the wide use of optical coherence tomography (OCT) and intravitreal drugs. Intravitreal injection of anti-vascular endothelial growth factors (anti-VEGF) and steroids result in the reduction of CME. However, the effect is transient, and multiple injections may be required. On repeated use, few patients become non-responders to these drugs. Nonetheless, anti-VEGF drugs may have potentially life-threatening complications because of systemic absorption. Intravitreal steroids may lead to severe ocular side effects such as cataract and glaucoma. Chances of endophthalmitis, retinal tear, and inflammation can occur with any of the intravitreal injections. We present a case of BRVO with recalcitrant CME following focal laser, multiple intravitreal anti-VEGF, and steroid injections. However, he had cardiovascular risk factors, so repeated anti-VEGF injections were not given. He was planned for hyperbaric oxygen therapy and showed favorable response. His visual acuity improved and macular edema reduced to more than half from baseline values on OCT.
Keywords: Hyperbaric oxygen therapy, intravitreal injection, macular edema, recalcitrant cystoid macular edema, retinal vein occlusion
How to cite this article:
Oli A, Bhirud R, Solanki KP, Joshi D. Hyperbaric Oxygen Therapy for Recalcitrant Macular Edema Following Branch Retinal Vein Occlusion. J Mar Med Soc 2022;24, Suppl S1:117-9 |
| Introduction | |  |
Cystoid macular edema (CME) is noted in almost one-third of patients with branch retinal vein occlusion (BRVO). Laser photocoagulation, intravitreal steroids, or vascular endothelial growth factor (VEGF) inhibitors are used for the treatment of CME.[1] Steroids and anti-VEGFs may have a transient effect on the resolution of CME; hence, repeated injections are required. The cost for repeated injections is a critical concern, along with the chances of life-threatening complications such as stroke and cardiac complications.[2] Hyperbaric oxygen (HBO2) therapy has been reported to reduce the macular edema in various vascular diseases of the retina like diabetic macular edema and retinal vein occlusion. HBO2 involves the administration of 100% oxygen at a pressure 2–3 times of the normal atmospheric pressure which increases tissue levels of oxygen. Based on available evidence, HBO2 has been recommended in central retinal artery occlusion, however, the evidence for other ocular indications is scant.[3] We present a case of recalcitrant macular edema in BRVO treated with HBO2 therapy.
| Case Report | | |
A 55-year-old male, a known case of primary hypertension, presented with reduced vision in the right eye (RE) for the past 2 years. He had received three doses of intravitreal ranibizumab and three dexamethasone implants along with focal laser.
His best-corrected visual acuity (BCVA) was 6/60 in the RE and 6/6 in the left eye. Anterior segment examination was normal except for the posterior chamber intraocular lens in the RE. His intraocular pressure in both eyes was 16 mmHg. Fundus examination in the RE showed sclerosed vein along the superotemporal arcade, old laser scars, multiple hard exudates, and fluid in the foveal region [Figure 1]a. Fundus fluorescein angiography showed leakage in the early phase with staining of laser scars in the late phase along with capillary nonperfusion areas and enlarged foveal avascular zone (FAZ) [Figure 1]b, [Figure 1]c, [Figure 1]d. Optical coherence tomography (OCT) showed cystoid changes, hard exudates arranged in the form of a necklace of pearl pattern, and distorted foveal contour in RE with macular edema of 780 microns [Figure 2]a. | Figure 1: (a) Fundus photograph in the right (right eye) showed sclerosed vein along the superotemporal arcade, old laser scars, multiple hard exudates and fluid in the foveal region. (b-d) Fundus fluorescein angiography showed leakage in the early phase with staining of laser scars in late phase along with capillary nonperfusion areas and enlarged foveal avascular zone
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 | Figure 2: (a) Optical coherence tomography showed cystoid macular edema with the distorted foveal contour in right eye with macular edema of 780 microns. (b) Optical coherence tomography showed reduced cystoid macular edema and resolution of fluid nasally
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Treatment
He was diagnosed as a case of recalcitrant macular edema RE following superotemporal BRVO. Meanwhile, he was already treated with three intravitreal anti-VEGF and steroid implant injections. With the addition of laser photocoagulation, he was given a trial of all the therapeutic modalities available in the armamentarium. When he reported to this center, he had taken intravitreal injection Ranibizumab 9 months back and was off medication for the last 9 months. He presented to us, with chronic CME and an enlarged FAZ, which was unlikely to respond to anti-VEGF injections and he was reluctant to receive any further intravitreal injections. Finally, the option to try HBO2 therapy was discussed with him and he was keen for the same.
