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Table of Contents
EDITORIAL  
Year : 2014  |  Volume : 17  |  Issue : 2  |  Page : 89-91
Postoperative vision loss during off-pump coronary artery bypass grafting


Department of Anaesthesiology, AIIMS Raipur, Chhattisgarh, India

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Date of Web Publication1-Apr-2014
 

How to cite this article:
Neema PK. Postoperative vision loss during off-pump coronary artery bypass grafting. Ann Card Anaesth 2014;17:89-91

How to cite this URL:
Neema PK. Postoperative vision loss during off-pump coronary artery bypass grafting. Ann Card Anaesth [serial online] 2014 [cited 2022 Dec 4];17:89-91. Available from: https://www.annals.in/text.asp?2014/17/2/89/129821


Postoperative vision loss (POVL) after anesthesia and surgery is a rare, unexpected, and devastating complication. [1] POVL has been reported after almost all kinds of surgery, including cardiac surgery with bypass, spine surgery, endoscopic sinus surgery, [2] arthroscopic shoulder surgery, [3] axillary femoral bypass grafting, [4] hemireplacement arthroplasty of the hip, [5] after lumbar epidural steroid injection, [6] liposuction, [7] and transurethral prostatectomy. [8] Shen et al.[9] examined the POVL prevalence in the US Nationwide Inpatient Sample (NIS); the highest frequencies were found after spine (3.09/10,000, 0.03%) and cardiac surgery (8.64/10,000, 0.086%). The four most commonly reported ocular events associated with POVL are anterior ischemic optic neuropathy (AION), posterior ischemic optic neuropathy (PION), central retinal artery occlusion (CRAO), and cortical blindness. [10]

The causes of POVL are primarily retinal vascular occlusion and ischemic optic neuropathy (ION). The ischemic damage to the optic nerve head (AION), to the optic nerve at its entry into the orbit (PION), and cortical blindness are the various clinical manifestations. PION generally involves the optic nerve between the optic foramen at the orbital apex and the point of entry of the central retinal artery, where it is most vulnerable to ischemia. [11] The definite mechanism operating in a particular patient and surgery cannot be defined well as multiple mechanisms are involved in the pathogenesis of POVL and also because it has a very low incidence.

Ischemic damage to the optic nerve is the final common pathway; hence, it is important to know the blood supply of the optic nerve and the factors that can compromise the O 2 delivery to the optic nerve. The anterior optic nerve includes the optic disc and the portion of the optic nerve lying within the scleral canal. [12] The optic nerve head (ONH) receives its blood supply through the central retinal artery and the posterior ciliary arteries, branches from the ophthalmic artery. The posterior ciliary arteries provide the majority of the blood supply through the short posterior ciliary arteries (SPCA), whereas the retinal arterioles provide partial perfusion of the superficial disc. [12] Additional contributions to its blood supply arise from choroidal arterioles and recurrent pial arterioles. [13] The later exhibits significant individual variation including the existence of watershed areas between the areas of distribution of the SPCA which may make an individual susceptible to ischemia. [14] The venous drainage of the inner retina occurs via the central retinal vein to the superior ophthalmic vein after which the blood passes into the cavernous sinus and out of the skull through the internal jugular vein. The outer retina, choriocapillaris, and choroid are drained through the vortex veins which join the central retinal vein in the superior ophthalmic vein to drain into the cavernous sinus and jugular vein circulation. The vortex veins drain the choroidal circulation via superior and inferior ophthalmic veins. The perfusion pressure for retina is described as the difference between mean arterial pressure in choroidal vessels and intraocular pressure (IOP). The blood supply and O 2 delivery to the optic nerve can be affected in several ways including hypotension, decreased O 2 content of the blood (low hematocrit), disease of the supplying artery (internal carotid artery), critical compression of the SPCA supply to the ONH due to raised IOP, embolic obstruction of central retinal artery, or its branch/branches. Pressure within the orbit can be increased internally after retrobulbar hemorrhage, associated with vascular injuries during sinus or nasal surgery. Prone position and long duration of surgery may predispose patients to ION and visual loss. It is postulated that the increase in IOP could be due to an increase in episcleral venous pressure (small veins in the sclera near the corneal margin). [9],[10] Increased episcleral venous pressure caused by vascular congestion may be a significant factor in the rise in IOP in the prone position. [15],[16] The raise in IOP thus produced may contribute to vascular occlusion in highly compromised eyes.

