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1. Portal hypertension results from increased resistance to portal blood flow and increased blood flow into the portal system, leading to complications like variceal bleeding and ascites. 2. Surgical management of portal hypertension aims to decrease portal pressure and treat complications. Procedures include devascularization to reduce variceal blood flow or decompression procedures to reduce portal venous pressure. 3. Decompression procedures include selective shunts that decompress only the variceal compartment or non-selective shunts like portocaval shunts that provide complete decompression. The distal splenorenal shunt is a commonly used selective shunt that preserves some portal flow to the liver.
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shmabhavi.pptx
- 1. Portal Hypertension management Dr. ShambhaviSharma 3rd year Resident PAHS Moderator : Dr Shantabir Maharjan
- 2. Introduction • Portal hypertensiondefined as portal vein pressure above 5-8mm Hg • Hepatic-portal vein pressure gradient(HVPG) more than 5 mm Hg
- 3. Pathophysiology of portalhypertension Structural changes (fibrosis, scarring, vascular thrombosis etc) Increased Hepatic Resistance Dynamic changes (vascular smooth muscle and stellate cell contraction) PORTAL HYPERTENSION Splanchnic Vasodilation Increased Portal Blood Inflow Effective Hypovolemia Activation Of Endogenous Vasoactive System Na Retention Hypervolemia Increased Cardiac Index
- 4. Clinical manifestations ofportal hypertension where surgery is required Cirrhotic 1. Uncontrolled or recurrent Variceal bleeding 2. Liver failure 3. Refractory ascites Non cirrhotic 1. Hypersplenism 2. Symptomatic splenomegaly 3. Growth retardation 4. Portal biliopathy 5. Uncontrolled or recurrent Variceal bleeding
- 5. Surgical approach • Primarytherapy : sinistral portal hypertension (isolated splenic vein thrombosis) • Rescue therapy : 1. Emergency 2. Elective
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- 7. Management for acutevariceal bleeding • Resuscitation • Achievement of hemostasis • Prevention of complications
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- 9. If bleeding cannotbe controlled or endoscopy delays Baloon tamponade • considered a temporary bridge to more definitive measures of variceal hemorrhage control • control refractory bleeding in up to 90% of patients Contraindications: • History of esophageal strictures • Recent gastric or esophageal surgeries
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- 11. • Potential forcomplications: • aspiration • airway obstruction • esophageal perforation due to overinflation or pressure necrosis Use should not exceed 36 hours to avoid tissue necrosis
- 12. • Sengstaken Blakemoretube • Minnesota tube Orthotropic liver transplantation Transjugular intrahepatic portosystemic shunt
- 13. Transjugular intrahepatic PortoSystemic shunt (TIPS) Involves implantation of a metallic stent • between an intrahepatic branch of the portal vein and a hepatic vein radicle • The needle track is dilated until a portal pressure gradient of ≤12 mmHg is achieved.
- 14. TIPS (contd.) • TIPSfor control of acute variceal bleeding: 93 - 95 % • 1-month actuarial probability of rebleeding : 22% • Operative mortality (30 days) : 28%.- 37% • Complications : 13% • massive hemoperitoneum • cardiorespiratory arrest & cardiac failure • acute renal failure • bacteremia Banares R, Am J Gastroenterol. 1998 Bosch J. J Hepatol 2001
- 15. Contraindications for TIPS Rightheart failure --most significant --acute death from total heart failure (Peron et al, 2000) • Older age of patient • High MELD or Child ough score • Cavernous transformation • Polycystic liver disease • Active spontaneous bacterial peritonitis (SBP)
- 16. TIPS Advantage • Non-operative approach •Ideal in short term portal decompression in patient requiring liver transplant until donor is available • Advanced hepatic functional decompensation who are unlikely to survive long enough for TIPS to malfunction Disadvantage Shunt stenosis or shunt thrombosis ( upto 50%) within first year Recurrent portal hypertensive bleeding Total shunt occlusion in 10-15% of patients
- 17. TIPS vs Endoscopictherapy • Rebleeding = 19 vs 47% • Encephalopathy = 34% in TIPS
- 18. TIPS vs Surgery(Distal splenorenal shunt) Randomised trial • 73 DSRS & 67 TIPS (Child Pugh A and B patients) • Follow-up: 2-8yrs • DSRS and TIPS similar in efficacy in the control of refractory variceal bleeding • rebleeding : DSRS, 5.5%; TIPS, 10.5%; P = .29 • Re-intervention: significantly greater for TIPS compared with DSR(DSRS, 11% v/s TIPS, 82%, p<0.001) • No difference in need for Liver Transplantation The choice is dependent on available expertise . Henderson JM, et al, Gastroenterology, May 2006
- 19. Devascularization procedures • Reduceblood flow to varices • Interrupt bleeding source • Eliminate the complications of splenomegaly (hypersplenism) Advantages : • Easy technique • Low mortality • Low recurrent variceal bleeding rate • Postoperative encephalopathy is rare - preserving of portal blood flow • Liver function well preserved
- 20. SUGIURA procedure • Disadvantage: •Thoracic approach • Abdominal approach • Mortality distribution: 4,3% (Child A, B), 17%(Child C) • Recurrent variceal bleeding rate < 5 % D.Vagotomy and pyloroplasty Modified sugiura procedure
- 21. Hassab operation • Gastro-esophagealdecongestion and splenectomy • Perhiatal devascularization of lower esophagus • Complete separation of the stomach from its bed • Ligation of the left gastric artery at the lesser curvature, peritonization of greater curvature and suction drainage of the splenic bed
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- 23. Indication for surgery Absolute •Symptomatic hypersplenism (recurrent bleeding or infection) • Severe thrombocytopenia (<10000) • Symptomatic or medically refractory hepatic encephalopathy • Hepatopulmonary syndrome • Portopulmonary syndrome Relative • Symptomatic splenomegaly (pain,rupture, infarction,restricting daily activities ) • Poor health related QOL • Large varices with poor access to health care or rare blood groups • Refractory LGI bleed due to ano-rectal varices or colopathy • Portal biliopathy • Growth failure • Delay In sexual development
