Transjugular intrahepatic portosystemic shunts: Postprocedure care and complications

INTRODUCTION — Transjugular intrahepatic portosystemic shunt (TIPS) is an important therapeutic tool for patients with complications of portal hypertension (eg, variceal bleeding, refractory ascites). TIPS placement reduces elevated portal pressure by creating a low-resistance channel between the hepatic vein and an intrahepatic branch of the portal vein using angiographic techniques. The tract is kept patent by deployment of an expandable stent across it, thereby allowing blood to return to the systemic circulation. An advantage of TIPS is that it functions like a surgical side-to-side portacaval shunt but is a minimally invasive procedure. However, TIPS insertion can be associated with a number of complications (eg, hepatic encephalopathy [HE], liver failure).

This topic will review postprocedure patient care and complications related to TIPS placement. The indications, contraindications, and pre-TIPS evaluation are discussed separately. (See "Overview of transjugular intrahepatic portosystemic shunts (TIPS)".)

The clinical manifestations and diagnosis of portal hypertension in adults are discussed separately. (See "Portal hypertension in adults".)

Management of patients with portal hypertension and acute variceal bleeding is discussed separately. (See "Overview of the management of patients with variceal bleeding" and "Methods to achieve hemostasis in patients with acute variceal hemorrhage".)

PATIENT CARE AFTER TIPS

Initial postprocedure care — Initial postprocedure care consists of observation, laboratory studies, and imaging [1]:

●Observation – Patients are observed for a minimum of six hours after TIPS placement for signs or symptoms of bleeding (hypotension, tachycardia), hepatic encephalopathy (HE), cardiac dysfunction, or pulmonary hypertension (eg, dyspnea). TIPS creates a rapid increase in venous return to the heart and can unmask cardiac dysfunction or pulmonary hypertension. (See 'Postprocedure complications' below.)

●Laboratory studies – We check laboratory studies (complete blood count, international normalized ratio, and liver biochemical and function tests) within 72 hours after TIPS placement or sooner if a complication such as acute liver failure is suspected. (See 'Liver failure' below and "Acute liver failure in adults: Etiology, clinical manifestations, and diagnosis".)

A decrease in hemoglobin, typically <3 g/dL, has been observed in some patients after TIPS and has been attributed to hemolysis [2].

●Imaging – A baseline ultrasound with Doppler of the liver is performed three to seven days after TIPS insertion to confirm shunt patency. Follow-up surveillance ultrasound studies are performed at one-, three-, and six-month intervals thereafter [3,4]. If ultrasound findings suggest TIPS stenosis, angiogram with portosystemic venous pressure gradient measurement is performed. (See 'Post-TIPS surveillance' below and 'TIPS dysfunction' below.)

Medication adjustments — Published data to guide medication adjustments after TIPS are lacking. Our approach is based on clinical experience and depends on the indication for TIPS:

●Patients with variceal bleeding – For patients who had TIPS for control of active variceal bleeding, we typically continue pharmacologic therapy (ie, octreotide) for 24 to 48 hours and then discontinue it if no further bleeding occurs. (See "Methods to achieve hemostasis in patients with acute variceal hemorrhage", section on 'Pharmacologic therapy'.)

●Patients with refractory ascites – For patients who had TIPS for refractory ascites, we resume sodium restriction and initially continue the pre-TIPS diuretic regimen. Diuretics are slowly tapered over the next several months, provided that ascites does not reaccumulate [5]. Diuretic therapy for patients with ascites, including specific regimens and patient monitoring, is discussed separately. (See "Ascites in adults with cirrhosis: Initial therapy", section on 'Diuretic therapy'.)

Post-TIPS surveillance — To assess TIPS patency, we obtain liver ultrasound with Doppler study between three and six months after TIPS and then at six-month intervals for long-term surveillance. Of note, most patients with cirrhosis have a liver ultrasound every six months to screen for hepatocellular carcinoma. (See "Surveillance for hepatocellular carcinoma in adults".)

The goal of surveillance is to detect TIPS stenosis before the patient develops recurrent symptoms of portal hypertension (eg, ascites), while data to support this practice are limited [1,6-8]. Detecting shunt stenosis prior to complete occlusion allows for early intervention, and treating shunt stenosis is typically more successful than treating shunt occlusion. (See 'TIPS dysfunction' below.)

