Interventional radiology in the management of portal hypertension

Abstract From being a mere (though important) diagnostic tool, radiology has evolved to become an integral part of therapy in portal hypertension today. Various procedures are currently available, the choice depending on the etiology and location of disease, the pathoanatomy, and the symptomatology. The main aim of any procedure is to reduce the portal pressure by either direct or indirect methods. This can be achieved with transjugular intrahepatic portosystemic shunt (TIPS), recanalization of the hepatic vein outflow, recanalization of the portal vein and its tributaries, recanalization of dysfunctional portosystemic shunts, partial splenic embolization, and embolization of arterioportal shunts. When any of these procedures cannot be performed due to anatomical or physiological reasons, the symptoms can often be controlled effectively with embolization of varices or balloon-occluded retrograde transvenous obliteration of varices (BRTO). This article briefly describes the procedures, their results, and their current status in the treatment of portal hypertension.

The role of the radiologist in the management of portal hypertension (PHT) has undergone a signiÞ cant metamorphosis over the last few decades.Initially, it was limited to determining the presence and cause of PHT, using angiographic techniques such as percutaneous splenoportography, transhepatic portography, and arterioportography.For many years these procedures were conducted frequently for planning surgical treatment; later, they were replaced by safer and equally reliable modalities such as USG, CT scan and CT angiography (CTA) and MRI and MRI angiography (MRA).
Progressively, the focus changed from diagnostic to therapeutic procedures.Interventions involving the portal venous system were introduced in the 1970s, beginning with transhepatic embolization for control of gastric and esophageal variceal bleeding.The subsequent decade saw an expansion in the variety of therapeutic interventions, with procedures such as transjugular intrahepatic portosystemic shunt, portal vein recanalization, balloonoccluded retrograde transvenous obliteration of varices, hepatic venous outß ow angioplasty, and revision of surgical shunts being rapidly introduced one aft er the other.Since then radiological interventions have become established methods in the treatment of PHT.

Interventions in PHT
The primary goal in treating portal hypertension is reduction in the portal venous pressure itself.This should mitigate the complications of portal hypertension such as bleeding from varices and congestive gastroenteropathy, accumulation of ascites and hydrothorax, or the hepatorenal syndrome, etc.When it is not possible to achieve this primary goal, various procedures can be off ered to palliate or control the symptoms related to portal hypertension.The procedure involves many steps: (1) puncture of the jugular vein, (2) cannulation of the hepatic vein, (3) passage of a long needle from the hepatic vein, through the liver parenchyma and into the portal vein, (4) dilatation, with an angioplasty balloon, of the parenchymal tract created by the needle, and (5) stent deployment to ensure patency of the tract.Usually an 8-10 mm diameter stent is chosen to adequately decompress the hypertensive portal circulation to achieve a final portosystemic gradient of less than 12 mm Hg [Figure 1].
TIPS was conceived as early as 1969, when Rösch reported this method in a series of dog experiments using Teß on tubes as stents. [1]It has since then matured from an experimental procedure into an established technique and has replaced surgical shunts in most centers where it is available.It has proved to be eff ective in treating various complications of PHT [Table 1]. [2]PS is contraindicated in patients with congestive heart failure, severe pulmonary hypertension, severe tricuspid regurgitation, hepatic failure, preexisting encephalopathy, unrelieved biliary obstruction, multiple hepatic cysts, and uncontrolled systemic infection.Relative contraindications include the presence of large liver tumors, hepatic vein thrombosis, portal vein thrombosis, thrombocytopenia (<20,000/cm 3 ) and severe coagulopathy (INR >5). [2]PS is successful in more than 95% of patients and is generally safe, with a procedural mortality of <1%.The 1-month mortality, however, is variable and can be as high as 40%, in patients with limited hepatic reserve.This poor outcome can be predicted using various prognostic indicators such as serum bilirubin ( >3 mg/dl), Child-Pugh score ( >12), modiÞ ed MELD score (>25), APACHE II score (>18), or Emory risk score (>3). [3][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21] The long-term results of TIPS are impaired by the high rate of shunt dysfunction from intimal hyperplasia and the resulting recurrence of symptoms [Figure 2].The primary patency rate at 1, 2, 3, 4, and 5 years is 25-66%, 5-42%, 21%, 13%, and 13%, respectively.If a regular Doppler or angiographic surveillance of TIPS is done, early shunt stenosis can be detected and patency enhanced by a secondary balloon dilation or restenting.The resulting primary assisted patency rates approximate 85%, 61%, 46%, 42%, and 36% at 1, 2, 3, 4 and 5 years, respectively, and the cumulative secondary patency rates increase to 85-96% and 64-90% at 1 and 2 years, respectively. [22]However, this calls for reliable follow-up, more interventions, and a cumulative increase in expenditure incurred.The introduction of stent-graft s has largely mitigated this problem, with 1-year primary patency rates of >80% [23,24] [Figure 3].In studies comparing bare stents and stent-graft s, the latt er have been shown to provide much bett er patency rates. [25]ke any other portosystemic shunt, TIPS can be responsible for encephalopathy in up to 50% of patients.Fortunately, most of these episodes are mild and only medical management is necessary.In 3-7% cases, this encephalopathy can be severe or recurrent, necessitating a shunt reduction. [26]

