肝硬化(Cirrhosis of Liver)

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肝硬化(Cirrhosis of Liver) Powered By Docstoc
					LIVER CIRRHOSIS

THE FIRST AFFILIATED HOSPITAL OF
     JIANGXI MEDICAL COLLEGE

 ZHANG KUN HE (张焜和)
  What is hepatocirrhosis
• It is a kind of common,chronic,progressive and diffusing
  liver disease.
• Its histological feature is nodular regeneration of liver cells,
  fibrosis and forming pseudo-lobule.
• Contracture of fibrous tissue makes liver deform and
  sclerosis.
• Manifestation: damage of liver cells and portal
  hypertension
• Many serious complications occur in later period
• It more occurs in males. Males:females=3.6~8:1
• It often occurs in forties(35~48)
ETIOLOGY
Etiologic classification

• Viral hepatitis hepatocirrhosis
• Alcoholic cirrhosis
• Schistosomiasis hepatocirrhosis
• Biliary cirrhosis
• Metabolic hepatocirrhosis
• Others
Viral hepatitis and liver cirrhosis
 • The commonest factor of hepatocirrhosis in China
 • Infection of HBV, HCV or HBV+HDV
 • Superinfection of several kinds of virus causes it most
   easily.
 • Viral infection can result in chronic hepatitis, especially
   chronic active hepatitis
 • Chronic damage of liver develops into post-hepatitis
   cirrhosis in the end.
 • HAV and HEV only cause acute hepatitis.They can not
   result in hepatocirrhosis.
HBV
   Chronic schistosomiasis
     and hepatocirrhosis
• Schistosomiasis is still a common factor of
  hepatocirrhosis in epidemic-stricken area
• Long-term or repeated infection of Japanese
  blood flukes
• Mass eggs deposit in portal area
• Mass fibrous tissues proliferate in portal area
• Ultimately it develops into schistosomiasis
  hepatic fibrosis.
• Portal hypertension is the major
  manifestation.Damage of liver is gentler
   Chronic alcoholism and
      hepatocirrhosis
• Liver is the unique organ where alcohol is
  metabolized
• Long-term drinking(>10 years)and mass
  alcohol(>80g) may cause hepatocirrhosis
• Metabolite(acetaldehyde) of alcohol can result in
  chronic lesion of liver
• Alcoholic hepatitis and alcoholic fatty liver are
  caused and develop into alcoholic cirrhosis later
alcoholic cirrhosis
Cholestasis and hepatocirrhosis
 • Intrahepatic or extrahepatic bile duct obstruction
   lasts for a long time resulting in long-term
   depositing bile
 • Depositing bile damages liver and stimulates
   fibers proliferation which cause biliary cirrhosis at
   last
 • The cause of primary biliary cirrhosis is indistinct
 • Secondary biliary cirrhosis is caused by choleith
   blocking bile duct
primary biliary cirrhosis
        Circulatory disorder
        and hepatocirrhosis

• Liver chronic congestion→hypoxia →
  hepatocyte necrosis →fibrous tissue
  proliferation → cirrhosis of liver
• Chronic congestive heart failure
  (constrictive pericarditis)→cardiac cirrhosis
• Obstruction of hepatic veins or inferior vena
  cava → cirrhosis of liver
       Toxicity hepatitis and
         cirrhosis of liver
• Hepatotoxicity poison:tetrachloride,
 phosphorum, arsenic
• Hepatotoxicity drug:isaphenin, methyl-
 DOPA、tetracycline
• Chronic toxicity hepatitis→cirrhosis of liver
     Metabolic disorders and
        cirrhosis of liver
• Inherited diseases
• Copper metabolic disorder: hepatolenticular
  degeneration→deposition of copper → fibers
  proliferation →cirrhosis of liver
• Ferrum metabolic disorder:hemachromatosis
  →deposition of iron → cirrhosis of liver
• a1-anti-trypsin deficiency syndrome
• Galactosemia
Malnutrition and liver cirrhosis

