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Portal hypertension
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- 2. Content • Definition • Pathophysiology •Classification • Clinical Features • Management
- 3. Definition-An elevation ofportal pressure above 10-12 mm Hg or 30 cm of saline or intrasplenic pressure>17 mm Hg or wedged hepatic venous pressure more than 4 mm Hg above inferior vena caval pressure.
- 4. Pathophysiology • portal systemincludes all veins,which carry blood from digestive tract,spleen pancreas and gall bladder to liver via portal vein • portal vein is formed by the union of superior mesenteric vein and splenic vein just posterior to neck of pancreas at level of L 2
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- 6. • portal veinabout 6-8 cm long and 12 mm in diameter • It dose not contain any valves and hence the pressure is same in all part of portal venous system. • it supplies the liver 80% of blood and 20 % of oxygen • the portal system is peculiar in that it begins as capillaries in mesentery of the intestine and spleen and end as capillaries in liver
- 7. classification of PHT 1Prehepatic PTH 2.Intra hepatic PTH- 1.pre sinusoidal 2.sinusoidal 3.post sinusoidal 3.post-hepatic PTH
- 8. Pre hepatic PHT 1.Upper GITbleeding 2.pallor 3.splenomegaly PRESINUSOIDAL SINUSOIDAL 1.upper GIT bleeding 2.splenomegaly 3.jaundice 4.hepatomegaly 5.ascites 6.hepatic encephalopathy PORTAL HYPERTENSION post sinusoidal post hepatic abdominal pain with vomiting massive ascites tender hepatomegaly upper GIT bleeding jaundice splenomegaly upper GIT BLEED the combination of GIT bleed and splenomegaly is pathognomonic of PTH. left lobe of liver enlarged in intr hepatic PTH and caudate lobe enlarged in post hepatic PTH
- 10. PRE HEPATIC PORTAL HYPERTENSION block in portal vein occurs before the blood reaches the liver. • Patients usually present with upper GIT bleeding, • normal liver function and, prognosis excellent.
- 11. AETIOLOGY 1. Developmental defects-Portalvein agenesis, atresia, stenosis, cavernoma. 2. umbilical sepsis-this is most important cause in developing countries umbilical vein left branch of portal vein portal vein infected thrombus
- 12. 3. trauma 4.Portal veinthrombosis 5.Intra-abdominal infections-like acute appendicitis and primary peritonitis and pancreatitis. 6.idiopathic-IN 50 % OF children with pre hepatic PTH etiology can not be found out.
- 13. CLINCAL FEATURE OFPRE HEPATIC PTH UPPER GIT BLEED- due to ruptured oesophageal varices Manifestation of upper GI bleed hematemesis-vomiting of fresh blood melaenemesis-vomiting of altered blood. melena-passage of black,tarry,sticky,offensive,loose stools.
- 14. On General Examination •pallor • splenomegaly • stunted growth-stunted growth due to the following factors- 1. massive splenomegaly compresses the stomach. 2.deprivation of hepatotrophic growth factors • no jaundice • no hepatomegaly • no ascites
- 15. Intra Hepatic PTH •TYPES- 1.pre sinusoidal 2.sinusoidal 3.post sinusoidal • the liver functions are usually normal in pre sinusoidal ,where they are dearrenged in sinusoidal and post sinusoidal.
- 16. pre sinusoidal PTH 1.chronic active hepatitis 2.congenital hepatic fibrosis 3.chronic myeloid leukemia 4.systemic mastocytosis 5.sarcoidosis 6.primary biliary cirrhosis 7. schistosomiasis
- 17. sinusoidal PTH thisis cause by cirrhosis due to hepatitis B and C ,metabolic disorders like wilson's disease,cholestasis disorders like biliary atresia,neonatal hepatitis,drugs like INH,methotrexate. feature-1.upper GIT bleed 2.splenomegaly 3.jaundice 4.ascites 5.hepatic encephalopathy 6.caput medusa 7.hepatomegaly
- 18. smith-Howard syndrome:- sometimesthe spleen become impalpable following a massive bleed,which may cause diagnostic confusion this condition is called smith-Howard syndrome. size of spleen dose not correlate well with portal hypertension. ascites is a frequent problem in sinusoidal and post sinusoidal PTH. It is not usually seen in pre hepatic and pre sinusoid PTH
- 19. POST SINUSOIDAL PHT (VENO-OCCLUSIVEdisease) • This is non thrombotic occlusion of terminal hepatic venous radicles without associated abnormality of hepatic vein or inferior vena cava. AETIOLOGY- TOXINS LIKE aflatoxins drugs like 6-mercaptopurine, cyclophosphamide,vincristine hypervitaminosis A.
