![Medical therapy
• Medical management should be started at the onset of variceal bleeding.
ANTIBIOTICS PROPHYLAXIS MUST BE GIVEN.
1. Vasopressin : Constricts splanchnic vessels, lowering portal pressure
2. Nitroglycerine : prevents coronary vasoconstriction and reduces portal
pressure [Nitroglycerin is used in conjunction with octreotide to prevent
adverse effects of vasopressin]
3. Terlipressin, Desmopressin : similar MOA but increased half-life and
fewer side-effects.
4. Somatostatin : reduces splanchnic and hepatic blood flow
5. Octreotide : decreases portal pressure and azygous blood flow
6. Propranolol : used as prophylaxis, decreases portal pressure
7. Metoclopramide : causes lower esophageal sphincter constriction](https://image.slidesharecdn.com/portalhypertension-230701090320-8c131eb6/75/Portal-Hypertension-pptx-26-2048.jpg)
![Surgeries for acute bleeding varices
Open esophageal stapler transection and esophago-gastric anastomosis
(Jhonston)
Borema-Crile operation [बोरमा सिलाउने ओपेरिन ] : The esophagus is
opened. Esophageal varices are under-run using Vicryl.
Sugiura-Futagawa operation: Esophagogastric transection and
devascularization, vagotomy, pyloroplasty and splenectomy.
Milnes-Walker thoracic esophageal transection [मिल्ने छामििा ]
Tanner’s abdominal esophagogastric resection [िान्ने पेटिा]
Hassab operation: It is a single abdominal operation and consists of
splenectomy, devascularization of the esophagus and the proximal part of the
stomach, vagotomy, and pyloroplasty. [सब मिसाब मिने ]
Shunt surgeries are not commonly used to control bleeding in acute stage.](https://image.slidesharecdn.com/portalhypertension-230701090320-8c131eb6/75/Portal-Hypertension-pptx-33-2048.jpg)
![Types of Shunts
1. Non-selective Shunts
• End-to-side portacaval shunt (ECK fistula)---prototype of non-selective shunt
• Side-to-side portacaval shunt
• Most effective anastomotic technique for relieving ascites as well as for preventing recurrent
variceal hemorrhage as both liver and colon are important contributors for ascites formation.
• Large-diameter interposition shunts
• Mesentericocaval shunt
• Mesentericocaval shunt with graft
• Proximal splenorenal shunt [@ NP]
• TIPS
2. Selective shunts
• Distal splenorenal Shunt – Warren’s shunt
• Inokuchi shunt between left gastric vein and IVS through a graft](https://image.slidesharecdn.com/portalhypertension-230701090320-8c131eb6/75/Portal-Hypertension-pptx-42-2048.jpg)
More Related Content
Similar to Portal Hypertension.pptx
Portal Hypertension.pptx
- 1.
- 2. Types of PortalHypertension • Cirrhotic PH • Non-cirrhotic PH
- 3. Portal Circulation Contributes approx.75% of blood and approx. 72% of oxygen supplied to the liver In average adult, 1000-1500ml/min portal venous blood is supplied to the liver. Portal venous system is without valves and drains blood from the spleen, pancreas, gall bladder & abdominal portion of the alimentary tract into the liver. Tributaries of the portal vein communicate with veins draining directly to systemic circulation.
- 4. Porto-systemic circulation Sites ofCollateral Communications Portal Circulation Systemic Circulation Lower end of esophagus Left gastric veins Lower branch of esophageal veins Upper part of anal canal Superior rectal veins Inferior and middle rectal veins Umbilicus Paraumbilical veins Epigastric veins/Anterior abdominal vein Bare area of the liver Intraparenchymal branches of right division of portal vein Retroperitoneal veins (Vein of Retzius) Hepatic and Splenic Flexures Omental and colonic veins Retroperitoneal veins (Vein of Retzius)
- 7. Portal Hypertension The normalportal venous pressure is 5-10 mm Hg. At this pressure, very little blood is shunted from the portal venous system into the systemic circulation. Gilbert and Villaret first coined the term “Portal Hypertension” in 1906. Portal hypertension is the sustained elevation of the portal venous pressure more than 10mm Hg. Portal hypertension (PHT) is a clinical syndrome defined by a portal venous pressure gradient between the portal vein (PV) and inferior vena cava exceeding 5 mmHg.
