Bilateral central retinal artery occlusion: An exceptional complication after frontal parasagittal meningioma resection

INTRODUCTION

Non-arteritic central retinal artery occlusion (CRAO) has an incidence of 0.85/100000/year. It has often been related to different surgical procedures; however, rarely to brain surgeries.[10] Furthermore, clinical presentation of bilateral CRAO is very uncommon and its incidence is about 1–2% of the cases and only isolated reported cases are associated with autoimmune vasculitis such as lupus, Wegener’s granulomatosis, and endocarditis.[4,9,21] CRAO leads to comorbidity, impacting on patient’s quality of life. At present, there is little evidence about which treatment can be effective in case of CRAO due to low tolerance to ischemia of the ophthalmic artery (OA) and to the irreversibility of this condition after short time.[20]

CASE PRESENTATION

Here, we reported a 41-year-old female with a medical history of obesity and diabetes type 2, who underwent surgical resection of a frontal parasagittal with no intraoperative surgical and anesthetic complications and developed complete blindness on awakening as a complication. Postoperative ophthalmological examination revealed bilateral mydriasis and non-reactive to light in both eyes, although bilateral mydriasis can occur after general anesthesia.[22] Fluorescein angiography showed adequate choroidal filling in both eyes with delayed arterial phase and all subsequent phases; as well as, in late phases an absence of bilateral optic nerve staining occurred, confirming a bilateral CRAO [Figure 1]. The photopic and scotopic electroretinogram showed a prolonged latency and decreased extent of the a and b waves. Postoperative digital subtraction angiography was performed showing adequate blood flow through both OAs and a significant decrease in bilateral choroidal blush [Figures 2]. The echocardiography performed did not reveal vegetations or other valvular alterations. Carotid Doppler showed mild non-obstructive diffuse atheromatosis and type I atheroma plaques in both common carotids, both with biphasic flow, without stenosis and with preserved flow velocities. Whole-body vessels CTA scans were not contributory. Different hematological tests were normal. Brain MRI showed no suggestive lesions of stroke in the DWI sequence and intra-orbital segment hyperintensity in T2-weighted sequences, suggesting for bilateral optic nerve infarction [Figure 2]. Patient started an early treatment with hyperbaric chamber sessions, continuing with this at discharge, even if patient reported only a very slight improvement in the visual deficit, referring only shadows in her peripheral visual field.

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Figure 1:: Preoperative (a) and postoperative (b) CT head scans show the site of a parasagittal meningioma and its subsequent complete resection. Bilateral electroretinogram in scotopic (c) and phototopic (d) protocols, which show prolonged latencies, decreased amplitudes and distortion in a and b waves, as signs of moderate to severe diffuse retinopathy in both eyes. Right (e) and left (f) eyes retinal fluorescein biography shows delay in the arterial phase as well as in the optic nerve head hypofluorescence in late phases. The macula is marked with black arrows while the absence of cilioretinal arteries with black arrowheads. Spectral domain optical coherence tomography (at 3 months after surgery) of the right eye (g) and left eye (h) show chronic changes caused by CRAO.

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Figure 2:: Postoperative right (a) and left (b) internal carotid digital subtraction angiography (DSA) shows ophthalmic artery (black asterisks) on the same side, the ciliary arteries (black arrows) and the attenuated choroidal blush of the eye (black arrowheads). Right (c) and left (d) external carotids DSA shows no choroidal blush nor the presence of some dangerous anastomosis of the ophthalmic artery with the middle meningeal artery (black arrows) or with the internal maxillary (black arrowheads). Postoperative DSA (e) shows the right ophthalmic artery (white arrow), the origin of the central retinal artery (white arrowhead), and the delay in filling in phase of the distal portion of the central retinal artery (black arrowheads), which is partially supplied by the vascular ring of Zinn (black arrow). (f) shows left ophthalmic artery (white arrow), the posterior ciliary artery (white arrowhead), in addition to a delay in the filling of the central retinal artery (black arrow heads) and partial replacement through the vascular ring of Zinn (black arrow). Sagittal (g) T2-weighted brain MRI shows hyperintensity of both optic nerves in its intra-orbital segment (white arrowhead), suggestive of bilateral optic nerve infarction. Right and left fundi (h) at 3 months follow-up after surgery. Axial (i) T2-weighted brain MRI shows hyperintensity of both optic nerves.

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DISCUSSION

CRAO is an ophthalmological emergency due to the short time retina tolerates ischemia (12–15 min) and this is due to the fact that the oxygen consumption rate (13 ml/100 g/min) of the retina is even greater than the brain (3.8 ml/100 g/min).[20] Although studies in animals found a 100 min tolerance to ischemia, it is very likely that the human retina tolerates arterial flow loss for less time.[8,20]

The supply of the internal and external retina is the central retinal artery and the posterior short ciliary arteries, respectively.[11] However, it is reported that only 5% of central retinal occlusions are due to occlusion of the OA; in addition, these arteries are not the only ones responsible for their irrigation in all cases since there are anatomical variants.[11] CRAO can be due to several conditions such as embolism, prothrombotic states, genetic diseases, infections, ophthalmological diseases, obstetric pathology, cancer, iatrogenesis, and cosmetic procedures, following a head trauma but also after surgical procedures such as spine, cardiac ophthalmology surgeries, radical neck debulking, and endovascular procedures.[1-3,5,6,13-19] The general incidence of visual loss as a postsurgical complication is 0.002% in non-ocular nor cardiac surgery.[19] Risk factors are high blood pressure, blood loss with high crystalloid reposition, prone position, long hours surgery, as also diabetes, and smoking habit.[12,19,23] A postoperative clinical presentation of bilateral CRAO secondary to elective brain surgery is uncommon and to the best of our knowledge we did not found any previously similar cases report. Given that all hematological tests performed were negative, we believe that our patient reported a bilateral CRAO due to several factors such as diabetes, anemia, microembolism, and/or hemodynamic instability during surgery, resulting in a multifactorial etiology, although the real cause remains unknown. One third of ocular ischemia are due to microemboli in the absence of severe carotid stenosis on Doppler echography,[7] and this kind of patient remain a high-risk patient (7%) for stroke during the peri-event CRAO period.

CONCLUSION

The present image report showed a rare case of bilateral CRAO as an acute complication of cranial surgery, which is extremely unusual according to the bibliography, reporting all clinical and neuroradiological exams performed to understand what the cause is, even if it remains unknown.