Ocular decompression retinopathy occurs when intraocular pressure (IOP) is lowered suddenly after trabeculectomy and other surgical or medical procedures. It has also been reported after paracentesis for uveitic glaucoma. The sudden lowering of IOP increases the choroidal and retinal blood flow beyond the control of retinal autoregulation causing features of decompression retinopathy such as retinal hemorrhages, disc hyperemia, and rarely exudative retinal detachment and choroidal detachment. Herein, we would like to report a case of ocular decompression retinopathy following paracentesis and intracameral bevacizumab (ICB) injection in neovascular glaucoma with PDR.
A 49-year-old diabetic female presented with a painful diminution of vision in the left eye for 10 days. On examination, her best-corrected visual acuity was 20/50p N18 in the right eye and 20/40p N6 in the left eye. Both eyes anterior segment examination showed a clear cornea while gonioscopy showed right eye open angles with neovascularization of the angle (NVA) in one quadrant whereas the left eye showed 360 closed angles, florid neovascularization of iris (NVI) with NVA in 2 quadrants. IOP in the right eye was 18 mmHg and in the left eye, it was 42 mmHg. Nuclear and posterior subcapsular cataract was seen in both eyes. Fundus examination of the right eye showed multiple dot-blot hemorrhages and flat neovascularization elsewhere (NVE) while the left eye showed elevated fibrovascular proliferation (FVP) near the disc, multiple flat NVE, multiple dot-blot hemorrhages, and inferior 180° sclerosed vessels [Fig. 1]. Both eyes showed healthy optic discs and no macular edema. Fundus fluorescein angiography confirmed the presence of new vessels in both eyes [Fig. 2]. Thus, a diagnosis of both eyes senile cataract, PDR, and neovascular glaucoma (NVG [rubeosis stage in the right eye and closed-angle stage in left eye]) with left eye inferior old branch retinal vein occlusion was made.
The patient was injected with intravitreal bevacizumab (IVB - 1.25 mg/0.05 mL) in the right eye but in view of the elevated FVP in the left eye, IVB was avoided and left eye first sitting of panretinal photocoagulation (PRP) was done in the inferior quadrant. Subsequently, the patient was started on oral and topical antiglaucoma medications (AGM) in both eyes (a combination of brimonidine tartrate 0.2% with brinzolamide 0.1% two times/day, a combination of travoprost 0.004% and timolol maleate 0.5% at night and oral acetazolamide 250 mg three times/day). Two days later, the left eye IOP was still raised at 38 mmHg and the cornea showed microcystic edema not allowing for further PRP sittings. At this visit, anterior chamber paracentesis with intracameral bevacizumab (ICB - 1.25 mg/0.05 mL) injection was performed for the left eye.
Three days following left eye ICB the visual acuity dropped to 20/200 N36, the corneal edema persisted and IOP was measured as 58 mmHg. The NVI had regressed completely and there was no hyphema but the fundus examination revealed multiple peripapillary white-centered flame-shaped and dot retinal hemorrhages with two patches of subhyaloid hemorrhage at the fovea along with inferior PRP marks [Fig. 3]. These peripapillary hemorrhages were not seen prior to the left eye intraocular intervention suggesting ocular decompression retinopathy following sudden and transient lowering of IOP during anterior chamber paracentesis prior to the ICB injection.
Despite regression of the left eye NVI and keeping the patient on maximum medical antiglaucoma therapy, the IOP was persistently raised. Thus, 6 days following the ICB injection the patient underwent left eye mitomycin C-augmented trabeculectomy with repeat ICB injection (1.25 mg/0.05 mL). Following the surgical intervention, vision improved to 20/125, cornea cleared and IOP normalized to 12 mmHg with no further change in the fundus picture. At 3 weeks follow-up, the left eye vision improved to 20/40, peripapillary hemorrhages reduced and the patient subsequently underwent left eye PRP completion in 2 sittings [Fig. 4].
At the last follow-up, 2 months following the initial visit, right eye had a visually significant cataract, no visible ocular NV and normal IOP on 4 topical AGM. The left eye had a superior conjunctival bleb, clear cornea, normal IOP on 3 topical AGM, senile cataract, no anterior segment NV, regressed FVP, and 360 PRP marks.
Ocular decompression retinopathy may occur after IOP lowering procedures such as glaucoma drainage implant insertion and trabeculectomy but may also occur after anterior chamber paracentesis, cataract surgery, vitrectomy, and silicone oil removal. The diagnosis of ocular decompression retinopathy is mainly clinically where about 80% of patients are asymptomatic. Clinical features include hemorrhages at multiple levels of optic nerve and peripapillary retina which resolve in as short as 2 weeks. In most of the cases the disease follows a benign course with visual acuity usually returning to preoperative levels without treatment. However, a few patients may require vitrectomy for nonresolving vitreous hemorrhage.
In our patient, the right eye had PDR with multiple flat new vessels along with NVG in the rubeosis stage and normal IOP, thus IVB was preferred as the initial treatment modality. Though the effect of PRP is long-lasting, it often takes several weeks to show effect during which progressive angle closure, raised IOP, and optic nerve damage may ensue resulting in loss of vision.
The left eye had PDR with an elevated FVP near the disc along with NVG in the closed-angle stage and raised IOP. In view of this elevated FVP, IVB was avoided as it may lead to development of tractional retinal detachment. Thus, as the cornea was clear at presentation despite the raised IOP, PRP 1 was done to the inferior retina on the same day. On subsequent follow-up, the left eye corneal edema developed in view of the raised IOP which prevented PRP completion. Thus, anterior chamber paracentesis along with ICB was done since ICB not only decreases iris neovascularization but also aids as a surgical adjunct for neovascular glaucoma. Also the half-life of ICB is considerably less which would prevent any prolonged effect on the posterior segment pathology. Hyphema is a common complication in NVG following anterior segment surgeries including anterior chamber paracentesis but it did not occur in our case. In a study by Nakatake et al., only 22% of patients of NVG undergoing an IOP reducing surgery developed hyphema. Following the intracameral anti-VEGF injection multiple retinal hemorrhages developed suggesting decompression retinopathy. A differential of central retinal vein occlusion and Valsalva retinopathy was kept but the absence of dilated and tortuous veins, absent hemorrhages up to retinal periphery, and absence of history suggestive of raised intra-abdominal or thoracic pressure with only uniocular changes ruled out these differentials. Subsequently, the patient underwent mitomycin C-augmented trabeculectomy along with a repeat dose of ICB following which the IOP normalized, cornea cleared, and the patient underwent PRP completion.
To conclude, though not the standard treatment procedure, ICB can be used in cases of PDR with NVG where there is an elevated FVP in the retina. Moreover, ocular decompression retinopathy can occur after anterior chamber paracentesis in cases of NVG where there is a sudden fall of raised IOP.
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