AASLD Practice Guidance on the use of TIPS, variceal embolization, and retrograde transvenous obliteration in the management of variceal hemorrhage

PURPOSE AND SCOPE OF THE GUIDANCE This is a comprehensive guidance on the use of interventional radiology endovascular techniques in the management of variceal hemorrhage from the American Association for the Study of Liver Diseases (AASLD). This guidance document is complementary to the AASLD "Risk Stratification and Management of Portal Hypertension and Varices in Cirrhosis" guidance1 and addresses the recent advancements in these invasive procedures. Although the use of TIPS dates back to the 1980s, several new technical refinements in TIPS stents have occurred in the last few years. The other major addition to the management of gastric variceal hemorrhage in North America has been the introduction of retrograde transvenous obliteration (RTO) in its different forms. The present document aims to equip care providers with an in-depth understanding of the use of TIPS and/or variceal embolization/obliteration in the management of variceal hemorrhage. The goal is to facilitate multidisciplinary discussions between hepatologists, gastroenterologists, interventional radiologists, and surgeons in the selection of endovascular treatments for patients with variceal hemorrhage. This document reviews first the anatomy of portosystemic collaterals, which is essential to understand the rationale for the use of these endovascular procedures. A second section describes the technical details of TIPS, RTO, and anterograde transvenous obliteration (ATO). The final section deals with the clinical use of endovascular treatments in the management of hemorrhage from esophageal, gastrofundal, and ectopic varices. Therefore, this AASLD Guidance provides a data-supported approach to the use of endovascular therapies for the management of variceal hemorrhage. It differs from the AASLD Guidelines, which are supported by systematic reviews of the literature, formal rating of the quality of the evidence, and strength of the recommendations. In contrast, this Guidance was developed by consensus of an expert panel and provides guidance statements based on comprehensive review and analysis of the literature on the topics, with oversight provided by the AASLD Practice Guidelines Committee. The AASLD Practice Guidelines Committee chose to perform a Guidance on this topic because, in most instances, a sufficient number of randomized controlled trials (RCTs) were not available to support meaningful systematic reviews and meta-analyses on this topic. ANATOMY OF PORTOSYSTEMIC COLLATERALS IN PORTAL HYPERTENSION Portosystemic collaterals develop between the portal and the systemic circulation as a consequence of portal hypertension. They represent an unsuccessful attempt by the body to decompress the portal circulation through the systemic circulation. Collaterals in the gastrointestinal lumen are referred to as varices. Varices develop commonly at the distal esophagus and proximal stomach i.e., the gastroesophageal region. Varices outside the gastroesophageal area such as the rectum, duodenum, and surgically created sites (e.g., stomal) are uncommon (≤5% of all variceal bleeding) and are referred to as ectopic varices.2–4Table 1 shows the location, supply, and drainage of common varices. TABLE 1 - Location, supply, and drainage of gastrointestinal varices (see also Fig. 1) Location Supply (afferent) Drainage (efferent) Gastroesophageal varices Esophageal varices Mid- and distal esophagus Left gastric vein Through azygos and hemiazygos vein into SVC Gastroesophageal varices (GOV): contiguous with esophageal varices GOV1 Lesser curvature of stomach Left gastric vein Through azygos and hemiazygos veins into SVC GOV2 Greater curvature of stomach/fundus Left gastric vein and posterior gastric vein Through azygos vein and hemiazygos veins into SVC and inferior phrenic vein into left renal vein (GRS) or IVC (gastrocaval shunt) Isolated gastric varices (IGV) IGV1 Fundus Short gastric veins, posterior gastric vein Through inferior phrenic vein into left renal vein (GRS) or into IVC (gastrocaval shunt) IGV2 Any location in stomach other than the fundus Short gastric veins, posterior