|Year : 2022 | Volume
| Issue : 3 | Page : 376-378
Suprachoroidal hemorrhage postintracameral bevacizumab injection: An unusual case report and review of literature
Karthikeyan Mahalingam, Dewang Angmo, Swechya Madhukar Neupane, Shorya Vardhan Azad
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, India
|Date of Submission||03-Sep-2021|
|Date of Decision||19-Oct-2021|
|Date of Acceptance||06-Apr-2022|
|Date of Web Publication||02-Nov-2022|
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Room 374, New Delhi
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Suprachoroidal hemorrhage (SCH) is a dreaded complication of intraocular surgery. We report a case of a 65-year-old male with left eye primary angle-closure glaucoma and idiopathic elevated episcleral venous pressure with neovascularization of the iris. Due to uncontrolled intraocular pressure even after maximum medical therapy, trabeculectomy with mitomycin C was planned. Preoperative intracameral bevacizumab was given to avoid intraoperative bleeding. Postinjection, localized SCH was noted, which settled spontaneously on conservative management. A combination of ocular and systemic risk factors, such as arteriosclerosis and idiopathic elevated episcleral venous pressure accentuated by intraoperative hypotony during intracameral injection, led to SCH. There are no previous reports of a localized SCH following intracameral bevacizumab.
Keywords: Hemorrhagic choroidal detachment, intracameral bevacizumab, suprachoroidal hemorrhage
|How to cite this article:|
Mahalingam K, Angmo D, Neupane SM, Azad SV. Suprachoroidal hemorrhage postintracameral bevacizumab injection: An unusual case report and review of literature. Oman J Ophthalmol 2022;15:376-8
|How to cite this URL:|
Mahalingam K, Angmo D, Neupane SM, Azad SV. Suprachoroidal hemorrhage postintracameral bevacizumab injection: An unusual case report and review of literature. Oman J Ophthalmol [serial online] 2022 [cited 2022 Dec 4];15:376-8. Available from: https://www.ojoonline.org/text.asp?2022/15/3/376/360407
| Introduction|| |
Choroidal detachment (CD) is defined as the separation of the choroid from the sclera. It can be serous or hemorrhagic, depending on whether there is an accumulation of serous fluid due to effusion or blood postrupture of choroidal vessels in the suprachoroidal space (SCS). Suprachoroidal hemorrhage (SCH), as the latter is known, is a dreaded complication of intraocular surgery. Most of the intraocular surgeries (such as extracapsular cataract extraction, intracapsular cataract extraction, phacoemulsification, penetrating keratoplasty, and trabeculectomy) have reported the occurrence of SCH. However, its occurrence postintracameral injection has not been reported so far, to the best of our knowledge. It can either occur early, during the intraocular procedure, known as expulsive SCH, or late/delayed when it develops in the postoperative period. Most bleed collects in entire SCS, yet cases of limited or localized SCH have also been described rarely.
Herein, we report a case of primary angle-closure glaucoma (PACG) with neovascularization of the iris (NVI) developing limited SCH postintracameral injection of bevacizumab, which was given before trabeculectomy.
| Case Report|| |
A 65-year-old male patient presented with diminution of vision in the left eye (LE) for 1 year, associated with redness. There were no known comorbidities. On examination, the patient had a best-corrected visual acuity of 6/9 in the right eye (RE) and hand movement close to the face with accurate projection of rays in the LE. Intraocular pressure (IOP) was 12 mmHg and 26 mmHg in RE and LE, respectively. On slit-lamp examination, both eyes had shallow anterior chamber (AC) and gonioscopy, revealing occludable angles in RE and closed angles in LE with no signs of neovascularization. In the LE, dilated tortuous episcleral vessels [Figure 1]a were noted with very fine NVI at 11 “0” clock near the pupillary border [Figure 1]b. Patent peripheral iridotomy was seen in both eyes. Relative afferent pupillary defect along with cataracts was noted in the LE. Fundoscopy revealed a cup–disk ratio of 0.3 in RE and near-total cupping with dot-blot hemorrhages in the superonasal quadrant in LE (media haze due to cataract). Fluorescein angiography (FA) of LE revealed superonasal capillary nonperfusion areas with perivascular hyperfluorescence [Figure 2]b, suggestive of superonasal branch retinal vein occlusion (BRVO). Iris FA confirmed neovascularization [Figure 2]a. After ruling out any other vascular pathology of the retina, a diagnosis of RE primary angle closure and LE PACG, BRVO with secondary NVI, and idiopathic elevated episcleral venous pressure was made. The blood pressure was in the hypertensive range (152/90 mmHg) on presentation with a deranged lipid profile. Carotid Doppler showed insignificant nonocclusive plaque in the distal right common carotid artery, and referral to internal medicine was sought. Due to uncontrolled IOP on maximal medical therapy, the patient was planned for LE intracameral bevacizumab injection followed by trabeculectomy. LE intracameral bevacizumab injection was given after AC paracentesis. NVI regressed completely 4 days postinjection, and the pupil was irregular [Figure 1]c, with shallow AC and IOP being 22 mmHg. Fundus examination revealed an inferotemporal CD. Ultrasonography confirmed the same and additionally revealed heterogeneous echoes inside the CD suggestive of hemorrhagic CD [Figure 3]a. Trabeculectomy was deferred, and the patient was managed conservatively. CD settled in 10 days [Figure 3]b with topical cycloplegics and oral steroids.