- 24. Patient preparation (1) underlyingliver disease and its severity (Child pugh score/ MELD Score ) (2) abdominal venous anatomy (imaging ) (3) overall performance status
- 25. Therapeutic goal: to decreaseportal pressure thus prevent and treat PH complications Aims : • Bypass the portal resistance site by creating portoportal or, more commonly, portosystemic shunts (PSS); • When not feasible, direct treatment of complications of NCPH (eg, ligation of varices)
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- 28. Surgical procedures • Devascularizationprocedures • Decompression procedures
- 29. Decompression procedures Aim • Reduceportal venous pressure • Maintain total hepatic and portal blood flow • Avoid the high incidence of complicating hepatic encephalopathy
- 30. Non selective shunts(complete porto systemic decompression ) decompress the entire portal system by diverting all portal flow Portocaval End to side or side to side anastomosis Mesocaval Side to side or with an interposition graft Mesoatrial Requires interposition PTFE graft Proximal splenorenal End to side anastomosis of proximal splenic vein to left renal vein Requires splenectomy Partial (incomplete portal system decompression) Non selective shunt with diameter <10mm
- 31. Portocaval shunt First describedby Eck in 1877, • either joins the portal vein to the IVC in an end-to-side fashion and completely disrupts portal vein flow to the liver • or joins it in a side-to-side fashion and thereby maintains partial portal venous flow to the liver.
- 32. Portocaval shunt • Helpto decrease variceal bleeding • Refractory ascites treatment • Decompresses the splanchnic venous circulation and intrahepatic sinusoid network • Performed when TIPS not available or fails Disadvantage • Rebleeding rate upto 70% • Encephalopathy 20-40% • Accelerated hepatic failure due to decrease in hepatic perfusion • Makes subsequent hepatic transplantation much more technically difficult
- 33. Mesocaval shunt • Usesan 8- or 10-mm PTFE graft • connect superior mesenteric vein to the IVC • Technically easier to perform • Ease hepatic transplantation. • Smaller caliber of the shunt : 1. avoids the deleterious effects of portal blood flow deprivation on hepatic function 2. reduce the incidence of encephalopathy Disadvantage : increased risks of shunt thrombosis and rebleeding
- 34. Partial (incomplete portalsystem decompression)
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- 36. Mesoatrial shunt portal veinto drain directly into the right atrium Use : Budd Chiari syndrome inferior venacava thrombosis can be present
- 37. Selective (variceal-bearing compartment decompression) decompressonly the variceal-bearing compartment of the portal venous system and preserve some portal flow to the liver Inokuchi's left gastric venous caval End to side anastomosis of left gastric vein vena cava, may require an autologous graft Splenocaval End-to-side anastomosis of distal splenic vein to cava, may require an interposition PTFE graft Small‐diameter H‐graft shunt. PTFE reinforced grafts that measure 8 mm in internal diameter and connects the superior mesenteric vein or portal vein to inferior vena cava. Warren's distal splenorenal End-to-side anastomosis of distal splenic vein to left renal vein, includes ligation of the coronary and pancreatic veins
- 38. Distal Spleno-Renal shunt •Aka Warren Shunt • Division of GE collaterals • End-to-side splenic to left renal vein anastomosis • allows venous drainage of the stomach and lower esophagus through the short gastrosplenic veins into the spleen • allowing the splenic vein to drain directly into the left renal vein • ultimately decompresses the left LUQ. Interruption of all collateral vessels
- 39. Selective shunt- DSRS Advantages: • SMV continues to perfuse liver • lower rate of hepatic encephalopathy and decompensation (<10%) • not interfering with subsequent liver transplantation. • Rate of recurrent bleeding (7-13%) Disadvantages: • Technically more demanding • Important lymphatic pathways transected- aggravates ascites • Gradual collateralizes- loss of portal flow in 50% in 1year • Complications : acute pancreatitis, pseudocyst • Mortality: 1-19%) Contraindication • Prior splenectomy • Splenic vein <7mm • Intractable ascites
- 40. Portoportal shunts Rex shuntConnects superior mesenteric vein or varix to the left portal system at the recessus of Rex (left portal vein system)
- 41. Rex Bypass • Directportal revascularization can be achieved by interposing a vascular graft between the SMV and the Rex recessus (left portal vein system) • very successful physiologic cure of chronic portal hypertension and restores the portal flow into and through the liver graft. • Primary revascularization of liver grafts • Managing early acute portal vein thrombosis episodes.
- 42. Selection of shuntsprocedure • Depends on hepatic functional reserve • patency of the splenoportal venous axis • Patient's transplant candidacy • Available surgical expertise - Portal blood containing hormones, nutrients and cerebral toxins diversion cause adverse reactions - Portosystemic encephalopathy - Accelerated hepatic failure
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- 44. Follow up • Regular6 monthly follow up to look for spleen size, growth, quality of life, school performance, development of jaundice, decompensation, portal biliopathy, hepato-pulmonary syndrome
- 45. References • Sabiston textbookof surgery, 20th edition • Consensus on EHPVO, SK Sarin et al., 2006 • ACG & AASLD Joint Clinical Guideline: Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis Am J Gastroenterol 2007;102:2086–2102 • Non-cirrhotic portal hypertension – Diagnosis and management.Journal of Hepatology 2014 vol. 60 j 421–441 439
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