The risk factors and the perioperative events associated with POVL are yet not well-documented because of its infrequent occurrence. Preoperative risk factors for patients include small disc on fundoscopic examination, male gender, age >40 years, obesity, diabetes, and preoperative anemia. [17],[18] The intraoperative factors that have been associated with POVL include hypotension, blood loss (>1,000 mL), facial edema, pressure on the eye, prone position, and prolonged surgery (>6 h). [17],[18] Certain procedural risks can be reduced by avoiding external pressure on the eye during operative procedures and minimizing emboli during cardiopulmonary bypass. [14] In high-risk patients head should be positioned at a level higher than the heart (Reverse Trendelenburg) or at the level of the heart and the head should be maintained in a neutral forward position. [17] The Recommendations of the ASA Task Force on Perioperative Blindness are available from http://www.asahq.org/publicationsAndServices/BlindnessAdvisoryFinal.pdf

In this issue of Annals of Cardiac Anaesthesia, Battu et al., in a retrospective analysis describes POVL in four patients out of 1442 patients (0.28%) after off-pump coronary artery bypass grafting (OPCABG). [19] All patients were male, over 50 years of age, and known diabetics on treatment, which was well-controlled prior to surgery. Of four patients, one had lost vision two years ago in one eye due to diabetes-related complications; one patient had mild nonproliferative diabetic retinopathy in both eyes, and the remaining two patients had no evidence of diabetic retinopathy. Three patients had triple vessel disease and one patient had double vessel disease. All the four patients had a significant decrease in hematocrit and mean arterial pressure intraoperatively, which decreased further during the postoperative period and all of them needed epinephrine intraoperatively and postoperatively for support of circulation. Arguably, all the four patients were at high-risk of developing POVL; however, the majority of the patients presenting for CABG carries similar risks. Hypotension can only be a rare cause of retinal ischemia as Little et al reported POLV in just three cases amongst 27930 cases of deliberate hypotensive anaesthetics reviewed by them. [20] Holy et al.[21] did not find an association of perioperative ION and hypertension, coronary artery disease, diabetes, or stroke. In a prospective study of nonsurgical patients, ION was not associated with carotid artery disease. [22] However, Shapira et al. [23] showed an association between prolonged epinephrine infusions or long bypass time and ION in patients undergoing open-heart surgery. One can possibly conclude that the presence of diabetes, intraoperative and postoperative low hematocrit and hypotension, need of epinephrine to support circulation independently need not necessarily cause POLV. But what if all these factors exist in concert!!!

It is important to understand hemodynamics during the construction of distal anastomosis during OPCABG and the management of hemodynamic disturbances associated with it. During distal anastomosis of obtuse marginal and ramus intermedius artery, the heart is lifted from its cradle and is verticalized, which cause folding of the right ventricle resulting in obstruction of inflow and outflow of the right ventricle. Similarly, lifting of heart during anastomosis of right coronary and posterior descending artery is associated with bradycardia and severe hemodynamic instability. In both the situations, the cardiac output is often severely decreased, and simultaneously there is a severe compromise of superior vena cava drainage resulting in central venous congestion [Figure 1]. The resulting hemodynamic instability is usually managed by Trendlenburg position, volume resuscitation and inotropes and vasoconstrictors. The Trendlenburg position aggravates the central venous congestion and also results in central retinal venous congestion. Volume resuscitation with crystalloids and/or colloids and ongoing blood loss results in lowering of hematocrit. Finally, compromised cardiac output and use of vasoconstrictors can impair blood supply to the optic nerves and the whole body. Evidently, the period of distal anastomosis of ramus intermedius, obtuse marginal, right coronary artery and posterior descending artery is critical and potentially harmful for the blood supply of optic nerves. The surgical stress continues during proximal anastomosis when the anastomosis are constructed using side-biting clamp, which can result in atheroembolic shower from the diseased aorta which may migrate to any site in the circulatory system. The hemodynamic instability often persists during the postoperative period and for circulatory support patients usually receive clear fluids and inotropes such as dopamine, dobutamine, and epinephrine. Large fluid replacement is generally reported in many case reports of ION. [24] Patients in the ASA Postoperative Visual Loss Registry received an average of 9.7 L of crystalloid intraoperatively, [25] and increased postoperative weight gain was identified in a case-control study of visual loss after heart surgery, [23] suggesting, although not proving, that fluid replacement might play a role. In the study presented by Battu et al, all the four patients suffered from severe decrease in hematocrit during intraoperative and postoperative period (30.50% ± 2.38%; 23.50% ± 5.00%), and all of them received epinephrine. Although, the authors have not described the surgical details regarding the vessels grafted, the hemodynamics during anastomosis and the management of hemodynamic instability, it is assumed that the perioperative course must have been similar to that described earlier. The severe decrease in hematocrit indicates resuscitation with clear fluids. In such situations, whether one should resuscitate these patients with clear fluids or replace the ongoing blood loss by blood or packed red cells blood is a point that needs immediate investigation. Needless to state, the hemodynamics and their management strategies during OPCABG are the important factors which may compromise the optic nerve blood supply. Perhaps echocardiography guided verticalization of the heart to minimize inflow-outflow obstruction, expeditious distal anastomosis, particularly, of ramus intermedius and obtuse marginal and short periods of reverse Trendlenburg position between anastomosis might help to reduce the incidence of this devastating complication.
Figure 1: Pathophysiology of optic nerve damage (see text for details)

