1. Introduction
Transient cortical blindness (TCB) is an infrequent yet intriguing postoperative complication following cardiac surgery. It is marked by the sudden, temporary loss of vision in both eyes, typically resolving within hours (1). This report of a rare occurrence of TCB following coronary artery bypass grafting (CABG) surgery aims to raise awareness among clinicians and researchers regarding this potential complication.
2. Case Presentation
A 54-year-old non-diabetic woman with a history of myocardial infarction (MI) and percutaneous coronary intervention approximately 13 years ago presented with complaints of chest pain. Her medications included nitroglycerin, atorvastatin, and aspirin. Preoperative evaluation showed an ejection fraction of 40%, with carotid Doppler revealing no abnormalities. Coronary angiography indicated 80%, 90%, and 60% stenosis in the left anterior descending (LAD), diagonal artery, and right coronary artery, respectively. Bypass grafts were placed, utilizing the left internal mammary artery to the LAD artery and a saphenous vein to the obtuse marginal and ramus arteries; however, bypass grafting for the right coronary artery was unsuccessful. During surgery, blood flow through the grafts was satisfactory. An iodinated contrast agent was used, with an operative time of 128 minutes and an aortic clamp duration of 70 minutes.
The patient remained asymptomatic immediately postoperatively but began experiencing bilateral blurred vision three days after surgery. Her vision progressively worsened over the following two weeks until she could only perceive light in both eyes. Her vision then gradually improved over the next two months. Postoperatively, her vital signs were stable, there were no changes in her electrocardiogram or cardiac enzymes, and her cardiac status remained stable.
Ophthalmologic examination revealed no causative ocular abnormalities aside from bilateral papilledema and reduced visual acuity to light perception. As an initial treatment, intravenous hydrocortisone was administered (100 mg twice daily for three days). A non-contrast computed tomography (CT) scan showed bilateral subarachnoid hyperdensities in the occipital and parietal lobes. Subsequently, magnetic resonance imaging (MRI) was performed to confirm the presence of cerebral hemorrhage, but no evidence of hemorrhage was detected. Evaluation of the carotid, vertebral, and ophthalmic arteries was normal. The patient was kept under close observation without further intervention, and her vision fully recovered after two months. No additional complications were noted during follow-up.
3. Discussion
Transient cortical blindness is an uncommon but potentially severe and stressful complication that has been primarily associated with cerebral and vertebral angiography (2, 3). Reports on TCB following CABG have also appeared in the literature since the 1990s (4, 5). The pathophysiology of TCB remains incompletely understood, but several proposed mechanisms may help explain its occurrence. Hyperosmolar iodinated contrast agents have been linked to TCB cases (1). These contrast agents may disrupt the blood-brain barrier, leading to the infiltration of contrast into the brain parenchyma. This localized infiltration, particularly in the occipital lobes, may induce an inflammatory response, which could contribute to the sudden onset of cortical blindness (6).
It is worth noting that not all TCB cases involve hyperosmolar iodinated contrast agents. Reports indicate that non-ionic contrast agents, considered less osmotically active, have also been associated with TCB occurrences (7). Although using non-ionic and hypoosmolar contrast agents was expected to reduce the risk of TCB, it is evident that this precaution does not provide complete prevention (7). This discrepancy suggests that factors beyond contrast agent osmolarity may contribute to TCB.
In the present case, bilateral subarachnoid hyperdensities in the occipital and parietal lobes were observed on a non-contrast CT scan. However, subsequent MRI findings showed no pathological abnormalities. This inconsistency raises questions about the nature of the observed hyperdensities and their relationship to TCB. A similar case reported by Lee and Arjan Singh also demonstrated acute subarachnoid bleeding in both occipital lobes on CT, with a normal MRI, further underscoring the transient nature of these changes and the absence of lasting damage associated with TCB (8). This highlights the importance of MRI in the evaluation of these patients, though the diagnosis of TCB remains largely based on clinical presentation. The prognosis for TCB is generally favorable, with most cases resolving within hours, as observed in this patient (9). In conclusion, clinicians should remain vigilant about the possibility of TCB following coronary angiography and CABG procedures. Additionally, patients undergoing these procedures should be informed of the potential risk of TCB, and close monitoring for signs and symptoms of this condition is advised.
