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Table of Contents
Year : 2014  |  Volume : 17  |  Issue : 2  |  Page : 92-97
Perioperative optic neuropathy in patients undergoing off-pump coronary artery bypass graft surgery

1 Department of Vitreoretina, Narayana Nethralaya, Institute of Medical Sciences, Bengaluru, Karnataka, India
2 Department of Anaesthesiology, Narayana Hrudayalaya Institute of Medical Sciences, Bengaluru, Karnataka, India

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Date of Submission11-Aug-2013
Date of Acceptance04-Mar-2014
Date of Web Publication1-Apr-2014


Aims and Objectives: Perioperative optic neuropathy (PON) is a rare, but devastating complication following coronary artery bypass graft surgery (CABG). We performed a retrospective study of PON associated with off-pump CABG (OPCABG) to identify possible risk factors. Materials and Methods: 1442 patients underwent OPCABG over a 10-month period from October 2008 to August 2009; PON was identified in four (0.28%) patients. A retrospective review of the charts was done to identify the patient characteristics, pre-operative status, intra-operative details, and ophthalmic examination details. Friedman test was used to compare the hematocrit (Hct) and the mean arterial pressure (MAP) values across the three time periods: Pre-, intra- and post-operative periods. Results: All four patients were male, diabetic, and in the age range 51-69 years. All patients noted unilateral or bilateral severe visual loss in the immediate post-operative period, which was permanent. All the four patients had statistically significant decrease in the Hct (P < 0.039) and mean arterial blood pressure (P < 0.018) in the intraoperative and post-operative period when compared to pre-operative value. Conclusions : PON is a rare but definite possibility in patients undergoing OPCABG. Diabetes mellitus may be a risk factor. Perioperative hemodynamic abnormalities like decrease in MAP and anemia may play a role in the development of PON in OPCABG.

Keywords: Coronary artery bypass grafting; Diabetes mellitus; Optic neuropathy

How to cite this article:
Battu R, Prasad A, Kanchi M. Perioperative optic neuropathy in patients undergoing off-pump coronary artery bypass graft surgery. Ann Card Anaesth 2014;17:92-7

How to cite this URL:
Battu R, Prasad A, Kanchi M. Perioperative optic neuropathy in patients undergoing off-pump coronary artery bypass graft surgery. Ann Card Anaesth [serial online] 2014 [cited 2023 Jan 30];17:92-7. Available from:

   Introduction Top

Visual loss following non-ocular surgery is a very rare, but dreaded complication. Perioperative visual loss (POVL) could be due to cortical infarction, retinal vascular occlusion, and anterior or posterior ischemic optic neuropathy. [1],[2] POVL has been described in a variety of operative procedures, the most common being spinal and cardiac surgeries. [1],[3],[4],[5],[6] Posterior ischemic optic neuropathy is more common following spinal surgeries, while anterior ischemic optic neuropathy (AION) has been described more often following cardiac surgeries. [1],[2],[3],[4] Most of the information about perioperative ischemic optic neuropathy is from case reports and a few case control studies. [1],[2],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15] The American Society of Anesthesiologists (ASA) post-operative Visual Loss Registry is the single largest series providing insight into post-operative visual loss. [16] The reported incidence of perioperative optic neuropathy (PON) varies between 0.028% and 1.3%. [6],[7],[8],[9],[12] Most cases of PON have bilateral simultaneous involvement, albeit asymmetrical, usually with very poor visual function. [16],[17] Typically, PON in cardiac surgery has been reported more often with conventional coronary artery bypass grafting (CABG), which uses cardiopulmonary bypass (CPB). [7],[8],[9],[12] There have been three reports of PON associated with off-pump cardiac surgery. [10],[11],[18] We report our experience in a series of patients who developed PON following off-pump CABG (OPCABG).

