Question 2 from the first paper of 2011 was the only SAQ to ever delve into this topic in any great detail, until Question 16 from the first paper of 2019. The candidates were expected to know what TIPS is, why it is used, what indications for it there might be, and which complications one might expect. In view of such detailed questions, a summary chapter was constructed which contains equally detailed answers. The most relevant literature source for this is probably the nostalgic review article by Martin Rössle, "TIPS: 25 years later" (Hepatology, 2013).
The transjugular intrahepatic portosystemic shunt procedure
TIPS is a conduit for portal venous blood to bypass the ineffective liver and thereby relieve portal hypertension. The transjugular variety of this procedure has existed for decades. After Joseph Rösch's group perfected the procedure in about 40 dogs, it took a further eleven years years unleashed the thing on cirrhotic humans (Colapinto et al, 1982). Obviously there is no natural law which requires for this concept to be limited to percutaneous radiologically guided affairs. Prior to TIPS being T, just IPS was available as a surgical procedure. Orloff (1966) describes this portocaval shunt as "the definitive treatment for portal hypertension and esophageal varices".
The procedure itself
in its modern form, the procedure takes 1-2 hours. Its history is well described by Harold Conn (1993). The first human study reported using a Grüntzig balloon catheter, which is a standard angioplasty balloon dilation device. A catheter is passed though the jugular vein (that's the "transjugular" component) and introduced into the middle hepatic vein. Over this catheter, a modified Ross needle (these days called a Colapinto needle) is stabbed through the liver parenchyma and into the left portal vein.
At this stage, one is able to measure the portal pressure directly, which is a rare opportunity. The hole between veins is then dilated with the balloon, usually 9-10mm in diameter. In the original paper, the balloon was left in situ for up to 12 hours, and then deflated. Colapinto et al would have called it a day at this stage. These days, we finish by placing a mesh stent through the defect, thereby maintaining patency of the shunt.
The procedure itself is improved if the patient has recently had their ascites drained (this places the liver in a more favourable position). A CT should be performed to map the anatomy. Furthermore, a TTE should be performed to confirm that there is no severe right heart failure, and that a vigorous tricuspid regurgitation jet is not going to contribute to portal hypertension by blowing right venticular ejecta back up the new shunt. It would be supremely ridiculous to perform a TIPS and suddenly discover that systemic central venous pressures were higher than the portal venous pressures. The general recommendation is to reduce the portal pressure to below 12mmHg (if you're trying to control varices, anyway) and so a CVP persistently in excess of 12mmHg is obviously going to be counterproductive.
Mechanism by which TIPS acts
The main objective of this procedure is a fairly crude mechanical one. In short, the rationale for a TIPS can be summarised as follows:
- Portal hypertension causes the majority of the morbidity from chronic liver disease
- This is due to raised portal pressure
- TIPS decompresses the portal circulation by allowing it to empty into the comparativbely lower central venous circulation
- Ergo, TIPs should relieve the majority of the morbidity from chronic liver disease
Indications for a TIPS procedure
Indications for TIPS include:
- Refractory ascites or hepatic hydrothorax
- Refractory rebleeding in variceal disease
- Hepatorenal syndrome
- Hepatopulmonary syndrome
- Bridge to liver transplant
- Hepatic vein thrombosis
- Hepatic veno-occlusive disease
- Portal vein thrombosis
Portal vein thrombosis is at the same time an indication for TIPS, a relative contraindication to TIPS and a complication of TIPS. This sort of doublethink (triplethink?) is made possible by the diversity of experience in interventional radiology. That is a kind way of saying that it should not be attempted by the novice, as it presents several technical challenges. Basically, there are three main problems.
One problem is the brutally stupid problem of a vessel blocked by bulky clot, i.e. the shunt can be deployed into the clot with zero flow across it. One might therefore consider the complete absence of any patent intrahepatic portal branches to be an absolute contraindication. One might then be tempted to delay the procedure until the clot dissolves somewhat, but then the result might be either the atrophy of the portal vein (i.e. it becomes a smaller target with more fragile walls) or - more likely - the formation of a portal cavernoma, which is basically like an intrahepatic caput medusae- multitudinous dilated collaterals snaking through the hepatic hilum to bypass the site of thrombosis. According to Perarnau et al (2010), this was the most common cause of TIPS failure in the group of patients with portal vein thrombosis. The successful stent deployment rate in the cavernoma group was only about 63%, as compared to 83% for the rest of the portally thrombosed patients and 99% for the patients with a patent portal vein. Overall the rate of successful deployment and complications was such that the authors were forced to include portal vein thrombosis in the list of indications for TIPS.
Complications and contraindications of TIPS
Friedman et al (1993) have complied a comprehensive review of the most common complications of TIPS. Some memorable specific complications include:
- Vascular access complications
- Hepatic damage (through-and-through puncture): risk of intraperitoneal haemorrhage is 1-2%
- Haemobilia (damage to the biliary tree)
- Shunt stenosis or thrombosis (it happens in up to 70%)
- Shunt migration
- Hepatic vein stenosis (this can sabotage a future transplant)
Complications from portal venous shunt:
- Worsening hepatic encephalopathy
- Shunt thrombosis or portal vein thrombosis (7-10%). If there is already a portal vein thrombosis, this risk appears to increase somewhat (Perarnau et al, 2010) - which probably reflects the overall prothrombotic diathesis.
- Bilirubin rise: the diseased liver doesn't even get a chance to metabolise it
- Ischaemic hepatitis: the liver gets much of its oxygen from the portal vein, and even in spite of the hepatic arterial buffer response there is a risk of ischaemic hepatitis.
- Right heart failure (the venous return to the heart is increased. The RV may not be prepared for this)
- Tricuspid endocarditis (organisms may now travel directly from the leaky gut into the systemic circulation)
- Haemolysis (due to the direct shearing effect of being in contact with the shunt)
- "Unmasked" cardiomyopathy: the TIPS returns splanchnic blood to the heart and acts as a volume challenge, and if there was pre-existing cardiomyopathy, it may be dramatically revealed in this manner.
- Shunt infection may occur, where the shunt may become the source of infection. The college refer to this as "endotipsitis", which (it turns out) is not a cute neologism but a serious part of medical language, even though technically speaking the synthetic shunt is not itself inflamed. Bouza et al (2004) attributed it to DeSimone et al (2000), who supposedly coined the term, but it does not appear anywhere in their paper. Instead, the first mention of it seems to be in earlier article by Sanyal & Reddy (1998). It is supposed to reflect the fact that persistent bacteraemia resembles bacterial endocarditis. The use of the term has increased in popularity, in spite of the fact that it is an abomination.
Contraindications for portal venous shunt (Boyer and Haskal, 2009)
- Absolute contraindications:
- Moderate to severe pulmonary hypertension
- Congestive heart failure
- Multiple hepatic cysts
- Uncontrolled sepsis
- Uncontrolled biliary obstruction
- Total portal vein thrombosis (in the absence of any patent intrahepatic branches)
- Relative contraindications:
- A MELD score above 18
- Central hepatocellular carcinoma
- Portal vein thrombosis (in the absence of an experienced operator)
- Hepatic vein thrombosis
- Severe coagulopathy or thrombocytopenia