Cirrhosis of the Liver

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					Cirrhosis of the Liver
         and
     Liver Failure
      Developed by
Cheryl McConnell RN MSN
             Pathophysiology
   Slow, insidious, progressive, chronic
   Fibrous bands replace normal liver
    structure
   Cell degeneration occurs
   Liver attempts to regenerate cells but cells
    are abnormal and disorganized
   Causes abnormal blood and lymph flow
   Results in more fibrous tissue formation
Normal Liver
         Incidence of Cirrhosis

   Tenth leading cause of death in US
   At least 25,000 deaths annually
   Higher death rates for men than women
      mortality in African Americans and
      Hispanics
              Types of Cirrhosis
   Laennec’s (alcoholic)

   Postnecrotic

   Biliary

   Cardiac
                   Laennec’s Cirrhosis

   Most common type of cirrhosis
   Also called alcoholic or portal
   Alcohol causes inflammation to liver cells
   Leads to fatty deposits and hepatomegaly
   Scarring formed and liver cells destroyed
   Malnutrition and more alcohol accelerate
    the damage
Postnecrotic Cirrhosis

   Caused by viral hepatitis or
    hepatotoxins
   Scar tissue destroys liver
    lobes
   Liver initially enlarges but
    then shrinks in size
   10 – 30% of all cirrhoses
                Biliary Cirrhosis
   Caused by chronic biliary obstruction
    or stasis of bile, biliary inflammation,
    or hepatic fibrosis
   Excessive bile leads to liver cell
    destruction and formation of nodules
    in the lobes
   5 – 10% of all cirrhoses
Cardiac Cirrhosis

   Seen with right sided heart failure
   Liver is engorged with venous blood
   Becomes enlarged, edematous, and
    dark
   Venous congestion results in anoxia
   Cell necrosis results
                     Diagnostic Data

    AST, ALT, LDH, Alk phos
    bilirubin, ammonia,
    coagulation studies
   Serum protein levels depend on disease
      with acute liver disease

      with chronic liver disease
             More Diagnostics
   Abdominal x-ray
   Upper GI series
   Angiography
   Abdominal CT
   EGD
   Liver biopsy
   Nuclear scan
Signs and Symptoms
   Neurological
     Asterixis             Paraesthesias
      LOC                 Sensory disturbances
      Behavorial changes   Cognitive changes
   Skin
    Spider angiomas        Palmar erythma
    Jaundice               Pruitis
     hair production      caput medusa
     pigmentation         Bruising
    White Nails
Caput Medusae
Spider Angiomas
Palmar Erythema
      More Signs and Symptoms
   GI
    Abdominal pain        Anorexia
    Ascites               Diarrhea
    Clay colored stools   Fetor hepaticus
    Gastritis             GI bleeding
    N/V                   Varices
    Malnutrition
“White Nails”
    More Signs and Symptoms

   Cardiovascular
     Dysrhythmias             Portal hypertension
     Collateral circulation   Fatigue
     Peripheral edema
   Endocrine
    Gynecomastia      Amenorrhea
     aldosterone, ADH, estrogens,
      glucocorticoids
More Signs and Symptoms
          Respiratory
            Dyspnea      Hypoxia

          Blood
            Anemia      DIC
            Thrombocytopenia  WBCs
            Hypokalemia Hypocalcemia
            Hypo/Hypernatremia
            Hypomagnesia
      More Signs and Symptoms
   Immune
      Susceptibility to infections
      Leukopenia
   Renal
      Urinary output
     Complications
    Portal hypertension
              Ascites
              Varices
  Coagulation defects
        Jaundice

  PSE (portal systemic
     encephalopathy)
 Hepatorenal syndrome
             Portal Hypertension

   Increased pressure within the portal vein
   Results in obstruction of blood flow
    through the portal vein
       Blood tries to find new ways around
        obstructed area = collateral circulation
   Causes venous distention in entire GI tract
                        Ascites
   Accumulation of plasma in the peritoneal cavity
       Caused by increased pressure forcing fluid out of
        intravascular space into cavity
       Plasma contains albumin so circulating proteins
        decreased
        serum osmotic pressure
       Intravascular fluid depletion stimulates kidney to
        conserve sodium and water =  hydrostatic pressure
        and creates more ascites
Ascites
                      Varices
   Occur anywhere in the GI tract
    especially
      Esophageal
        Hemorrhoids
   Bleeding esphageal varices
      Caused by thin walled veins that
       are irritated, distended and
       eventually rupture
        Chemical irritants
                 Mechanical trauma
         Esophagus pressure
   Prone to hemorrhage – medical
    emergency
Esophageal Varices
           Coagulation Defects
   Susceptible to bleeding
   Bruises easily
   Does not clot
      Esophageal varices bleeding
                      Jaundice

