Overview

Surgical shunts for portal hypertension and variceal hemorrhage are rarely undertaken today, in large part as a result of the recent popularity gained by transjugular intrahepatic portosystemic shunting (TIPS) (see Chapter 76E), a general lack of interest by surgeons, and the rising number of liver transplant centers across the United States. As a result, the number of hepatobiliary surgeons who have expertise in surgical shunting is declining, which is not to imply that this is appropriate, but it is true. Although current data document that surgical shunting is superior to TIPS in regard to patency, survival, risk of rebleeding, and maintaining effective hepatic blood flow, TIPS now predominates current therapy for variceal bleeding, likely because of its less invasive nature. The scope of this chapter is to describe the technical aspects of performing a native side-to-side portacaval shunt and a small-diameter prosthetic H-graft portocaval shunt. Unlike an end-to-side portacaval shunt, these shunts potentially preserve effective hepatic blood flow and are not ascitogenic.

Variceal hemorrhage secondary to portal hypertension presents an enormous challenge and responsibility to surgeons. Varices that are actively bleeding should be treated pharmacologically and endoscopically, if possible, prior to surgical management (see Chapters 75A and 75B). In the opinion of most providers, it should be a priority to stabilize the patient with nonoperative measures rather than attempt an emergency surgical shunt. The primary goal of surgery is to control ongoing hemorrhage and to prevent future life-threatening hemorrhage without inducing hepatic dysfunction. Patients should not be candidates for imminent liver transplantation (i.e., within 6 months), and an optimal candidate should have a Model for End-Stage Liver Disease (MELD) score less than 14 or have a Child-Turcotte-Pugh (CTP) class of A or B. However, for patients with advanced liver disease without prospects for transplantation, shunting is advocated for resource conservation and control of hemorrhage, albeit with increased risk of hepatic decompensation. With a recent episode of hemorrhage, the total bilirubin may be elevated, which increases the MELD score at the time of hospitalization. In these circumstances, it is helpful to extrapolate the patient’s MELD score or CTP class back to a time prior to the most recent hospitalization and/or hemorrhage.

A side-to-side portacaval shunt, as well as a small-diameter prosthetic H-graft portacaval shunt (HGPCS), is constructed for bleeding esophageal or gastric varices as a result of portal hypertension, most commonly caused by cirrhosis. Side-to-side portacaval shunts are placed electively or as an emergency in patients with a history of bleeding esophageal and/or gastric varices not amenable to or failing endoscopic therapy; prophylactic shunts are not recommended. In patients with acute bleeding, every effort is made to correct underlying coagulopathy and metabolic disorders, as well as to control active bleeding, using pharmacologic and endoscopic measures or balloon tamponade. An absolute contraindication to side-to-side portacaval shunt is the presence of portal vein (PV) thrombosis; therefore, PV patency is assessed preoperatively to document patency using color-flow Doppler ultrasound or other tests, such as magnetic resonance angiography (MRA) or computed tomography (CT). Side-to-side portacaval shunts are indicated for Budd-Chiari syndrome or other disorders that severely impair hepatic outflow. Contraindications to use include PV or inferior vena cava (IVC) thrombosis, multiple previous abdominal operations, morbid obesity, severe mitral regurgitation and/or aortic stenosis, and poor cardiopulmonary reserve. In contrast to large-diameter side-to-side portacaval shunts, a small-diameter (8 to 10 mm), calibrated, side-to-side portacaval shunt preferentially maintains hepatopetal flow and a normal (6 to 8 mm Hg) pressure gradient between the PV and IVC.

A focused preoperative investigation should include a determination of MELD score and CTP class; assessment of underlying cardiac dysfunction—such as mitral regurgitation or aortic stenosis—and cardiorespiratory reserve; evidence of current alcohol abuse; nutritional status; and presence of ascites and/or encephalopathy. If cardiac dysfunction is suspected, an echocardiogram should be obtained to avoid postoperative heart failure. A transabdominal color-flow Doppler ultrasound or other test is mandatory to assess portasplanchnic patency, directional flow, and patency of the vena cava.