Recanalization of Hepatic Venous Outß ow
Budd-Chiari syndrome includes all obstructions to the hepatic vein outß ow at the level of the hepatic vein and/or the inferior vena cava.This causes hepatic congestion which, when left untreated, progresses to hepatic necrosis and Þ brosis.The aim of treatment is to restore physiological ß ow, i.e., to recanalize the hepatic vein and/or the inferior vena cava by balloon angioplasty and stenting thus relieving the hepatic congestion and preventing progression to irreversible liver damage. [27]This is feasible if the obstruction is over a short segment [Figures 4 and 5].Long segment hepatic vein occlusion is diffi cult to reopen and even if restored the reocclusion rates are extremely high.This subgroup of patients would need a portosystemic shunt.Surgical     portocaval shunts are diffi cult to create, due to the large caudate lobe not allowing easy access to the portal vein.Also, portocaval shunts may not be successful, as the shunt oft en opens into a hypertensive cava due to caval compression by an enlarged caudate lobe.TIPS has increasingly been performed in such patients as it is associated with much less morbidity and can provide very gratifying results [Figures 6  and 7].In addition, TIPS opens high into the inferior vena cava and is not aff ected by any compression by the enlarged caudate lobe.In the few published case series, ascites control is close to 100%, and there is improvement in liver function, obviating the need for transplantation in most cases. [28,29]

Recanalization of the Portal Vein and Its Tributaries
Extrahepatic obstruction of the portal vein or its branches can induce a focal PHT; this accounts for 5-10% of all cases of PHT.The cause of obstruction can be benign or malignant, and patients usually present with variceal bleeding, ascites, or abdominal pain.Recanalization of the blocked vein by angioplasty and stenting will reduce these symptoms and can be done either via a transjugular or a percutaneous transhepatic route [Figure 8]. [30,31]

Embolization of Arterioportal Fistulae
Arterioportal fistulae (APF) are a rare cause of PHT.They may be congenital or secondary to trauma, surgery, percutaneous biopsy or other liver procedures, and liver tumors.Although silent most of the times, some patients with large APFs can present with features of PHT such as bleeding, ascites, and splenomegaly.The preferred treatment is transarterial embolization of the feeding artery, using coils, detachable balloons, or glue.The procedure is usually successful, provided the Þ stula is not too large and is accessible. [32]rtial Splenic Embolization (PSE) PSE is performed to diminish inß ow of blood into the portal vein, with secondary reduction of the portal venous pressure.The procedure involves superselective catheterization and embolization of the intrasplenic arterial branches, usually with polyvinyl alcohol particles.This achieves reduction of portal vein pressure, reduction in splenic size, and improvement in hypersplenism-induced thrombocytopenia. [33]The results of treatment are good and the rate of serious complications (e.g., splenic abscess or sepsis) with current techniques is low.