• Lose of nutrien and malabsorption:IBD

• Long-term deficiency in food:malnutrition

• Fatty degeneration of liver→necrosis

 →cirrhosis of liver
        Hepatocirrhosis of
        unknown etiology

• The etiology is difficult to define

• Parts of them are of viral hepatitis
PATHOLOGY
Pathogenesis of hepatocirrhosis

     extensive necrosis of liver cells
                   ↓
           regenerated node
                   ↓
             pseudo-leaflet
                   ↓
          portal hypertension
Pathologic classification of
     hepatocirrhosis
• Lesser tubercle cirrhosis:portal cirrhosis
• Greater tubercle cirrhosis:necrotic
 cirrhosis
• Mixed cirrhosis
• Others
Lesser tubercle cirrhosis

• Commonest,caused by chronic hepatitis

• Smaller nodes: Ø0.3~0.5cm

• The size of nodes is similar

• Pseudo-lobules are also similar in size
Lesser tubercle cirrhosis
Greater tubercle cirrhosis

• Caused by serious hepatic necrosis
• Greater nodes : Ø1~3cm
• Discrepancy in size
• Broder fibrous spetum,and vary in width
• Different size of pseudo-lobules
Greater tubercle cirrhosis
Mixed nodular cirrhosis

greater tubercle + lesser tubercle
Unconspicuous regenerated
    nodular cirrhosis
• Significant proliferation of fiber
• Fibrous spetum extend into hepatic lobules,
  but not completely cut apart hepatic lobule
• Fibrous tissues wrap many hepatic lobules
  and form multi-lobule nodes
• Unconspicuous regeneration in nodes
• Seeing in schistosomiasis hepatic fibrosis
 Pathologic features of liver
         cirrhosis
• Hepatomegaly early, evidently decreased in
  size later
• Fibers increase and become hard, so called
  “sclerosis”
• Nodular surface, so called “pineapple liver”
• Section shows islanded, wrapped by gray
  fibrous tissues
    Histologic features of
        liver cirrhosis
• Consisted of several non-integrality hepatic
  lobules, containing 0~3 central veins
• Consisted of regenerated nodes, irregular
  arrangement of cells
• Degeneration, necrosis and regeneration of liver
  cells
• Portal area significantly becomes broader
  because of proliferation of fibrous tissues and
  have infiltration of inflammatory cells and
  pseudo-bile duct
fibrous tissues
    Pathologic features of
        other organs
• Collateral circulation forming in esophagus,
  gastric fundus and abdominal wall varicosis
• Splenomegaly: hyperemia, proliferation of
  splenic pulp, hyperplasia of fibers
• Portal hypertension gastropathy: congestion,
  edema and erosion of gastric mucosa
• Others
   CLINIC
PRESENTATION
      Compensatory phase
        of liver function
• Symptoms mild, no specificity
• Digestive symptoms:anorexia, mild diarrhea
• Systemic symptoms:characterized with fatigue
• Signs:mild hepatomegaly, mildly hard quality,
  tenderness,mild~moderate splenomegaly
• Liver function tests:basically normal or mildly
  abnormal
Decompensatory phase of
     liver function
• Clinical presentations evident
• Divided into two categories
  • Presentations of liver function disfunction
  • Presentations of portal hypertension
• Presentations of complications
    Systemic symptoms of
  subsidence of liver function
• Malnutrition, weight loss
• Bad spirit, fatigue
• Facial features of liver disease, no politure,
  kraurotic skin
• Jaundice, suggesting significant necrosis of
  liver cells
• Irregular fever
     Digestive symptoms
• Poor appitite, nausea or epigastric distention after
  having food
• Diarrhea, induced when intaking unhealthful or
  fatty food
• Abdominal distention
• serious distention when with a great quantity of
  ascites
• Major causes of symptoms
   • Gastrointestinal congestion and edema,
     dysfunction of digestion and absorption
   • Dysbacteriosis of intestinal tract
          Manifestations of
          the blood system
• Hemorrhagic tendency:gingival bleeding, skin
  ecchymosis
   • Decreased synthesis of coagulation factors
   • Thrombocytopenia caused by hypersplenism
   • Increased capillary fragility
• Anemia, with different degrees based on causes
   • Malnutrition caused by dysfunction of digestion
     and absorption
   • Hypersplenism
   • Blood loss: gastrointestinal bleeding
 Endocrine disturbance
• Decreased inactivation of estrogen
   • sexual disturbance
   • spider nevus, liver palm, capillary
     telangiectasia
• Decreased inactivation of aldosterone:
  increased reabsorption of sodium, sodium
  retention
• Decreased inactivation of antidiuretic hormone:
  increased reabsorption of water
• Hypoadrenocorticism(feedback suppression):
  skin pigmentation, especially on face
        Splenomegaly
• Mild~moderate splenomegaly
• Spleen can temporarily shrink,even
  cannot be touched when upper digestive
  tract haemorrhages
• Hypersplenia may exist when three series
  of blood cells decrease
• Those with splenomegaly must exclude
  liver cirrhosis
   Collateral circulation
• When portal venous pressure exceeds
  200mmH2O,collateral circulation is formed
  between portal vein and systemic vein
  • Varicosis of esophagus and gastric
    fundus
  • Varicosis of abdominal wall
  • Phlebectasia of hemorrhoid
Portal hypertension: ascites
• The most significant presentation in
  decompensatory phase
• See in more than 75% patients
• Distention often prior to ascites
• Frog belly
• Part of patients with pleural fluid, mostly in
  right-sidedness
• Caused by excessive accumulation of
  sodium and water
         Causes of ascites
• Portal hypertension
• Hypoallbuminemia
• Increased hepatic and possibly splanchnic lymph
  fluid formation
• Secondary aldosteronism:increased
  reabsorption of sodium
• Antidiuretic hormone increased:water
  reabsorption increased
• Deficiency of effective circulating blood volume
     Palpation of liver
• Relatively hard quality