- 20. fibroblastic proliferation endothelial edema phlebosclerosis toxinand drugs, and hypervitaminosis occlusion of vein
- 21. POST HEPATIC PTH (Budd-chiari syndrome) thrombosis of hepatic vein. etiology- A.Thrombosis complicating- 1.abdominal trauma 2.polycythemia rubra vera 3.neoplasms 4.S.L.E 5.cirrhosis 6.sickle cell anaemia B.membranous obstruction of supra hepatic vena cava
- 22. • acute buddchiari syndrome- 1. sever abdominal pain with vomiting 2. mild jaundice 3.ascites chronic budd chiari syndrome 1.massive ascites 2.hepatomegaly 3.upper GI bleed 4.hypertrophy of the caudate lobe. 5.compression of the intrahepatic portion of the IVC, leading to lower extremity edema
- 23. MANAGEMENT of UpperGIT BleedMANAGEMENT of Upper GIT Bleed
- 24. INVESTIGATION • CBC • LFT-dearrengedin sinusoidal,post sinusoidal and post hepatic portal hypertension.normal in pre sinusoidal and pre hepatic PHT.. USG • portal vein diameter >17mm • portal vein not increases in diameter during inspiration. • demonstration of collaterals • splenomegaly color Doppler-assess the blood flow within the portal vein
- 25. Upper GIT ENDOSCOPY •demonstration of oesophageal varices, gastric varices
- 26.
- 27. primary prophylaxis propranolol- dose-:1-2 mg /kg/day mechanism of action-it lowers the venous pressure and portal venous pressure by decreasing the heart rate by 25% and the blood pressure by 15 mm Hg.It also causes splanchnic vasoconstriction.
- 28. Treatment of bleeding esophagealvarices • fluid resuscitation- i.v. fluids and blood transfusion to correct hypovolemia in a patient with massive upper GIT bleeding. • The first step is to assess the degree of blood loss by the following methods:- 1.disproportionate tachycardia,suggest that the patient has lost about 20 % of blood volume.
- 29. 2.TILT TEST-the basalpulse rate and BP are measured.The head end of the patient is then tilted or raised to 45 degree, so as to produce postural hypertension. if the pulse rate rises by more than 20/min or if the diastolic BP falls by more than 10 mm of mercury,the patient has suffered about 25% blood loss. 3. Capillary refill sign In a normal person if the nail bed is compressed and the pressure released, the blood column comes back almost immediately. But if the patient has lost the blood 25% blood volume it take more than 5 sec to come back. 4. If the patient is in shock, he has lost about 40% blood volume.
- 30. • use ofNasogastric tube to confirm active bleeding • normal saline at room temperature is best for gastric lavage • chilled or iced saline gastric wash does not stop bleed and may cause central hypothermia.
- 31. Pharmacological therapy 1.vasopressin 0.33 u/kgin 20 min than iv infusion of 0.33U/kg/hr 2.octreotide administered by continuous intravenous infusion of 1.0-5.0 µg/kg/hr H2 blocker/PPI I.V. vit k
- 32. Endoscopic therapy variceal band ligation-itis gold standard treatment for esophageal varices.less bleeding,fewer complication and requires fewer treatment sessions to achieve variceal eradication than sclerotherapy.
- 33. B.variceal sclerotherapy-via endoscope sclerosingagent is injected in lumen of each varix,causing thrombosed.endoscopy is usually repeated with in 48 hr than weekly interval. • sclerosant used in esophageal varices- 1.ethalonamide oleate 2.absolute alcohol 3.phenol 4.butyl cyanoacrylate
- 34. Disadvantage of sclerotherapy •chances of re bleeding is high (>25%) hence repeated injections are necessary • multiple esophageal ulceration • esophageal stricture • paraplegia
- 35. Trans jugular IntrahepaticPorto- systemic Shunt
- 36. • TIPSS ispercutaneous technique creates communication between the right hepatic vein and the right or left branch of the portal vein • performed if failed medical and endoscopic management
- 37. Surgical procedure • Surgicalporto-systemic shunts (often spleno-renal) • De vascularization surgery • Liver transplantation
- 38. • creation ofan anastomosis between portal and systemic venous system. • most common anastomosis between splenic vein and left renal vein. Surgical porto-systemic shunts
- 39.