- 8. Portal Hypertension Cirrhotic PHTis associated with an elevated hepatic venous pressure gradient (HVPG) predominantly due to raised sinusoidal resistance, while in the non- cirrhotic PHT (NCPH), HVPG is normal or only mildly elevated and is significantly lower than PV pressure.
- 9. Portal Hypertension As theportal venous pressure increases, however the collateral communication with the systemic circulation dilate, and a large amount of blood may be shunted around the liver and into the systemic circulation. Pressure > 10 mmHg are required to begin stimulating the development of porto-systemic collaterization. In absence of liver disease, if portal vein is thrombosed, hepatopetal portal collaterals develop to restore perfusion. This is called as the cavernous transformation of portal vein. Portal hypertension may also follow thrombosis of splenic vein from pancreatitis or tumor. This phenomenon is called Left-sided portal hypertension (segmental portal hypertension). If partial channels are present within splenic vein, it is called as splenic vein cavernoma. Here, liver is normal and splenectomy alone will correct the condition When splenic vein thrombosis occurs, left gastroepiploic vein becomes a major collateral and gastric varices develop rather than esophageal varices.
- 10. Measurement of PortalVenous Pressure Most accurate method of determining portal hypertension is Hepatic Venography. Transfemoral-hepatic vein catheterization with a balloon tip catheter is the best method to estimate the gradient. Most commonly used procedure involves placing a balloon catheter directly into the Hepatic vein and measuring free hepatic venous pressure (FHVP), with the balloon deflated. The wedged hepatic venous pressure(WHVP) with the balloon inflated to occlude hepatic vein.
- 11. Measurement of PortalVenous Pressure The Hepatic venous pressure gradient (HVPG) is then calculated by subtracting the free from the wedged venous pressure. HVPG represents the pressure in hepatic sinusoids & portal vein and is a measure of portal venous pressure. Clinically significant portal hypertension is evident when HVPG exceeds 10mm Hg. HVPG = WHVP - FHVP
- 12. When HVPG is> 10mm Hg : Porto-systemic shunting develop When HVPG is > 12mm Hg : Risk of Variceal bleeding increases When HVPG is ≥ 20mm Hg : Bleeding esophageal varices
- 13. Causes of Non-CirrhoticPortal Hypertension • The diseases leading to NCPH are primarily vascular in nature and classified anatomically on the basis of site of resistance to blood flow. 1. Pre-hepatic 2. Hepatic a) Pre-sinusoidal b) Sinusoidal c) Post-sinusoidal 3. Post-hepatic
- 14. Pre-hepatic causes ofNCPH (Normal WHVP & FHVP with Normal HVPG) Extrahepatic portal vein obstruction (EHPVO) Portal vein thrombosis Splenic vein thrombosis Splanchnic arteriovenous fistula Massive splenomegaly • Infiltrative diseases : Lymphoma, myeloproliferative disorders • Storage diseases : Gaucher’s disease
- 15. Hepatic causes ofNCPH (Increased WHVP, Normal FHVP and Increased HVPG)
- 16. Post-hepatic causes ofNCPH (Increased WHVP & FHVP and Normal HVPG) Inferior vena cava obstruction – web, thrombosis, tumor, enlarged caudate lobe Constrictive pericarditis Tricuspid regurgitation Severe right-sided heart failure Restrictive cardiomyopathy
- 17. Clinical Features ofPortal Hypertension As portal hypertension per se produces no symptoms, it is diagnosed following presentation with decompensated CLD & encephalopathy, ascites or variceal bleeding. (Triad of Portal Hypertension) 1. Esophageal varices (most common) responsible for 1/3rd of the death due to Portal HTN. EHPVO patients rarely die because of variceal bleeding. Risk of rebleeding is highest within first few days. If no hemorrhage occurs risk returns to pre- hemorrhage rate after 6 weeks 2. Splenomegaly 1. Frequently associated with functional hypersplenism causing leukopenia, thrombocytopenia and anemia. 3. Ascites; severe PTH with Hepatocyte dysfunction (hepatic decompensation)
- 18. Clinical Features ofPortal Hypertension • Jaundice • Generalized anasarca • Features of encephalopathy • Recurrent infection • Coagulopathy • Hepatorenal Syndrome
- 19. Assessment of portalhypertension • Diagnosis of underlying disease • Estimation of hepatic reserve • Defining the portal venous anatomy • Hepatic hemodynamic evaluation • Identification of sites of UGI bleeding (if present): Gastric vs Esophageal
- 20. Imaging of PortalVenous System • Before undertaking Porto-systemic shunts, hepatic resection or hepatic transplantation, an understanding of portal vein patency & anatomy is crucial. The patency of the portal vein & nature of the collateral circulation should be established. • The simplest initial investigation is abdominal ultrasonography (USG). • Doppler ultrasound is capable of outlining the anatomy of portal vein; excluding the presence of thrombosis & identifying the direction of portal venous blood flow.
