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TIPS procedure in the management of portal hypertension and variceal hemorrhage. C. Matthew Mitchell M.D. Portal Hypertension. Defined as a portal-systemic pressure gradient of 12mm Hg or greater.
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TIPS procedure in the management of portal hypertension and variceal hemorrhage. C. Matthew Mitchell M.D.
Portal Hypertension • Defined as a portal-systemic pressure gradient of 12mm Hg or greater. • Portal hypertension results from increased vascular resistance within the portal system. As portal pressure increases, up to 90% of portal blood flow is shunted through portal-systemic collateral pathways resulting in the formation of varices over time. • Classified as pre-sinusoidal, sinusoidal, and post-sinusoidal.
Portal Hypertension • Pre-sinusoidal causes: • Portal vein thrombosis/cavernous transformation, splenic vein thrombosis, extrinsic compression of portal vein (tumor, polycystic disease, granulomatous disease. • Sinusoidal causes: • Cirrhosis of any etiology, schistosomiasis, veno-occlusive disease. • Post-sinusoidal causes: • Right sided heart failure, constrictive pericarditis, Budd-Chiari syndrome
Portal Hypertension • Cirrhosis is by far the most common cause of portal hypertension. In the United States, alcoholic cirrhosis is the most common subtype, with chronic hepatitis the second most common. • In cirrhosis the increased vascular resistance occurs at the hepatic microcirculation (sinusoidal portal hypertension). This is not only a mechanical consequence of hepatic architectural distortion, but a dynamic component also exists due to the active contraction of myofibroblasts, activated stellate cells, and vascular smooth-muscle cells of the intrahepatic veins. • Portal blood flow is also increased due to excessive physiologic release of endogenous splanchnic vasodilators.
Portal Hypertension • Varices are a common manifestation of portal hypertension. • Prevalence of gastroesophageal varices in cirrhosis varies between 30% (patients with compensated cirrhosis) and 70% (patients with decompensated cirrhosis). • Risk of hemorrhage is approximately 30% within the first year after their identification.
Portal Hypertension • Acute variceal hemorrhage is life threatening and requires a multidisciplinary approach for effective treatment. • Management may involve gastroenterologists, hepatologist, critical care physicians, surgeons, and interventional radiologists.
Portal Hypertension • The principle components of therapy include airway management, hemodynamic stabilization, control of variceal hemorrhage, and alteration of the hemodynamic effects of portal hypertension (decompressive procedures).
Portal Hypertension • Endoscopy is performed early in the course of management in an attempt to localize the bleeding and treat the varices. • Generally two types of endoscopic therapies are available; variceal banding and sclerotherapy. • Endoscopy has limitations including failure to localize all bleeding sites secondary to excessive hemorrhage, inability to treat all bleeding sites, and the failure of banding/sclerotherapy to control hemorrhage.
Portal Hypertension • Other adjunctive medical therapies include the use of B-blockers, octreotide, and vasopressin to decrease portal blood flow and portal pressures. • Sengstaken-Blakemore tube is used for tamponade of variceal hemorrhage. • Most often endoscopy either alone or in combination with adjunctive therapies is effective in controlling acute variceal hemorrhage. Patients who do not respond are referred for flow diversion therapies (TIPS, DIPS.)
Varices Sengstaken-Blakemore tube.
TIPS • Transjugular Intrahepatic Portosystemic Shunt • Interventional radiology is generally the next step in management after failed endoscopic treatment of variceal hemorrhage. • Typical patient has tenuous hemodynamic status, is intubated, with marginal liver function or fully decompensated cirrhosis. • Never presents during daylight hours.
TIPS • Pre-TIPS workup generally involves review of available cross sectional imaging, pertinent lab data, and patient history. • Complete blood count, renal function parameters, liver function tests, ammonia levels, and coagulation profiles are essential. • Imaging studies allow pre-procedural assessment of portal vein and liver anatomy, portal vein patency, and the presence of varices or other portosystemic shunts which may compete with the TIPS shunt.
