To report a case of bitemporal hemianopsia due to ischemic chiasmopathy after mechanical thrombectomy of a right distal internal carotid artery (ICA) occlusion.
A 60-year-old female presented with left sided weakness and difficulty speaking and was found to have suffered a right internal carotid artery occlusion 10 days after tricuspid valve replacement for severe symptomatic tricuspid valve disease. She underwent mechanical thrombectomy and in hospital and at further follow ups was noted to have a bitemporal hemianopsia, consistent with an ischemic optic chiasmopathy.
Conclusions and importance
The optic chiasm is vascularized by multiple arteries of the Circle of Willis. As such, ischemic optic chiasmopathy is rare. Clinicians should consider ischemic chiasmopathy following cardiac and other surgical procedures including mechanical thrombectomy of the ICA or its branches.
Bitemporal hemianopsia usually occurs from compression of the optic chiasm.
The optic chiasm is supplied by multiple arteries – ischemic chiasmopathy is uncommon.
This case describes ischemic chiasmopathy post mechanical thrombectomy.
A bitemporal hemianopic visual field defect typically indicates a lesion of the optic chiasm due to involvement of the crossing nasal fibers in both eyes. The most common causes of a bitemporal hemianopsia are compressive lesions (e.g., pituitary adenoma) but ischemic etiologies have been reported previously as a rare cause of chiasmopathy. We report a case of presumed ischemic chiasmopathy after mechanical thrombectomy of the internal carotid artery. To our knowledge, this is the first such case to be described in the English language, ophthalmic literature.
A 60-year-old female with severe, symptomatic tricuspid valve disease underwent surgical tricuspid valve replacement (TVR). Ten days post-operatively, she presented with acute left-sided hemiplegia, dysarthria, right gaze preference, and a left facial droop. Past medical history included idiopathic hypertrophic subaortic stenosis (IHSS) for which she had undergone pacemaker placement. Following the TVR, she developed atrial fibrillation requiring anticoagulation with apixaban.
Computerized tomography (CT) and CT angiogram (CTA) of the head revealed a right-sided distal internal carotid artery (ICA) occlusion and acute right middle cerebral artery (MCA) territorial infarction involving the insula and temporal lobe. She did not receive intravenous thrombolysis as she was anticoagulated with apixaban. Mechanical thrombectomy was performed with stent retriever and suction. Fig. 1 illustrates the presence of an occlusion of the right cavernous segment of the ICA. There was an anomalous origin to the right MCA with no proper M1 segment, and the anterior and posterior divisions of the MCA originating separately from the bifurcation. Fig. 2 shows complete revascularization of the right ICA following thrombectomy. One day after thrombectomy, the patient reported ptosis of the right eye (OD), diplopia, and loss of peripheral vision in both eyes (OU).
On examination at the bedside, near vision was 20/60 OU. There was no anisocoria or relative afferent pupillary defect (RAPD). There was a mild ptosis (1 mm) OD and a mild abduction and supraduction limitation OD. Anterior segment examination showed mild conjunctival chemosis OD and dilated fundus examination was normal OU. A CT scan of the orbit with contrast was unremarkable. CT head demonstrated no change in the prior MCA infarct, specifically, no chiasmal lesion was identified. Magnetic resonance imaging (MRI) could not be obtained due to patient’s non-MRI compatible cardiac pacemaker.
Eight months after discharge from the hospital, the patient was seen in the Houston Methodist Hospital neuro-ophthalmology clinic. The ptosis OD, ophthalmoplegia, and diplopia had resolved spontaneously. The bitemporal visual field loss OU remained unchanged. On examination, her best corrected visual acuity was 20/25 OD and 20/40 in the left eye (OS). Color vision tested with Ishihara plates was 14/14 OU. The pupils were isocoric with no RAPD. The extraocular motility exam, intraocular pressure, and slit lamp biomicroscopy were normal OU. Automated perimetry (Humphrey visual field 24-2), Fig. 3 , demonstrated an incomplete bitemporal hemianopsia, denser inferiorly. There was no evidence of a left homonymous hemianopsia due to the prior right MCA infarction. Optical coherence tomography (OCT) and optic nerve head photos revealed nasal and temporal atrophy (“band atrophy”) OD greater than OS consistent with a chiasmal etiology ( Fig. 4 A and 4B ). OCT of the macular ganglion cell layer also demonstrated loss in the papillomacular bundle corresponds with a chiasmal lesion ( Fig. 4 C). Repeat CT imaging of the sella showed no chiasmal or pituitary lesion. There was no evidence for suprasellar hemorrhage or chiasmal or pituitary apoplexy. No demyelinating lesions were seen on neuroimaging to suggest multiple sclerosis (MS). Serum antibody tests for syphilis, tuberculosis, aquaporin 4 in neuromyelitis optica (NMO) and myelin oligodendrocytic glycoprotein (MOG) were negative. A presumptive diagnosis of bitemporal hemianopsia following ischemic chiasmopathy following mechanical thrombectomy of the right ICA was made. Serial follow up of the patient has shown no change over time.