Ophthalmic Surgery, Lasers and Imaging Retina

Case Report 

Macular Hole Following Subretinal Tissue Plasminogen Activator for Submacular Hemorrhage Secondary to Neovascular AMD

Anthony Obeid, MD, MPH; Katherine E. Talcott, MD; Ferhina S. Ali, MD; Xinxiao Gao, MD, PhD; Kareem Sioufi, MD; Turner D. Wibbelsman, BS; Allen C. Ho, MD

Abstract

A full-thickness macular hole (FTMH) is a rare sequela to submacular hemorrhage. Herein, the authors report a case of an 80-year-old man actively being treated for neovascular age-related macular degeneration who presented with sudden vision loss in the right eye. Examination with optical coherence tomography (OCT) imaging revealed submacular hemorrhage. The patient underwent vitrectomy with subretinal tissue plasminogen activator (tPA) with no intraoperative complications. Dilated fundus examination and OCT imaging revealed a FTMH at postop week 1. Possible causes for MH development include the submacular hemorrhage itself and subretinal administration of the tPA infusion.

[Ophthalmic Surg Lasers Imaging Retina. 2019;50:e257–e259.]

Abstract

A full-thickness macular hole (FTMH) is a rare sequela to submacular hemorrhage. Herein, the authors report a case of an 80-year-old man actively being treated for neovascular age-related macular degeneration who presented with sudden vision loss in the right eye. Examination with optical coherence tomography (OCT) imaging revealed submacular hemorrhage. The patient underwent vitrectomy with subretinal tissue plasminogen activator (tPA) with no intraoperative complications. Dilated fundus examination and OCT imaging revealed a FTMH at postop week 1. Possible causes for MH development include the submacular hemorrhage itself and subretinal administration of the tPA infusion.

[Ophthalmic Surg Lasers Imaging Retina. 2019;50:e257–e259.]

Introduction

Submacular hemorrhage, a complication that can occur secondary to neovascular age-related macular degeneration (nAMD), often presents with sudden and severe vision loss. Vitrectomy with subretinal tissue plasminogen activator (tPA) has been previously used to treat submacular hemorrhage by both dissolving and displacing the clot.1 Chang et al.2 previously demonstrated improved visual outcomes over 12 months in patients undergoing the procedure for submacular hemorrhage secondary to nAMD. Some of the complications of this procedure include retinal detachment, vitreous hemorrhage, and recurrent subretinal hemorrhage.2 In this report, we provide a unique case of a postoperative macular hole (MH) that developed after vitrectomy and subretinal tPA for submacular hemorrhage secondary to nAMD.

Case Report

An 80-year-old man presented with sudden vision loss in the right eye for approximately 2 days. Best-corrected visual acuity (BCVA) was count fingers at 3 feet. Ophthalmic history was notable for bilateral nAMD with active choroidal neovascularization being treated with intravitreal aflibercept (Eylea; Regeneron Pharmaceuticals, Tarrytown, NY), active hypertensive retinopathy, and primary open-angle glaucoma. Surgical history included bilateral cataract extraction with posterior capsule intraocular lens insertion approximately 1 year prior to presentation. Dilated fundus examination and fundus photography revealed a dense submacular hemorrhage (Figure 1A). Optical coherence tomography (OCT) revealed subretinal fluid with retinal thickening consistent with submacular hemorrhage (Figure 2A). The decision was made to proceed with surgery, and the patient underwent a 23-gauge vitrectomy with subretinal tPA (10 μg/0.1 mL) administration using a 41-gauge cannula. Several peripheral retinal breaks were noted and treated with endolaser. A soft tip extrusion cannula was then used for a complete air-fluid exchange followed by 20% SF6 gas tamponade. No complications were noted intraoperatively. There was no MH visualized on final inspection, nor was there leakage of the tPA into the vitreous cavity.

Fundus photograph of submacular hemorrhage secondary to neovascular age-related macular degeneration (nAMD). Fundus photograph of (A) the right eye with submacular hemorrhage secondary to nAMD. The eye is seen (B) 10 days after subretinal tissue plasminogen activator administration and vitrectomy with the hemorrhage well displaced but a macular hole present. The patient then underwent a repeat vitrectomy with an internal limiting membrane peel.

Figure 1.

Fundus photograph of submacular hemorrhage secondary to neovascular age-related macular degeneration (nAMD). Fundus photograph of (A) the right eye with submacular hemorrhage secondary to nAMD. The eye is seen (B) 10 days after subretinal tissue plasminogen activator administration and vitrectomy with the hemorrhage well displaced but a macular hole present. The patient then underwent a repeat vitrectomy with an internal limiting membrane peel.

Optical coherence tomography (OCT) of submacular hemorrhage secondary to neovascular age-related macular degeneration (nAMD). OCT of (A) the right eye reveals submacular hemorrhage secondary to nAMD. Imaging revealed subretinal fluid (SRF) with retinal thickening consistent with macular edema. Postoperative imaging at (B) 10 days and (C) week 3 after vitrectomy with tissue plasminogen activator administration demonstrated a macular hole (MH) with persistent SRF and a pigment epithelial detachment (PED). The eye then underwent MH repair with vitrectomy and an internal limiting membrane peel. At postoperative week 1 (D), the MH is closed with resolution of the SRF but persistence of the PED.