   Materials and Methods Top

After obtaining approval for the study from the Institutional Review Board, we retrospectively analyzed the case records of patients who underwent OPCABG over a 10-month period from October 2008 to August 2009 at our tertiary care cardiac center. The following information was abstracted from the case records: Pre-operative comorbidities, including diabetes, hypertension, peripheral vascular disease [Table 1]; intra-operative anesthesia, and monitoring details of hemodynamic parameters including mean arterial pressure (MAP), arterial blood gas analysis, blood glucose level, hematocrit (Hct), temperature, urine output, inotropic support agent (s), blood and blood component administered; surgical information such as use of myocardial stabilizer, heparin-protamine administered, number of vessels grafted, episodes and duration of hypotension and intra-operative events if any.
Table 1: Pre-operative data

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Anesthesia techniques were as per institutional practice. In general, patients were premedicated with oral diazepam (0.05-0.1 mg/kg) and beta-blocking agent (dose adjusted after considering the baseline heart rate and left ventricular ejection fraction). Propofol (~1 mg/kg), midazolam (0.1 mg/kg) and fentanyl (5-10 μg/kg) was used for induction. Pancuronium or vecuronium in appropriate doses was administered to facilitate oral endotracheal intubation. Intermittent positive pressure ventilation (volume control mode) was used; the lungs were ventilated to maintain PCO 2 at approximately 35 mmHg. Intra-operatively, fentanyl (up to a total 15 μg/kg) was administered. Anesthesia was maintained by isoflurane in air-oxygen mixture to maintain end tidal anesthetic concentration of 1-1.2%. Electrocardiogram, oxygen saturation, end-tidal carbon-di-oxide level, invasive arterial blood pressure, and central venous pressure were monitored in all patients. At intermittent intervals, blood gas analysis, blood sugar level in diabetics and urine output were measured. Heparin 400 U/kg was administered, and an activated clotting time of > 480 s was targeted. All patients underwent OPCABG using myocardial-stabilizing device (Octopus, Medtronic USA) for distal coronary anastomosis and side-biting clamp on the aorta for proximal anastomosis. MAP of 70-90 mmHg in normotensives and higher in hypertensive patients was aimed. In order to maintain MAP during grafting, continuous infusion of epinephrine (0.02-0.05 μg/kg/min) was started after optimizing the preload and the afterload, in compliance with the institutional protocol, the transfusion trigger was based on Hct < 25% with clinical assessment.

   Results Top

PON was identified in four (0.28%) patients out of 1442 patients. All patients were male, over 50 years of age, and known diabetics on treatment, which was well-controlled prior to surgery. Patient 1 had lost vision in the right eye (RE) due to diabetes-related complications 2 years ago, and he developed PON in the left eye (LE), patient 4 had mild non-proliferative diabetic retinopathy in both eyes, patients 2 and 3 had no evidence of diabetic retinopathy. Two patients had bilateral acute AION [Figure 1] and [Figure 2]; one patient (patient 1) had unilateral AION with contralateral advanced diabetic retinopathy, and another (patient 2) had unilateral AION with contralateral optic atrophy due to a previous PON [Table 2].
Table 2: Ophthalmic examination at the onset and during follow - up

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Figure 1: Fundus pictures of the right eye and left eye (LE) of patient 3 at presentation. Note the bilateral optic disc edema (black arrows) and cotton wool spots (white arrows). Note also the hemorrhages along the disc margin in the LE

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Figure 2: Humphrey visual fields (30-2) of the right eye (RE) and left eye (LE) of the same patient as in Figure 1. Note the advanced visual field loss in the RE and the loss of inferior field in the LE

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In all these cases, a significant decrease in MAP (73.00 ± 10.89 mmHg) and Hct (30.50 ± 2.38%) occurred in the intra-operative period, which further decreased significantly in the post-operative period (MAP 61.00 ± 11.34 mmHg and Hct 23.50 ± 5.00%, which further decreased significantly in the post-operative period) [Table 3] and [Table 4]. The average nocturnal MAP was noted to be lower than that during the day. All these patients received adrenaline infusion (0.02-0.05 μg/kg/min) intraoperatively and post-operatively. They also received packed red cell transfusion in the post-operative period. Patient 4 suffered pulseless ventricular tachycardia and was resuscitated as per AHA guidelines. He had a return of spontaneous circulation in 2 min and received increased dose of adrenaline (up to 0.1 μg/kg/min) for an hour. He also had prolonged post-operative ventilation. All the four patients complained of vision loss following tracheal extubation [Table 3] in the intensive care unit. All the four patients underwent an evaluation of their visual acuity, pupils, and fundus and MRI of the brain within 24 h, to rule out associated intracranial co-morbidities. Serial measurements of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also done to rule out arteritic AION. One patient (patient 2) gave a history of vision loss in the RE following a previous CABG, he suffered PON in the LE after his second CABG; this patient underwent a temporal artery biopsy after the second episode (which was negative for features of temporal arteritis).
Table 3: Pre-operative, intra-operative and post-operative data

