Sudden, severe bilateral vision loss after coronary artery bypass grafting

Abstract

We describe a rare complication of coronary artery bypass grafting (CABG) in a young man who presented with sudden, severe, bilateral visual loss after surgery. His ophthalmological examination was non-revealing; however, MRI of the brain revealed bilateral occipital lobe infarction. His infarction was presumed to be secondary to emboli arising from surgical manipulation within the atherosclerotic ascending aorta or from a cardiogenic thrombus formed due to perioperative arrhythmia.

Background

Sudden vision loss in the perioperative setting is a challenging situation that requires a thorough neuro-ophthalmic assessment. In this case, we review the approach to diagnosis in a patient with postoperative visual loss and highlight the rare yet significant presentation of bilateral occipital lobe infarction as a complication of coronary artery bypass grafting (CABG).

Case presentation

A 46 year-old man underwent uneventful CABG. During the procedure, he was noted to have diffuse coronary artery disease without intraoperative arrhythmias. He had a history of type 1 diabetes mellitus and diabetic nephropathy that led to end-stage renal disease requiring peritoneal dialysis. He was found to have severe coronary artery disease during recent investigations to determine suitability for kidney-pancreas transplantation. After awaking on the second postoperative day, he noticed blurry vision in each eye. He was able to see well before CABG. He had a history of panretinal photocoagulation (PRP) for proliferative diabetic retinopathy in each eye and underwent a vitrectomy in the right eye 8 years ago for non-clearing vitreous haemorrhage. There were no other focal neurological symptoms or signs. When assessed at the bedside, vision was counting fingers in both eyes. It did not improve with pinhole. Pupils were reactive to light with no relative afferent pupillary defect. Anterior segment examination and extraocular motility were unremarkable. Dilated fundus examination showed normal appearing optic nerves and multiple PRP scars in the posterior pole with no evidence of active retinopathy. It was found that the patient’s blood pressure remained within the normal range during the perioperative period, and no vascular bruit in the neck was appreciated.

Investigations

An urgent MRI of the brain with diffusion-weighted imaging (DWI) is the investigation of choice in this case. An MRI of the brain will allow for identification of optic nerve ischaemia by demonstrating restricted diffusion within the optic nerves. As well, an MRI will also be able to detect acute stroke involving the brain parenchyma that would manifest as an area of restricted diffusion with low signal on the associated diffusion coefficient (ADC) map. Posterior reversible encephalopathy syndrome (PRES) is also readily apparent on MRI and can be distinguished from infarction by increased diffusion and a bright signal on ADC sequences corresponding to areas of extracellular oedema. This patient’s MRI demonstrated multiple areas of diffusion restriction including the bilateral occipital lobes, pons and cerebellum, consistent with ischaemic strokes most likely secondary to an embolic source (figure 1). The patient’s CT angiography demonstrated atherosclerosis though no evidence to support an anterior circulation embolic source. An echocardiogram done immediately postoperatively demonstrated normal biventricular size and systolic function without significant valvulopathy.

Figure 1.

(A) Diffusion-weighted imaging demonstrating an extensive area of restricted diffusion involving both occipital lobes. (B) Apparent diffusion coefficient map demonstrating low signal in the same area confirming acute ischaemia. (C) Fluid-attenuated inversion recovery sequence confirming a large area of ischaemia in both occipital lobes.

Differential diagnosis

There is a limited differential diagnosis for bilateral vision loss in the immediate perioperative setting. When the ocular examination is normal, the possibilities are narrowed to bilateral posterior ischaemic optic neuropathy (PION), bilateral occipital lobe infarction and PRES.

Ischaemic optic neuropathy should always be considered in patients with postoperative vision loss. If ischaemia involves the short posterior ciliary arteries, anterior ischaemic optic neuropathy results, with oedema of the optic nerve head seen on ophthalmoscopy. When the vascular supply of the posterior optic nerve is compromised, the fundus examination is normal.¹ PION is typically confined to two settings: severe perioperative hypotension and giant cell arteritis. Surgery-related PION is bilateral in more than half of patients and visual loss is catastrophic in almost all cases with visual acuity typically in the range of hand motion to no light perception (NLP).^{2 3} If vision is NLP, the pupils are typically minimally or non-reactive to light, and in unilateral cases there will be a brisk RAPD.^{2 3} Given that there was no clinical suspicion of giant cell arteritis and that the operative notes did not detail any perioperative hypotension, the risk of PION remained less likely.