Figure 2.

Optical coherence tomography (OCT) of submacular hemorrhage secondary to neovascular age-related macular degeneration (nAMD). OCT of (A) the right eye reveals submacular hemorrhage secondary to nAMD. Imaging revealed subretinal fluid (SRF) with retinal thickening consistent with macular edema. Postoperative imaging at (B) 10 days and (C) week 3 after vitrectomy with tissue plasminogen activator administration demonstrated a macular hole (MH) with persistent SRF and a pigment epithelial detachment (PED). The eye then underwent MH repair with vitrectomy and an internal limiting membrane peel. At postoperative week 1 (D), the MH is closed with resolution of the SRF but persistence of the PED.

The patient then presented 10 days later for a postoperative examination. BCVA was count fingers at 4 feet. Fundus photo (Figure 1B) demonstrated resolution of the submacular hemorrhage. OCT (Figure 2B) revealed a full-thickness MH (FTMH) with subretinal fluid and a retinal pigment epithelium elevation consistent with a pigment epithelial detachment (PED). The patient was positioned appropriately (face-down) and instructed to return for follow-up. The patient returned at postoperative week 3 with a BCVA of 20/400. OCT revealed persistent findings (Figure 2C). The decision was made to proceed with surgical repair of the MH. The patient underwent vitrectomy with an internal limiting membrane peel using indocyanine green and a Tano scraper, followed by air-fluid exchange and 20% SF6 gas tamponade. At the postoperative week 1 exam, vision was 20/200. Fundus photography and OCT imaging revealed a closed MH with a persistent PED (Figure 2D).

Discussion

To the best of our knowledge, there has been only one reported case of a MH that developed after subretinal tPA administration for nAMD with submacular hemorrhage.3 The MH in the previously reported case appeared to form intraoperatively after administering tPA via a small peripheral access retinotomy, with the tPA infusion observed to have entered the vitreous cavity via the hole. Following liquefaction of the clot, the MH closed with postoperative OCT confirming the resolution of the hole without the need for further intervention.3 In our specific case, the MH was not observed intraoperatively, with no escape of tPA into the vitreous cavity and no resolution of the hole postoperatively. There is no definitive explanation as to why the MH formed; however, it is possible that the complication was secondary to the force of infusion from the subretinal injection of tPA.3 There has been one documented case of a MH forming 5 months after an episode of subretinal hemorrhage secondary to nAMD with no history of surgery.4 This suggests that there might be a different etiology responsible for forming the full-thickness defect.4 Other cases of MHs forming after submacular hemorrhage have been documented with ruptured retinal artery macroaneurysms (RAM).5–7 Although previously thought to be a rare complication, the incidence of MH after ruptured RAM on either presentation or follow-up could be as high as 5.3%.5 It is hypothesized that tangential and anteroposterior forces occur secondary to the vitreous hemorrhage, which induces traction from a contracted posterior vitreous cortex.7 These forces could be responsible for the formation of the MH. Alternatively, it could be a result of structural damage secondary to the accumulated blood underneath the retina. The accumulated blood is a rich source of fibrin, which has been found to cause tearing of photoreceptor layers early during contact and degeneration of all layers of the retina with lengthier exposures.8 This fibrin-mediated damage may facilitate the formation of a MH, especially post-surgical manipulation.

MHs are a rare complication of submacular hemorrhage. Previous cases suggest that this is not necessarily a sequela of surgical repair, and it might indeed be mediated by alternative mechanisms associated with the submacular hemorrhage. However, the MH we observed may indeed have developed intraoperatively. Given this possibility, we recommend the surgeon injects the subretinal tPA slowly. Finally, early surgical intervention appears effective in closing the MH and restoring functional anatomy.

References

  1. Haupert CL, McCuen BW 2nd, Jaffe GJ, et al. Pars plana vitrectomy, subretinal injection of tissue plasminogen activator, and fluid-gas exchange for displacement of thick submacular hemorrhage in age-related macular degeneration. Am J Ophthalmol. 2001;131(2):208–215. doi:10.1016/S0002-9394(00)00734-0 [CrossRef]11228297
  2. Chang W, Garg SJ, Maturi R, et al. Management of thick submacular hemorrhage with subretinal tissue plasminogen activator and pneumatic displacement for age-related macular degeneration. Am J Ophthalmol. 2014;157(6):1250–1257. doi:10.1016/j.ajo.2014.02.007 [CrossRef]24531021
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  8. Toth CA, Morse LS, Hjelmeland LM, Landers MB 3rd, . Fibrin directs early retinal damage after experimental subretinal hemorrhage. Arch Ophthalmol. 1991;109(5):723–729. doi:10.1001/archopht.1991.01080050139046 [CrossRef]2025175
Authors

From The Retina Service, Wills Eye Hospital, Philadelphia.

Dr. Ho reports grants and personal fees from Alcon, Allergan, and Genentech, as well as grants from Iconic outside the submitted work. The remaining authors report no relevant financial disclosures.

Address correspondence to Allen Ho, MD, The Retina Service of Wills Eye Hospital, Mid Atlantic Retina, 840 Walnut St., Suite 1020, Philadelphia, PA 19107; email: acho@midatlanticretina.com.

Received: September 18, 2018
Accepted: March 26, 2019

10.3928/23258160-20190905-18

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