Spontaneous hyphema and pupillary block in a patient with a left ventricular assist device

Abstract

SummaryThe left ventricular assist device (LVAD) has been a standard of care for the management of patients with advanced heart failure since the 1990s. An increased risk of spontaneous bleeding related to the device has been noted, ranging from minor epistaxis to major thoracic and mediastinal hemorrhages. To our knowledge, intraocular hemorrhage has not been previously reported. We report a 72-year-old patient with an LVAD who subsequently developed a spontaneous intraocular hemorrhage that manifested as hyphema, pupillary block, and acute intraocular pressure elevation. Case ReportA 72-year-old man with a history of ischemic cardiomyopathy with prior 5-vessel coronary artery bypass and a continuous-flow left ventricular assist device (LVAD) placed 6 months prior awoke with 10/10 pain and loss of vision in the right eye. Recent medical history included an ischemic stroke suffered 1 week after the LVAD procedure and 2 episodes of gastrointestinal (GI) bleeding with arteriovenous malformations (AVMs) found on endoscopy. Ocular history included uneventful bilateral cataract extraction and intraocular lens (IOL) implantation approximately 10 years prior and non-exudative, age-related macular degeneration in both eyes. There was no recent trauma. His medicines included 2 mg warfarin daily with a goal international normalized ratio (INR) of 1.8-2.5, which had been reduced to 1.8-2.2 after the GI bleeds.On initial evaluation, visual acuity in the right eye was light perception; intraocular pressure (IOP) in the right eye by Tono-Pen (Reichert Technologies, Depew, NY) was 87 mm Hg. The anterior chamber was deep with a 1.5 mm crescent-shaped layering hyphema. The iris was flat, without neovascularization, and the angle was open, with a deep chamber by Van Herick slit-lamp examination. The pupil was unreactive, and the entire pupillary aperture was filled with a blood clot obstructing the view to the posterior segment (Figure 1). B-mode ultrasonography revealed a vitreous opacity consistent with blood in the anterior vitreous. The left eye was unremarkable, with an open angle. The IOP dropped to 46 mm Hg 1 hour after administration of oral acetazolamide 500 mg and topical timolol 0.5%, 1 drop times 2 doses every 5 minutes. Two hours later, IOP was 17 mm Hg; the patient's pain abated with additional oral acetazolamide and topical brimonidine 0.2%, timolol 0.5%, latanoprost 0.005%, prednisolone, and atropine solutions. INR on admission was found to be elevated at 1.7, slightly below the goal therapeutic range for the LVAD. Prothrombin time was 14.9. In collaboration with cardiology, warfarin was stopped because of the ocular bleed. Computed tomography imaging was negative for intracranial hemorrhage. The patient was admitted to the coronary care unit and monitored closely for signs and symptoms of thrombosis.Twelve hours later, the patient's 10/10 eye pain returned. The IOP measured 58 mm Hg, with a shallow anterior chamber and 360 degrees of anterior iris bowing. Repeat B-scan was unchanged. An acute angle closure second...