Bilateral vision loss secondary to stroke is rare and always secondary to bilateral occipital infarction. While the more common unilateral visual cortex lesions produce contralateral homonymous visual field defects with spared central vision, bilateral lesions cause severe reduction of central visual acuity.

The hallmark of PRES is extracellular oedema, as opposed to intracellular ischaemia in stroke. If the inciting source is removed, the oedema typically resolves on its own. Though this syndrome is most often seen in the context of severe hypertension, PRES is a possibility in this case, as it has also been reported in dialysis patients and postcardiac surgery.^{4 5}

Outcome and follow-up

As the patient was already on acetylsalicylic acid 81 mg daily, no further treatment was offered. He was started on atorvastatin 20 mg daily as a secondary prevention strategy. He was referred for low vision rehabilitation. Clinical examination at 1 month postoperatively was stable, with an unchanged visual acuity and ocular examination. He remained systemically well with no focal neurological deficits.

Discussion

Periprocedural stroke has been reported in 2% of patients undergoing CABG.⁶ Embolic stroke post-CABG usually occurs either as a consequence of surgical manipulation within an atherosclerotic ascending aorta or is secondary to cardiogenic thrombus due to perioperative arrhythmia.⁷

Bilateral occipital strokes as a complication of CABG are exceedingly rare. In a case series evaluating the incidence of postoperative stroke after CABG, out of 1631 consecutive cases, 19 (1.16%) patients suffered postoperative strokes, of which only two (0.12%) were reported as unilateral occipital lobe infarcts and another two (0.12%) as unilateral strokes in the vertebrobasilar artery distribution.⁸ Only one case (0.06%) was identified as possibly involving bilateral occipital lobes, although the clinical details of the case were not reported. In another similar series of 1380 CABG cases, 16 (1.15%) postoperative strokes were identified, of which 4 (0.29%) were reported as occurring in either a unilateral occipital lobe or posterior cerebral arterial distribution.⁹ No cases of bilateral occipital lobe infarcts were identified. In yet another large series of 2029 patients who underwent CABG by Hise et al, postoperative unilateral posterior cerebral arterial infarct occurred in 5 (0.25%) patients, while bilateral posterior cerebral arterial infarcts occurred in only 1 (0.05%) case.¹⁰

Secondary prevention strategies in patients with ischaemic strokes include dual antiplatelet therapy as well as a cholesterol lowering agent, while in patients with embolic strokes, the therapy is aimed at eliminating the source of the emboli (ie, treating bacterial endocarditis or addressing severe carotid stenosis either medically or surgically). If the source of emboli is permanent, such as in patients with prosthetic heart valves, life long anticoagulation is employed.¹¹

In summary, we describe a rare case of bilateral occipital stroke as a complication of CABG surgery and review an approach to vision loss in perioperative setting. Detailed ophthalmological examination is essential in ruling out retinal ischaemia and bilateral optic nerve head infarcts. When the optic nerve and retina appear normal in both eyes, the possibilities are limited to ischaemia in the bilateral occipital lobes or posterior optic nerves (PION) and PRES. MRI of the brain and orbits with DWI is essential in determining the correct diagnosis in these entities.

Learning points.

• In patients with bilateral sudden vision loss in the postoperative setting and normal ocular examination, MRI of the brain with diffusion-weighted imaging is the investigation of choice.

• The differential diagnosis in these cases is limited to bilateral posterior ischaemic optic neuropathy, bilateral occipital lobe infarction and posterior reversible encephalopathy syndrome.

• An acute stroke involving the brain parenchyma would manifest as an area of restricted diffusion with low signal on the associated diffusion coefficient (ADC) map on MRI.

• Posterior reversible encephalopathy syndrome can be distinguished from infarction by increased diffusion and a bright signal on ADC sequences corresponding to areas of extracellular oedema.

• In patients with diabetes and renal dysfunction presenting with vision loss, detailed neuro-ophthalmic examination and evaluation of the vertebral artery circulation is warranted.

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