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MANAGEMENT OF LIVER CIRRHOSIS: PRACTICE ESSENTIALS AND PATIENT SELF - MANAGEMENT Sherona Bau, ACNP The Pfleger Liver Institute 200 UCLA Medical Plaza, Suite 214 Los Angeles, CA 90095 September 30, 2017

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  • MANAGEMENT OF LIVER CIRRHOSIS:

    PRACTICE ESSENTIALS AND PATIENT SELF-MANAGEMENT

    Sherona Bau, ACNP

    The Pfleger Liver Institute

    200 UCLA Medical Plaza, Suite 214

    Los Angeles, CA 90095

    September 30, 2017

  • DISCLOSURE

    • I have no disclosure.

  • OBJECTIVES

    • What is liver cirrhosis

    • Causes of liver cirrhosis

    • Management of liver cirrhosis

    • Patient Self-Management of liver cirrhosis

  • LIVER CIRRHOSIS

    • A late stage of progressive hepatic fibrosis characterized by distortion of the hepatic architecture and the formation of regenerative nodules.

    • It is generally considered to be irreversible in its advanced stages

    • The ideal treatment for decompensated liver cirrhosis may be liver transplantation. 4

  • LIVER DISEASES THAT LEAD TO LIVER CIRRHOSIS

    • Hepatitis B• Hepatitis C• Autoimmune hepatitis• Primary biliary cholangitis• Primary sclerosing cholangitis• Alcoholic liver disease• Nonalcoholic steatohepatitis• Hemochromatosis 5

  • PHYSICAL EXAMINATION• Spider angiomata

    • Palmar erythema

    • Scleral icterus or jaundice

    • BLE edema

    • Ascites

    • Anorexia 6

  • SPIDER ANGIOMATA

    7

  • PALMAR ERYTHEMA

    8

  • SCLERAL ICTERUS

    9

  • EDEMA

    10

  • ASCITES

    11

  • Liver Biopsy Elastography

    Serum Biomarkers

    TESTS FOR LIVER CIRRHOSIS ASSESSMENT

    Routine Imaging

    Physical Examination

  • Histologic Staging Hepatitis C

    Normal Cirrhotic

    Stage 1 2 3 4

  • LAB FINDINGS

    • Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are usually moderately elevated.

    • Normal AST and ALT do not preclude cirrhosis

    • Low platelet counts < 150,000

    • Low albumin < 3.5

    • Bilirubin may be normal or elevated in cirrhosis progresses

  • SEROLOGIC TESTS

    15

  • IMAGING OR EGD FINDINGS

    • Ultrasound of abdomen can show • Nodular liver• Portal hypertension• Splenomegaly • Ascites

    • Upper endoscopy may show esophageal varices

    • MRElastography

  • PREDICTION OF PROGNOSIS

    • Child-Pugh Classification

    • MELD score (Model for end-stage liver disease)

  • CHILD-PUGH CLASSIFICATION OF CIRRHOSIS

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    Parameter 1 2 3

    Point 1 point 2 points 3 points

    Prothrombin 1-3 4-6 >6

    Albumin >3.5 2.8-3.4

  • MELD-NA SCORE

  • MANAGEMENT OF CIRRHOSIS

    • Treatment goals for patients with cirrhosis:• Slow the progression of liver damage • Manage symptoms and reduce the risk for complications

    • Treatment by a multi-disciplinary team is the ideal approach.

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  • MANAGEMENT OF LIVER CIRRHOSIS

    • Hepatocellular Carcinoma screening (US of abdomen + AFP) every 6 months

    • EGD to screen esophageal varices • Low sodium diet• No raw fish or raw shellfish to prevent Vibrio vulnificus infection• Avoid constipation • Alcohol abstinence• Small snacks between meals to maintain nutrient

  • DECOMPENSATED LIVER CIRRHOSIS

    • Ascites• Portal Hypertension• Esophageal varices bleeding• Encephalopathy• Jaundice• Muscle wasting• Thrombocytopenia

    22

  • ASCITES

    • Diuretics

    • Sodium monitoring• Low sodium diet, < 2 gram per day

    • Paracentesis as needed

    23

  • ASCITES

    • Diuretics • If kidney function and electrolytes allow, single morning doses

    of oral spironolactone 100mg and furosemide 40mg.

    • Spironolactone can increase potassium versus furosemide can lower potassium.

    • The doses of both drugs an increased at the same time every 5-7 days.

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  • ASCITES

    • Amiloride 10-40mg per day can be substituted for spironolactone in patients with tender gynecomastia.

    • Hydrochlorothiazide can cause rapidly development of hyponatremia when using with spironolactone and furosemide, it should be used extreme caution.

