THE most commonly reported cause of sudden, devastating postoperative visual loss is anterior ischemic optic neuropathy (ION), resulting from decreased oxygen delivery to the optic nerves. 1Postoperative blindness has been previously reported in association with pressure-induced eye-injury, arterial hypotension, low hematocrit concentration, and obstruction of venous outflow. One cause of venous obstruction, superior vena cava syndrome (SVCS), is a reported but uncommon complication of liver transplantation in patients with a history of central venous thrombosis, indwelling catheters, or peritoneovenous shunts. 2–7 

A 43-yr-old man with hepatitis C cirrhosis had intractable ascites and a history of repeated placement of peritoneojugular shunts and placement of a transjugular intrahepatic portosystemic shunt. At the time of liver transplantation, induction of anesthesia with thiopental, fentanyl, and succinylcholine was achieved, and femoral and radial arterial catheters were placed. Because of poor peripheral venous access, insertion of peripheral, larger bore catheters was not successful. Several attempts were necessary to place central lines. Ultimately, large-bore intravenous catheters (8.5 French) were inserted into both internal jugular veins and the subclavian veins. An oximetric pulmonary artery catheter was inserted through the right internal jugular catheter. Anesthesia was maintained with isoflurane, fentanyl, and pancuronium.

The transplant operation was uneventful until the third hour, when it was aborted (just before recipient hepatectomy) because malignancy within the donor organ was revealed by postmortem examination. Stable hemodynamic parameters recorded throughout the procedure included central venous pressure (8 to 9 mmHg), pulmonary artery pressure (22–25/10–15 mmHg), and cardiac index (3.2–4.0 l/m2). The administered fluids included 4 l of crystalloids, 1 l of 5% albumin, 4 units packed erythrocytes, and 4 units fresh frozen plasma. No antifibrinolytic agents were administered to the patient during the operation.

During the closure of the aborted transplantation, the previously placed, nonfunctional peritoneojugular shunt was removed by sliding the venous end from the subcostal incision. Swelling and cyanosis of the patient’s face and neck were noted thereafter. The positions of all intravenous catheters were reconfirmed by the ability to draw back blood easily. Intravenous fluid maintenance was limited, and the patient was placed in the 30° reverse Trendelenburg position. Postoperatively in the intensive care unit, the head, face, and upper extremities became markedly edematous and cyanotic. A diagnosis of acute SVCS was determined, and three of four larger bore catheters were removed; the right internal jugular pulmonary artery indwelling catheter was left in place. Doppler study revealed total occlusion of both subclavian veins and the left and right internal jugular veins and a clot in the superior vena cava (SVC). Because of the facial edema, the patient remained intubated in the surgical intensive care unit, and maintenance fluid was continued through a freshly inserted femoral catheter. The patient required intermittent use of vasopressors and β-blockers to control tachycardia. By the second postoperative day, the patient had become hemodynamically stable, but there was little improvement in the signs of SVCS.

A second liver allograft was identified, and liver transplantation was performed successfully 48 h later using the piggyback technique. Intravenous access for this procedure was secured through large-bore femoral vein catheters. The procedure proceeded routinely except for a 2-min extreme hypotensive episode (systolic blood pressure, 50–60 mmHg) because of acute blood loss, which was rapidly corrected with massive-volume resuscitation. Total blood loss was estimated to be approximately 6 l and during the procedure the patient received 12 l of crystalloids, 1 l albumin, 5%, 13 units packed erythrocytes, 10 units fresh frozen plasma, and 20 units platelets. The postoperative course initially was uneventful, and the patient was extubated on the third postoperative day. On the fourth postoperative day, the patient verbalized that he was unable to see, and examination showed for the first time that his pupils were fixed and dilated, with no reaction to light. Fundoscopic examination performed by the ophthalmology consultant showed bilaterally elevated, pale, and blurred optic disks. The retina in both disks was flat, and the macula and vessels seemed to be normal. Computed tomography of the head showed no evidence of acute intracranial hemorrhage or infarction. The ophthalmology consultant diagnosed the patient with bilateral anterior ION. Facial and upper extremity congestion and edema resolved as the patient recovered from the transplant procedure. Subsequent eye examinations showed no significant changes and that the patient was unable to see. The patient was discharged from the hospital on postoperative day 21, with complete bilateral blindness and resolving SVCS.