If ultrasound findings suggest TIPS stenosis, we obtain an angiogram with portosystemic venous pressure gradient measurement to confirm the presence of shunt stenosis prior to TIPS revision. Portosystemic venous pressure gradient (PSG) measures the gradient in pressure between the portal vein and the systemic circulation (ie, inferior vena cava or right atrium), and if the PSG is ≥12 mmHg, patients are at risk for variceal bleeding and ascites. (See "Portal hypertension in adults", section on 'Hepatic venous pressure gradient'.)

Liver ultrasound with Doppler is the primary surveillance tool because it is noninvasive and widely available, and its accuracy is comparable to invasive methods (venography) [9,10]. In a study including 43 patients who had undergone TIPS, the sensitivity and specificity of liver ultrasound with Doppler study for detecting TIPS stenosis was 92 and 72 percent, respectively [10].

POSTPROCEDURE COMPLICATIONS

Issues related to portosystemic shunting

Hepatic encephalopathy

Incidence and etiology — Hepatic encephalopathy ([HE], also referred to as portosystemic encephalopathy [PSE]) is a complication of TIPS due to shunting of blood from the portal to systemic circulation. The incidence of HE following TIPS ranges from 30 to 50 percent, and chronic HE may occur in up to 25 percent of patients [11-16]. For example, in patients with variceal bleeding, the risk of HE was higher after TIPS insertion compared with endoscopic therapy. In a meta-analysis of 12 trials including 883 patients with variceal bleeding, patients with TIPS were more likely to develop HE compared with endoscopic sclerotherapy (odds ratio [OR] 2.21, 95% CI 1.61-3.03) [14]. Shunting of portal venous blood through the liver limits the metabolic filtering process of the liver parenchyma, and this contributes to new or worsening HE for patients after TIPS [1].

Risk factors for post-TIPS HE include:

●Hyponatremia [17]

●Sarcopenia [18]

●Older age [11]

●Prior history of HE [11,12]

●Larger shunt diameter (eg, >10 mm) [19,20]

●Alcohol-associated cirrhosis [16]

●Covert HE or cognitive impairment on testing [11,12]

According to Poiseuille's equation, resistance to flow can be defined as:

Where r is the radius of the stent, n is the coefficient of viscosity, and l is the length of the vessel. Thus, the resistance to flow through the shunt decreases exponentially with increasing shunt diameter, resulting in increases in shunt flow and portosystemic shunting. As a result, the risk of HE would be expected to increase with larger shunt diameters. However, one trial that assigned 45 patients to receive either 8 or 10 mm diameter stents failed to show an increased incidence of HE in patients with larger diameter stents [20]. At one year, the probability of being free of HE was not significantly different in patients with an 8 mm stent compared with a 10 mm stent. In addition, the trial was stopped early because of a higher portosystemic pressure gradient in patients who received the 8 mm stent (8.9 versus 6.5 mmHg). This correlated with a lower rate of having no complications related to portal hypertension in patients with smaller shunts (42 versus 83 percent).

Clinical presentation — HE usually becomes clinically apparent two to three weeks after TIPS insertion [21,22], while the occurrence of HE ≥6 weeks after TIPS insertion is typically precipitated by gastrointestinal bleeding. Additional precipitating factors for and symptoms of HE are similar to those that occur in patients with cirrhosis but without TIPS (eg, altered sleep pattern, confusion, disorientation), and these are discussed separately. (See "Hepatic encephalopathy in adults: Clinical manifestations and diagnosis".)

Prevention — Rifaximin prophylaxis may be reasonable for patients with risk factors for post-TIPS HE (eg, sarcopenia, older patient age, alcohol-associated cirrhosis). (See 'Incidence and etiology' above.)

However, we do not routinely use pharmacologic prophylaxis for preventing post-TIPS HE because data on the benefits of prophylaxis have been mixed [16,23-25]. In a trial including 197 patients with alcohol-associated cirrhosis who were scheduled for TIPS placement and were followed for six months, rifaximin prophylaxis resulted in lower rates of post-TIPS HE compared with no prophylaxis (34 versus 53 percent; OR 0.48, 95% CI 0.27-0.87) [16]. Rates of other liver disease-related complications (eg, bleeding) were not significantly different between the groups. In an earlier trial of 75 patients with cirrhosis who had TIPS placement, rates of post-TIPS HE were not significantly different for patients given prophylaxis with rifaximin or lactitol compared with no prophylaxis [24]. Additional trials are needed to determine if rifaximin is beneficial for preventing post-TIPS encephalopathy in most patients, while balancing the potential barriers to its use (eg, duration of therapy, cost).