- 40. child-pugh scorechild-pugh score features1 2 3 bilirubin(mg%) 1-2 2-3 >3 ascites absent slight moderate prothrombin time <4 sec 4-6 sec >6 sec serum albumin >3.5g 2.8-3.5g <2.8g encephalopathy (stage) none 1-2 3-4 child's criteria are useful guide for deciding the suitability of a patient for shunt surgery and prognosis
- 41. grading points prognosis gradeA 5-6 liver function is maintained.<10% mortality in surgical procedure grade B 7-9 intermediate grade C 10-15 poor. >90% mortality in surgical procedure
- 42. Devascularization surgery • transthoracicpara-esophageal devascularization is combined with esophageal transection, splenectomy, esophagogastric devascularization, truncal vagotomy and pyeloplasty.
- 43. Liver transplantation • Orthotopicliver transplantation represents a much better therapy for portal hypertension resulting from intrahepatic disease and cirrhosis
- 44. portal hypertension PRIMARY Prophylaxis propranolol-dose1 mg /kg/day Bleeding esophageal varices iv fluids and blood transfusion vit k H2 blocker or PPI after bleeding episode or bleeding is not stop pharmacological drugs sengstaken-blackemore tube surgical procedure de vascularization porto-systemic shunt liver transplantation bleeding persists TIPSS EST/ EVL
- 45. Pathophysiology Of AscitesIn Portal Hypertension portal hypertension hypovolaemia activation of renal angiotensin-aldosterone system(RAAS) increase Na and water reabsorption from DCT renin Ascitesexpansion of plasma increase pressure in sinusoid protein rich fluid from sinusoids into hepatic lymphatics causing increased hepatic lymph excess lymph enter into the peritoneal cavity
- 46. Management OF Ascites •In 80% of cases ,ascites is caused by cirrhosis • in portal hypertension transudate ascites occur. • Serum -Ascites Albumin Gradient (SAAG) is useful for distinguishing ascites caused by portal hypertension from non-portal hypertension ascites. • SAAG=(ascites albumin -serum albumin). • SAAG>1.1g/dl :- presence of portal hypertension.
- 47. SAAG >1.1 g/dl Ascitic protein<2.5g/dl cirrhosis late budd-chiari syndrome massive metastases Ascitic protein_>2.5g/dl congestive heart failure/constrictive pericarditis early budd-chiari syndrome IVC obstruction post sinusoidal PTH <1.1g/dl biliary leak nephrotic syndrome pancreatitis peritoneal carcinoma tuberculosis
- 48. Management of ascites- BedRest Bed rest : • Upright posture activates sodium retaining mechanisms , impairs renal perfusion and sodium excretion.
- 49. Sodium Restriction Sodiumrestriction : A negative Na balance can attained by restricting oral intake of salt 2 g/day.
- 50. WATER RESTRICTION • Centralhypovolaemia - > stimulates ADH receptors - > decreases free water clearance - > dilutional hyponatraemia. • Restriction of water worse> central hypovolaemia.
- 51. DIURETICS • potassium -sparingdiuretics is considered the diuretic of choice in portal hypertension. • hyper aldosteronism promotes sodium retention in distal tubules and collecting ducts in portal hypertension • this action is inhibited by spironolactone. • loop diuretics act on thick ascending limb of henle by inhibiting Na-k-2Cl symport,preventing the reabsorption of Na and water.there is hperaldosteronism In portal hypertension.so Na and water absorbed from the DCT.so loop along is not effective. • spironolactone is not a powerful natriuretic agent .As mono therapy,it takes several days to induce weight loss.hence it is preferable to use a combination of spironolactone and furosemide.
- 52. • Dose ofspironolactone-start with 1mg/kg and increase at rate of 1mg/kg/day to a maximum of 6 mg/kg/day. Assess response to diuretics • Weight loss of 0.5kg/day in absence of edema and 1kg/day when edema present. • Use Spironolactone & Furosemide 100mg/40mg ratio
- 53. Refractory ascites • Definition-ascitesdoes not respond to salt restriction and diuretics. • Therapeutic options in refractory ascites-: 1.Serial Paracentesis 2.Peritoneovenous Shunts 3.TIPSS 4.Liver Transplantation
- 55. Peritoneo-venous shunt • asciticfluid is shunted from the high pressure peritoneal cavity to the low pressure superior vena cava by 1.Le veen shunt 2.denver shunt