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Portal hypertension DR/ Walid Elshazly

Portal hypertension DR/ Walid Elshazly. Portal hypertension. Portal hypertension is an increase in the blood pressure within a system of veins called the portal venous system Normal portal pressure is generally defined between 5 and 10 mm Hg. Portal hypertension.

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Portal hypertension DR/ Walid Elshazly

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  1. Portal hypertension DR/ Walid Elshazly

  2. Portal hypertension • Portal hypertension is an increase in the blood pressure within a system of veins called the portal venous system • Normal portal pressure is generally defined between 5 and 10 mm Hg.

  3. Portal hypertension The portal vein drains blood from the small and large intestines, stomach, spleen, pancreas, and gallbladder.

  4. Portal Vein Anatomy

  5. Portal hypertension The superior mesenteric vein and the splenic vein unite behind the neck of the pancreas to form the portal vein.

  6. Etiology • Functional • Organic • Pre-sinusoidal extra-hepatic • Pre-sinusoidal intra-hepatic ( Fibrosis) • Post-sinusoidal intra-hepatic ( Cirrhosis) • Post-sinusoidal extra-hepatic

  7. Etiology • Presinusoidal • Extrahepatic • Cavernomatous malformation • Malignant portal & splenic vein obstruction • Intrahepatic • Schistosomiasis • Congenital hepatic Fibrosis • Sarcoidosis

  8. Etiology • Post sinusoidal • Intrahepatic • Cirrhosis • Venoocclusive disease • Extra hepatic • Hepatic vein obstruction • Budd Chiari syndrome • Constrictive pericadritis

  9. Pathogenesis • Backward resistance theory (to initiate) • It denotes increase resistance in the liver bed through a • constant component (liver fibrosis and regenerating nodules) • variable component through the action of humoral substances (endothelin, prostaglandins, adrenergic sububstances, and serotonin)

  10. Pathogenesis • Forward flow theory (to maintain) • It denotes increase in inflow to the liver through the action of humoral substances that cause • hyperdynamic and • hypervolemic circulation (nitric oxide, glucagon and, prostacylin)

  11. Mechanism of portal hypertension In Shistosomiasis • Peri-portal fibrosis • Portal hyper-volaemia • Release of vaso-spastic substances • Angiomatous mass • Endo- arterial obstruction

  12. Complication of portal hypertension • Spleno-megally • GIT congestion • Ascites • Opening of porto-systemic collaterals • Hepatocelluar failure • Portosystemic encephalopathy

  13. Splenomegally • Mechanisms • RES hyper-plasia • Opening of A/V shunts • Venous congestion • hypersplenism

  14. Splenomegally • Clinical picture • Pressure manifestations • Splenic pain • Hypersplenism • Psychic trauma

  15. GIT congestion • Gastric dyspepsia related to type of food • Haematemesis dt gastropathy which cause sever form of bleeding

  16. Ascites • etiology of ascites • Hormonal factors lead to salt and water retention • Hypo-proteinaemia • Portal hypertension • Lymphorrhoea • Disturbed renal function

  17. Ascites ( treatment) • Bed rest • Diet • Albumin infusion • Fresh frozen plasma • Diuretics • Refractory ascites require • Therapeutic para-centesis • Recirculation therapy • Peritoneo-venous shunt • Sapheno-peritoneal shunt

  18. Porto-systemic Collaterals • Cephalic • Lower end of esophagus • Bare area of liver • Caudal • Around umbilicus • Rectal • Retro-peritoneal

  19. Portal Vein Collaterals • Five Principle Routes • EsophagealVarices • Umbilical Vein • Hemorrhoids • Veins of Retzius • Adhesions

  20. 1 4 2 3

  21. Lower end of esophagus There is four rather than three plexuses of veins (intraepithelial, superficial, sub mucus and periesophageal) with the intraepithelial plexus in excess

  22. Lower end of esophagus In the palisade zone the veins are oriented in a special way, different from the gastric, perforator or truncal zones

  23. Lower end of esophagus The veins are condensed in the superficial plexus, rather than in the submucosal plexus opposite to the distribution in other zones

