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Cirrhosis & Portal Hypertension

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Slide 1 :

Cirrhosis & Portal Hypertension Sanjay Munireddy Sinai Hospital of Baltimore Feb 13, 2007

Slide 2 :

CIRRHOSIS Term was 1st coined by Laennec in 1826 Many definitions but common theme is injury, repair, regeneration and scarring NOT a localized process; involves entire liver Primary histologic features: Marked fibrosis Destruction of vascular & biliary elements Regeneration Nodule formation

Slide 3 :

Cirrhosis: Pathophysiology Primary event is injury to hepatocellular elements Initiates inflammatory response with cytokine release->toxic substances Destruction of hepatocytes, bile duct cells, vascular endothelial cells Repair thru cellular proliferation and regeneration Formation of fibrous scar

Slide 4 :

Cirrhosis: Pathophysiology Primary cell responsible for fibrosis is stellate cell Become activated in response to injury and lead to ?ed expression of fibril-forming collagen Above process is influenced by Kupffer cells which activate stellate cells by eliciting production of cytokines Sinusoidal fenestrations are obliterated because of ?ed collagen and EC matrix synthesis

Slide 5 :

Cirrhosis: Pathophysiology Prevents normal flow of nutrients to hepatocytes and increases vascular resistance Initially, fibrosis may be reversible if inciting events are removed With sustained injury, process of fibrosis becomes irreversible and leads to cirrhosis

Slide 6 :

Causes of Cirrhosis Alcohol Viral hepatitis Biliary obstruction Veno-occlusive disease Hemochromatosis Wilson’s disease Autommune Drugs and toxins Metabolic diseases Idiopathic

Slide 7 :

Classification of Cirrhosis WHO divided cirrhosis into 3 categories based on morphological characteristics of the hepatic nodules Micronodular Macronodular Mixed

Slide 8 :

Micronodular Cirrhosis Nodules are <3 mm in diameter Relatively uniform in size Distributed throughout the liver Rarely contain portal tracts or efferent veins Liver is of uniform size or mildly enlarged Reflect relatively early disease

Slide 9 :

Macronodular & Mixed Cirrhosis Nodules are >3 mm in diameter and vary considerably in size Usually contain portal tracts and efferent veins Liver is usually normal or reduced in size Mixed pattern if both type of nodules are present in equal proportions

Slide 10 :

Cirrhosis - Alcohol Also known as Laennec’s cirrhosis >50% of pts. with alcoholic cirrhosis die within 4 yrs of diagnosis Develops in only 10% to 30% of heavy drinkers Morphologically, micronodular pattern Multifactorial - genetic, nutritional, drug use and viral

Slide 11 :

Cirrhosis - Alcohol Fatty liver, alcoholic hepatitis Histology - megamitochondria, Mallory bodies, inflammation, necrosis, fibrosis Key mediator is acetaldehyde (ADH), the product of alcohol metabolism by alcohol dehydrogenase ADH directly activates stellate cells, inhibits DNA repair and damage microtubules

Slide 12 :

NAFLD/NASH Nonalcoholic Fatty Liver Disease and Steatohepatitis Becoming more common Infiltration of the liver with fat ± inflammation Pathologically similar to alcoholic liver but in absence of alcohol Associated with obesity, hyperlipidemia, NIDDM,

Slide 13 :

Viral Hepatitis Most common cause of cirrhosis worldwide (>50% of cases) Incidence of cirrhosis in Hepatitis B pts. is 1% and 10% in Hepatitis C pts. Incidence increases to 70-80% in HBV +ve pts. who are superinfected with HDV

Slide 14 :

DIAGNOSIS Can be asymptomatic for decades History Physical findings: Hepatomegaly, jaundice, ascites, spider angioma, splenomegaly, palmar erythema, fetor hepaticus, purpura etc. Elevated LFTs, thrombocytopenia,

Slide 15 :

DIAGNOSIS Definitive diagnosis is by biopsy or gross inspection of liver Noninvasive methods include US, CT scan, MRI Indirect evidence - esophageal varices seen during endoscopy

Slide 16 :

Manifestations of Cirrhosis Hepatorenal syndrome Hepatic encephalopathy Portal hypertension Water retention Hematologic Hepatocellular carcinoma

Slide 17 :

Portal Hypertension (PH) Portal vein pressure above the normal range of 5 to 8 mm Hg Portal vein - Hepatic vein pressure gradient greater than 5 mm Hg (>12 clinically significant) Represents an increase of the hydrostatic pressure within the portal vein or its tributaries

Slide 18 :

Pathophysiology of PH Cirrhosis results in scarring (perisinusoidal deposition of collagen) Scarring narrows and compresses hepatic sinusoids (fibrosis) Progressive increase in resistance to portal venous blood flow results in PH Portal vein thrombosis, or hepatic venous obstruction also cause PH by increasing the resistance to portal blood flow

Slide 19 :

Pathophysiology of PH As pressure increases, blood flow decreases and the pressure in the portal system is transmitted to its branches Results in dilation of venous tributaries Increased blood flow through collaterals and subsequently increased venous return cause an increase in cardiac output and total blood volume and a decrease in systemic vascular resistance With progression of disease, blood pressure usually falls