- 21. Imaging of PortalVenous System • Doppler ultrasound is also useful in evaluating blood flow though surgical shunts & TIPS. • Abdominal CT & MR angiography both are capable of revealing portal vein anatomy as well as patency. • Visceral angiography & portal venography are reserved for the cases that cannot be evaluated satisfactory by non-invasive methods and require further clarification of portal patency or anatomy.
- 22. Investigations Complete bloodcount Liver function test Renal function test AFP and other relevant markers • Serum iron • Α1-antitrypsin • Autoantibodies Esophagogastroscopy Liver Biopsy
- 23. Management of PortalHypertension • General measures • Secure airway (especially in an encephalopathic patient) • Ensure adequate IV access • Fluid infusion • Blood typing and products transfusion • Restrictive strategy is useful as it reduces risk of rebleeding and better survival at 6-weeks • As per this strategy transfusion is given only when hemoglobin levels is below 7g/dl • Nutrition supplementation Inj. Vitamin K – 10mg IM for 5days
- 24. Management of PortalHypertension B. Specific measures Treatment of esophageal varices Prevention of hepatic encephalopathy Treatment of ascites Measures to reduce portal pressure Surgeries – Portosystemic Shunt • Non-selective • Selective TIPSS Drugs to reduce the portal pressure like propranolol, nadolol, isosorbide-5-mononitrate Liver transplantation
- 25. Management of Esophagealvarices • Medical therapy (Drugs) • Endoscopic therapy • Balloon tamponade • TIPSS • Surgeries for acute bleeding varices • Shunt surgery
- 26. Medical therapy • Medicalmanagement should be started at the onset of variceal bleeding. ANTIBIOTICS PROPHYLAXIS MUST BE GIVEN. 1. Vasopressin : Constricts splanchnic vessels, lowering portal pressure 2. Nitroglycerine : prevents coronary vasoconstriction and reduces portal pressure [Nitroglycerin is used in conjunction with octreotide to prevent adverse effects of vasopressin] 3. Terlipressin, Desmopressin : similar MOA but increased half-life and fewer side-effects. 4. Somatostatin : reduces splanchnic and hepatic blood flow 5. Octreotide : decreases portal pressure and azygous blood flow 6. Propranolol : used as prophylaxis, decreases portal pressure 7. Metoclopramide : causes lower esophageal sphincter constriction
- 27. Endoscopic therapy 1. EndoscopicVariceal banding : Band-ligation. Gold standard and ideal for esophageal varices. 80-90% of acute variceal bleeding are successfully controlled by endoscopic measures. Early endoscopy, preferably within 12 hours of admission, with an attempt at control of bleeding is recommended. 2. Endoscopic Variceal sclerotherapy : Easier and cheaper. Both intra variceal and Para variceal or only intravariceal injections are given. Esophageal banding>> sclerotherapy 3. Endoscopic gluing using tissue adhesives : Done for gastric varices. Needle tip is placed into the gastric varix and adhesive is injected 4. Endoscopic thrombin/dilute adrenaline injection
- 28. Luminal (Balloon) Tamponade@ Balloon of 40 • Variceal bleed is controlled using Sengstaken-Blakemore tube, when medical and endoscopic measures have failed. • It will control up to 90% refractory bleeding but is only temporary measure of hemorrhage control. • It’s possible complications include aspiration, airway obstruction and esophageal perforation due to over-inflation or pressure necrosis. • Therefore, the use of Sengstaken-Blakemore tube should not exceed 36 hours to avoid tissue necrosis. • X-ray should be taken to confirm the position of the balloons. • Esophageal balloon is inflated with 40mm Hg pressure of air, gastric balloon with 400ml of air.
