Postoperative visual loss following cerebral arteriovenous malformation surgery: a case report

Introduction

Postoperative visual loss (POVL) is a known complication of surgery and anesthesia; its incidence varies from 0.03% after spine surgery to 0.086% after cardiac surgery¹. Typically, this involves ischemic optic neuropathy (ION), and is clinically characterized by the acute or subacute loss of visual acuity and/or visual field. Both anterior (diffuse optic disc swelling) and posterior (no optic disc swelling) ION have been reported after general anesthesia in spinal and other non-ocular surgeries^1,2. It can present as both unilateral and bilateral. An association with systemic diseases, such as hypertension, diabetes, hypercholesterolemia, or atherosclerosis, is not well documented. The management of this entity has been described by an American Society of Anesthesiologists (ASA) task force³. The incidence of POVL in a general surgical population is low (0.0012%)¹; to our knowledge, only one case has previously been reported in intracranial neurovascular surgery, and was included in the POVL registry of the ASA⁴.

Case report

A 46 year-old woman initially presented with paresthesia in hands and legs, and was diagnosed with a right frontal, Spetzler-Martin grade 1, superficial, arteriovenous malformation (AVM). She was classified as ASA physical status 3, and underwent surgical excision of the AVM. The patient’s personal medical history revealed arterial hypertension, as well as a coronary artery disease with previous myocardial infarction (MI) and percutaneous coronary angioplasty (PTCA). Preoperative transthoracic echocardiography showed a grade II left ventricular function (ejection fraction 50–55%) and mild distal anteroseptal and distal anterior wall hypokinesia. The patient ceased to smoke one year ago with a 30 pack-year history. Medication consisted of metoprolol 12.5 mg twice daily, aspirin 81 mg and clopidogrel 75 mg. Aspirin and clopidogrel were stopped 7 days prior to the intervention. The patient’s preoperative blood pressure was 130/90 mmHg, and hemoglobin concentration was 14.2 g/dl. After induction of general anesthesia with midazolam 2 mg, fentanyl 150 µg, and propofol 150 mg, followed by neuromuscular blockade with rocuronium 50 mg, the patient’s trachea was orally intubated. Anesthesia was maintained with sevoflurane and a remifentanil infusion during the 4-hour surgical procedure. Surgery was performed in the supine position, with the head elevated to 30 degrees with fixation in a head frame. The patient’s intraoperative blood pressure was maintained stable around 100 mmHg systolic, and there was minimal blood loss (300 ml). Total crystalloid infusion was 2 l. Emergence from anesthesia was uneventful, and the patient was extubated while awake and obeying commands. There was no sign of external compression of the eyes during and after surgery.

On awakening in the recovery room, the patient complained of blindness in her right eye. Immediate computer tomography of the brain was inconclusive. Ophthalmological examination of the right eye showed a posterior ION in association with a relative afferent pupillary defect (RAPD), but fundoscopy was normal without optic disc edema or cherry-red spot. Upon diagnosis of ION, the patient immediately received digital massage of the right eye once for a few minutes. Anti-glaucoma treatment (timolol maleate ophthalmic solution 0.5% applied to the affected eye twice daily for 2 days) was given to decrease intraocular pressure (IOP). On the following day, her vision had somewhat improved; however, the right temporal visual field was still missing. Examination of the retina was again normal, and no further treatment was administered. She was discharged from the hospital 2 days after surgery. In a follow-up visit after 3 months, she was neurologically intact, and her vision was better. Her visual field had returned to normal with just some blurring of vision in the right eye.

Discussion

This patient experienced acute unilateral loss of visual acuity and visual field after AVM surgery in the supine position. Findings were consistent with the diagnosis of POVL due to posterior ION with RAPD. Fundo- and retinoscopy of the affected eye were normal, and there was no sign of external pressure on the ocular globe. In a review of the literature, we only found one case of unilateral visual loss after intracranial aneurysm surgery (ASA POVL Registry)⁴, suggesting that POVL is a very rare complication of intracranial neurovascular surgery in the supine position.

Several potential causes of POVL have been described. Intraoperative corneal trauma may result in irritation, abrasion, or even laceration of the eye. Preventive measures include taping the eyes shut and careful patient positioning. Intraoperative stroke involving the visual tracts or the visual cortex may lead to hemianopsia and cortical blindness. Cerebral ischemia may be due to prolonged systemic hypotension or thromboembolism. Arteriosclerosis-related embolism also plays an important role in the etiology of central retinal artery occlusion (CRAO)⁵; however, CRAO may be caused by an acute and severe rise of IOP found in trauma or direct external pressure to the ocular globe as well. Clinical findings in CRAO are the unilateral painless loss of vision with signs of external periorbital swelling or ecchymosis, and a pathognomic cherry-red spot at the macula. Recently, posterior reversible encephalopathy syndrome (PRES) has also been proposed as potential cause of POVL⁶.

Risk factors that have been implicated in the development of ION in spine surgery include male sex, obesity, prolonged intraoperative hypotension, long duration of surgery, substantial intraoperative blood loss, and the excessive use of intravenous replacement fluids, or anemia^7,8.

The majority of POVL cases are reported after lumbar spine surgery^1,2,5–9, suggesting a greater incidence of POVL associated with prone positioning. Increases in IOP during surgery in the supine position were thought to be an important factor for the development of visual loss; the current recommendation of the ASA task force³ is to keep the head elevated higher than the heart and in neutral position whenever possible. Intraoperative blood loss and prolonged arterial hypotension should be avoided. Intravenous administration of colloid solutions and avoidance of excessive crystalloid infusion has been recommended. Excess crystalloid may cause tissue edema, and compromise tissue oxygenation in the orbital cone. If prolonged duration of surgery in the prone position is necessary, the eyes should be examined for external compression or swelling at regular intervals.

Conclusion

POVL involving ION remains a rare, but devastating condition. Unfortunately, our limited knowledge of the pathophysiology restricts the treatment options. Type of surgery, patient-related and intraoperative risk factors have been identified, but absent in this case. Recognition of high-risk cases such as major spine surgery, intraoperative head elevation, use of colloids, avoidance of excessive crystalloid infusion, correction of anemia, and staging of surgery are preventive measures recommended by the ASA task force on POVL³. Cases of permanent loss of vision have occurred, therefore early diagnosis and treatment are paramount to increase chances of visual recovery in the event of POVL.

Patient consent

Written informed consent for publication of their clinical details was obtained from the patient.