• Sharp edge

• Nodular or granular

• No tenderness without hepatitis, but
 tenderness with active hepatitis
Cirrhosis type & presentations

 • Lesser tubercle liver cirrhosis

 • Greater tubercle liver cirrhosis

 • Schistosomiasis liver cirrhosis
COMPLICATIONS
   Upper gastrointestinal
        hemorrhea
• The commonest complication
• Hematemesis and melena(tarry)
• Often evoking hepatic encephalopathy
  and greatly increased ascites
• Etiology
   • Esophageal and gastric varices
   • Erosive gastritis
   • Peptic ulcer disease
 Hepatic encephalopathy

• The most serious complication
• The commonest cause of death
• Based on metabolic disorder
• Symptoms of central neural system:
 abnormal behavior,disorder of
 consciousness and even coma
                  Infection
• Patients with liver cirrhosis are easily infected because
  of poor immunity
• Spontaneous peritonitis is serious infection
   • Abdominal pain
   • Ascites quickly increased or intractable ascites
   • Abdominal tenderness or peritoneal irritation sign
   • Fever
   • Mostly Gram-negative septicemia infection
   • Higher mortality rate
    Hepatorenal syndrome
• Massive ascites:deficiency of circulating blood
  volume→renal blood flow decreased→renal
  failure characterized with functional failure
• Clinical feature:spontaneous oliguresis or
  anuresis, azotemia, dilutional hyponatremia
• Complicated pathogenesis
   • Excitability of sympathetic nerve increased
   • Activity of renin-angiotensin system increased
   • Prostaglandin↓, thromboxane A2 ↑
   • Endotoxemia
   • Leukotriene increased
      Primary hepatocellular
           carcinoma
• With the background of liver cirrhosis in 80% of
  patients, especially post-hepatitis cirrhosis
• Often occurs in greater tubercle cirrhosis or mixed
  nodular cirrhosis
• Warning symptoms
  • Lasting hepatic region aching
  • Obviously emaciation recently
  • Newly developed hepatomegaly
  • touched mass on liver surface, hard like stone
  • bloody ascites
 Disturbance of acid-base balance
• Hyponatremia
   • Decreased dietary sodium:long-trem dietary salt
     restriction
   • Massive loss of sodium:diuresis, paracentesis
   • Dilutional hyponatremia:water retention exceed sodium
     retention
• Hypopotassaemia and hypochloraemia and metabolic
  alkalosis
   • Intake deficiency
   • Excessive loss:vomiting,diarrhea,diuresis
   • Secondary aldosteronism
   • Hypopotassaemia and hypochloraemia result in
     metabolic alkalosis,evoke hepatic encephalopathy
LABORATORY
   TESTS
Routine blood counts and
   Routine urine test
• Routine blood counts
  • Anemia :caused by bleeding or
    malnutrition
  • Three series blood cells decreased:
    hypersplenia
• Routine urine test
  • Bilirubin:jaundice
  • Increased urobilinogen:jaundice
  • Albuminuria, hematuria
    Liver function tests
• No significant abnormity in compensatory phase
• Overall lesion in decompensatory phase
  • Transaminase increased,AST>ALT
  • Bilirubin increased
  • GGT increased
  • Decreased albumin, globulin increased
  • Protein electrophoresis:albumin decreased,-
    globulin increased
  • Prothrombin time elongation
  • Liver backlog decreased:ICG clearance
    decreased
  Increased markers of liver
           fibrosis
• Hepatic fibrosis is pathologic foundation of
  liver cirrhosis
• Increased fibrosis index of active liver
  cirrhosis
   • P-III-P
   • HA
   • Laminin
   • Fibronectin
      Immunologic tests
• Decreased T lymphocytes, including CD3, CD4,
  CD8
• IgG obvious increased, paralleling to -globulin
  increased
• Marks of virus infection
   • HBV or HCV
   • HBV+HDV or HBV+HCV+HDV
• Nonspecific autoantibody
