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Table of Contents
Year : 2014  |  Volume : 17  |  Issue : 2  |  Page : 97-99
Perioperative vision loss: What's the cause?

Department of Ophthalmology, Neurology, and Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, India

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Date of Web Publication1-Apr-2014

How to cite this article:
Subramanian PS. Perioperative vision loss: What's the cause?. Ann Card Anaesth 2014;17:97-9

How to cite this URL:
Subramanian PS. Perioperative vision loss: What's the cause?. Ann Card Anaesth [serial online] 2014 [cited 2020 Apr 7];17:97-9. Available from:

Perioperative visual loss (POVL) is a devastating, but fortunately rare event after nonophthalmic surgery. While, there are extraordinary cases of direct eye injury or severe bilateral occipital lobe infarction causing permanent damage and central vision loss, most POVL occurs from optic nerve or retinal ischemia, producing ischemic optic neuropathy (anterior or posterior) or central/branch retinal arterial occlusion, respectively. Optic neuropathy is thought to be the more common outcome and has been studied more extensively. The proximate cause of ischemia is not usually identifiable, and the vision loss may be unilateral or bilateral. It is often profound (vision worse than 20/400 in each eye) and leaves patients functionally devastated. Because it occurs so infrequently, it is difficult to determine its incidence with certainty. POVL has been reported after a number of surgical procedures, including liposuction, [1] various orthopedic surgeries, [2] laparoscopic and robot-assisted urological surgeries, [3],[4] and extensive skin grafting. [5] Nonetheless, the cases with the highest apparent risk for POVL appear to be cardiac and spine cases, and these procedures are the most studied with respect to the incidence and potential risk factors for its occurrence.

A very large database study from the Mayo Clinic, in which over 400,000 noncardiac surgical cases were reviewed, revealed only four cases of permanent visual loss without direct surgical injury to the eye or visual pathways. [6] The authors concluded that the rarity of POVL made it impossible to identify meaningful risk factors. However, the perception that POVL had an increasing incidence as surgeons were undertaking more complex and prolonged surgical procedures led researchers to investigations showing a 0.113% incidence of perioperative optic neuropathy after cardiac surgery [7] and an even lower incidence of 0.028% after spine surgery, [8] with both studies at the same institution. Kalyani et al. concluded that postoperative hemoglobin levels of <10 g/dL were a potential risk factor for optic neuropathy after cardiac surgery and suggested that packed red blood cell transfusion to a hemoglobin concentration greater than this threshold value should be considered in patients with acutely recognized vision loss. [7] A similar finding was not found in spine surgery patients. Contemporaneously the American Society of Anesthesiologists (ASA) maintained a POVL database, and analysis of the registered cases confirmed the rarity of the disorder. [9]

The mechanism by which POVL occurs remains unknown. A parallel may exist with shock optic neuropathy, a condition recognized since ancient times in which profound vision loss occurs after massive hemorrhage and hypotension. [10] Nonetheless, a definitive link to absolute blood loss was not found in a recent retrospective review of over 126,000 surgical cases in which 17 cases of POVL (0.013% incidence) were identified. [11] One of the best systematic efforts to assess POVL and its risk factors can be found in the American Society of Anesthesiologists (ASA Practice Advisory for perioperative vision loss associated with spine surgery. [12] This document, which was prepared with the participation of anesthesiologists, spine surgeons, and neuro-ophthalmologists, presents evidence regarding the etiology and possible prevention of POVL, generally occurring as ischemic optic neuropathy. In reading this document, we are struck by the paucity of substantive evidence to support any of the theories regarding POVL. For instance, although intraoperative hypotension is thought to lead to optic nerve hypoperfusion, there is no evidence that the use of deliberate hypotension (used to reduce blood loss) increases the risk of POVL. The authors do recommend the use of crystalloid and colloid solutions together to maintain perfusion in the setting of intraoperative blood loss, based on some evidence that colloids may better maintain intravascular volume. The authors were unable to establish a threshold value for blood transfusion and advised an individualized approach for each patient. Of note, they make a clear statement that facial edema cannot lead to ischemic optic neuropathy, although direct globe compression could lead to retinal arterial occlusion.