Treatment — Treatment of post-TIPS encephalopathy is similar to that of HE in other settings. When HE develops de novo or worsens after TIPS insertion, the patient is evaluated for precipitating factors (eg, gastrointestinal bleeding, dehydration, infection), and these coexisting conditions are treated when possible. (See "Hepatic encephalopathy in adults: Clinical manifestations and diagnosis", section on 'Evaluation for precipitating causes'.)

Initial medical management of HE typically includes lactulose, along with nutritional support. The management of HE, including the approach to patients who do not respond to initial therapy, is discussed separately. (See "Hepatic encephalopathy in adults: Treatment".)

For patients with TIPS and HE that is refractory to medical therapy, options also include revising the shunt to reduce the diameter or occluding the shunt, although this approach reverses the benefits of the procedure [26,27]. While consensus is lacking, reducing shunt diameter is generally an option for patients who have ≥3 HE episodes that were not precipitated by other factors and that required hospital admission [28].

In one series, an attempt was made to quantify and follow the severity of encephalopathy after TIPS using a PSE index [21]. The PSE index rose sharply within 7 to 10 days after TIPS placement (figure 1). Over time, the PSE index declined, but at six months, it remained higher compared with baseline values and values in concurrent matched controls who underwent sclerotherapy. The decline in PSE index may be attributed to both treatment of HE and the development of stent stenosis, due to pseudointimal hyperplasia, which reduced the degree of portosystemic shunting. Subsequent studies using cognitive tests have demonstrated declining performance on these tests following TIPS, especially in selected patients (eg, those with sarcopenia or pre-TIPS cognitive impairment) [11,12]. Patients may also undergo such testing prior to TIPS placement to assess risk for post-TIPS HE. (See 'Incidence and etiology' above.)

Cardiac failure — Cardiac decompensation and/or failure is a complication of TIPS and results from a large-volume blood shift from the splanchnic circulation to the systemic circulation, increasing venous return to the heart, cardiac output, and right heart pressures [29]. In some patients, this increased venous return acts as a volume challenge and can unmask a previously undiagnosed cirrhotic cardiomyopathy or worsen portopulmonary hypertension [30]. (See "Definition and classification of the cardiomyopathies", section on 'Cirrhotic cardiomyopathy' and "Portopulmonary hypertension".)

However, despite initial volume overload, cardiovascular stabilization occurs during the first several months for most patients after TIPS placement, and specialty consultation (eg, cardiology, pulmonary) is obtained to help guide management [31,32].

The approach to pre-TIPS cardiac evaluation is discussed separately. (See "Overview of transjugular intrahepatic portosystemic shunts (TIPS)", section on 'Pre-TIPS evaluation and planning'.)

Pre-TIPS cardiac evaluation may help to identify patients at risk for cardiac decompensation after TIPS insertion. In a cohort study including 100 patients with cirrhosis (primarily alcohol-related disease), 20 patients (20 percent) developed cardiac decompensation requiring hospitalization after a median follow-up of 316 days. Risk factors for cardiac decompensation included aortic stenosis, diastolic dysfunction based on echocardiography, prolonged QTc interval, and elevated pre-TIPS brain natriuretic peptide (BNP) and N-terminal pro-BNP [33]. (See "Natriuretic peptide measurement in heart failure".)

Liver failure — Liver failure after TIPS insertion has been defined as ≥3-fold increase in total bilirubin and/or ≥2-fold international normalized ratio elevation that is associated with need for further intervention (eg, liver transplantation) or worse outcome (ie, mortality). The reported incidence of post-TIPS liver failure is 20 percent [14,34]. Pre-TIPS risk factors for liver failure include high Model for End-stage Liver Disease (MELD) score (ie, MELD >20) and underlying cardiovascular disease. (See "Model for End-stage Liver Disease (MELD)".)

Precipitants of acute liver failure after TIPS include:

●Sepsis.

●Gastrointestinal bleeding.

●Iatrogenic liver injury.

●Inability to increase arterial blood flow to the hepatic sinusoids (eg, reduced cardiac contractility) [35]. Hepatic arterial blood flow is often increased after creation of a portosystemic shunt, and patients who cannot increase arterial flow after diverting portal venous flow through the shunt may be predisposed to liver failure. The management of liver failure includes supportive care and treating reversible factors (eg, infection). For patients who do not respond to these measures and who are unlikely to have hepatic recovery, liver transplantation is the only viable option for long-term survival. (See "Acute liver failure in adults: Management and prognosis".)

