|Year : 2017 | Volume
| Issue : 4 | Page : 141-142
Delayed retrobulbar hemorrhage after reconstruction of inferior orbital wall fracture: a case report
Bahram Eshraghi1, Ali Torkashvand1, Ramon Katoozpour1, Pasha Anvari2
1 Department of Opthalmology, Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Iran
2 Department of Opthalmology, Eye Research Center, Rassoul Akram Hospital, University of Medical Sciences, Tehran, Iran
|Date of Submission||27-Aug-2016|
|Date of Acceptance||12-Oct-2017|
|Date of Web Publication||8-Mar-2018|
Eye Research Center, Rassoul Akram Hospital, Iran University of Medical Sciences, Tehran
Source of Support: None, Conflict of Interest: None
A 25-year-old man presented with enophthalmos and hypophthalmos in the left eye, underwent orbital floor reconstruction. Three days after the initial surgery, the patient’s visual acuity (VA) reduced to finger counting at 3 m, intraocular pressure increased to 32 mmHg, and relative afferent pupillary defect was detected. Further, spiral computed tomography demonstrated retrobulbar hemorrhage. After cantholysis and canthotomy, the VA was 20/200, 4 h postoperatively. Within 3 days, VA improved to 10/10. Physicians should have a heightened index of suspicion and awareness of this uncommon complication.
Keywords: delayed retrobulbar hemorrhage, medpor implant, orbital wall fracture
|How to cite this article:|
Eshraghi B, Torkashvand A, Katoozpour R, Anvari P. Delayed retrobulbar hemorrhage after reconstruction of inferior orbital wall fracture: a case report. J Egypt Ophthalmol Soc 2017;110:141-2
|How to cite this URL:|
Eshraghi B, Torkashvand A, Katoozpour R, Anvari P. Delayed retrobulbar hemorrhage after reconstruction of inferior orbital wall fracture: a case report. J Egypt Ophthalmol Soc [serial online] 2017 [cited 2019 May 26];110:141-2. Available from: http://www.jeos.eg.net/text.asp?2017/110/4/141/226938
| Introduction|| |
Retrobulbar hemorrhage (RBH) is an infrequent vision-threatening complication that results from blood accumulation in the orbital cavity. The estimated incidence rates vary from 0.44 to 0.77%. As no natural mechanism exists for decompression, a compartment syndrome may develop where blood accumulation leads to an increased intraocular pressure. This elevated pressure cuts off the blood flow to the optic nerve, causes ischemic damage, and blocks ocular perfusion leading to venous or arterial occlusive process. The RBH occurrence might be spontaneous, as a consequence of retrobulbar injections, surgery, or trauma.
| Case report|| |
A 25-year-old man who had undergone orbital inferior wall reconstruction for a blow-out fracture 2 years ago, presented to our hospital. On examination, visual acuity (VA) was 20/20 OU with 4 mm of enophthalmos and 5 mm hypophthalmos in the left side. Relative afferent pupillary defect was absent. Slit-lamp examination and fundoscopy were unremarkable. There was no evident limitation of eye movement, diplopia, or hypoesthesia.
A spiral computed tomography showed the inferior orbital wall fracture line without entrapment of the orbital soft tissue ([Figure 1]a). To correct the enophthalmos and hypophthalmos, orbital floor reconstruction was performed through a subciliary incision with a Medpor (Stryker, Kalamazoo, Michigan, USA) enophthalmos wedge (22×30 in diameter and 7 mm in thickness) in the subperiosteal space that fully covered the fracture site. At the end of surgery, complete definitive hemostasis was achieved without any active bleeding in the surgical field.
|Figure 1 (a) Orbital computed tomographic scan before reconstruction shows inferior wall discontinuity. (b, c) Orbital computed tomographic scan 24 h after reconstruction demonstrates proptosis and retrobulbar hemorrhage threatening the optic nerve.|
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On the third postoperative day, the patient experienced periocular discomfort, followed by decreased VA to finger counting at 3 m, a positive relative afferent pupillary defect, and elevated intraocular pressure to 32 mmHg. Spiral computed tomography showed the blood clot accumulation within the orbital region, exerting a compressive force on the optic nerve ([Figure 1]b and [Figure 1]c). To relieve the compression with allowing the orbital volume expansion, inferior cantholysis and lateral canthotomy were immediately performed. The surgical site in conjunctiva was reopened and the blood was suctioned out. Thereafter, the probable source of hemorrhage was cauterized.
Within 4 h, the symptoms were satisfactorily resolved and VA improved to 20/200. There was no significant proptosis and limitation of eye movement. After 3 days, the patient VA improved to 10/10 and remained stable along the follow-up period.
The patient has provided permission to publish these features of his case, and the identity of the patient has been protected.
| Discussion|| |
The RBH is a medical emergency that presents clinically as proptosis, circumbulbar pain and pressure, eyelid discoloration, periocular lid skin tightness, mydriasis, visual impairment, diplopia, and increased intraorbital and intraocular pressure. Intraocular damages are more frequently observed in small fractures compared with large fractures .
RBH can develop within the first days following a facial fracture. Our patient had a delayed RBH within 36 h postoperatively. There are few similar cases with delayed RBH. Cheon et al.  have presented two cases of RBH following blow-out fracture repair. Postoperative RBH in these patients, manifested within 8 days and 29 h, respectively. While one of their patients, permanently lost vision, the other had undergone immediate decompression surgery. Notably, 0.242–0.3% of surgical repairs of facial fractures are followed with postoperative blindness , and 48% of blindness cases following orbital surgery have been linked to RBH. Even a 90–120 min delay in surgery can lead to permanent vision, prompt recognition of RBH and surgical intervention is required .
Wood  reported a case of delayed RBH following an orbital floor fracture. The patient developed RBH signs 72 h postoperatively. With an occurrence of virtual total loss, he was treated with 100 g of mannitol, 500 mg of acetazolamide, and 200 mg of hydrocortisone. Afterwards, the VA improved with no surgical decompression. The severity of vision loss and ischemic damage can be mitigated by adjunct treatments to surgical decompression and evacuation, including a megadose of corticosteroids, acetazolamide, mannitol, and topical timolol.Complications arising from the use of alloplastic orbital floor include the formation of hematic, dacryocystitis, fistula, proptosis, infection and cyst formation, globe elevation motility restriction and hemorrhage. Michael et al.  described a case of RBH that occurred within 10 days following orbital floor blow-out fracture reconstruction with an implant. In this case, the implant might have impeded the fluid drainage.
Since RBH may occur late, following orbital floor fracture repair, the patient should be informed and instructed upon discharge regarding the warning symptoms of pain and blurred vision, to seek prompt medical care.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
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Wood CM. The medical management of retrobulbar haemorrhage complicating facial fractures: a case report. Br J Oral Maxillofac Surg 1989;27:291-295.
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