   • antinuclear antibody, antimitochondria
     antibody, smooth muscle antibody
            Ascites tests
• Typical: transudate
• Spontaneous peritonitis: between transudate and
  exudate
• Associated with peritoneal tuberculosis:
  significantly increased lymphocytes
• Associated with liver cancer: bloody ascites
         X-rays findings
• Esophagogram with barium swallow
  • Esophageal varices
  • Gastric varices
• CT(MRI)findings
  • Imbalance of liver lobes: right lobe atrophy, left
    lobe enlargement
  • Irregular liver surface
  • Splenomegaly
  • Ascites
       Ultrasonography
• B type ultrasound
  • Irregular liver contour, uneven echo, thicker
     spot, indistinct blood vessel
  • Splenomegaly
  • Portal vein >13mm, spleen vein >8mm
  • Ascites
  • Cholecyst wall coarse, increased thickness
• Ultrasound Doppler
  • Change of portal vein flow-rate, direction and
     blood flow
                Endoscopy
• Gastroscopy
   • Direct observation of the sites and degrees of
     esophagus and fundus varicosis
   • Diagnosis portal hypertension gastropathy
• Laparoscope
   • Direct observation of the liver contour, color and
     luster, edge
   • Direct observation of spleen
   • Feeling of liver rigidity with rod
   • Aspiration Biopsy under direct observation
 Liver aspiration biopsy
• Final diagnosis of liver cirrhosis
  • Detection of pseudo-lobule
• Diagnosis of liver cirrhosis activity
  • Silence: no obvious liver cells
    degeneration and necrosis
  • Activity: liver cell degeneration and
    necrosis
DIAGNOSIS AND
 DIFFERENTIAL
   DIAGNOSIS
Diagnosis of liver cirrhosis
• History :viral hepatitis,long-term drinking, etc
• Clinical situation:liver function decline, portal
  hypertension
• Palpation of liver:rigidity, sharp edge, nodular
• Abnormality of liver function test :-globulin
  increased obviously
• Imaging studies:liver deformation,
  splenomegaly, ascites
• Aspiration biopsy:pseudo-lobule
Differentiated with diseases
     with hepatomegaly
• Chronic hepatitis
• Primary liver carcinoma
• Clonorchiasis sinensis
• Hepatic echinococcosis
• Liver glycogenosis
• Hematologic diseases
Differentiated with diseases
    with abdominal bulge
• Peritoneal tuberculosis
• Constrictive pericarditis
• Chronic nephritis
• Enormous tumor in abdominal cavity
• Enormous ovarian cyst
    Differentiation of liver
   cirrhosis complications
• Upper gastrointestinal hemorrhage
  • Peptic ulcer
  • Erosive hemorrhagic gastritis
  • Gastric carcinoma
• Hepatic encephalopathy
  • Hypoglycemia
  • Uremia
  • Diabetic ketoacidosis
• Hepatorenal syndrome
  • Chronic nephritis
  • Acute renal tubular necrosis
MANAGEMENT
 Therapeutic principle
• No specific effective therapy
• Compensatory phase
  • Etiology therapy
  • emphasis of general therapy
• Decompensatory phase
  • Allopathy
  • improvement of liver function
  • Control of complications
       General therapy
• Rest
  • Relieving laboring strength, gentle work
  • Bed rest as major treatment in
    decompensatory phase
• Diet
  • Enough calorie, vitamins, protein
  • no alcohol
• Support therapy
  • give glucose, amino acid, vitamin, etc
    through vein
        Drug treatment
• No patent medicine
• Liver protection therapy
   • Vitamins
   • Liver protection medicine
• Anti-hepatic fibrosis
   • Colchicine
   • Dan-shen root, peach seed
• Chinese traditional medicine
  Therapy of ascites(1)
• Salt restriction:no salt or low salt diet(NaCl
  1.2~2.0g/d)
• Water restricton:500~1000ml/d
• Diuresis:
  • Moderate diuresis:weight loss <0.5kg/d
  • Moderate dosage:initiation with small
    dosage,
  • Combination of medication
    spironolactone+Furosemide: 100mg:40mg