  24. Endoscopic Views

  25. Cirrhosis Childs-Pugh Classification System Endoscopy No Varices Varices b-blocker Parameter 1 Point 2 Points 3 Points Bilirubin <2 2-3 >3 Albumin >3.5 2.8-3.5 <2.8 D PTT 1-3 4-6 >6 Ascites None Slight Moderate Encepha- None 1-2 3-4 lopathy 1st Variceal Bleed Endoscopy q 2 years Banding Evaluation Medical Tx Banding Rebleeding Childs A or B Childs C / Liver Failure Surgical Shunt / TIPS Transplant 5 – 6 Class A 7 – 9 Class B > 10 Class C

  26. Hepato-cellular failure ( etiology) • Infection • Bleeding • Drugs • Anesthesia • surgery

  27. Hepato-cellular failure (C/P) • Weakness • Jaundice • Fetor hepaticus • Palmer erytems • Spider angioma • Gynaecomastia • Loss of axially and pubic hair • Testicular atrophy • Acute liver failure

  28. Gynecomastia

  29. Hepato-cellular failure (R) • Treat precipitating factors • Diet • Drugs • Renal failure • Correct clotting abnormalites • If no response • Exchange transfusion • Cross circulation between donor and patient • Extra-corporeal perfusion through pigs liver

  30. Porto-systemic encephalopathy • Due to materials that by pass the liver with its toxic effect over the brain (GABA, ammonia, methionine & short chain FA ) • Clinically • Personality changes • Disorientation • Slurring speech • Flappy tremors • Cogwheel rigidity • Ankle clonus • coma

  31. Porto-systemic encephalopathy • Treatment • Chemical • Intestinal antiseptic • Lactulose • Mechnical • Liver support • Nerve cell support glutamic acid

  32. Investigations • Laboratory • Stool • Urine • CBC • Kidney function • Liver function • Synthesis (proteins, prothrombin) • Excretory ( bilirubin, dye excretion) • Cell insult (SGOT, SGPT, alk phospatase, LDH)

  33. Investigations • Radiological • U/S • Doppler • B swallow • B enema • Portography • CT scan • MRI • Radio-isotope • Instrumental • Upper endoscopy • Laparscopy • Laparscopic U/S

  34. Child-Pugh Classification Grade A, 5-6 points; Grade B, 7-9 points; Grade C, 10-15 points

  35. Angio-graphy • Indirect trans-femoral porto-grapgy • Direct portigraphy • Per-cutaneous trans-splenic • Per-cutaneous trans-hepatic • Umbilical catherization • Direct operative • Wedged hepatic venograpgy

  36. Active bleeder Resusitation Specific measures Non-operative Naso-gastric Tr-iluminal tube Edo-scopic injection Operative Measures to prevent encephalopathy Cold case Child C injection sclerotherapy liver transplantation Child A&B Non shunt Hassab Sugura Tanner Shunt Non selective selective Treatment (Bleeder)

  37. Huge splenomegally or hyper-splenism Decongestion Small spleen No varices conserve Varices Sclerotherapy Decongestion prophylactic ?? Treatment (Non-Bleeder)

  38. Active bleeder Resusitation Specific measures Non-operative Naso-gastric Tr-iluminal tube Edo-scopic injection Operative Measures to prevent encephalopathy Treatment (Bleeder)

  39. Active bleederResusitation On patient admission and after clinical evaluation three lines are installed • I.V. line for blood sample, blood and fluid replacement • Urinary catheter for monitoring tissue perfusion together with pulse and BP • Nasogastric tube or Sangestaken Blackmore tube for monitoring the bleeding, and doing gastric lavage to prepare for endoscopy

  40. Active bleederResusitation Resuscitation with transfusion of • Colloids (blood) and • Crystalloids (Ringer, or lactated Ringer or saline solutions) at the same time with monitoring the blood pressure, pulse and urinary output.

  41. Active bleederResusitation • Sandostatin infusion (0.25 microg in 500 ml glucose over 4 to 8 hours, with or without an intramuscularly administered shot) • Sangestaken tube to arrest the bleeding • Sclerotherapy • can be done immediately, however, • it is better to be postponed until the hemodynamics of the patient are corrected and the stomach is washed from the retained blood which obscure the procedure and make it very difficult

  42. Endoscopic Banding

  43. Endoscopic Sclerotherapy Intravariceal Paravariceal

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