Percutaneous Transhepatic Variceal Embolization (PTE)
PTE was the earliest intervention performed for portal hypertension and was Þ rst described by Lunderquist and Vang in 1974 to treat intractable variceal bleeding.In this technique, the portal vein is catheterized by a percutaneous transhepatic approach and the gastric vein feeding the varix is embolized with ethanol, steel coils, or cyanoacrylate glue [Figure 9].When Þ rst described, PTE appeared to be a highly eff ective procedure, successfully controlling bleeding in 70-90% of patients.However, the underlying PHT was unaff ected and, consequently, bleeding recurred in 38-70% of patients within 6 months and in 71-90% aft er 2 years.In addition, it carried a failure rate of 9%, particularly in patients with portal vein thrombosis or small livers with marked ascites. [34]PTE itself was responsible for inducing portal vein thrombosis in up to 36% of patients. [35]All these factors, and the emergence of endoscopic therapy (EST), led to a decline in the procedure; EST had bett er survival rates and lower rebleeding rates.The introduction of TIPS and BRTO further antiquated the procedure, and PTE is now very rarely performed.

Balloon-occluded Retrograde Transvenous Obliteration of Varices (BRTO)
BRTO is a technique that is popular in Japan for control of gastric varices through a natural gastrorenal shunt.
The technique involves advancing a balloon catheter from the femoral vein into the outlet of the gastrorenal shunt.Following balloon occlusion of the shunt, sclerosant (5% ethanolamine oleate) is injected retrogradely to Þ ll the gastric varices.Aft er adequate contact of the sclerosant with the variceal wall, the sclerosant is aspirated and the balloon catheter withdrawn.Considered by many to be as eff ective as TIPS in controlling gastric variceal bleeding, it has an added advantage in that it augments portal blood ß ow by occluding the natural shunt that takes blood away from the portal vein.This improves liver function in cirrhotic patients and also prevents encephalopathy, a problem commonly associated with TIPS. [36]However, occlusion of the gastrorenal shunt may aggravate existing esophageal varices or lead to the development of new ones, and this is one the most signiÞ cant complications of BRTO. [37]rcutaneous Peritoneovenous Shunt Surgical peritoneovenous shunts have been replaced by TIPS in most centers but are still off ered to patients who cannot tolerate a TIPS.However, surgery in this high-risk group is associated with the morbidity of general anesthesia.These shunts can now be inserted by radiologists with less risk as the procedure is done under local anesthesia.In addition, venous entry puncture can be more precise, and access is easier, with USG guidance. [38]

Conclusion
There are various interventional procedures that can be off ered to patients with PHT.The choice of the procedure is based on the etiology of PHT, the symptoms, the clinical status, and the results of imaging studies.Most procedures now off er high success rates, good mid-and long-term results, and signiÞ cantly less morbidity than the corresponding surgical procedures, and this has led to the emergence of interventional radiology as the procedure of choice in controlling PHT and its complications.

Figure 1 (
Figure 1 (A, B): TIPS performed in a patient with uncontrolled variceal bleed.Portal venogram (A) obtained after puncture of the portal vein shows retrograde fi lling of the left gastric vein and feeding of a large junctional varix.The portosystemic gradient was recorded at 21 mm Hg.The post-TIPS venogram (B) shows good fl ow across the TIPS.Adequate decompression is evident from the non-fi lling of the left gastric vein and varices and reduction of the portosystemic gradient to 4 mm Hg

Figure 2 :
Figure 2: Mid-shunt stenosis (arrow) in a Wallstent, causing reappearance of varices and ascites.This was treated by balloon dilatation

Figure 4 (Figure 5 (Figure 6 (
Figure 4 (A, B): Budd-Chiari syndrome due to membranous obstruction of the inferior vena cava in the suprahepatic segment.Cavogram (A) shows a 4-cm long occlusion (arrow) of the inferior vena cava above the right hepatic vein (arrowhead); after needle fenestration of the occluded inferior vena cava through the femoral route, a stent is deployed across the occluded segment (B).The inferior vena cava is widely patent after stenting

Figure 3 :
Figure 3: The Viatorr stent-graft device has a bare lower end that lies in the portal vein (arrow) and an upper covered end that bridges the liver parenchymal tract (arrowheads); the transition between the two is marked by an opaque ring (open arrow).When appropriately positioned, the bare end in the portal vein allows fl ow into the intrahepatic portal veins and the covered segment prevents intimal hyperplasia from blocking the shunt

Figure 7 (Figure 8 (Figure 9 (
Figure 7 (A, B): Contrast-enhanced CT scan of a patient with Budd-Chiari syndrome, before TIPS (A) and after TIPS (B), showing improvement in enhancement pattern of the liver parenchyma and regression of ascites following TIPS