TIPS • Absolute contraindications to TIPS include right heart failure and pulmonary arterial hypertension, rapidly progressing liver failure. • Relative contraindications include encephalopathy, polycystic liver disease (hemorrhagic complications), active sepsis, and chronic organized portal vein thrombosis. • TIPS is of unclear survival benefit in patients with sever liver disease (Child-Pugh C or MELD >22), however procedure is often done as only alternative is exsanguination.
TIPS • Post procedure outcome is heavily governed by the pre-TIPS condition of the patient. Liver function parameters and presence of other co-morbidities greatly influence outcome. • Patients with advanced liver disease generally will not tolerate further deprivation of nutrient portal flow that occurs with shunt creation, which can lead to accelerated liver failure. Thus, salvage therapy with TIPS is important in the acute setting but may not prolong midterm survival.
TIPS • One report of pooled data from 509 acute variceal hemorrhages treated with TIPS described control of variceal in bleeding in 93.6 % +/- 6.7%, with an early rebleeding rate of 12.4% +/- 6.1%. In spite of this, the same study reported a 6 week mortality of 35.8% +/- 16%, reflecting the presence of severe comorbidities (advanced liver disease, multi-organ system failure, ARDS).
TIPS • Once variceal hemorrhage as occurred and the patient survives the herald bleed, risk of rebleeding is at least 50%. • Portal decompressive procedures are much more effective than endoscopic treatments at lowering rebleeding risk, although the risk of hepatic encephalopathy is higher. • Multiple randomized trials have shown the rebleeding rate for TIPS was approximately 16% versus 44% for endoscopic therapy. Survival was rarely improved however, again pointing to the progressive nature of advanced liver disease and ultimate need for transplantation.
TIPS • There is no evidence to support the use of portal decompressive procedures for primary prophylaxis of variceal bleeding following initial diagnosis of varices. • TIPS results in higher rates of encephalopathy versus medical management, at a higher cost. Bleeding rates are lower, but no clear survival benefit is shown.
TIPS • Reported major complication rate is 2-3%. • Hemoperitoneum • Stent migration • Hemobilia • Radiation skin burn • Hepatic infarction • Renal failure • Death • Severe uncontrolled hepatic encephalopathy • Liver failure • Bowel or gallbladder injury • Right heart failure/CHF
TIPS • Reported minor complication rate is 3-4%. • Transient renal failure • Encephalopathy controlled with medication • Hepatic arterial injury • Fever • Access site hematoma • Transient pulmonary edema
TIPS • Technical success rate is above 90%. There are instances where portal vein anatomy and orientation relative to the hepatic veins makes the procedure extremely challenging, and occasionally it is not possible to successfully perform the procedure in the standard fashion. Cirrhosis may cause significant segmental and lobar atrophy, altering the size of the vessels as well as their spatial relationship.
Hepatic Vein Anatomy • Normal (Classic) anatomy. • 3 main hepatic veins (right, middle, and left) drain into the IVC approximately 1 cm below the diaphragm and 2cm below the right atrium. • Accessory hepatic veins drain the caudate lobe (segment I) directly into the IVC.
Hepatic Vein Anatomy • The right hepatic vein is the largest vein, draining the largest hepatic volume (segments V-VIII), and entering along along the posterolateral aspect of the IVC. • The middle hepatic vein drains the inferior aspect of the anterior segments (V and VIII) and the inferior aspect of the medial segment of the left lobe (IVB). It forms a common trunk with the left hepatic vein in 85% of the population, entering into the anterolateral aspect of the IVC. • The left hepatic vein is the smallest vein, draining the left lateral segments (II and III) and superior medial segment (IVA).
Portal system functions to conduct nutrient venous return from the GI tract to the liver. Approximately 2/3 blood supply to the liver is via the portal system, with the remainder supplied by the hepatic artery. Portal Vein Anatomy
Portal Vein Anatomy • The main portal vein enters the liver at the porta hepatis enveloped in a thick fibrous peritoneal reflection, where it then divides into the right and left portal veins. The MPV bifurcation is extrahepatic in 48% of the population, which has clinical implications in TIPS. • The right portal vein divides into anterior and posterior branches. • The left portal vein is longer, dividing into medial and anterior branches.