gastric vein Left and right gastric vein Ectopic varices Rectal varices Rectum Superior rectal vein Through middle and inferior rectal vein into internal iliac vein Duodenal varices Duodenum Superior or inferior pancreaticoduodenal veins5,6 Through gonadal or renal capsular vein into IVC Stomal varices Surgically created ostomies Mesenteric branches from the superior mesenteric vein7 Through systemic venous collaterals in abdominal wall into iliofemoral vein Abbreviations: GRS, Gastrorenal shunt; SVC, superior vena cava. Esophageal varices are located in the mucosa and submucosa of the mid- and distal esophagus. They are supplied by the left gastric vein and drain into the azygos and hemiazygos veins through periesophageal veins (gastroesophageal venous system) (Fig. 1). Esophageal varices are most likely to bleed at the gastroesophageal junction because they are more superficial in this location and are unable to decompress through the azygos vein because of lack of communication with the periesophageal veins. Based on subjective endoscopic appearance, esophageal varices can be classified into (1) small: straight varices that collapse on insufflation, (2) medium: enlarged, tortuous varices that occupy less than one third of the lumen, or (3) large: coil-shaped varices that occupy more than one third of the lumen.8 In practice, medium and large varices are grouped together as high-risk varices because they require prophylactic therapy to prevent variceal bleeding.8 Owing to their superficial location, esophageal varices are amenable to endoscopic variceal ligation (EVL), i.e., placing of rubber bands for variceal obliteration, or sclerotherapy.FIGURE 1: Supply and drainage of varices. Esophageal varices and GOV1 are supplied by the left gastric vein (LGV) and drain through the azygous vein (AV) into the superior vena cava (SVC). Gastrofundal varices are supplied by the LGV (not shown in the figure), posterior gastric vein (PGV), and/or short gastric vein (SGV). Gastrofundal varices can drain into the left renal vein (LRV) through a gastrorenal shunt (GRS). Rectal varices are supplied by the superior rectal vein (SRV) and drain into the middle rectal vein (MRVs) and inferior rectal veins (IRV). Duodenal varices are supplied by the superior or inferior pancreaticoduodenal veins and drain into the IVC through the gonadal or the renal capsular vein.Gastric varices can be grouped based on their endoscopic location as (1) gastroesophageal varices type 1 (GOV1): lesser curvature, (2) gastroesophageal varices type 2 (GOV2): greater curvature, (3) isolated gastric varices type 1: gastric fundus (IGV1), and (4) isolated gastric varices type 2: any location in the stomach other than the gastric fundus (IGV2).9 Gastric varices are supplied by the left gastric vein (feeds GOV1, GOV2), or short gastric veins, and posterior gastric vein (feed IGV1, IGV2, GOV2) (Fig. 1). Like esophageal varices, GOV1 and sometimes GOV2 drain into the gastroesophageal venous system (Fig. 1). GOV2 and IGV1, also known as "cardio-fundal varices," drain through the gastrophrenic venous system, which is through the inferior phrenic vein into the left renal vein (gastrorenal shunt [GRS]) or the IVC (gastrocaval shunt) (Fig. 1). These can be seen frequently in patients with portal and/or splenic vein thrombosis. The accompanying large gastrorenal/-caval shunts provide an opportunity for transvenous obliteration. Gastric varices tend to be submucosal and may not be amenable to EVL. From an interventional radiology perspective, several classifications of gastric varices have been proposed based on characteristics important for planning interventional radiology procedures such as the type of varices and presence of shunts,4,10 the anatomy of the feeding and drainage vessels,11 visualization during venography,12 and the flow dynamics of the circuit13 (Table 2). Regardless of the classification, intraoperative flow dynamics are most important in determining the technique of embolization. TABLE 2 - Classifications of gastric varices Basis of classification Description Sarin Classification9 Endoscopic location Gastroesophageal varices (GOV) type 1: lesser curvature Gastroesophageal varices (GOV) type 2: greater curvature Isolated