In this setting, Battu et al. report on the incidence of POVL in coronary artery bypass grafting (CABG) surgeries performed without cardiopulmonary bypass. It is somewhat surprising that in their cohort of 1442 patients, there were four cases of POVL, providing a 0.28% rate. This result is statistically indistinguishable from studies of POVL in cardiac surgery with bypass and is 10 times higher than the rate found by Chang and Miller for spinal surgery. [8] All four patients with POVL had diabetes mellitus, but it is not known if their glycemic control was different from that of patients without POVL. The ASA Task Force did not find diabetes to be a POVL risk factor in spine surgery. [12] Similarly, a drop in mean arterial pressure was recorded in all four patients, but there is no evidence that this drop was significantly greater than in matched control subjects without POVL. Perhaps of greatest interest is the finding that one patient suffered POVL in his right eye 11 years earlier during CABG surgery with bypass and then had vision loss in the fellow eye during the off-bypass CABG procedure. This observation suggests that there are anatomic risk factors that may predispose a particular patient to POVL. We do not know what these factors might be, and identifying them may shed additional light onto the mechanism of POVL.

The most frustrating aspect of POVL for physicians and patients alike remains its seemingly random occurrence. When studies of POVL, including the one in this issue by Battu et al., are read critically, it becomes apparent that patients with identical vascular risk factors, surgical histories, and intraoperative management techniques may have widely disparate visual outcomes. A prospective study of cases in which the ASA Practice Advisory recommendations have been implemented systematically remains to be done, but statistical power to find a difference in outcomes, if it is present, may be unachievable in the context of the very rare occurrence of POVL in any surgical procedure. Nonetheless, we as physicians owe it to our patients to try to identify and mitigate preventable causes of POVL. Because the vision loss is often bilateral and may reduce vision to below the 20/400 level, patients are left functionally blind and must cope with this extreme challenge in addition to recovering from major cardiac or spinal surgery. For this reason, we must continue the research efforts to understand how POVL occurs and to determine if we can prevent it, and Battu et al. are to be congratulated for exploring such issues in a surgical population in which POVL might not have been anticipated.

   References Top

1.Ribeiro Monteiro ML, Moura FC, Cunha LP. Bilateral visual loss complicating liposuction in a patient with idiopathic intracranial hypertension. J Neuroophthalmol 2006;26:34-7.  Back to cited text no. 1
2.Berg KT, Harrison AR, Lee MS. Perioperative visual loss in ocular and nonocular surgery. Clin Ophthalmol 2010;4:531-46.  Back to cited text no. 2
3.Weber ED, Colyer MH, Lesser RL, Subramanian PS. Posterior ischemic optic neuropathy after minimally invasive prostatectomy. J Neuroophthalmol 2007;27:285-7.  Back to cited text no. 3
4.Metwalli AR, Davis RG, Donovan JF. Visual impairment after laparoscopic donor nephrectomy. J Endourol 2004;18:888-90.  Back to cited text no. 4
5.Price TP, Ivashchenko A, Schurr MJ. Perioperative visual loss after excision and autografting of a thermal burn to the back. Burns 2014; Jan 24. pii: S0305-4179 (14) 00006-0.  Back to cited text no. 5
6.Warner ME, Warner MA, Garrity JA, MacKenzie RA, Warner DO. The frequency of perioperative vision loss. Anesth Analg 2001;93:1417-21.  Back to cited text no. 6
7.Kalyani SD, Miller NR, Dong LM, Baumgartner WA, Alejo DE, Gilbert TB. Incidence of and risk factors for perioperative optic neuropathy after cardiac surgery. Ann Thorac Surg 2004;78:34-7.  Back to cited text no. 7
8.Chang SH, Miller NR. The incidence of vision loss due to perioperative ischemic optic neuropathy associated with spine surgery: The Johns Hopkins Hospital Experience. Spine (Phila Pa 1976) 2005;30:1299-302.  Back to cited text no. 8
9.Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008;145:604-10.  Back to cited text no. 9
10.Foroozan R, Buono LM, Savino PJ. Optic disc structure and shock-induced anterior ischemic optic neuropathy. Ophthalmology 2003;110:327-31.  Back to cited text no. 10
11.Holy SE, Tsai JH, McAllister RK, Smith KH. Perioperative ischemic optic neuropathy: A case control analysis of 126,666 surgical procedures at a single institution. Anesthesiology 2009;110:246-53.  Back to cited text no. 11
12.American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Practice advisory for perioperative visual loss associated with spine surgery: An updated report by the American Society of Anesthesiologists Task Force on Perioperative Visual Loss. Anesthesiology 2012;116:274-85.  Back to cited text no. 12

Correspondence Address:
Prem S Subramanian
Department of Ophthalmology, Neurology, and Neurosurgery, The Johns Hopkins University School of Medicine, 600 N Wolfe St., Woods 457, Baltimore, MD 21287
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Source of Support: None, Conflict of Interest: None

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