- 30. Trans jugular intrahepaticportosystemic shunt • The TIPSS procedure involves implantation of a metallic stent in between an intrahepatic branch of the portal vein and a hepatic vein radicle. • The needle track is dilated until a portal pressure gradient of ≤ 12mm Hg is achieved. • Controls variceal bleeding in >90% of cases refractory to medical treatment and should not affect subsequent hepatic transplantation. • Complications include bleeding (intra-abdominally or via biliary tree), infections, renal failure, decreased hepatic function and hepatic encephalopathy.
- 31. Frequent follow-up with repeated interventionssuch as dilation or restenting often are needed to maintain TIPSS patency.
- 32. Operative approaches • Reservedfor situations in which TIPS is not indicated or available. • Selection of the operative techniques are mainly guided by the experience of the surgeon. • An emergency operation is promptly carried out when less invasive measures fail to control hemorrhage and are not indicated. • Situations in which emergency or urgent surgery are required are • Failure of acute endoscopic treatment • Failure of long-term endoscopic therapy • Hemorrhage from gastric varices • Portal hypertensive gastropathy • Failure of TIPS placement
- 33. Surgeries for acutebleeding varices Open esophageal stapler transection and esophago-gastric anastomosis (Jhonston) Borema-Crile operation [बोरमा सिलाउने ओपेरिन ] : The esophagus is opened. Esophageal varices are under-run using Vicryl. Sugiura-Futagawa operation: Esophagogastric transection and devascularization, vagotomy, pyloroplasty and splenectomy. Milnes-Walker thoracic esophageal transection [मिल्ने छामििा ] Tanner’s abdominal esophagogastric resection [िान्ने पेटिा] Hassab operation: It is a single abdominal operation and consists of splenectomy, devascularization of the esophagus and the proximal part of the stomach, vagotomy, and pyloroplasty. [सब मिसाब मिने ] Shunt surgeries are not commonly used to control bleeding in acute stage.
- 35. EPCS Emergency portocavalshunting LT Liver transplantation BEV Bleeding Esophageal Varices EST Endoscopic sclerotherapy
- 36. Prevention of recurrentvariceal hemorrhage • Likelihood of repeated episode of bleeding is > 70% • Rebleeding is most frequent during the first year and reduces @ 15% annually • Challenge for long-term management is prevention of recurrent bleeding and maintenance of satisfactory hepatic function • Effective treatment of recurrent hemorrhage requires two or more therapies in sequence • In most centers the therapy involves • Pharmacotherapy or endoscopic therapy • Portal decompression by TIPS • Operative shunt (reserved for failure of first-line treatment) • Hepatic transplantation
- 37. Pharmacotherapy • Non-selective β-adrenergicblocker OR β-blocker + long-acting nitrate (isosorbide 5-mononitrate) • Combination therapy is more effective than variceal ligation • Long term pharmacotherapy is useful only to patients who are compliant for follow up. Endoscopic therapy • Variceal ligation preferred over sclerotherapy. • Variceal ligation with pharmacotherapy (non-selective β-blockade) is more effective than variceal ligation alone • Predictors of failure of endoscopic therapy • Uncontrolled hemorrhage • Multiple episodes of major bleeding • Hemorrhage from gastric varices • Hypertensive gastropathy • Chronic endoscopic therapy should not be undertaken for noncompliant patients and patients living a long distance from advanced medical care.