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Table 4: Perioperative hematocrit and mean arterial pressure

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Once ambulatory, all these patients underwent a thorough ophthalmic examination in the clinic including a visual field assessment and fundus photography [Figure 1], [Table 2]. Vision loss was bilateral in two patients and unilateral in the other two. The vision loss ranged from severe visual loss (perception of light only) to altitudinal visual field loss at presentation [Figure 2]. These patients were followed up over a time period of 2 weeks to 3 years. At the last examination, only one patient (patient 3) had recovered partial vision in one eye although the severe visual field defects persisted.

   Discussion Top

This is the first series of patients with PON following OPCABG. Non-surgical AION is primarily a hypotensive disorder and occurs due to transient hypoperfusion of blood vessels due to any cause. [19] Hypotension may play a causal role even in post-surgical optic nerve ischemia as observed in PON. [1] PON has been mostly described in patients who have undergone cardiac surgery with CPB. Microembolization, inflammation, absolute/relative hypotension, anemia, hemodilution, hypothermia and pump-related platelet dysfunction have been considered as risk factors. [1],[7],[8],[9],[12] Newman observed that many of these factors may be epiphenomena of the procedures themselves and not necessarily causal. [1] OPCABG theoretically reduces the risk of embolization by reducing the manipulation of the aorta [20] and risk of microembolization by eliminating extracorporeal circuit. Rainio et al. studied the neuroprotective efficacy of OPCABG over conventional CABG and concluded that the risk of retinal embolism can be minimized by the use of OPCABG. [21]

Three isolated reports of PON following OPCABG have been reported. Frey et al. described a patient who underwent uncomplicated off-pump cardiac surgery for triple vessel disease. [18] Tidow-Kebritchi et al. postulated severe anemia, atrial fibrillation, hypotension, a small optic disc and uncontrolled diabetes as risk factors in a patient, who developed PON in the RE 3 days after an uncomplicated OPCABG. [11] Onorati postulated multiple risk factors in a 63-year old man who developed bilateral PON on the 3 rd day following an uneventful OPCABG. [10] Anemia and hypotension seem common risk factors for PON. Our patients showed a significant decrease in both the Hct and MAP from the pre-operative period. Hypotension decreases the perfusion pressure in the optic nerve and may lead to ischemic injury due to abnormal auto-regulation. Age-related changes, systemic co-morbidities like diabetes and hypertension may contribute to this abnormal auto-regulation. The clinical significance of a lower average nocturnal MAP is difficult to comment. Nocturnal arterial hypotension is an important risk for non-arteritic AION. [19] It is possible that similar factors are at play in the surgical setting. The MRI of brain of all four patients was normal. Nonsurgical ischemic optic neuropathy is seen in the clinic often in patients with an underlying systemic risk factor. This could be arteritic due to giant cell arteritis or non-arteritic due to other causes such as diabetes mellitus, arterial hypotension, arterial hypertension, blood loss or sleep apnea. [19]

Diabetes can cause intrinsic small vessel disease and is generally accepted as a risk factor for AION. [2],[14],[19] Kalyani et al., in their series of patients with CPB-associated PON, did not find an increased risk in diabetics. [7] They found that patients with vascular disease and those who had an absolute drop in hemoglobin had an increased risk of PON. Nuttall et al. and Shapira et al. in their studies did not find diabetes to be significantly associated with PON after CPB. [8],[9] Diabetes has been implicated as a possible risk factor in patients with non-cardiac ischemic optic neuropathy. [19] In a diabetic, it is not difficult to imagine that the optic nerve with an already-compromised circulation is further susceptible to even minor circulatory/ischemic changes that occur in the setting of CABG. It may be therefore prudent to identify these patients as being at a higher risk for PON following cardiac surgery. Efforts can be made to obtain one ophthalmic consult prior to a potential CABG that could possibly identify additional local risk factors like a small cup/disc ratio or severe atherosclerotic changes in the retinal arterioles. It may also be imperative to explain the possible risk of visual loss following cardiac surgery in these high-risk patients.