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   References Top

1.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. 1
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2.Murthy TV, Bhatia P, Gogna RL, Prabhakar T. An unusual incidence of postoperative visual loss. Indian J Anaesth 2006;50:145-7.  Back to cited text no. 2
    
3.Bhatti MT, Enneking FK. Visual loss and ophthalmoplegia after shoulder surgery. Anesth Analg 2003;96:899-902.  Back to cited text no. 3
    
4.Remigio D, Wertenbaker C. Post-operative bilateral vision loss. Surv Ophthalmol 2000;44:426-32.  Back to cited text no. 4
    
5.Pandey V, Rao PS, Rao SK, Acharya KK. Monocular blindness due to central retinal artery occlusion in bipolar hemireplacement arthroplasty of the hip. Singapore Med J 2008;49:e96-7.  Back to cited text no. 5
    
6.Purdy EP, Ajimal GS. Vision loss after lumbar epidural steroid injection. Anesth Analg 1998;86:119-22.  Back to cited text no. 6
    
7.Minagar A, Schatz NJ, Glaser JS. Liposuction and ischemic optic neuropathy. Case report and review of literature. J Neurol Sci 2000;181:132-6.  Back to cited text no. 7
    
8.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. 8
    
9.Shen Y, Drum M, Roth S. The prevalence of perioperative visual loss in the United States: A 10-year study from 1996 to 2005 of spinal, orthopedic, cardiac, and general surgery. Anesth Analg 2009;109:1534-45.  Back to cited text no. 9
    
10.Dickemper RL, Griffin AT. Vision loss as a complication of nonophthalmologic surgery: Implications for care for the perianesthesia nurse. J Perianesth Nurs 2010;25:29-35.  Back to cited text no. 10
    
11.Rupp-Montpetit K, Moody ML. Visual loss as a complication of nonophthalmologic surgery: A review of the literature. AANA J 2004;72:285-92.  Back to cited text no. 11
    
12.Grant GP, Szirth BC, Bennett HL, Huang SS, Thaker RS, Heary RF, et al. Effects of prone and reverse trendelenburg positioning on ocular parameters. Anesthesiology 2010;112:57-65.  Back to cited text no. 12
    
13.Levin LA. Optic nerve. In: Kaufman PL, Alm A, editors. Adler's Physiology of the Eye. 10 th ed. St. Louis: Mosby; 2003. p. 617-9.  Back to cited text no. 13
    
14.Williams EL. Postoperative blindness. Anesthesiol Clin North America 2002;20:605-22, viii.  Back to cited text no. 14
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15.Cheng MA, Todorov A, Tempelhoff R, McHugh T, Crowder CM, Lauryssen C. The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology 2001;95:1351-5.  Back to cited text no. 15
    
16.Hunt K, Bajekal R, Calder I, Meacher R, Eliahoo J, Acheson JF. Changes in intraocular pressure in anesthetized prone patients. J Neurosurg Anesthesiol 2004;16:287-90.  Back to cited text no. 16
    
17.American Society of Anesthesiologists Task Force on Perioperative Blindness. Practice advisory for perioperative visual loss associated with spine surgery: A report by the American Society of Anesthesiologists Task Force on Perioperative Blindness. Anesthesiology 2006;104:1319-28.  Back to cited text no. 17
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18.Tempelhoff R, Yoder J. A new look at ischemic optic neuropathy. Curr Rev Nurs Anesth 2008;31:65-76.  Back to cited text no. 18
    
19.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.  Back to cited text no. 19
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20.Little DM Jr. Induced hypotension during anesthesia and surgery. Anesthesiology 1955;16:320-32.  Back to cited text no. 20
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21.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. 21
    
22.Fry CL, Carter JE, Kanter MC, Tegeler CH, Tuley MR. Anterior ischemic optic neuropathy is not associated with carotid artery atherosclerosis. Stroke 1993;24:539-42.  Back to cited text no. 22
    
23.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. 23
    
24.Roth S. Postoperative visual loss. In: Miller RD, editor. Miller's Anesthesia, 7 th ed. New York: Elsevier; 2010. p. 2821-41.  Back to cited text no. 24
    
25.Lee LA, Roth S, Posner KL, Cheney FW, Caplan RA, Newman NJ, et al. The American Society of Anesthesiologists Postoperative Visual Loss Registry: Analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 2006;105:652-9.  Back to cited text no. 25
    

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Correspondence Address:
Praveen Kumar Neema
Department of Anaesthesiology, AIIMS Raipur - 492 099, Chhattisgarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.129821

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