|Figure 1: (a) Slit-lamp photo of the patient's LE showing dilated tortuous episcleral vessels. (b) Slit-lamp photo (×25) of the LE iris prebevacizumab showing very fine iris neovascularization (NVI - black arrow). (c) Slit-lamp photo (×25) of the LE iris postbevacizumab, in the same area showing regression/absence of neovascularization. LE: Left eye, NVI: Neovascularization of the iris|
Click here to view
|Figure 2: (a) Fluorescein angiography of LE iris showing leakage superiorly corresponding to the NVI area (b) suggestive of iris neovascularization. (b) Fundus fluorescein angiography of LE showing superonasal capillary nonperfusion areas with perivascular hyperfluorescence, suggestive of superonasal branch retinal vein occlusion. LE: Left eye, NVI: Neovascularization of the iris. White arrow: Shows area of hyperflourescence|
Click here to view
|Figure 3: (a) Ultrasound B-scan showing inferotemporal hemorrhagic choroidal detachment in LE. (b) Ultrasound B-scan showing resolved choroidal detachment in LE. LE: Left eye. Black arrow: Shows area of hemorrhagic choroidal detachment|
Click here to view
| Discussion|| |
In PACG, glaucoma filtration surgery is often required if IOP cannot be controlled on maximum medical therapy. More so, raised levels of vascular endothelial growth factor in PACG may lead to NVI, further jeopardizing outcomes of filtering surgery. To counter it, injection bevacizumab is given widely, either intracameral or intravitreal for regression of anterior and posterior segment neovascularization. Furthermore, intracameral bevacizumab is not only effective in terms of NVI regression but superior in terms of IOP control when compared to intravitreal injection. Thus, intracameral bevacizumab followed by trabeculectomy is the preferred practice for glaucoma with NVI, as it decreases intraoperative bleeding and improves our surgical outcomes.
In our case, uncontrolled IOP, despite maximal medical therapy, prompted the need for filtering surgery. Prior intracameral bevacizumab (after AC paracentesis) was given to reduce the risk of intraoperative hemorrhage. Of all intraocular surgeries, SCH is most frequently associated with glaucoma surgeries, as alterations in IOP are a major precipitating factor. It is postulated that the inciting event is hypotony, leading to choroidal effusion with subsequent stretching and rupture of necrotic choroidal vessels. In our case, AC paracentesis may have led to a transient but sudden decrease in IOP, leading to rupture of a choroidal vessel and bleed. The transient nature of IOP drop and a closed system led to only a localized SCH which resolved conservatively. It has been shown that eyes with idiopathic elevated episcleral venous pressure are more prone to choroidal effusions postfiltration surgery, further supporting our findings.
Apart from ocular risk factors, systemic factors such as hypertension, arteriosclerosis, and diabetes have shown a predisposition to SCH. Thus, undiagnosed hypertension and deranged lipid profile, supported by the presence of plaques in the common carotid artery, show that no single mechanism can explain SCH in our patient. Hence, we contend that a combination of ocular and systemic risk factors such as arteriosclerosis and idiopathic elevated episcleral venous pressure accentuated by sudden and transient intraoperative hypotony during intracameral injection could have led to SCH [Figure 4]. Thus far, there is a single case report of massive hemorrhagic CD after intravitreal bevacizumab. However, to the best of our knowledge, none have mentioned SCH after intracameral bevacizumab injection.
|Figure 4: Flow diagram showing the possible mechanism of choroidal detachment in our patient|
Click here to view
| Conclusion|| |
Our case highlights the rare and localized presentation of SCH after intracameral bevacizumab. Patients with systemic comorbidities and ocular risk factors need careful administration of intracameral injection to prevent intraoperative hypotony. Nonetheless, the transient nature of IOP drop often leads to localized and limited bleeds, which resolve spontaneously.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given her consent for images and other clinical information to be reported in the journal. The guardian understands that her names and initials will not be published and due efforts will be made to conceal the patient's identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Chu TG, Green RL. Suprachoroidal hemorrhage. Surv Ophthalmol 1999;43:471-86.
Eriksson A, Koranyi G, Seregard S, Philipson B. Risk of acute suprachoroidal hemorrhage with phacoemulsification. J Cataract Refract Surg 1998;24:793-800.
Augsburger JJ, Coats TD, Lauritzen K. Localized suprachoroidal hematomas. Ophthalmoscopic features, fluorescein angiography, and clinical course. Arch Ophthalmol 1990;108:968-72.
Huang W, Gao X, Chen S, Li X, Zhang X, Zhang X. Vascular endothelial growth factor is increased in aqueous humor of acute primary angle-closure eyes. J Glaucoma 2016;25:e647-51.
Bhagat PR, Agrawal KU, Tandel D. Study of the effect of injection bevacizumab through various routes in neovascular glaucoma. J Curr Glaucoma Pract 2016;10:39-48.
Manschot WA. The pathology of expulsive hemorrhage. Am J Ophthalmol 1955;40:15-24.
Maumenee AE, Schwartz MF. Acute intraoperative choroidal effusion. Am J Ophthalmol 1985;100:147-54.
Rhee DJ, Gupta M, Moncavage MB, Moster ML, Moster MR. Idiopathic elevated episcleral venous pressure and open-angle glaucoma. Br J Ophthalmol 2009;93:231-4.
Saxena RC, Kumar D. Choroidal detachment (a clinico-aetiopathological study). Indian J Ophthalmol 1983;31:238-41.
] [Full text]
Brouzas D, Koutsandrea C, Moschos M, Papadimitriou S, Ladas I, Apostolopoulos M. Massive choroidal hemorrhage after intravitreal administration of bevacizumab (Avastin) for AMD followed by controlateral sympathetic ophthalmia. Clin Ophthalmol 2009;3:457-9.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]