      Ascites therapy(2)
• Merely tap the abdomen
   • Relieving compression symptom
   • ≤2~3L∕every time
• Tap the abdomen +infusion of albumin
   • Treatment of refractory ascites
   • 4~6L every time, meanwhile infusion of
     albumin 40~60g
• Rise of plasm colloid osmotic pressure
   • infusion of albumin or fresh plasm every
     week
       Ascites therapy(3)
• Back importation of concentrated ascites
   • Treatment of refractory ascites
   • releasing ascites (4~10L),concentrating to 500ml,
     then back importation through vein
   • Complication:fever,infection, electrolyte disturbance
• Peritoneojugular shunts
   • Placement non-return valve silictube between
     abdominal cavity and internal jugular vein
   • Impel by abdomen-pectoral cavity pressure difference
   • Complication:ascites leak, pulmonary
     edema,DIC,infection
     Ascites therapy(4)
• Transjugular intrahepatic portocaval shunt(TIPS)
   • Invasive radiologic procedures
   • Creation of diffluent way between portal vein and
     hepatic vein
   • Effectively decreased portal venous pressure,
     simple and safe operation
   • Serve to esophageal variceal hemorrhage and
     refractory ascites
   • Easy occurrence of hepatic encephalopathy
   • Obstruction of duct in short time
Operational therapy of portal
       hypertension
• Aim
   • Reduce portal venous pressure
   • Resolve hypersplenia
• Method
   • Bypass, cutoff
   • splenectomy
• Indication
   • Schistosomiasis hepatocirrhosis——bypass
   • Hepatitis hepatocirrhosis——cutoff
   • Contraindicates: jaundice, ascites, serious damage
     of liver function
     Therapy of upper
gastrointestinal hemorrhage
• Prohibition of food, bed rest, intensive care
• Supplement of blood volume: transfusion, fresh blood
• Effective hemostasia
   • Pituitrin,GIH
   • Balloon tamponade
   • Endoscopic hemostasia
   • Emergency operation or TIPS
• Prevention of rehemorrhage
   • Endoscopic injection of sclerosing agent or variceal
     ligation
   • Long-term intake of propranolol
 Therapy of spontaneous
       peritonitis
• Active treatment
• Earlier, sufficient, and associated
  application of antibacterial
   • Immediate medication after diagnosis
   • Cephalothin + quinolone
   • Enough dosage, lasting above two
     weeks
• effective support therapy
         Therapy of hepatic
          encephalopathy
• Eliminate the precipitating factors
• Promote reduction of poisonous products in the gut
• Deceased blood ammonia
• Branched-chain amino acids
• GABA/BZ receptor antagonists
• Artificial liver
• Allopathy
• Liver transplantation
     Therapy of hepatorenal
          symdrome
• Absence of efficient therapy, placing emphasis on
  prevention
• Liver protection
• Quick control of precipitating factors such as
  hemorrhage, infection
• Strict control of transfuse dose
• Balance water-electrolyte imbalance
• Diuresis after increasing circulating blood volume
• Blood vessel active medicine, improving RBF
Transplantation of liver
• The unique effective therapy for
  terminal hepatopathy
• Higher therapeutic demand
• Expensive cost
• Rejection
• Reinfection of HBV
Prognosis of liver cirrhosis
• Related with classification
   • Poor prognosis of virus cirrhosis, good of alcohol’s
• Related with disease activity
   • Poor prognosis of active cirrhosis, good of silence
• Related with Child-pugh grade
   • Best prognosis of A grade, worst of C grade
• Death cause
   • Hepatic encephalopathy, upper gastrointestinal
     hemorrhage, infection, hepatorenal syndrome
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posted:11/9/2011
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