Pre-existing optic nerve morphology and presence of a "disc at risk" may predispose a patient to PON. [1] We could not comment on the optic discs in our patients because of bilateral involvement and contra-lateral optic atrophy in the unilateral ones. One of our patients (patient 2) had suffered AION in the RE after the first cardiac bypass surgery 11 years ago (no details available); he suffered PON in the LE after the second CABG. It is likely that there are individual susceptibility risk factors that may predispose a patient under duress to PON. Patients in a single family have been described to have non-arteritic AION, un-related to surgery. [22] It is similarly possible that patients may have a genetic predisposition to PON. One of our patients (patient 3) had a partial recovery of central visual function in one eye, with no specific treatment. It is likely that subclinical or spontaneously recovered PON may be more common than noted; a subsequent diagnosis of partial optic atrophy would miss the correlation.

Of interest are the raised ESR and CRP levels in our patients; this is not unexpected in the immediate post-operative period. We did not look for any other markers of inflammation. Although speculative, it is likely that inflammation may play a role in the development of PON, which has recently been postulated in ION following spinal surgeries. [23]

Cardiac arrest in the post op period may have been an additional risk factor for PON in the patient 4. The patient remained hypotensive after resuscitation and required increased dosage of adrenaline (up to 0.1 μg/kg/min) for approximately an hour. It is possible that the hypotension and vasoconstriction sustained during this period may have been contributory to the optic nerve ischemia.

The ASA POVL Practice Advisory has suggested guidelines for the management of visual loss in patients undergoing spinal surgery. [16],[24] They have advised optimizing hemoglobin levels, hemodynamic status, and arterial oxygenation. In addition, there are several guidelines for blood transfusions. [24],[25] Avoiding factors like arterial hypotension, excessive fluid replacement, pressure on the eye or orbit and dependent position of the head have been advocated as possible prophylactic measures to avoid PON. [23]

Our study has several limitations. This is a small retrospective study from a single tertiary care cardiac center, where the majority of surgeries are done as OPCABGs. It is also possible that the subset of patients operated here belong to a higher-risk group systemically. Our statistical analysis was very limited owing to the very small number of patients. We emphasize the need for a case-control study in the future, to obtain a statistically significant analysis.

   Conclusion Top

PON is a rare, but definite possibility in patients undergoing OPCABG. A low Hct and low MAP appears important risk factors, Individual risk factors such as diabetes mellitus, disc-at-risk, possible inflammation, and a genetic predisposition may contribute. The study highlights the fact that patients undergoing OPCABG, despite avoiding the risks of CPB are not completely immune to this unfortunate complication.

