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VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION
Portal hypertension occurs when blood flow through the liver is blocked, increasing pressure in the portal vein and spleen. This causes collateral veins to develop like esophageal varices, which can bleed if ruptured. Diagnosis involves blood tests, ultrasound, and endoscopy. Treatment depends on severity but may include medications, band ligation, TIPS procedure, or liver transplant. Managing variceal bleeding quickly through fluid resuscitation, medications, and endoscopic therapy can help prevent complications from progressive liver disease.
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Presentation introduction by Dr. Sadia Nazneen at Malda Medical College on 22.02.2017.
Gasatroesophageal varices in over 90% cases, with hypertensive portal gastropathy less than 5%.
Portal hypertension defined as hepatic venous pressure gradient ≥ 10 mm Hg.
Normal hepatic venous pressure gradient at 6-8 mm Hg; in cirrhosis >10 mm Hg indicates risks.
Mechanism of portal hypertension, vasodilation response, and collateral circulation.
Development of collaterals and veins involved in portal circulation like gastric and oesophageal veins.
Pre, intra, and post hepatic causes including thrombosis and cirrhosis.
Complications include splenomegaly, varices, ascites, and more.
Methods for assessing liver function and portal circulation.
Indicators of liver function including hypoalbuminaemia and raised liver enzymes.
Use of duplex scan or Doppler ultrasound for assessing portal circulation.
Upper GI endoscopy to detect gastroesophageal varices.
Diagnosis involves immunological tests, serological markers, and liver biopsy.
CT and MR angiography utilization in diagnosing liver and portal circulation issues.
MELD score assessment based on bilirubin and albumin levels, prothrombin time, ascites.
Score for predicting liver function based on creatinine, bilirubin, and INR.
Pharmacotherapy and endoscopic approaches for managing acute variceal bleeding.
Use of beta blockers and somatostatin analogues along with antibiotic prophylaxis.
Sclerotherapy and endoscopic banding as treatment options for varices.
Detailed explanation of Transjugular Intrahepatic Portosystemic Shunt (TIPS) procedure.
Indications for TIPS including refractory cases and liver dysfunction.
Classification of portal shunts and their utility in managing portal hypertension.
Overview of small diameter shunts and their advantages in managing portal hypertension.
Surgical approach aiming to disconnect varices from bleeding sources.
Treatment strategies for patients categorized based on Child-Pugh score.
Description of gastropathy, its connection to cirrhosis, and treatment methods.
Clinical features and treatment options for gastric varices.
Emphasis on early intervention and treatment progression for variceal bleeding.
Closing remarks and gratitude for audience participation.
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VARICEAL HAEMORRHAGE WITH SPECIAL ATTENTION TO PORTAL HYPERTENSION
- 1. Dr. Sadia Nazneen 22.02.2017,MALDA MEDICAL COLLEGE
- 2. Gasatroesophageal varices> 90% Hypertensive portal gastropathy <5% Isolated gastric varices – rare.
- 3. Portal hypertensionis defined as a hepatic venous pressure gradient equal to or greater than 10 mm of Hg.
- 4. Normal 6-8mmHg In cirrhosis >10mm Hg HVPG <12 mm Hg unlikely to develop variceal bleeding. Useful for assessing medical treatment.
- 6. Block toportal flow increased portal pressure Splanchnic vascular bed response : (a) Initial increased vasoconstrictor and decreased vasodialator response intrahepatic response (b)Secondarily vasodialator response dominates with increase in splanchnic inflow Collaterals develop. Plasma volume expansion Systemic hyperdynamic circulation
- 8. Portal inflow Systemicoutflow Collaterals Left gastric veins Short gastric veins Intercostal, diaphragmatic and oesophageal veins Gastro- oesophageal varices Superior haemorrhoidal vein Middle haemorrhoidal vein Inferior haemorrhoidal vein haemorrhoids Left portal vein via falciform ligament Umbilicus and abdominal wall veins Caput medusa Liver via lienorenal ligament Left renal vein Retroperitoneal collaterals
- 9. Pre hepatic: Portalvein thrombosis Splenic vein thrombosis Congenital thrombosis of Portal vein Arteriovenous fistula Intra hepatic: Primary biliary cirrhosis Cirrhosis Infiltrative liver disease Congenital hepatic fibrosis Polycystic liver disease Veno – occlusive disease Post hepatic: Budd – Chiari syndrome Inferior vena cava webs or thrombosis Congenital heart failure Constrictive pericarditis Tricuspid valve diseases
- 11. Splenomegaly Oesophagealvarices Caput medusa. Haemorrhoids. Complications : Ascites. Spontaneous bacterial peritonitis. End-stage renal disease. Hepatopulmonary syndrome. Encephalopathy
- 12. Assessment ofthe liver function. Assessment of the portal circulation. Upper GI endoscopy.
- 13. Assessment of liverfunction: Hypoalbuminaemia. ALT & AST are moderately raised. Prothrombin time and INR are disturbed. Blood picture anaemia, leucopenia, thrombocytopenia or pancytopenia.
- 14. Assessment of portalcirculation: Duplex scan or Doppler ultrasound: To assess the hepatic artery, hepatic vein and portal vein. Patency of portal vein.
- 15. Upper GI Endoscopyor EGD To detect gatroesophageal varices Gold standard for diagnosing variceal bleeding
- 16. Diagnosis of theaetiology of liver disease is performed by: (a) Immunological tests for hepatitis markers. Other specific serological markers are alpha foeto protein, ceruloplasmin,alpha 1 antitrypsin, antimitochondrial antibodies,and iron studies. (b) Liver biopsy.