Portal Vein Anatomy • Anatomic portal vein variations are found in 10-20% of the population. Trifurcation occurs in 10.8-12.4%; right posterior segment branch arises from the MPV in 4.7-9.2%; right anterior segment branch arises from the LPV in 4.3%. Clinical significance is that there are several smaller branches instead of 1 main larger right trunk, making TIPS creation more challenging.
Portal Vein Tributaries • Superior mesenteric V. • • Intestinal veins • • Ileocolic vein • • Right colic vein • • Middle colic vein • • Inferior pancreaticoduodenal • • Right gastroepiploic vein • Splenic vein • • Inferior mesenteric vein • • Left colic vein • • Sigmoid veins • • Superior hemorrhoidal veins • • Pancreatic veins • • Left gastroepiploic vein • • Short gastric veins • Coronary vein • Cystic vein • Paraumbilical veins
Portocaval anastamoses • Esophageal anastomosis: coronary or short gastric (portal)- azygos (caval). • Paraumbilical anastomosis: paraumbilical vein (portal) - epigastric veins (caval). • Rectal anastomosis: sup. hemorrhoidal (portal) - inferior and middle hemorrhoidal veins (caval). • Retroperitoneal anastomosis: visceral vein of Retzius (portal) - parietal vein (caval).
Hepatic anatomy • Spatial relationship between the hepatic and portal veins. • The RPV is anterior and medial to the RHV, and posterior and lateral to the MHV. • The LPV is inferior to the MHV, and inferior and medial to the LHV. • Knowledge of spatial orientation and associated anatomic landmarks are critical for successful completion of TIPS procedure.
TIPS • TIPS procedure is performed under general anesthesia, with careful hemodynamic monitoring and attention to volume status. Aggressive volume resuscitation may complicate post procedure outcome and contribute to congestive failure once shunt is created. • Coagulation parameters are corrected if necessary with platelets or fresh frozen plasma. 2 units PRBC should be on standby during the procedure.
TIPS • Paracentesis performed prior to case if large volume ascites is present. This reduces the risk of infection and potential bleeding should the liver capsule be inadvertently punctured during the procedure.
TIPS • Minor inter-operator variations exist on how the procedure is performed; the fundamental aspects of the procedure such as portal vein access and stent deployment are basically standard among operators. • Several TIPS kits exist from different manufacturers, primarily differing in their portal vein access needle/sheath combination.
TIPS Colopinto needle Rosch-Uchida needle
TIPS • Jugular vein access obtained under ultrasound guidance. • Access sheath exchanged for 12 fr vascular sheath. • Hepatic vein accessed using catheter and guidewire (operator dependent). • Right hepatic vein preferred over middle and left. Anatomic variations or clinical circumstances dictate which hepatic vein is used.
TIPS • Wedged portal venogram performed using either CO2 or iodinated contrast with balloon occlusion catheter. • Excessive force when performing the wedged venogram may lacerate the liver and rupture the capsule.
TIPS • Portal access needle and sheath advanced into hepatic vein. • Portal vein is accessed using needle-sheath combination under fluoroscopic guidance. • Knowledge of hepatic and portal vein anatomy critical during this step.
Injection of contrast through access needle opacifying right portal vein
TIPS Portovenograms showing coronary and short gastric varices, retrograde IMV flow
TIPS Splenic vein, short gastric varices Gastric coronary, pyloric, and short gastric varices
TIPS • Once access into the portal vein is confirmed, a measuring pigtail catheter is advanced over a guidewire into portal vein. A calibrated portogram for stent measurement is performed. • Periportal fibrosis may necessitate use of angioplasty to dilate portal vein wall for advancement of catheter/sheath.
TIPS • Right atrial and portal venous pressure measurements are obtained. • Angioplasty of the hepatic parenchymal tract between the hepatic vein and portal vein performed to facilitate sheath advancement and stent deployment. • 10 fr sheath advanced into main portal vein for stent deployment.