Surgical Shunts in the Age of Tips

TIPS is a “definitive” nonsurgical treatment option for portal hypertension, often coined a “bridge to transplantation,” but with many critical issues. The most common causes of TIPS failure are shunt thrombosis and stenosis, both of which lead to variceal rehemorrhage. Numerous reports have shown that hepatic decompensation is unacceptably common after TIPS. In addition, the survival data after TIPS are not comparable to surgical shunts, most notably small-diameter prosthetic HGPCSs (Clark et al, 2010). Of concern is that TIPS excessively diverts nutrient effective hepatic blood flow (EHBF) from liver parenchyma that is already compromised by increased sinusoidal resistance to portal blood flow (Rosemurgy et al, 1995, 2003), thus potentially accelerating hepatic decompensation. Although TIPS does successfully partially decompress the PV and corrects the abnormal physiologic pressure gradient between the PV and IVC, its failures and shortcomings should be recognized, as this treatment option is undertaken frequently, without thorough consideration of its consequences. Although TIPS is viable for portal pressure decompression and temporary relief from variceal bleeding, the “bridge” to transplantation built by this procedure is seldom crossed; less than 10% of patients who undergo TIPS undergo liver transplantation.

Both TIPS and surgical shunts decompress the portal system, but surgical shunts—notably small, calibrated, side-to-side portacaval shunts and HGPCSs—relatively preserve effective hepatic blood flow. With TIPS, a decompression of portal venous pressure, along with the ensuing decrease in sinusoidal pressure, results in a concomitant increase in arterialization of the liver. However, after TIPS, increases in arterial blood flow, or “arterialization of the liver,” are not sufficient to compensate for relative excessive diversion of portal blood flow from the hepatocytes. Excessive decreases in total nutrient blood flow (EHBF) to hepatocytes result after TIPS relative to small-diameter calibrated and reinforced side-to-side portacaval shunts, such as an HGPCS (Rosemurgy et al, 2003). The critical, life-threatening issues of decreased EHBF and variceal rehemorrhage loom over an otherwise successful TIPS decompression.

Variceal hemorrhage after TIPS is relatively common and often results from shunt stenosis or thrombosis. Despite strict follow-up and assessment, TIPS patients experience more shunt occlusion and stenosis, although occlusion can usually be corrected by interventional radiology. The issue is that patients require multiple interventions to maintain shunt patency, whereas with an HGPCS, occlusion is less common. Vigilance with follow-up is necessary after TIPS; often the first sign of TIPS malfunction is variceal rehemorrhage (Rosemurgy et al, 2005).

The long-term complications of nonpatency, shunt stenosis, and thrombosis associated with TIPS are well documented. In 2005, a randomized controlled trial of 132 patients undergoing TIPS versus HGPCS was reported (Rosemurgy et al, 2005). The data demonstrated that stenosis and thrombosis after TIPS placement occurred in significantly more patients, and with greater frequency, compared with HGPCS. In the 32 patients who received TIPS, 66 interventions and/or revisions were required to maintain shunt patency during a 1-year follow-up period. In this study, only seven patients required intervention for patency after HGPCS, and five patients had irreversible TIPS occlusion. Most importantly, irreversible shunt occlusion often presented as major variceal hemorrhage. Of the 32 patients who underwent revisions for TIPS stenosis or thrombosis, 20 of these patients had major variceal rehemorrhage within 30 days, two patients rehemorrhaged after 30 days, and none of the patients had stenotic or thrombosed shunts following HGPCS (Rosemurgy et al, 2005). Also, TIPS has proven to be more expensive than pharmacologic, endoscopic, or surgical shunt treatments, owing to the number of interventions necessary to maintain patency (Kravetz, 2007). Indeed, the “Achilles heel” of TIPS is its lack of patency, and the success of TIPS as a portal decompression procedure is masked by continuing stenosis and thrombosis, requiring more cost for intervention and follow-up. Proponents of TIPS believe this has changed with the advent of covered stents.

A critical issue of TIPS is subsequent mortality. Median time to death after shunting was 29 months (41 ± 39.4 months) after TIPS compared with 56 months (53 ± 40.1 months) after H-graft shunts. Predicted survival was identical in both groups, and actual survival was significantly better for each shunt than predicted, using survival data at 3, 6, 12, and 24 months after shunting (Table 76B.1). However, actual survival with H-graft shunts was superior to survival after TIPS. Furthermore, the time to failure for patients undergoing TIPS or HGPCS was significantly different. For all patients of all CTP classes, TIPS had a median time to failure of 14 months (29 ± 33.2) compared with a median time to failure of HGPCS of 43 months (48 ± 41.9). In a patient with a severely impaired liver, a difference of nearly 30 months is critical, as that time could be utilized to undergo transplantation, if such were indicated and possible.