In patients with recurrent ascites after peritoneovenous shunt placement, total and partial occlusion of the SVC is seen in 53 and 17% of patients, respectively. 6,7Patients with partial SVC obstruction may be asymptomatic preoperatively, but overt SVCS may develop after transplantation and placement of large-bore lines into the subclavian or jugular vein. Several cases of acute SVCS associated with peritoneovenous shunt have been reported in patients undergoing liver transplantation; however, without any alteration in vision in the postoperative period. 2–5 

The most commonly reported cause of postoperative visual loss is acute optic nerve ischemia. 1Visual loss as a result of ischemic injury to the optic nerve are labeled as anterior and posterior ION because these parts of the optic nerve have different blood supplies, different predisposing factors for injury, and varying clinical pictures. 1Anterior ION is characterized by sudden, progressive and painless visual-field deficit and defect in a pupillary light reaction, from a slight decrease in visual acuity to no light perception (as in the presented case). Ophtalmoscopic examination initially shows optic disk edema, which usually resolves in several weeks and is replaced by optic atropy. There are vascular causes of postoperative loss of vision other than ION. Cortical blindness, retinal occlusion, and ophthalmic venous obstruction therefore should be excluded. Cortical blindness is characterized by loss of visual sensation with retention of papillary reaction to light and normal fundoscopic examination results. Computerized tomography or magnetic resonance imaging abnormalities in the parietal or occipital lobe confirm the diagnosis. Central retinal artery occlusion presents as painless, monocular blindness. Ophthalmoscopic examination of eyes with retinal artery occlusion shows a pale edematous retina, a cherry-red spot at the fovea, and platelet–fibrin or cholesterol emboli in the narrowed retinal arterioles. Obstruction of venous drainage from the eye may occur intraoperatively when patient positioning results in external pressure on the eyes. In severe cases, ophthalmoscopic examination shows normal or dilated retinal arterioles, engorgement of the veins, and edema of the macula and the retina surrounding the optic disk. Another rare causes of postoperative blindness in liver transplantation is cyclosporine-induced neurotoxicity, which results in usually reversible cortical blindness. 8 

Postoperative anterior ION is the result of multiple causes of decreased oxygen delivery. It is usually associated with hypotension and blood loss. However, often there are other contributing variables, such as venous obstruction or vascular abnormalities. In a recent retrospective study of 350 patients who experienced massive trauma, anterior ION developed in 2.6%, and there was a significant association among ION, massive fluid resuscitation, and prolonged ventilatory support. 9Importantly, most of the patients in this study and those in our study were placed in the supine position.

Increased venous pressure was cited previously as a contributor to postoperative anterior ION after head and neck surgery as a result of local obstruction of venous outflow. 1It is speculated that changes in central venous pressure concomitant with changes in body position result in venous stasis in the drainage of the optical nerve. Patients with SVCS or predisposition to SVCS perhaps should be positioned in the reverse Trendelenburg position. The potential for SVC thrombosis and ION should be considered in patients with a history of peritoneovenous shunt placement.

Williams EL, Hart WM, Tempelfhoff R: Postoperative ischemic optic neuropathy. Anesth Analg 1995; 80: 1018–29
Kang Y, Videira R, DeWolf AM, Casavilla A, Freeman JA, Aggrwal S, DeRiso B: The superior vena caval syndrome during orthotopic liver transplantation: A complication of LeVeen shunt and venovenous bypass. Transpl Proceed 1991; 23: 1998–9
Pinna AD, Sugitani A, Thistlethwaite P, Kang Y, Marongiu L, Todo S, Starzl TE, Fung JJ: Venous-right atrial bypass for superior vena thrombosis during orthotopic liver transplantation. Transplantation 1997; 15: 471–2
Haussmann R, Motsch J, Otto G, Martin E: Acute jugular engorgement in liver transpantation: Anesthetist 1992; 41: 702–3
Suriani RJ, Abel M: Acute superior vena cava syndrome resulting from inferior vena cava cross-clamping: J Cardiothorac Vasc Anesth 1997; 11: 197–200
Smadja C, Tridard D, Franco D: Recurrent ascites due to central venous thrombosis after peritoneojugular (LeVeen) shunt. Surgery 1986; 100: 535–41
Foley WJ, Elliott JP, Smith RF, Reddy DJ, Lewis JW Jr, Hageman JH: Central venous thrombosis and embolism associated with peritoneovenous shunts. Arch Surg 1984; 119: 713–20
Wijdicks EF, Wiesner RH, Krom RA: Neurotoxicity in liver transplant recipients with cyclosporine immunosuppression. Neurology 1995; 45: 1962–4
Cullinane DC, Jenkins JM, Reddy S, VanNatta T, Eddy VA, Bass JG, Schwartz M, Lavin P, Morris JA Jr: Anterior ischemic optic neuropathy: A complication after system inflammatory response syndrome. J Trauma 2000; 48: 381–6