   References Top

1.Newman NJ. Perioperative visual loss after nonocular surgeries. Am J Ophthalmol 2008;145:604-10.  Back to cited text no. 1
2.Roth S. Perioperative visual loss: What do we know, what can we do? Br J Anaesth 2009;103 Suppl 1:i31-40.  Back to cited text no. 2
3.Moura FC, Cunha LP, Monteiro ML. Bilateral visual loss after liposuction: Case report and review of the literature. Clinics (Sao Paulo) 2006;61:489-91.  Back to cited text no. 3
4.Sadaba LM, Garcia-Layana A, Maldonado MJ, Berian JM. Bilateral ischemic optic neuropathy after transurethral prostatic resection: A case report. BMC Ophthalmol 2006;6:32.  Back to cited text no. 4
5.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. 5
6.Sweeney PJ, Breuer AC, Selhorst JB, Waybright EA, Furlan AJ, Lederman RJ, et al. Ischemic optic neuropathy: A complication of cardiopulmonary bypass surgery. Neurology 1982;32:560-2.  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.Nuttall GA, Garrity JA, Dearani JA, Abel MD, Schroeder DR, Mullany CJ. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: A matched case/control study. Anesth Analg 2001;93:1410-6.  Back to cited text no. 8
9.Shapira OM, Kimmel WA, Lindsey PS, Shahian DM. Anterior ischemic optic neuropathy after open heart operations. Ann Thorac Surg 1996;61:660-6.  Back to cited text no. 9
10.Onorati F, De Feo M, Santè P, Renzulli A, Cotrufo M. Perioperative optic neuropathy following off-pump coronary artery bypass grafting. J Cardiovasc Surg (Torino) 2006;47:585-7.  Back to cited text no. 10
11.Tidow-Kebritchi S, Jay WM. Anterior ischemic optic neuropathy following off-pump cardiac bypass surgery. Semin Ophthalmol 2003;18:166-8.  Back to cited text no. 11
12.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. 12
13.Larkin DF, Wood AE, Neligan M, Eustace P. Ischaemic optic neuropathy complicating cardiopulmonary bypass. Br J Ophthalmol 1987;71:344-7.  Back to cited text no. 13
14.Mansour AM, Awwad ST, Najjar DM, Sibai AN, Sibai AM, Medawar WA, et al. Anterior ischaemic optic neuropathy after coronary artery bypass graft: The role of anaemia in diabetics. Eye (Lond) 2006;20:706-11.  Back to cited text no. 14
15.Williams I. Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: A matched case/control study., by G. A. Nuttall, J. A. Garrity, J. A. Dearani, M. D. Abel, D. R. Schroeder, and C. J. Mullany. Anesth Analg 93:1410-6, 2001. Surv Ophthalmol 2003;48:237-8.  Back to cited text no. 15
16.Lee LA, Roth S, Posner KL, Cheney FW, Caplan RA, Newman NJ. The American Society of Anesthesiologists postoperative visual loss registry preliminary analysis of factors associated with spine operations. ASA Newsl 2003;67:7-8.  Back to cited text no. 16
17.Buono LM, Foroozan R. Perioperative posterior ischemic optic neuropathy: Review of the literature. Surv Ophthalmol 2005;50:15-26.  Back to cited text no. 17
18.Frey ME, Schwartz HW. Bilateral anterior ischemic optic neuropathy after an off-pump bypass: A case report. Am J Phys Med Rehabil 2000;79:206.  Back to cited text no. 18
19.Hayreh SS. Ischemic optic neuropathies-Where are we now? Graefes Arch Clin Exp Ophthalmol 2013;251:1873-84.  Back to cited text no. 19
20.Shroyer AL, Grover FL, Hattler B, Collins JF, McDonald GO, Kozora E, et al. On-pump versus off-pump coronary-artery bypass surgery. N Engl J Med 2009;361:1827-37.  Back to cited text no. 20
21.Rainio A, Hautala N, Pelkonen O, Palosaari T, Heikkinen J, Mosorin M, et al. Risk of retinal microembolism after off-pump and on-pump coronary artery bypass surgery. J Cardiovasc Surg (Torino) 2007;48:773-9.  Back to cited text no. 21
22.Hayreh SS, Fingert JH, Stone E, Jacobson DM. Familial non-arteritic anterior ischemic optic neuropathy. Graefes Arch Clin Exp Ophthalmol 2008;246:1295-305.  Back to cited text no. 22
23.Postoperative Visual Loss Study Group. Risk factors associated with ischemic optic neuropathy after spinal fusion surgery. Anesthesiology 2012;116:15-24.  Back to cited text no. 23
24.Practice Guidelines for blood component therapy: A report by the American Society of Anesthesiologists Task Force on Blood Component Therapy. Anesthesiology 1996;84:732-47.  Back to cited text no. 24
25.Society of Thoracic Surgeons Blood Conservation Guideline Task Force, Ferraris VA, Brown JR, Despotis GJ, Hammon JW, Reece TB, et al. 2011 update to the Society of Thoracic Surgeons and the Society of Cardiovascular Anesthesiologists blood conservation clinical practice guidelines. Ann Thorac Surg 2011;91:944-82.  Back to cited text no. 25

Correspondence Address:
Rajani Battu
Narayana Nethralaya, 121/C, Chord Road, Rajajinagar, Ist R Block, Bengaluru - 560 010, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.129823

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