Infection — Infections involving TIPS are uncommon and include endovascular shunt infection and periprocedural sepsis, and they are managed with intravenous antibiotics [36-38]. Selecting antibiotic therapy in this setting is similar to other intra-abdominal infections, and this is discussed separately. (See "Antimicrobial approach to intra-abdominal infections in adults", section on 'Empiric antimicrobial therapy'.)

Bacteremia (or fungemia) associated with endovascular TIPS infection (referred to as endotipsitis) is a rare complication but may occur after TIPS insertion or revision [38-41]. Sources of most infections include the gastrointestinal tract and skin, and endotipsitis was associated with a high mortality rate. In a review of case reports and small case series including 56 patients with infected TIPS, the mortality rate for patients with bacteremia with an infected TIPS was 32 percent (18 out of 56 patients) [38].

Preprocedure preparation including antibiotic prophylaxis is discussed separately. (See "Overview of transjugular intrahepatic portosystemic shunts (TIPS)", section on 'Pre-TIPS evaluation and planning'.)

TIPS dysfunction — TIPS dysfunction is defined as a loss of decompression of the portal venous system due to occlusion or stenosis of the TIPS. Patients with TIPS dysfunction typically present with symptoms of recurrent portal hypertension (eg, ascites, variceal bleeding). If TIPS dysfunction is suspected, liver ultrasound with Doppler study is performed to evaluate for stent narrowing or occlusion.

Causes of TIPS dysfunction include [1]:

●Thrombosis – Extensive thrombosis of the TIPS, portal vein, or splenic vein has been reported in up to 12 percent of patients after TIPS insertion. However, the available data reflect the era of bare metal stents, while the thrombosis risk with covered stents is uncertain [6,42-45]. In addition, no specific risk factors for thrombosis have been identified [6]. (See "Acute portal vein thrombosis in adults: Clinical manifestations, diagnosis, and management".)

Pharmacologic prophylaxis with anticoagulation is not required after TIPS insertion for maintaining shunt patency.

If thrombosis does occur, patients typically present within the first month after TIPS. Treatment options include thrombolysis, anticoagulation, or suction thrombectomy [46]. In those who are transplant candidates, liver transplantation is definitive treatment. We have used both suction thrombectomy followed by urgent liver transplant and thrombolysis followed by long-term anticoagulation in this setting.

●Stenosis or occlusion – Data have suggested that use of polytetrafluoroethylene (PTFE)-covered stents reduced the risk of shunt stenosis [47-49]. In a trial of 258 patients with cirrhosis who underwent TIPS placement, use of PTFE-covered stents resulted in lower risk of shunt dysfunction (defined as >50 percent reduction in shunt lumen or by portosystemic pressure gradient >12 mmHg) after five years compared with bare metal stents (risk ratio [RR] 0.42, 95% CI 0.28-0.61) [48,49]. In an earlier trial of 80 patients who underwent TIPS placement followed by Doppler ultrasound every three months for two years, rates of TIPS patency were higher in patients with covered stents compared with bare metal stents (76 versus 36 percent) [47].

TIPS stenosis or occlusion is caused by pseudointimal hyperplasia within the parenchymal tract or within the outflow hepatic vein. The occluded stent is coated with a collagenous matrix, covered by endothelial cells [50,51].

Other complications — TIPS is very rarely associated with hemolytic anemia in the setting of stents covered with PTFE (rather than bare metal stents) [2,52]. TIPS-associated hemolytic anemia is defined as new onset hemolysis with or without anemia in the absence of alternate causes (eg, spur cell anemia). (See "Non-immune (Coombs-negative) hemolytic anemias in adults".)

When TIPS-associated hemolysis occurs, it typically presents within 7 to 14 days after stent placement with an increase in serum bilirubin that is mostly unconjugated [2,53]. This is accompanied by reticulocytosis and a decrease in serum haptoglobin. Whether overt anemia develops depends upon the balance between red cell production and destruction. Most patients have a mild (<2 g/dL) reduction in hemoglobin concentration, but severe anemia with high-output heart failure can occur. The diagnosis of hemolytic anemia is discussed separately. (See "Diagnosis of hemolytic anemia in adults".)