Informed consent was taken for the treatment with HBO2 and the use of clinical findings and images for research and this publication.
He underwent a total of 13 sessions of HBO2 at 2.4 absolute atmospheres with 100% oxygen through a tight-fitting mask. The HBO2 was given as per treatment tables, and each session lasted for about 90 min. At 1 month follow-up, he showed two-line improvement in visual acuity to 6/24 and a significant decrease in intraretinal fluid and macular edema from 780 to 380 μ(reduced to less than half, = 50%) which was maintained for 9 months [Figure 2]b.
| Discussion | | |
We present a case of BRVO with recalcitrant macular edema following multiple anti-VEGF, steroid implant intravitreal injections, and laser photocoagulation. The macular edema was recalcitrant and partially responded to treatment. He responded favorably to HBO2 with the improvement in BCVA by two lines and reduction in macular edema to more than half from baseline values.
Ocular indications of HBO2 include central retinal artery occlusion, radiation optic neuropathy, radiation-induced scleritis, and specific orbital cellulitis. HBO2 is also indicated in macular edema caused by diabetes, retinal vein occlusion, postcataract surgery, and uveitis.[4]
The exact pathogenesis of macular edema following BRVO is not known, but hypoxia and backpressure changes play an essential role. HBO2 causes retinal vasoconstriction which leads to a decrease in venous pressure and capillary leakage, thus reducing fluid transudation. Besides, HBO2 causes choriocapillaris to supply more oxygen to the inner retinal layers by increasing oxygen tension at the tissue level.[5] This may, in turn, decrease the tissue hypoxia and production of VEGF. Furthermore, increased tissue oxygenation leads to the efficient functioning of the RPE pump, which drives the fluid out of retinal layers.
The literature on the role of HBO2 in macular edema is sparse. In one such study on macular edema due to diverse causes, HBO2 improved vision from 2 to 4 lines. However, this study was done almost two decades back, without an objective assessment of macular edema on OCT.[6]
In our patient, multiple treatment modalities were tried over 2 years, and the CME became chronic, which might have affected the viability of photoreceptors. The macular edema in this patient reduced by more than 50% which was maintained for 9 months. The enlarged FAZ signifying macular ischemia which was reduced by HBO2 could be important factor in this case for a favorable response. However, reduction in macular thickness did not fully translate into an improvement in visual acuity but, the visual acuity did improve by two lines and did not worsen further over the follow-up period, and remained static after two-line improvement.
Significant limitations of HBO2 include the availability of the chambers and the lack of robust evidence. HBO2 is associated with complications of high oxygen tension toxicity affecting multiple organ systems and is contraindicated in patients with pneumothorax, pregnancy, preexisting respiratory illness, and claustrophobia.[4]
The experience from this case indicates that HBO2 can be used to treat CME in BRVO as adjuvant therapy, especially in cases who are nonresponders to intravitreal injections or have systemic or ocular contraindications. It is recommended to conduct a randomized controlled trial to establish the adjuvant role of HBO2 in CME due to BRVO.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
There conflict of interest
There are no conflict of interest.
| References | | |
| 1. | Kumar P, Banarji A, Patyal S, Gurunadh VS, Ahluwalia TS, Oli A, et al. A clinical study to evaluate the efficacy of intravitreal anti-VEGF therapy in treating macular edema due to retinal venous occlusions. Med J Armed Forces India 2013;69:260-7.  |
| 2. | CATT Research Group; Martin DF, Maguire MG, Ying GS, Grunwald JE, Fine SL, et al. Ranibizumab and bevacizumab for neovascular age-related macular degeneration. N Engl J Med 2011;364:1897-908. |
| 3. | Mathieu D, Marroni A, Kot J. Tenth European consensus conference on hyperbaric medicine: Recommendations for accepted and non-accepted clinical indications and practice of hyperbaric oxygen treatment. Diving Hyperb Med 2017;47:24-32. |
| 4. | Oguz H, Sobaci G. The use of hyperbaric oxygen therapy in ophthalmology. Surv Ophthalmol 2008;53:112-20. |
| 5. | Kiryu J, Ogura Y. Hyperbaric oxygen treatment for macular edema in retinal vein occlusion: Relation to severity of retinal leakage. Ophthalmologica 1996;210:168-70. |
| 6. | Krott R, Heller R, Aisenbrey S, Bartz-Schmidt KU. Adjunctive hyperbaric oxygenation in macular edema of vascular origin. Undersea Hyperb Med 2000;27:195-204. |
[Figure 1], [Figure 2]
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