gastric varices type 1: fundus Isolated gastric varices type 2: anywhere in the stomach other than fundus Saad-Caldwell Classification4 Type of varices and presence and absence of shunts Type 1: Supply (afferent flow) through left gastric vein 1(a): Drainage through small portosystemic collaterals 1(b): Drainage mainly through GRS Type 2: Supply (afferent flow) through short gastric veins 2(a): Drainage through small portosystemic collaterals 2(b): Drainage mainly through GRS Type 3: Supply (afferent) through left gastric and short gastric veins 3(a): Drainage through small portosystemic collaterals 3(b): Drainage mainly through GRS Type 4 4(a): Type 3(a) with PVT 4(b): Type 3(b) with PVT Kiyosue Classification11 Patterns of supplying (afferent) and draining (efferent) veins Supply Type 1: Single gastric vein Type 2: Multiple gastric veins Type 3: Single or multiple gastric veins with coexistent gastric veins that are contiguous with a shunt but do not contribute to the varices Drainage Type A: Single shunt Type B: Single shunt and collateral veins Type C: Both gastrorenal and gastrocaval shunts Type D: A shunt which cannot be catheterized Hirota Classification12 Visualization during venography Grade 1: No evidence of collateral veins, gastric varices are well opacified Grade 2: Few small collateral veins, contrast remains in gastric varices for >3 min Grade 3: Few medium to large collateral veins, partial opacification of gastric varices, contrast remains in gastric varices <3 min Grade 4: Large collateral veins, gastric varices are not well opacified Grade 5: Large GRS with rapid flow; left adrenal vein cannot be occluded with balloon catheter Matsumoto Classification13 Flow dynamics of the circuit Type 1: Gastric veins communicate with GRS 1(a): Hepatopetal blood flow 1(b): Hepatofugal blood flow Type 2: No evidence of communication between gastric veins and GRS 2(a): Hepatopetal blood flow 2(b): Hepatofugal blood flow IGVs (IGV1 > IGV2) can form in sinistral or segmental portal hypertension from a focal splenic vein thrombosis or stenosis related to an inflammatory process such as pancreatitis. Unlike in cirrhosis, in which IGVs represent portosystemic collaterals, IGVs in sinistral portal hypertension are porto-portal collaterals that are supplied by the short and posterior gastric veins but drain back into the portal vein through the left and right gastric veins. It is important to differentiate sinistral portal hypertension from systemic portal hypertension because the pathophysiology and management of the two entities differ. Rectal varices form at the junction of the superior rectal vein with middle and inferior rectal veins and differ from hemorrhoids because they do not extend to the dentate line. Bleeding from rectal varices and other ectopic varices is uncommon, and management should be considered on a case-by-case basis based on vascular anatomy. TIPS TIPS creation is a procedure in which a percutaneously created portosystemic shunt is used to treat the complications of portal hypertension such as variceal hemorrhage, refractory ascites, and hydrothorax. Since its inception in the 1990s, the TIPS procedure has advanced in technique, applications, and devices (e.g., polytetrafluoroethylene [PTFE]–covered stent-grafts). Physiological effects of TIPS A TIPS is an endovascular shunt placed under radiographic guidance connecting the portal system with the systemic circulation and aiming to decrease the portal venous pressure gradient. Portal flow is diverted to the systemic circulation, resulting in an increase of about 50%–100% in right atrial pressure, cardiac preload, and central blood volume and about 10%–15% in cardiac output owing to improved cardiac inotropy.14,15 Meanwhile, systemic vascular resistance and, consequently, cardiac afterload decrease. Right ventricular pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure also increase after TIPS. Heart rate, although initially unchanged, may increase after several months. Plasma copeptin, aldosterone, and renin levels decrease, whereas norepinephrine levels increase after TIPS. Renal function may improve after TIPS through improved renal perfusion.14 Technique TIPS procedure TIPS procedure is usually performed by