- 38. Interventional therapy • TIPSis being increasingly used for definitive treatment of patients who bleed from portal hypertension. • A major limitation of TIPS however is high incidence of shunt stenosis or shunt thrombosis • Shunt stenosis is due to neo-intimal hyperplasia which can be resolved by balloon dilation of the TIPS or placement of second shunt • PTFE covered stents used nowadays have lower incidence of stenosis and occlusion • Incidence of encephalopathy is 34% • Ideal for patients when a short-term portal decompression is required.
- 39. Indications of TIPS •Liver transplantation patients who fail to respond to endoscopic therapy or pharmacotherapy are well suited for TIPS followed by transplantation when donor becomes available. • Advanced hepatic functional decompensation • Medically intractable ascites.
- 40. Surgical therapy • Portosystemicshunts are clearly the most effective means of preventing recurrent hemorrhage in patients with portal HTN • These procedures decompress portal venous system. • Divided into various types depending upon • Complete decompression • Compartmentalization/ partial decompression of the portal venous circulation • Shunts may be • Non-selective shunts • Selective shunts or partial shunts
- 41. • Even thoughthe survival benefit is similar in both, the shunt group have advantages of • Reliable bleeding control
- 42. Types of Shunts 1.Non-selective Shunts • End-to-side portacaval shunt (ECK fistula)---prototype of non-selective shunt • Side-to-side portacaval shunt • Most effective anastomotic technique for relieving ascites as well as for preventing recurrent variceal hemorrhage as both liver and colon are important contributors for ascites formation. • Large-diameter interposition shunts • Mesentericocaval shunt • Mesentericocaval shunt with graft • Proximal splenorenal shunt [@ NP] • TIPS 2. Selective shunts • Distal splenorenal Shunt – Warren’s shunt • Inokuchi shunt between left gastric vein and IVS through a graft
- 43. Splenorenal shunt Proximal splenorenalshunt Distal splenorenal shunt (Warren’s shunt)
- 44. Non selective shunt •In summary non selective shunt effectively decompresses esophageal varices • Complications include postoperative encephalopathy, accelerated hepatic failure • Presently, non-selective shunts are rarely indicated and are created only when a TIPS cannot be performed or when a TIPS fails.
- 46. Selective shunts • Hemodynamicand clinical shortcomings of nonselective shunts stimulated the development of concept of selective variceal decompression • Consists of • Distal splenic vein-left renal vein anastomosis • Interruption of all collaterals • Coronary vein • Gastroepiploic vein
- 47. • Other contraindicationsof distal splenorenal shunt oPrior splenectomy oSplenic vein diameter < 7 mm as incidence of thrombosis is high when small diameter vessel is used. Drawbacks/Limitations of the surgery • Although the distal splenorenal shunt results in portal vein flow preservation in more than 85% patients during early post-operative interval, high-pressure mesenteric venous system gradually collateralizes to the low-pressure shunt resulting in loss of portal flow in approximately 50% of patients by 1 year. • Although portal flow is maintained in most patients with non-cirrhotic/ non- alcoholic portal hypertension, the flow rapidly collateralizes to the shunt in patients with alcoholic cirrhosis.
- 50. Hepatic transplantation • Notconsidered for treatment of variceal bleeding • Considered for patients who present with end-staged hepatic failure. • Those fulfilling the transplantation criteria should be managed acutely for hemorrhage and name listed as transplant candidate • Indications • Non-alcoholic cirrhotic patients • Abstinent alcoholic cirrhotic patients • Child Pugh C patients • Patients with poor quality of life due to disease (encephalopathy, fatigue, bone pain)
- 53. References • Bailey andLove’s Short Practice of Surgery, 26th Edition • Schwartz Textbook of Surgery, 11th Edition • Khanna R, Sarin SK. Non-cirrhotic portal hypertension–diagnosis and management. Journal of hepatology. 2014 Feb 1;60(2):421-41.