Unusual Cause of Postoperative Blindness

A 71-yr-old, 74-kg, female patient was scheduled to undergo exploratory laparotomy for a diagnosis of acute abdomen. She had a history of colon cancer, hypertension, and stable coronary artery disease, and a week previously, she had undergone an exploratory laparotomy to remove colon cancer. Her acute abdomen was presumed to be the result of bowel perforation.

Baseline laboratory work on the day of surgery, including a complete blood count and chemistry panel, was normal. A stress cardiac echo study performed 3 months previously showed a normal ejection fraction of 60%. An electrocardiogram showed normal sinus rhythm. Preoperative vital signs included blood pressure of 164/76 mmHg, heart rate of 116 beats/min, respiratory rate of 20 breaths/min, and temperature of 38.8°C.

Monitors included standard monitors, a radial artery catheter, and a Bispectral Index monitor. Anesthesia was induced using lidocaine, propofol, fentanyl, and rocuronium and was maintained with desflurane in air and oxygen. The patient was found to have a perforated cecum, and a wedge resection was performed. Blood pressure was stable during the entire case. Estimated blood loss was approximately 100 ml. She received a total of 2,900 ml crystalloid and 500 ml hetastarch over 4 h intraoperatively. Urine output was 200 ml. At the end of the case, the patient was taken to the recovery room and extubated approximately 3 h later when fully awake. After extubation, she was oriented to name and place and was aware of her surgery. She did not report anything unusual. She was transferred to the intensive care unit 70 min later.

More than 1 h after arriving in the intensive care unit, the patient casually reported being unable to differentiate between light and darkness since awakening from her operation. Examination revealed binocular vision loss. Given the uneventful operative and immediate postoperative course, the patient's lack of anxiety, and the timing, a presumptive diagnosis of hysterical conversion reaction was made. Neurology consultation was obtained, confirming binocular loss of vision, and cranial magnetic resonance imaging was obtained (fig. 1). Review of the imaging revealed bilateral occipital lobe ischemia believed to be secondary to an embolic event and consistent with a posterior cerebral circulation stroke. Neurology recommended anticoagulation, and the patient received a heparin infusion. On the day after acute vision loss and on anticoagulation, the patient reported a modest improvement in her vision (able to distinguish between light and dark). A cardiac echo was obtained and ruled out the heart as a source of the embolic event. Magnetic resonance angiogram of the intracranial arteries demonstrated bilateral posterior cerebral artery occlusions.

The patient was diagnosed with posterior cerebral artery infarction due to basilar artery embolus with cortical blindness. At the time of discharge and on follow-up in the neurology clinic, the patient continued to improve and was left with a right homonymous hemianopsia as her only neurologic deficit.

Visual loss after anesthesia for nonocular surgery is a devastating and fortunately uncommon event. In 1996, Roth et al.  2reported that 34 of 60,965 (0.056%) patients sustained eye injuries after anesthesia. The most common injury was corneal abrasion, and only 1 patient had permanent blindness from ischemic optic neuropathy after spine surgery. In 2001, Warner et al.  3reported 405 cases of vision loss or changes after 501,342 anesthetics. Of these, only 4 patients (0.0008%) developed prolonged vision loss after nonophthalmologic or neurosurgical procedures. In 2003, a report from the American Society of Anesthesiologists Postoperative Visual Loss Registry on 79 cases of postoperative visual deficit after nonophthalmologic surgery revealed that the most common associations were spine operations (67%) and cardiac bypass procedures (10%).4In the spine surgery cases, ophthalmologic diagnoses included ischemic optic neuropathy (81%) and central retinal artery occlusion (13%).

Postoperative visual loss caused by cortical infarction after routine noncardiovascular surgery is rare. Gelinas et al.  5reported a 51-yr-old woman who developed cortical blindness as a consequence of fat embolism during hip arthroplasty. There are also reports of cortical blindness in eclamptic obstetric patients.6,7Amar et al.  8reported a case of cortical blindness as an iatrogenic consequence of subclavian artery surgery. We found no reports of cortical blindness after routine abdominal procedures.

Basilar artery syndrome  is a stroke syndrome affecting the basilar artery, brainstem arterial perforators, and posterior cerebral arteries. The basilar artery is the dominant artery in the posterior circulation of the brain, formed by confluence of both vertebral arteries. Embolic strokes predominate in the posterior circulation and, in particular, the posterior cerebral arteries. Atherosclerosis is less common in this location and predominantly affects the proximal and middle segments of the basilar artery. Posterior circulation stroke risk factors include elderly age, peripheral arterial disease, previous stroke or transient ischemic attack, hypertension, diabetes mellitus, hypercholesterolemia, hyperhomocysteinemia, coronary artery disease, and smoking. Heralding symptoms include encephalopathy, brainstem syndromes, cortical blindness, gaze palsies, cranial neuropathies, and neurobehavioral disorders. The mortality rate varies and is a function of infarct volume.

Cortical blindness consists of complete loss of visual function including perception of light and dark due to injury to both occipital lobes. Cortical blindness is often associated with an encephalopathy, neurobehavioral abnormalities, and vertical gaze palsy. In most cases of cortical blindness due to ischemia, the associated encephalopathy is brief, after which the full extent of visual loss is often appreciated.

Diagnostic evaluation in a patient with a suspected embolic stroke is directed at possible embolic sources. These sources may be cardiac, aortic arch, or carotid or vertebral–basilar arteries, depending on whether an anterior or posterior circulation stroke has occurred. Cardiac sources are determined by history, electrocardiogram, and echocardiogram. Imaging studies include magnetic resonance imaging of the brain and magnetic resonance angiography of both extracranial and intracranial arteries. Magnetic resonance of the brain must include diffusion-weighted imaging because this sequence is most sensitive for early stroke detection. Computed tomography of the brain often underestimates ischemic stroke but is useful to exclude hemorrhagic stroke. In situations where a magnetic resonance angiography cannot be performed, e.g. , if a pacemaker is in place, computed tomographic angiography is an excellent substitute. Contrast angiography has an additional benefit as a therapeutic instrument for recanalization of the occluded artery.

Various treatment modalities have been suggested for patients with basilar artery syndrome, including treatment with thrombolytic agents (i.e. , prourokinase, streptokinase, and tissue plasminogen activator) given either intravenously or intraarterially. Patients should not be treated with thrombolytics if recent surgery has been performed, if they are taking anticoagulants, if more than 3 h have elapsed since stroke onset, or if there are large-volume ischemic changes on brain computed tomography (in the instance of middle cerebral infarcts). Anticoagulation with heparin or low-molecular-weight heparin has been advocated and used successfully.