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The Cirrhosis Tsunami are we ready?

The Cirrhosis Tsunami are we ready?. Mary Patricia Pauly MD FACP AGAF Kaiser Permanente Sacramento Medical Center. Diagnosis. 45 year old elementary school teacher with cirrhosis calls in to clinic Trouble focusing Slow Slurred speech Confused. Outline. Cirrhosis Definition ,

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The Cirrhosis Tsunami are we ready?

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  1. The Cirrhosis Tsunamiare we ready? Mary Patricia Pauly MD FACP AGAF Kaiser Permanente Sacramento Medical Center

  2. Diagnosis

  3. 45 year old elementary school teacher with cirrhosis calls in to clinic • Trouble focusing • Slow • Slurred speech • Confused

  4. Outline Cirrhosis Definition , Survival w and wo Decompensation causes Physical signs and lab signs Portal hypertension--Anatomy and physiology Manifestation of decompensated cirrhosis – how it fits with portal hypertension Ascites, variceal bleed , encephalopathy Only a certain percentage, TREATMENT OF complications of cirrhosis and portal hypertension- cancer surveillance Making the diagnosis Prognosis – Childs class, MELD Treatment may decrease incidence of cirrhosis

  5. Cirrhosis • Late stage of progressive hepatic fibrosis • Distortion of hepatic architecture • Regenerative nodules • Irreversible in advanced stages • Patients with cirrhosis • Decreased life expectancy • Susceptible to complications • Decompensation • Ascites, Variceal bleeding and encephalopathy • Cancer • HCC and • Cholangiocarcinoma

  6. Survival in Cirrhosis Survival Probability Compensated 100 After first major complication 80 60 Patients (%) 40 20 0 0 12 24 36 48 60 72 84 96 108 120 Mos Pts at Risk, n 38465 37639 34221 28811 2367 1654 1264 793 523 392 251 Fattovich G, et al. Gastroenterology. 1997;112:463-472.

  7. NAFLD Hepatitis B 350 million worldwide HBsAG positive 15 – 40% -> cirrhosis or HCC 15% progress to NASH xx% -> cirrhosis 170 million infected worldwide Up to 40% cirrhosis after 40 years

  8. The Cirrhosis Tsunami

  9. Spider angiomata Pathogenesis incompletely understood Possibilities: Alterations in sex hormone metabolism- increase in estradiol to free testosterone ratio in men. Note the central pulsating arteriole surrounded by many smaller vessels or “legs.” Number and size correlate with severity of disease

  10. Palmar erythema Pathogenesis: It is thought to be caused by altered sex hormone metabolism

  11. Gynecomastia Pathogenesis: increased conversion of androstenedione ( produced in adrenals) -> estrone -> estradiol.

  12. Dupuytren’s contractures Due to thickening and shortening of the palmar fascia Fibroblastic proliferation and disorderly collage deposition --> fascial thickening and flexion deformities of the fingers.

  13. Caput medusae In portal hypertension the umbilical vein ( normally obliterated at birth) can dilate Blood is shunted from periumbilical veins-> to the umbilical vien -> abdominal wall.

  14. Physicial findings in cirrhosis • Physical findings • Stigmata of portal hypertension: • Spider angiomata • Caput medusae • Palmar erythema • Dupuytren’s contracture • Gynecomastia • Ascites • Signs of encephalopathy • Jaundice --- does not necessarily indicate cirrhosis • acute hepatitis • CBD obstruction

  15. Laboratory Finding consistent with cirrhosis Laboratory findings Low platelet count < 100 K Low WBC and Anemia. Splenic sequestration Low albumin Elevated prothrombin time Elevated Bilirubin Liver biopsy Non invasive markers of Fibrosis Fibrosure/fibrospect  F3-4 Fibroscan and similar technologies  measures elasticity >12.5 Kpa APRI > 2

  16. APRI • APRI = • (AST elevation/platelet count) x 100 • Example • AST = 90 IU/L • ULN = 45 IU/L • Platelet count =120,000/mm3 APRI = 90/45=2 (2/120) x 100 = 1.67 APRI > 2 correlates with cirrhosis <0.5 correlates with no cirrhosis.

  17. The Liver: Progression of Disease TIME course 10 --> 40 years .

  18. Hepatic Fibrosis: Metavir score

  19. Portal Hypertension • More than mechanical obstruction • Vasodilation • increased • Glucagon • Nitrous oxide • Decreased SVR • Decreased MAP • Increased collaterals • Increased CO • Increased portal blood flow • Hyperdynamic circulation

  20. Cirrhosis Increased resistance to portal flow Decreased splanchnic arteriolar resistance Increased portal pressure Increased portal blood flow Varices

  21. Clinical Cirrhosis

  22. 50% of patients with cirrhosis 5-15% Risk of bleeding per year Directly related to portal pressure SIZE if most important predictor of bleeding * Large varices 30% Small varices 7% Recommended EGD Surveillance for varices in cirrhosis If no varices – Recheck 2-3 y If small varices Recheck 1-2 y If large varices Primary prophylaxis Gastro esophageal varices *over 2 years