interventional radiologists under real-time fluorosocopic and ultrasound (US) guidance. It is typically created using a transjugular venous approach under general anesthesia or deep sedation. A hepatic vein is catheterized, and, from within that vein, the portal vein is punctured using a long-curved needle. Once the portal vein is accessed, portal venography and hemodynamic assessments are performed, followed by dilation and measurement of the intrahepatic parenchymal tract. Finally, an expandable PTFE-covered stent-graft is used to line the tract, from portal vein entry to the hepatic vein ostium (Fig. 2). A shunt can be created between the IVC and portal vein as well, termed the direct intrahepatic portosystemic shunt (DIPS). DIPS is indicated when the hepatic veins are occluded or unsuitable, as can occur with Budd-Chiari syndrome. Bare metallic stents are no longer used in TIPS because of their higher rate of stenosis and occlusion compared with PTFE-covered stents, the use of which has also been shown to associate with decreased bleeding and improved survival.16FIGURE 2: TIPS. The stent should cover the hepatic vein up to its ostium into the IVC to prevent dysfunction. The covered portion of the stent covers the parenchymal tract and the hepatic vein, whereas the uncovered portion of the stent is located in the portal vein.Pre-TIPS workup should ideally include cross-sectional imaging to have an adequate anatomical map of the portal vein and hepatic veins. In emergent situations, bedside Doppler-US might be an alternative. An echocardiogram should be performed to assess for the presence and severity of systolic and diastolic dysfunction and pulmonary hypertension. Recent AASLD guidance provides recommendations for preprocedural correction of coagulopathy.17 The goal of portosystemic diversion is to optimize the balance between improvements in ascites, nutrition, renal function, and bleeding against the risk of worsening hepatic encephalopathy, cardiac overload, and liver function. Thus, creating the smallest-necessary caliber shunt to balance those outcomes is desirable. Recent studies suggest that an 8-mm-diameter PTFE-lined TIPS may be sufficient to prevent variceal rebleeding and potentially decrease the incidence of hepatic encephalopathy18–21 while lessening the possibility of worsened hepatic decompensation compared with larger shunts. In fact, the use of the 8-mm stent may lead to a survival advantage compared with those of the 10-mm stent.21,22 Additionally, the use of the 8-mm diameter stent has been found to be superior to medical therapy in the prevention of rebleeding from esophageal varices.19 Distinct from previously available stents, which had a fixed diameter, a more recently introduced TIPS stent-graft (so-called "controlled expansion") allows a range of operator-determined shunt diameters to be created with a single shunt, between 8 and 10 mm. Hemodynamic Pressure Measurements and Goals The HVPG refers to the difference in intravascular pressure between the portal vein and the hepatic vein. During TIPS placement, direct portal pressures are measured and used to calculate the portosystemic pressure gradient (PSPG). As recommended by two recent consensus conferences,23,24 PSPG should be calculated by subtracting the suprahepatic (intra-abdominal) IVC pressure from portal pressure to better correlate with clinical outcomes.25 When the IVC pressure cannot be measured because of technical difficulty, the right atrial pressure is often used in lieu of IVC pressure, but this may lead to an overestimation of the PSPG because atrial pressure is generally lower than IVC pressure.23,24 Additionally, portal and systemic hemodynamics recorded during general anesthesia or conscious sedation, which are generally done in fasting conditions, may not reflect the "real" PSPG.26 Post-TIPS PSPG level is predictive of rebleeding risk because lower values are associated with lower bleeding recurrence and, inversely, predictive of post-TIPS complications such as hepatic encephalopathy and worsened liver function (lower values are associated with higher rates of complications).27 Thus, the PSPG decrease target must balance bleeding control with safety in an individualized approach by