   Due to hepatocellular destruction or
    hepatic obstruction
       Hepatocellular – cannot metabolize bilirubin
        so it builds up
       Obstruction – clogs bile ducts so excretion is
        not possible
Jaundice
                       PSE
   Also known as hepatic
    coma
   Seen in end stage
    hepatic failure
   Can be insidious or
    rapid onset depending
    on the severity of
    liver disease
   Caused by impaired
    ammonia metabolism
               PSE Continued
   Usually protein breaks down into ammonia
    in GI tract, then ammonia into urea ---
    excreted by the kidneys
   Liver cannot convert ammonia into urea
       Results in  serum ammonia levels
       Toxic to the central nervous system
           PSE Continued
   Other factors that add
    to PSE:
     High protein diet
        Infection
     Hypovolemia
        Constipation
     GI bleeding
        Medications
Stages of PSE
   #1 - Prodomal – very
    subtle changes
       Personality/behavior
        changes
       Impaired
        thinking/concentration
       Emotional highs and
        lows
       Fatigue, drowsiness
       Slurred or slow speech
       Sleep pattern
        disturbance
               Stages of PSE
   #2 – Impending
     Continued mental
      deterioration
     Confusion

        Disoriented

     Asterixis
                Stages of PSE
   #3 – Stuporuous
     Marked mental
      confusion
     Drowsy but
      arousable
     Abnormal EEG

     Muscle twitching

     Hyperreflexia

     Continued asterixis
                Stages of PSE
   #4 – Comatose (85%
    mortality rate)
     Unresponsive
     Responds to painful
      stimuli only
     No asterixis
     Positive Babinski’s sign
     Muscle rigidity
     Fetor hepaticus
     Seizures
          Hepatorenal Syndrome
   A primary cause of death with hepatic
    failure/cirrhosis
   Kidneys cannot excrete ammonia and
    bilirubin
       Results in acute tubular necrosis
   Signs/symptoms
    Sudden  urinary output
     BUN, Cr, urine osmolarity        Urine Na
                        Treatment

   Diet
        Sodium (< 2 grams)
       Carbohydrate, moderate fats
        Protein
            Unless PSE present then  protein
       Fluid restriction (total of ≤ 1500cc/day)
       Vitamin supplements
            Treatment Continued
   Medications
      Diuretics

      Electrolyte replacement

      Antacids

         Must be low sodium – Riopan

      Lactulose

         Facilitates evaculation of
           ammonia
      Neomycin

         Eliminates intestinal flora = 
           protein breakdown
      Levadopa

         For PSE – repairs damaged
           neurotransmitters
               More Treatments
   Ascites control
      Paracentesis

      Shunts

         Le Veen Shunt - drains ascites fluid
          into superior vena cava
         Denver Shunt – subcutaneous pump
          that is manually compressed
             Post op care: same as with any
              abdominal surgery, watch for fluid
              volume overload and bleeding
              disorders, measure abdominal girth
              every shift
Le Veen Shunt
                    More Treatments
   Hemorrhage from varices
       Esophagogastric balloon tamponade
            Sengstaken-Blakemore tube – balloon inflates in esophagus and
             puts pressure on varices
       Blood transfusions
       Medications
            Beta blockers to decrease HR and BP
            Pitressin (vasopressin) IV or into superior mesenteric artery (via
             endoscopy)
       Sclerotherapy
            Sclerosing agents injected into varices during EGD
       Transjugular intrahepatic portal systemic shunt (TIPS)
            Shunt between portal and hepatic vein to  pressure =  bleeding
       Other portal system shunts – poor prognosis
Sclerosing Procedure
Blakemore Tube
Another Blakemore Tube
               More Treatments
   PSE
      Low protein diet

         May need TPN

      Control GI bleeding

      Medications

      Neuro checks

      Look for signs and symptoms of the stages
       of PSE
                     Home Care
   Diet
       calories, vitamins, protein
       (unless PSE)
       sodium

   Medications
      Diurectics

      Antacids, H2-receptor
       antagonists
      No OTC medications

   No alcohol consumption
    activity – rest periods
   Home care equipment
           Evaluation Outcomes
   Patient will
       in ascites

      Electrolytes WNL

      B/P WNL

      No bleeding or
       complications from
       bleeding
      PSE managed
       immediatley
      Optimal quality of life
                                 EVOLUŢIE
Ciroză compensată  ciroză
decompensată vascular şi
parenchimatos
Rezerva funcţională – Clasificarea Child
 Parametru    1 pct.   2 pct.     3 pct.
Pugh
Albumina serică    >3,5      2,8-3,5        < 2,8
     Ascita        Abs      Moderată       Mare
 Encefalopatia     Abs      Grd. I, II   Grd. III, IV
   Bilirubina       <2         2-3           >3
 Indicele Quick   > 70%     40-70%         < 40%

      A: 5-6 pct., B: 7-9 pct., C: 10-15 pct.

				
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posted:7/27/2012
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