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  • ASCITES

    • Paracentesis

    • Paracentesis can be performed as needed if a patient developed refractory ascites (diuretics-resistant tense ascites).

    • Transjugular intrahepatic portosystemic shunt (TIPS) – for refractory ascites

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  • PORTAL HYPERTENSION

    Portal hypertension is resistance to portal blood flow and is aggravated by increased portal collateral blood flow.

    The resistance most often occurs within the liver (as is the case in cirrhosis), but it can also be prehepatic (eg, portal vein thrombosis) or posthepatic (eg, Budd-Chiari syndrome).

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  • MANIFESTATIONS OF PORTAL HYPERTENSION

    • Variceal hemorrhage

    • Portal hypertensive gastropathy

    • Ascites

    • Hepatorenal syndrome

    • Hepatic hydrothorax

    • Hepatopulmonary syndrome

    • Pulmonary hypertension28

  • MANAGEMENT OF PORTAL HYPERTENSION

    • Transjugular intrahepatic portosystemic shunt (TIPS)

    • Purpose of a TIPS is to • Decompress the portal venous system • Prevent rebleeding from varices• Stop or reduce the formation of ascites

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  • TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT

  • COMPLICATIONS OF TIPS

    31

  • ESOPHAGEAL VARICES

    • As a result of portal hypertension

    • Screening for esophageal varices through upper endoscopy

    32

  • ESOPHAGEAL VARICES

  • MANAGEMENT OF ESOPHAGEAL VARICES

    • Esophageal varices non-bleeding• Primary prophylaxis – beta blockers

    • Esophageal varices bleeding• Esophagogastroduodenoscopy (EGD) with banding • TIPs with rebleeding

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  • ENCEPHALOPATHY

    • Hepatic Encephalopathy (HE)

    • HE is a brain dysfunction caused by liver insufficiency and/or Portal Systemic Shunting

    • Wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma

    • Clinically overt HE will occur in 30%-40% of those with cirrhosis and in most patients repeatedly

    • Subjects with recurrent overt HE have a 40% cumulative risk of another recurrence within 6 months, despite standard treatment

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  • GRADE OF ENCEPHALOPATHY

    Grade Definition

    I Changes in behavior with minimal change in level of consciousness

    II Gross disorientation, drowsiness, possibly asterixis, inappropriate behavior

    III Marked confusion, incoherent speech, sleeping most of the time but arousable to vocal stimuli

    IV Comatose, unresponsive to pain, decorticate or decerebrate posturing

  • FAMILY/PATIENT EDUCATION FOR ENCEPHALOPATHY

    • Being confused

    • Memory problems

    • Mood changes

    • Trouble speaking, drawing, and writing clearly

    • Problems with sleep – Some people have trouble falling asleep. Others sleep too much.

    • Moving more slowly than normal

    • Flapping hands

  • ASTERIXIS

  • PRECIPITATING CAUSES

    • Dehydration

    • Urinary tract infection

    • Large volume paracentesis

    • Constipation

    • Large amount of red meat consumption

    • Sleeping medication

  • MANAGEMENT OF ENCEPHALOPATHY

    • Lactulose 30cc bid• Goal 2 to 3 bowel movements per day

    • Rifaximin 550mg po bid

    • Avoid benzodiazepines

    • Avoid pain medication 40

  • PATIENT SELF-MANAGEMENT FOR LIVER CIRRHOSIS

    • Avoid• NSAIDs • Ok to take Tylenol no more than 2g/day• Alcohol • Constipation• Raw shellfish • Herbal supplement

  • PATIENT SELF-MANAGEMENT FOR LIVER CIRRHOSIS

    • Daily weight

    • Strict low sodium diet – less than 1500mg per day. Low sodium should be < 140mg / serving

    • Small snack between meals

  • FOOD HIGH IN SODIUM

  • FOOD HIGH IN SODIUM

  • FOOD HIGH IN SODIUM

  • FOOD HIGH IN SODIUM

  • FOOD HIGH IN SODIUM

  • FOOD HIGH IN SODIUM

    • Deli meats – hot dog - 700mg/serving

    • Vegetable juices – tomato juice - 700mg/serving

    • Canned vegetable – 1300mg/can

    • Frozen meals – 1800mg/serving

    • Ketchup - 150mg/tablespoon, Soy sauce – 1000mg/tablespoon

    • Bread or tortillas – 250 mg per serving

    • Daily products – cottage cheese, buttermilk or American cheese up to 400mg/ounce

  • CONCLUSION

    • Liver cirrhosis is late stage of hepatic fibrosis – potentially irreversible

    • Manage symptoms and prevent decompensations

    • Screening for hepatocellular carcinoma every 6 months

    • Patient and family members play an important roles for prognosis of liver cirrhosis

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