indication and patient profiles. In patients with acute, uncontrolled esophageal variceal bleeding, the desired post-TIPS PSPG is <12 mm Hg26,27 or a reduction ≥50% from baseline PSPG.28 However, the ideal post-TIPS PSPG for the management of gastric variceal bleeding is not well defined. The desired PSPG for secondary prevention of gastroesophageal variceal bleeding is <12 mm Hg. In a recent study, patients with a PSPG ≥12 mm Hg after TIPS had a 35% risk of recurrence of portal hypertension complications at 2 years, as compared with <5% in those with a PSPG <12 mm Hg.26 A PSPG >12 mm Hg at any time during follow-up was associated with 8.5-fold increase in the rate of recurrence of portal hypertension complications (bleeding and/or ascites).26 In patients not achieving a PSPG <12 mm Hg despite dilation of the stent to a maximum 10 mm of diameter, the addition of nonselective beta-blockers (NSBBs) should be considered because they might reduce portal pressure by an additional 20%–25%.29,30 Presence of PVT Acute or chronic bland (noncancerous) PVT are not a contraindication to TIPS, although the complexity of shunt creation and thrombectomy may require specialized technical skills. Various techniques such as transhepatic and trans-splenic approaches have proven useful in facilitating shunt creation, venous thrombectomy, and vascular recanalization.31,32 The success of TIPS in PVT is high, with 84% 1-year TIPS stent patency rate and 78% 1-year portal vein patency rate, although the incidence of major complications is 10%.33,34 TIPS failure and shunt dysfunction in the setting of PVT are affected by the degree of portal vein and superior mesenteric vein thrombosis and the presence of underlying thrombophilia.35 Portal vein recanalization and TIPS may also improve a patient's candidacy for liver transplantation36 by restoring patency to the portal vein, making it suitable for surgical anastomosis and graft perfusion. Variceal Embolization Embolization of gastric, esophageal, or ectopic varices may be performed during TIPS creation (see also the section on 4.2 on ATO). The indications for embolization include actively bleeding varices or persistent fugal variceal filling. In addition, embolization of enlarged portosystemic shunts (with or without varices) may be considered to prevent severe hepatic encephalopathy in patients receiving TIPS.37 Rebleeding may decrease with adjunctive antegrade embolization of residual varices in patients treated with TIPS for bleeding indications,38 but the results of two RCTs have been inconsistent.39,40 Ectopic and gastrofundal varices typically require embolization independent of shunt creation because downhill portosystemic flow through the varix may be incompletely diverted at target PSPG levels suitable for esophageal varices.Guidance statements PTFE-coated TIPS stents should be considered standard of care. When the indication for TIPS is variceal hemorrhage (treatment of acute hemorrhage or prevention of recurrence), TIPS should be progressively dilated (starting at 8 mm of diameter) to the minimum diameter needed to achieve a PSPG below 12 mm Hg. In patients whose PSPG does not decrease below 12 mm Hg despite maximum dilation of TIPS (10 mm), NSBBs should be added to further decrease portal pressure. Bland PVT does not preclude creation of a TIPS. Referral to experienced centers should be considered. In patients with large spontaneous portal systemic collaterals, collateral embolization at the time of TIPS placement may be considered because it may decrease the risk of hepatic encephalopathy. Contraindications Absolute contraindications for TIPS include congestive heart failure (stage C or D, or a documented ejection fraction <50%), severe pulmonary arterial hypertension (mean pulmonary artery pressure of >45 mm Hg), severe uncontrolled hepatic encephalopathy, and systemic infection or sepsis41 (Table 3). Untreated biliary obstruction and uncorrectable severe coagulopathy are relative contraindications. Creating a TIPS may be difficult in patients with polycystic liver disease, hepatic or portal vein occlusion, and intrahepatic tumors, although successful TIPS creation has been reported in these settings. Although higher model for end-stage liver