- 17. CT ANGIOGRAPHY MRANGIOGRAPHY
- 18. Points 1 2 3 Bilirubin(mg/dL) < 2 2 – 3 > 3 Albumin (g/dL) > 3.5 2.8 – 3.5 < 2.8 Prothrombin time (seconds) 1 – 3 4 – 6 > 6 Ascites None Slight Moderate Encephalopathy None Minimal Advanced Grade A, 5-6 points; Grade B, 7-9 points; Grade C, 10-15 points
- 19. Score =0.957 × loge creatinine (mg/dL) + 0.378 × loge bilirubin (mg/dL) + 1.120 loge INR
- 20. Prophylaxis –Pharmacotherapy and endoscopic therapy Acute variceal bleeding Resuscitaion and pharmacotherapy Endoscopic therapy Decompressive shunts Devascularisation Liver transplantation Prevention of rebleeding Level I evidence
- 21. Pharmacotherapy: Non-cardioselective betablockers Endoscopic variceal ligation
- 23. Admit patientin ICU Fluids and blood products judiciously administered Somatostatin or its analogues octreotide or terlipressin administered and continued for 3-5 days Non-selective beta blockers like propanol or nadolol Current recommendation is to administer an antibiotic prophylaxis upto 7days, specifically a fluoroquinolones. Initial bolus 100 microgram continuous infusion of 25 microgram / h for 24 hrs. Dose 20-60 mg bid
- 24. Sclerotherapy Intra- orPara-Variceal. 1-3 ml sclerosant (ethanolamine oleate). Multiple sessions (2 weekly). Control bleeding in 80-95 %. About 50% rebleed. Intravariceal Paravariceal
- 25. Endoscopic Banding Occludes venous channels Sessions< sclerotherapy Same results as sclerotherapy Endoscopic treatment of choice
- 28. Transjugular intrahepaticportosystemic shunt or (TIPS) is a procedure that involves the creation of an artificial anastomosis between the hepatic and portal veins under fluoroscopic guidance with the use of a covered stent, shunting away blood from the hepatic sinusoids and relieving portal pressure.
- 29. Indications forTIPSS: Refractorybleeding Prior to transplant Child C Refractory ascites
- 30. Porta –systemic shunts. Non Shunt surgery – Devascularisation. Liver transplantation.
- 31. Classification: Non-selective shunts: Total shunts: Portacaval Mesocaval Proximal spleno-renal Partial shunts: Small diameter porta-caval (Sarfeh) Selective shunts: Distal spleno renal shunt
- 32. Portal bloodis completely redirected into IVC below the liver. Two types: end to side and side to side Side to side shunt is useful in preventing portal hypertension in Budd – Chiari syndrome .
- 33. Anastomosis ofthe side of the SMV to the proximal end of the divided IVC, for control of portal hypertension; The incidence of thrombosis is high.
- 34. Indication: EHPVO. Advantage: Theincidence of encephalopathy is less than after porta caval shunt. Disadvantage: Less effective In rebleeding. If the splenic vein is less than 1 cm the anastmosis is liable to thrombosis.
- 35. A small diameter interposition (8-10mm) porta – caval shunt. Advantage: Partially decompress the portal venous system. Hepatic portal flow is preserved. Drawback: Increasaed incidence of thrombosis. Recurrence of bleeding.
- 36. Types : •The distalsplenorenal shunt (Dean Warren shunt) •Inokuchi splenocaval shunt (IMV to IVC) •Interposition shunts with the left gastric vein to IVC
- 37. An anastomosisof the splenic vein and the left renal vein, created to lower portal hypertension Merits: •The incidence of encephalopathy is low •Liver functions remain normal.
- 39. Devascularisation: Aim: Direct disconnection between theportal and azygos vein done by disconnecting the varices from their bleeding vessels. Components: Splenectomy Gastric and oesophageal devascularisation Oesophageal transection
- 40. Good-risk patients—Child’s Apatients or MELD less than 10. Pharmacotherapy +/- Banding If they rebleed or have failure to obliterate their varices banding, they may be a candidate for decompression with TIPS or DSRS. Indeterminate patients—Child’s B or MELD 10–16. Majority of patients Initial treatment is with endoscopic banding and a beta-blocker. Subsequent treatment depends on the course of their liver disease.
- 41. End-stage liver disease—Child’sC or MELD greater than16. Liver transplantation Patients with any of the above scenarios, who also have advanced liver disease, are candidates for liver transplantation, possibly using TIPS as a bridge.
- 42. Portal hypertensivegastropathy refers to changes in the mucosa of the stomach in patients with portal hypertension Most common cause of this is cirrhosis of the liver. Investigations: Endoscopy Treatment: Medications: o Non-selective beta blockers (such as propranolol and nadolol) o Octreotide Procedural: o Argon plasma coagulation. o TIPS. o Cryotherapy.
- 43. Most commonlyfound in patients with portal hypertension. Gastric varices may also be found in patients with thrombosis of the splenic vein. Clinical features: Hematemesis, melena, shock Treatment: Injecting cyanoacrylate glue, TIPS. Intravenous octreotide Splenectomy Liver transplantation.
- 44. Variceal bleedinghas high morbidity and mortality rate. Endoscopy is both diagnostic and therapeutic. Beta blockers and EVL are first line of treatment. TIPSS and DSRS are used as bridge to Liver Transplant. Liver transplant though last resort may be curative.
- 45.