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Our first case involves a 50-year-old woman who was admitted for an acute-onset left anterior cerebral artery stroke. She received tissue plasminogen activator and underwent emergent mechanical thrombectomy complicated by intraoperative rupture of the left internal carotid artery with subsequent embolization. Postoperative computed tomography angiography demonstrated poor filling of the left suprasellar carotid artery. Three days later, the left globe was noted to be collapsed, and ophthalmology was consulted to assess the patient while she remained intubated and sedated (Fig. 1). Examination of the right eye was unremarkable. Examination of the left eye revealed mild injection, a fixed 4 mm pupil with 3 clock hours of iris neovascularization, diffuse Descemet's folds, and severe corneal edema that prevented viewing of the posterior segment. Tonopen pressures were 14 mm Hg in the right eye and nondetectable in the left eye. On reexamination 2 weeks later, the globe remained collapsed. The patient was subsequently lost to follow-up.
Fig. 1Case 1 with collapsed left globe with mild injection (A), a fixed 4 mm pupil with 3 clock hours of iris neovascularization from prolonged ischemia, and diffuse Descemet's folds and severe corneal edema (B).
Our second case involves a 65-year-old woman with a history of poorly controlled hypertension and recent right thalamic intraparenchymal hemorrhage who was incidentally found during stroke work-up to have an unruptured 6 mm inferiorly directed posterior communicating artery aneurysm with a 3-mm-wide neck. No anisocoria or motility deficits suggesting compression of the third cranial nerve were present. One month later, the patient underwent elective right pterional craniotomy via a transsylvian approach for aneurysm clipping. The surgery was performed in routine fashion with the patient in the standard supine position with her head tilted to the left and secured with a Mayfield head clamp. No intraoperative complications were noted by neurosurgery. Ophthalmology was notified immediately by neurosurgery that the right globe was found to be “wrinkled and deflated” on undraping of the patient in the operating room (Fig. 2). The anterior chamber was diffusely flat with iridocorneal touch 360 degrees. Tonopen pressure of the left eye was 7 mm Hg. Posterior segment examination of both eyes was within normal limits. The patient was seen 24 hours later in the clinic with best corrected visual acuity of 20/25 in both eyes and intraocular pressures of 17 and 18 mm Hg, respectively. She reported being asymptomatic and at her baseline vision. (See also Supplementary Video 1, available online.)
Fig. 2Case 2 with collapsed right globe with “wrinkled and deflated” cornea and iridocorneal touch 360 degrees (A). The globe was re-formed within 24 hours (B).
Acute hypotony in the absence of intraocular pathology is an uncommon event that has previously been reported immediately after hypothermic cardiopulmonary bypass and coronary artery bypass graft surgery.
In these cases, the authors proposed that severe anemia and large fluctuations in central venous pressure may have caused transient ischemia of the ciliary body and reduced episcleral venous pressure.
reported unilateral orbital infarction syndrome following mechanical thrombectomy that resulted in complete ophthalmoplegia, blindness, and orbital pain but without globe collapse. This was secondary to iatrogenic embolic occlusion of the ophthalmic artery and multiple branches of the external carotid artery.
In our first case, we believe that acute iatrogenic ophthalmic artery occlusion resulted in permanent and profound collapse of the globe—a finding not previously described with orbital infarction syndrome. In our second case, although the patient experienced large intraoperative fluctuations in blood pressure and received mannitol, we believe that transient ophthalmic artery occlusion could explain ciliary body shutdown with subsequent acute globe collapse in the right eye. The left eye had mild hypotony, suggesting that osmotic effect and blood pressure fluctuations may have been contributory, but the globe collapse in the right eye suggests an additional mechanism, mainly transient vascular insufficiency, as the main cause for the globe collapse. Positioning of the patient was routine and felt to be noncontributory in this case. Anatomically, ischemia of the ciliary body at the level of the anterior ciliary arteries and long posterior ciliary arteries seems necessary to cause globe collapse in both cases. Acute globe collapse, permanent and transient, should be recognized as a rare complication of invasive neurovascular procedures.
Ethics approval and consent to participate
Written consent for publication was obtained from the patients’ next of kin for publication of these case reports and any accompanying images. Full adherence was maintained to the Declaration of Helsinki and all federal and state laws.
Author contributions
Joseph W. Fong, writing and reviewing; John P. Coleman, writing and reviewing; Riley N. Sanders, reviewing; Sami H. Uwaydat, writing and reviewing. all authors have read and approved the manuscript.
Footnotes and Disclosure
The authors have no proprietary or commercial interest in any materials discussed in this article.
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