Traumatic acute retrobulbar haemorrhage complicated with central retinal artery occlusion

Abstract

AbstractPurpose: To present the vascular complications of traumatic acute retrobulbar haemorrhage and describe its management through a case report.Methods: A case report of a patient having an acute retrobulbar haemorrhage complicated with central retinal artery occlusion (CRAO).Results: A 50‐year‐old male patient exposed to blunt orbital trauma two hours prior was referred to the emergency with complaints of pain and loss of vision in the left eye. The negative light perception was noted in this eye. A tense hematoma, proptosis, ophthalmoplegia, and a non‐reactive pupil were also noted. Biomicroscopic examination, revealed corneal edema, subconjunctival haemorrhage, and chemosis. The fundus examination was not possible. Intraocular pressure (IOP) was 60 mmHg. The patient was diagnosed with acute retrobulbar haemorrhage. Computerized tomography was performed immediately showing a fracture of the left medial orbital wall and haemorrhage within the retrobulbar space. Intravenous mannitol and topical dorzolamide‐timolol associated with oral corticosteroid were administered. IOP decreased to 30 mmHg, but the patient's visual acuity did not improve. The fundus examination revealed a total CRAO confirmed by the fluorescein angiography and OCT‐A showing massive ischemic edema and occluded perimacular arterioles with interruption to the choroidal blood flow. OCT images demonstrated an increased reflectivity and thickness of the inner retina and subretinal fluid, which corresponds to the acute phase of CRAO. The time of surgical treatment was missed, and as a result, the patient missed their chance for visual recovery.Conclusions: Retrobulbar haemorrhage is a complication from ocular trauma that may cause permanent vision loss. Retrobulbar haemorrhage can potentially lead to dangerous increases in intraorbital pressure, a condition that is also described as orbital compartment syndrome. This increase in pressure is sufficient to cause vision loss, whether through direct compression of the optic nerve leading to optic neuropathy, a central retinal artery occlusion, or compression of the vessels that provide nutrition to the optic nerve.