disease (MELD) score is associated with higher mortality,42,43 no specific MELD threshold can be recommended to contraindicate TIPS. Most trials assessing the use of TIPS for variceal bleeding excluded patients with a Child-Pugh score >13 points. Patients over 75 years old have been also excluded from RCTs, and performing TIPS in patients over 70 has been infrequent.44 A recent study suggests acceptable outcomes of TIPS in highly selected patients over 70 years old.44 TABLE 3 - Summary of endovascular therapies in the management of variceal hemorrhage Variceal obliteration techniques RTO TIPS BRTO PARTO CARTO ATO Technique Percutaneously created portosystemic shunt connecting portal vein with hepatic veinTIPS can be performed with ATO.Might complement RTO Balloon occlusion of a GRS and retrograde injection of sclerosant agent, with ensuing gastric variceal obliterationBalloon occlusion maintained up to 36 hNeed for ICU monitoring The GRS is occluded with a vascular plug, and Gelfoam is injected retrogradely to obliterate the gastric varices. The GRS is occluded with coils, and Gelfoam is injected retrogradely to obliterate the gastric varices. Percutaneous transhepatic or trans-splenic embolization of portomesenteric veins supplying esophageal, gastric or ectopic varices using various embolic materialsATO can be performed with TIPS or RTO. Technical limitations Challenging in patients with PVT, biliary dilation, hepatic tumors, and polycystic liver Need for prolonged balloon occlusion (up to 36 h), with ICU monitoring during this periodMight not be possible in patients with shunts larger than available balloon diameters Might not be possible in patients with shunts larger than available plugs (<18 mm)Might not be possible in challenging anatomy, such as a very tortuous course from IVC to renal vein to GRS (Z-path) Might not be possible in patients with giant shunts larger than available coils (<30 mm)No anatomical limitation Might not be able to embolize multiple collateral veins supplying varices, resulting in early rebleeding from collateralsMore invasive than RTO because it requires direct percutaneous access through the liver or spleen or through TIPS Physiological effects Decrease in PSPGIncrease in COIncrease in cardiopulmonary pressures Decrease in portosystemic shuntingRedirection of flow through portosystemic collaterals to the liver, with potential improvement in liver function and hepatic encephalopathyIncrease in PSPG with the possibility of new complications of portal hypertension (ascites or esophageal variceal hemorrhage) Clinical context of use Variceal hemorrhage because of esophageal and GOV1, gastrofundal varices or ectopic varicesPreemptive TIPSSalvage TIPSRescue TIPS Secondary prevention Gastrofundal variceal hemorrhage with a GRS allowing retrograde access:Treatment of acute hemorrhage Prevention of rebleeding Treatment of ectopic varices with favorable anatomy (large and accessible efferent shunt) Variceal hemorrhage because of Esophageal varicesGastric varicesEctopic varices Contraindications Congestive heart failure (Stage C/D or EF <50%)Severe pulmonary hypertension with mPAP >45 mm HgSevere uncontrolled hepatic encephalopathyUncontrolled sepsis Splenic and/or portal vein thrombosis (needs sufficient hepatopedal flow capacity for blood flow redirection)Active sepsisUncontrolled esophageal variceal hemorrhage (would require simultaneous TIPS)Poor liver function or hepatic encephalopathy are not a limitation and might improve with RTO CoagulopathySplenic and/or portal vein thrombosis (unable to access these vessels)Active sepsis Procedural or short-term complications <5% frequencyIntraperitoneal bleedingArterial injuryLiver infarctCapsular punctureHemobiliaSepsisTIPS thrombosis/dysfunction Related to sclerosant escape to systemic and/or portal circulation:Renal vein thrombosisPVTPulmonary embolismAnaphylactic shockDisseminated intravascular coagulationAcute kidney injury Related to Gelfoam escape to systemic and/or portal circulation (rare)Renal vein thrombosisPVTPulmonary embolismPlug or coil migration into renal vein and causing nontarget embolization (rare) Related to embolic materials escape to systemic and/or portal circulation (rare)Renal vein thrombosisPVTPulmonary