Slide 20 :

Portal Vein Collaterals Coronary vein and short gastric veins -> veins of the lesser curve of the stomach and the esophagus, leading to the formation of varices Inferior mesenteric vein -> rectal branches which, when distended, form hemorrhoids Umbilical vein ->epigastric venous system around the umbilicus (caput medusae) Retroperitoneal collaterals ->gastrointestinal veins through the bare areas of the liver

Slide 21 :

Slide 22 :

Etiology of PH Causes of PH can be divided into Pre-hepatic Intra-hepatic Post-hepatic

Slide 23 :

Pre-hepatic PH Caused by obstruction to blood flow at the level of portal vein Examples: congenital atresia, extrinsic compression, schistosomiasis, portal, superior mesenteric, or splenic vein thrombosis

Slide 24 :

Post-hepatic Caused by obstruction to blood flow at the level of hepatic vein Examples: Budd-Chiari syndrome, chronic heart failure, constrictive pericarditis, vena cava webs

Slide 25 :

Budd-Chiari Syndrome Caused by hepatic venous obstruction At the level of the inferior vena cava, the hepatic veins, or the central veins within the liver itself result of congenital webs (in Africa and Asia), acute or chronic thrombosis (in the West), and malignancy

Slide 26 :

Budd-Chiari Syndrome Acute symptoms include hepatomegaly, RUQ abdominal pain, nausea, vomiting, ascites Chronic form present with the sequelae of cirrhosis and portal hypertension, including variceal bleeding, ascites, spontaneous bacterial peritonitis, fatigue, and encephalopathy Diagnosis is most often made by US evaluation of the liver and its vasculature Cross-sectional imaging using contrast-enhanced CT or MRI

Slide 27 :

Budd-Chiari Syndrome Gold standard for the diagnosis has been angiography Management has traditionally been surgical intervention (surgical decompression with a side-to-side portosystemic shunt) Minimally invasive treatment using TIPS may be first-line therapy now Response rates to medical therapy are poor

Slide 28 :

Portal Vein Thrombosis Most common cause in children (fewer than 10% of adult pts.) Normal liver function and not as susceptible to the development of complications, such as encephalopathy Diagnosis by sonography, CT and MRI Often, the initial manifestation of portal vein thrombosis is variceal bleeding in a noncirrhotic patient with normal liver function

Slide 29 :

Portal Vein Thrombosis - Causes Umbilical vein infection (the most common cause in children) Coagulopathies (protein C and antithrombin III deficiency), Hepatic malignancy, myeloproliferative disorders Inflammatory bowel disease pancreatitis trauma Most cases in adults are idiopathic

Slide 30 :

Portal Vein Thrombosis Therapeutic options are esophageal variceal ligation and sclerotherapy Distal splenorenal shunt Rex shunt in patients whose intrahepatic portal vein is patent (most commonly children)

Slide 31 :

Splenic Vein Thrombosis Most often caused by disorders of the pancreas (acute and chronic pancreatitis, trauma, pancreatic malignancy, and pseudocysts) Related to the location of the splenic vein Gastric varices are present in 80% of patients Occurs in the setting of normal liver function Readily cured with splenectomy (variceal hemorrhage), although observation for asymptomatic patients is acceptable.

Slide 32 :

Complications of PH GI bleeding due to gastric and esophageal varices Ascites Hepatic encephalopathy

Slide 33 :

Varices Most life threatening complication is bleeding from esophageal varices Distal 5 cm of esophagus Usually the portal vein-hepatic vein pressure gradient >12 mm Hg Bleeding occurs in 25-35% of pts. With varices and risk is highest in 1st yr.

Slide 34 :

Prevention of Varices Primary prophylaxis: prevent 1st episode of bleeding Secondary prophylaxis: prevent recurrent episodes of bleeding Include control of underlying cause of cirrhosis and pharmacological, surgical interventions to lower portal pressure

Slide 35 :

Prevention of Varices Beta blockade: Beta blockade (Nadolol, Propranolol) Nitrates:Organic nitrates Surgery: No longer performed* Endoscopy: Sclerotherapy (no longer used*) and variceal ligation * Refers to primary prophylaxis

Slide 36 :

Treatment of Varices Initial Management: Airway control Hemodynamic monitoring Placement of large bore IV lines Full lab investigation (Hct, Coags, LFTs,) Administration of blood products ICU monitoring

Slide 37 :

Pharmacologic Treatment of Varices Decreases the rate of bleeding Enhances the endoscopic ability to visualize the site of bleeding Vasopressin - potent splanchnic vasoconstrictor; decreases portal venous blood flow and pressure Somatostatin: decrease splanchnic blood flow indirectly; fewer side effects Octreotide: Initial drug of choice for acute variceal bleeding

Slide 38 :

Endoscopic Therapy for Varices Endoscopic Sclerotherapy: complications occur in 10-30% and include fever, retrosternal chest pain, dysphagia, perforation Endoscopic variceal ligation: becoming the initial intervention of choice; success rates range from 80-100%

Slide 39 :

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