The typical course of TIPS-associated hemolysis for most patients is spontaneous resolution within 8 to 12 weeks; however, the mechanism for recovery is unclear [2]. It may reflect covering of the metal wires with endothelium and smoothing the edges of the parenchymal tract, thereby reducing shear stress. Severe hemolysis rarely persists beyond 12 weeks, although one case report suggests that orthotopic liver transplantation was required for refractory hemolytic anemia [52].

Hemolysis may result from injury to red cells from shear stress or direct mechanical trauma in the shunt with culling of abnormal cells in the spleen [2,53].

PROGNOSIS

Survival — Mortality rates directly related to TIPS insertion have ranged from 0 to 2 percent [42], while overall mortality (measured at 30 days in most studies) ranged from approximately 5 to 50 percent [42,54-58].

Factors associated with higher mortality risk included [57,58]:

●Child-Pugh C class cirrhosis

●Hemodynamic instability and/or active bleeding at the time of TIPS insertion

●Urgent procedure (ie, acute variceal bleeding)

●Elevated serum bilirubin level (eg, >3 mg/dL)

Mortality after TIPS was usually related to underlying liver disease and liver failure, multiorgan failure, and/or sepsis [1,59].

However, TIPS was not associated with a higher mortality rate than other treatments for variceal bleeding. In a meta-analysis of 12 trials including 883 patients with variceal bleeding, there were no significant differences in mortality rates for patients treated with TIPS compared with endoscopic sclerotherapy (25 versus 22 percent) [14].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Portal hypertension and ascites".)

SUMMARY AND RECOMMENDATIONS

●Background – Transjugular intrahepatic portosystemic shunt (TIPS) is an important therapeutic tool for patients with complications of portal hypertension (eg, variceal bleeding, refractory ascites). TIPS insertion reduces elevated portal pressure by creating a low-resistance channel between the hepatic vein and an intrahepatic branch of the portal vein (figure 2). The tract is kept patent by deployment of a stent across it, thereby allowing blood to return to the systemic circulation. (See 'Introduction' above.)

●Postprocedure care – For patients who undergo TIPS insertion, initial postprocedure care consists of observation for signs/symptoms of complications (eg, bleeding, cardiac dysfunction) and laboratory studies (eg, complete blood count, international normalized ratio, liver biochemical and function tests). Imaging (liver ultrasound with Doppler study) is typically performed in three to seven days after the procedure. (See 'Initial postprocedure care' above.)

●Post-TIPS surveillance – For patients with TIPS, we perform surveillance imaging to assess shunt patency. Liver ultrasound with Doppler study is performed between three and six months after TIPS insertion and then at six-month intervals for long-term surveillance.

The goal of surveillance is to detect TIPS stenosis before recurrent symptoms develop (eg, ascites, variceal bleeding). (See 'Post-TIPS surveillance' above.)

●Issues related to portosystemic shunting – Hepatic encephalopathy (HE) is a complication of TIPS due to shunting of blood from the portal to systemic circulation. The incidence of HE following TIPS ranges from 30 to 50 percent. (See 'Incidence and etiology' above.)

For most patients who undergo TIPS placement, we suggest no pharmacologic prophylaxis of post-TIPS HE (Grade 2C). However, rifaximin prophylaxis may be reasonable for patients with risk factors for post-TIPS HE (eg, sarcopenia, older age, alcohol-associated cirrhosis). (See 'Prevention' above.)

Cardiac decompensation and/or failure is a complication of TIPS and results from a large-volume blood shift from the splanchnic circulation to the systemic circulation, increasing venous return to the heart, cardiac output, and right heart pressures. In some patients, this increased venous return acts as a volume challenge and can unmask a previously undiagnosed cirrhotic cardiomyopathy or worsen portopulmonary hypertension. (See 'Cardiac failure' above.)

●TIPS dysfunction – Patients with TIPS dysfunction or occlusion typically present with symptoms of recurrent portal hypertension (eg, ascites, variceal bleeding). If TIPS dysfunction is suspected, liver ultrasound with Doppler study is performed to evaluate for stent narrowing or occlusion. (See 'TIPS dysfunction' above.)

●Prognosis – Mortality rates directly related to TIPS insertion have ranged from 0 to 2 percent. Overall mortality (measured at 30 days in most studies) for patients after TIPS ranged from approximately 5 to 50 percent and was usually related to liver failure, multiorgan failure, and/or sepsis. (See 'Survival' above.)