embolism Long-term complications Related to an increase in portal systemic shunt:New or worsening hepatic encephalopathyWorsening liver functionRelated to cardiac overloadCongestive heart failurePulmonary hypertension Related to the increase in PSPG New or worsening esophageal or ectopic varicesNew or worsening ascites and/or hepatic hydrothorax Follow-up Doppler-US study in1–4 weeks3 months6 months and6 months thereafter Contrast CT venogram or EUS in2–3 days prior to dischargeEndoscopic evaluation of gastric and esophageal varices in 1–2 months If normal, further imaging and endoscopic follow-up according to existing guidance Abbreviations: CO, cardiac output; EF, ejection fraction; EUS, endoscopic ultrasound; GOV1, gastroesophageal varices type 1; GRS, gastrorenal shunt; mPAP, mean pulmonary artery pressure; PVT, portal vein thrombosis. It is important to note that risk-benefit tradeoffs are different when TIPS is a last resort, life-saving procedure (e.g., uncontrolled variceal hemorrhage) versus when alternative treatments exist (e.g., secondary prevention of variceal hemorrhage or refractory ascites). Futility criteria for TIPS placement in the context of variceal hemorrhage are discussed later in this document. Complications Procedural complications during TIPS are rare (<5%) in contemporary series45,46 but may include intraperitoneal bleeding, arterial injury, liver infarct, hepatic capsular puncture, hemobilia, immediate TIPS thrombosis, and sepsis.47,48 Procedure-related deaths occur in <1%.46 The most relevant long-term complications are those related to shunting, mainly hepatic encephalopathy, deterioration in liver function, and complications related to cardiac overload (Table 3). The probability of developing at least one episode of hepatic encephalopathy ranges between 30% and 50%49–51 and that of severe, disabling encephalopathy is approximately 8%.50 Risk factors for hepatic encephalopathy are previous hepatic encephalopathy, older age, advanced liver dysfunction, kidney dysfunction, hyponatremia, sarcopenia, and a post-TIPS low PSPG.52 As mentioned previously, 8-mm TIPS stents (which are associated with higher post-TIPS PSPG) are associated with lower incidence of hepatic encephalopathy compared with that of 10-mm TIPS stents while maintaining similar effectiveness against variceal rebleeding and TIPS patency.19 In general, post-TIPS encephalopathy can be managed with medical therapy using lactulose and rifaximin in the vast majority of cases. In a recent double-blind multicenter RCT, prophylactic rifaximin, starting 2 weeks before TIPS placement, reduced the risk of overt hepatic encephalopathy.49 In 81% of the patients included in the trial, TIPS was performed to treat ascites, and the etiology of cirrhosis was alcohol-related in 86% of the cases. This leaves some uncertainty regarding the extrapolation of these results to patients with a bleeding indication for TIPS and with causes of liver disease other than alcohol. If encephalopathy is refractory to medical therapy, endovascular reduction techniques can be used to reduce TIPS diameter (TIPS recalibration).53 If the PSPG after TIPS reduction is greater than 12 mm Hg, the patient should be treated with NSBBs or undergo screening/surveillance endoscopy with endoscopic treatment of varices as appropriate. Portosystemic shunting might lead to a deterioration in liver function, but the incidence of this complication is difficult to estimate in the context of the natural progression of the underlying liver disease. TIPS induces a slight increase in bilirubin and international normalized ratio,54 without a signal for increased liver failure-related deaths.51,54,55 A recent prospective study showed a rate of cardiac decompensation of 20% after TIPS,56 but half of the patients experiencing decompensation had a previously diagnosed cardiomyopathy. Post-TIPS mortality related to heart decompensation was 5% within 1 year, which emphasizes the relevance of pre-TIPS cardiac evaluation. In a retrospective series, TIPS was associated with a new development of pulmonary hypertension in 4% of the patients.57 Follow-up after TIPS placement TIPS dysfunction, defined as the loss of portal venous decompression (resulting in