A Rare Complication of Vertebral Artery Angiography: Transient Cortical Blindness

Dear Editor, Transient cortical blindness (TCB) is marked by temporary blindness affecting both eyes, with structurally normal corneas, retinas, and optic nerves.[1] This is a rare complication after cerebral angiography, occurring in 10% to three per thousand cases.[2] Although the precise mechanism of TCB remains unclear, contrast toxicity is a leading hypothesis.[3] Contrast material has been shown to induce vasodilation, disrupt endothelial tight junctions, and result in toxicity.[2] Several risk factors contribute to TCB, including angiograms in the posterior system, excessive contrast material, low patient weight, chronic hypertension, and diabetes.[4,5] Supportive treatment, including hydration, dexamethasone, and mannitol, has demonstrated benefits in resolving symptoms.[6,7] The typical recovery period spans 2 h–4 days, sometimes up to 5 days.[8,9] Differential diagnoses for transient blindness in both eyes may include various conditions, such as epileptic seizures, vasospasm following subarachnoid hemorrhages, migraine, posterior reversible encephalopathy syndrome (PRES), infective endocarditis, myocardial infarction, head injury, and preeclampsia.[10] We aim to review and discuss the presentation and treatment strategies of our patient who developed TCB after vertebral angiography and relate our findings to existing literature. A 37-year-old male presented with dizziness, nausea, and left-sided visual impairment following an attempt to lift a heavy object to a high place, during which he experienced right arm strain and neck pain. Digital subtraction angiography (DSA) images revealed a right vertebral artery dissection and two 7-mm false aneurysms in the V3 segment of the right vertebral artery, with a hypoplastic left vertebral artery. An initial neurologic examination indicated left homonymous hemianopia and slightly distorted left cerebellar tests, no motor deficit exists, and no pathologic reflexes. Cranial magnetic resonance imaging (MRI) revealed bilateral millimetric cerebellar infarction. In a follow-up assessment 2 months after the initial examination, DSA images revealed two 7-mm false aneurysms in the V3 segment of the right vertebral artery [Figure 1]. In addition, a hypoplastic left vertebral artery was observed. After 6 months, recanalization was achieved, but the false aneurysm remained. We decided to proceed with placing a vertebral stent in our patient.Figure 1: Digital subtraction angiography images, two false aneurysms in the right vertebral artery. (a) preprocedural, (b) postproceduralThe patient consented to the procedure, and the neuroradiology department accessed the radial artery using ultrasonography guidance for the flow diverter stent placement. During the procedure, 600 mL of iohexol 350 mg/mL contrast agent was used. During the procedure, the patient’s blood pressure and vital signs remained stable, and no complications arose. After the procedure, the patient regained consciousness and demonstrated full orientation, cooperation, and no motor deficits. However, he reported complete blindness and no light perception. Following the procedure, the patient was placed under intensive care observation. Blood tests, routine biochemistry tests, and computed tomography scans showed normal results. The cranial diffusion MRI at the 12th h postprocedure revealed no diffusion-restricting areas or other pathologic findings [Figure 2]. Ophthalmology examination yielded normal findings related to eye structures, but the left homonymous hemianopia persisted. Dual antiplatelet treatment (acetylsalicylic acid and clopidogrel) was initiated. Simultaneously, supportive treatment commenced, including hydration at a rate of 150 mL/h, methylprednisolone at a dose of 1 mg/kg, and mannitol at 1 mg/kg. Hyperbaric oxygen therapy (HBO) was initiated, considering potential benefits for the patient experiencing sudden vision loss. By the 24th h after treatments, the patient regained the ability to perceive only light, and by the 40th h, visual improvement was noted. A follow-up examination at 64 h after the onset of symptoms showed that he had recovered and mirrored the baseline: left homonymous hemianopia and slightly distorted left cerebellar tests, with no motor deficits and no pathologic reflexes. During this period, the patient received methylprednisolone for 4 days and underwent five sessions of HBO. A decision was made to discharge the patient with a prescription for dual antiplatelet therapy to reduce the risk of thromboembolic events.[11]Figure 2: Postprocedural magnetic resonance imaging images including diffusion, apparent diffusion coefficient (ADC), and fluid-attenuated inversion recovery (FLAIR) sequences. (a) Diffusion weighted imaging, (b) FLAIR, (c) ADC, (d) T2-weighted imagesOur patient, a young individual with no other comorbid diseases, developed TCB following a standard angiography procedure for a posterior system aneurysm. The administration of supportive treatment was effectively managed, with the patient collaborating with the medical teams, resulting in a successful resolution. Contrast toxicity remains a prominent theory for TCB.[3] Studies indicate that contrast material can induce vasodilation, disrupt tight junctions in the endothelial barrier, and lead to neurotoxicity.[2] Although our patient had a body mass index between 25 and 30 kg/m2, which does not specifically elevate the risk associated with contrast dosage, caution is still warranted.[10,12] This is particularly relevant in posterior circulation procedures and in patients with anatomic variations[10,12] In this case, our patient presented with a hypoplastic left vertebral artery, and contrast was administered from a single dominant vertebral artery [Figure 1]. These factors may be regarded as predisposing elements contributing to the development of TCB. In addition to contrast agent neurotoxicity, vertebrobasilar vasospasm and reduced blood flow in the vertebrobasilar system could affect the occipital lobes and contribute to visual impairment.[13] Blood–brain barrier disturbance, resulting from contrast agents, may cause cerebral edema and further complicate the condition.[2] Another important differential diagnosis to consider is PRES, which can present with visual disturbances and is associated with conditions such as hypertension and renal failure and results from endothelial dysfunction leading to vasogenic edema in the posterior regions of the brain.[8] In managing this case, we implemented a supportive treatment approach involving hydration, methylprednisolone, mannitol, and HBO therapy.[2,6,7] The primary goal was to reduce cerebral edema and sustain optimal cerebral perfusion.[7] Although contrast-induced neurotoxicity is typically self-limiting, there are no established guidelines for its treatment.[6] Given the acute nature of the patient’s vision loss, which did not resolve within the first 12 h, we promptly initiated these additional interventions to stabilize cerebral pressure. Although the treatment was administered to alleviate the condition, it proved to be a demanding and distressing experience for the patient, transitioning from an initial state without visual impairment to a temporary and complete loss of vision in both eyes. Hence, we emphasize the importance of healthcare professionals prioritizing patient comfort during such interventions and ensuring clear communication about the temporary nature of the process. The neuroprotective effect of HBO therapy has been recognized, attributed to its ability to attenuate brain damage through various mechanisms.[14] These include enhanced tissue oxygenation, decreased blood–brain barrier permeability, decreased inflammation, reduced cerebral edema, and lowered intracranial pressure.[15,16] In our case, we administered HBO therapy to the patient, resulting in a successful recovery. Given the urgency of the sudden visual loss, we used HBO therapy as part of a rapid response. However, due to the transient nature of TCB, it remains challenging to definitively ascertain if HBO treatment accelerates the recovery process and the extent of its influence. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands his that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.