  23. Esophageal varices • Non bleeding varices • Primary prophylaxis • Non cardioselective beta- blockers • Propranolol • Nadolol • Titrate to 25% decrease in HR from baseline • EVBL • if intolerant of BB

  24. Treatment of varices Actively bleeding Band ligation Octreotide ->Splanchnic vasoconstriction and Decreased portal blood flow Inhibits release of vasodilator hormones (glucagon) IV Antibiotics Active variceal bleed 20% mortality 60 – 80% rebleeding within 2 years Secondary prophylaxis Band ligation Non cardioselective beta blockers

  25. Prophylactic antibiotics improve outcomes in cirrhotic patients with GI Hemorrhage Barnard et al J Hepatology 1998; 29: 1685

  26. Ascites • Increased vasodilaton affects the kidneys • Increased CO and decreased MAP-> • Stimulates endogenous vasoconstrictors -> • Salt and water retention • Ascites and edema • Dilutional hyponatremia

  27. Ascites • Most common complication of cirrhosis • Pathologic accumulation of fluid in peritoneal cavity • Risk of developing ascites • 50% - 70% within 10 years of diagnosis of cirrhosis • Requirements for Ascites in cirrhosis • Portal hypertension • Actually sinusoidal Hypertension

  28. Management of Ascites • Dietary Sodium restriction • 88 meq sodium daily • 2000 mg sodium daily • Diuretics • Combination of lasix and spironolactone • Spironolactone (aldactone) • Aldosterone antagonist • Weak diuretic • More effective than lasix alone in cirrhosis • Furosemide (Lasix) • Loop diuretic • Must enter the lumen of the tubule to work • Proximal tubular secretion is impaired in cirrhosis

  29. Refractory ascites • Diuretic resistant • No weight loss • Despite adequate doses of diuretics • And salt restriction • Diuretic intractable • Something precludes the use of effective doses of diuretics • Hyponatremia • Elevated creatinine Hepatorenal syndrome

  30. Large Volume Paracentesis Beware of post paracentesis circulatory dysfunction Can cause renal failure and Decreased survival Many advocate IV Albumin to prevent PPCD. Terlipressin * Vasoconstrictor Splanchnic and systemic Increases effective blood volume Decreases renin and angiotensin secretion Increases renal vasodilation and perfusion Improves creatinine Treatment of Refractory Ascites * Not yet approved in US

  31. Presence of VARICES and ASCITES determines prognosis patients with cirrhosis

  32. Hepatic Encephalopathy • Definition • A spectrum of potentially reversible neuropsychiatric abnormalities seen in patient with liver dysfunction and / or porto systemic shunting. • Overt Hepatic Encephalopathy • 30-45% of patients with cirrhosis • Minimal Hepatic Encephalopathy • Up to 80% with cirrhosis

  33. High index of suspicion Physical exam Clinical setting Rule out other causes of mental status changes Intracranial process Check for precipitating factor Infection SBP GI Bleed Drugs Renal Insufficiency Worsening liver function Encephalopathy work up and diagnosis

  34. Increases stool volume Increased acetate and lactate change acid base balance pH = 5 NH3 -> NH4 Increases excretion of fecal nitrogen Problems Side effects -> Increased number of BMs Loose stools Gas  Non compliance Lactulose

  35. Treatment of encephalopathy Rifaximin Nonabsorbable antibiotic Comparable efficacy to lactulose Wide bacterial activity against aerobic and anaerobic gram-negative and gram-positive Superior safety profile compared with neomycin

  36. Treatment of encephalopathy

  37. Surveillance recommended in all with cirrhosis Incidence HCC varies with cause of cirrhosis Up to 5% per year Surveillance decreases mortality detects small HCC HCC 1-2 cm can be cured in >50% of cases Patients listed for transplant with HCC Get Priority on list Exception points for certain cases are available Must be small One lesion < 5 cm or < 3 lesions None greater than 3 cm No vascular invasion No extrahepatic lesions Hepatocellular carcinoma

  38. Causes of Cirrhosis Most common Chronic viral hepatitis HBV HCV Alcoholic liver disease Hemochromatosis NASH Non alcoholic steatohepatitis Less common causes Autoimmune hepatitis Primary and secondary biliary cirrhosis Primary sclerosing cholangitis Medications Wilson disease Alpha-1 antitrypsin deficiency Granulomatous liver disease Polycystic liver disease Right-sided heart failure Veno-occlusive disease.

  39. Impact of Antiviral Treatment* on Risk of HCV-related Complications P<0.01 P<0.01 HR=2.59 Bruno S, et al Hepatology 2007; 45:579. *Pts with compensated cirrhosis treated with IFN monotherapy between 1992 and 1997.

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