Hepatic Cirrhosis
Professor Wang Ji-yao
Department of Internal Medicine
Division of Gastroenterology,
Zhongshan hospital,Fu Dan university,
Cirrhosis---definition
chronic,progressed,diffuse
hepatocellular injury
fibrosis
nodular regeneration
Incidence,17/100000/y
Age,20-50 yr,
Hepatic cirrhosis
,
Etiology
Liver function Injury,Portal hypertension
Diffuse,chronic liver injury
Hepato-cellular
necrosis,collapse of
hepatic lobules
regenerative
nodules formation
Formation of
diffuse
fibrous septa
Complations,Upper GI Bleeding,
Hepatic coma,infections,primary liver cancer,
Functional renal failure
1.Chronic viral hepatitis (慢性病毒性肝炎 ),
[HBV,HCV,HBV+HDV]
2,Long-term alcoholism(慢性酒精中毒 )
[80g/d,10 yr.]
3,Prolonged cholestasis(长期胆汁郁积 ),intra-and
extra-hepatic,[primary biliary cirrhosis,PBC]
/[secondary biliary cirrhosis]
4,Drugs and toxins(药物和毒物 )
[toxic hepatitis---chronic active hepatitis---
cirrhosis]
5,Nonalcoholic steatohepatitis (NASH)(非酒精性
脂肪性肝炎 )
Etiology of cirrhosis(I)
Etiology of cirrhosis(II)
6,Hepatic venous outflow obstruction(肝血液循环
障碍 )
veno-occlusive disease,Budd-Chiari syndrome,constrictive
pericarditis
7,Metabolic disorders (遗传代谢性疾病 )
hemochromatosis(血色病 ); Wilson‘s disease(肝豆状核变性 );
8,Autoimmune hepatitis (AIH)(自身免疫性肝炎 )
9,Schistosomiasis (血吸虫病 )
10,Cryptogenic (隐原性 )
11,Mixed,alcohol+virus,HBV+HCV,HBV+schistosomiasis
Hepatic stellate cell activation
Liver fibrosis
accumulation of
extracellular
matrix in liver
synthesis
of matrix
proteins
degradation
of matrix
proteins
Collagens type I and III
constitute more than
95% of the total content
of increased collagen in
fibrotic liver
Pathogenesis,chronic,progressed,
diffuse
? Hepatocyte injury leading to necrosis,
? Chronic inflammation - (hepatitis),
? Capillarization (肝窦毛细血管化 ) of the space of
Disse is a key event,
? Bridging fibrosis,
? Regeneration of remaining hepatocytes
proliferate as round nodules surrounded by
fibrous septa,
? Loss of vascular arrangement results in
regenerating hepatocytes ineffective,
? Cirrhosis may lead to liver failure,portal
hypertension,or development of hepatocellular
carcinoma
Histopathologic classification
? micronodular
uniformly small nodules (< 3 mm in diameter) and
regular bands of connective tissue
? macronodular
nodules that vary in size (3 mm to 5 cm in diameter)
? mixed macro and micronodular
(incomplete septal cirrhosis) combines elements
of micronodular and macronodular cirrhosis,
Consequences of portal hypertension[I]
1.Splenomegaly (脾肿大 )
2.Formation and open of portal-
systemic collateral’s (门体侧支循环
开放 )
--Esophageal/gastric varices (食管 /胃静脉曲张 )
(short gastric/coronary veins)
--Rectal collateral‘s(痔静脉丛 )
(Suphemorrhoidal/middle & inf,hemorrhoidal)
--Caput medusae(水母头 )( umbilical/epigastric)
--abdominal wall varices (腹壁静脉曲张 )
--Portal system and left renal
Consequences of portal hypertension[II]
3,Ascites (腹水 )
Theories of ascites formation
? Underfilling theory (灌注不足假说）
? Overflow theory (泛溢假说 )
? Arterial vasodilation theory (动脉扩张假说 )
Ascites
? Sodium retention
---Renin angiotension aldosterone system(RAAS)?
---sympathetic nerve system ?,norepinephrine?
--- Intrarenal factors,Kallikrein-kinin system,
Adenosine,
? Water retention
---Antidiuretic hormone(ADH)?
---Impaired renal synthesis of PGs (PGE2?)
? Renal vasoconstriction
--- RAAS,AngiotensionII?
---SNS
---ADH?
---ET?
Endocrine system
?gynecomastia(男性乳房发育 ),
telangiectases (毛细血管扩张症 ),
spider nevi(蜘蛛痣 ),
palmar erythema(肝掌 )
testicular atrophy(睾丸萎缩 )
menstrual irregularities (月经失调 )
Pulmonary manifestations
?Hepatic hydrothorax (肝性胸水 )
?Hepatopulmonary syndrome
(HPS,肝肺综合征 )
HRS is characterized clinically by the triad of
pulmonary vascular dilatation causing arterial
hypoxemia in the setting of advanced liver
disease,
HRS(Hepatorenal syndrome,肝肾综合征 )
? Occurred in the setting of,
---chronic liver disease
---advanced hepatic failure
---portal hypertension
? characterized by,
---impaired renal function
---marked abnormalities in arterial circulation
---activation of endogenous vasoactive system
? Classified into 2 different types,
---Type I,Rapidly progressive
---Type II,Not rapidly progressive,Often results in
mild renal insufficiency causing diuretic resistant ascites
Mechanisms of HRS[II]
Clinical features[I]
Compensated cirrhosis (代偿期 )
Many people experience few symptoms at the onset of
cirrhosis,symptoms are typically vague and nonspecific,
---Fatigue and loss of energy,
---Loss of appetite and nausea,
---Spider angiomas
---liver function is normal
Decompensated cirrhosis (失代偿 )
? Symptoms caused by loss of functioning
liver cells
--- System,fatigue,weakness,weight loss,malnutrition
--- Digestive System:Loss of appetite,nausea,diarrhea,
Clinical features[II]
---Tendency to hemorrhage(出血倾向 ) and
anaemia(贫血 ),Due to reduced synthesis of
coagulation factors (II,V,VII,IX,X),
hypersplenism(脾亢 ),low platelet count,poor
absorption,gastrointestinal bleeding,
---Hormonal abnormalities
gynecomastia(男性乳房发育 ),telangiectases
(毛细血管扩张症 ),spider nevi(蜘蛛痣 ),palmar
erythema(肝掌 )
---Jaundice(黄疸 )
Clinical features[III]
Portal hypertension (门静脉高压 )
1,Splenomegaly,anemia,leukopenia,
thrombocytopenia due to hypersplenism
2,development and open of collateral vessels in
portal hypertension
a,Esophageal varices
b,Rectal collateral's
c,Caput medusae
d,Abdominal wall varices
e,Portal system and left renal
3,Ascites,hepatic hydrothorax
Clinical features[IV]
? Palpation of liver
firm,hard,irregular,enlargement
rounded or sharp edge
below the right lower ribs,
? The spleen is often palpable,and
may be very large,
The clinical
manifestations
found in
cirrhosis
,
Complications[I]
?Upper gastrointestinal bleeding(上消
化道出血 ),
Hematemesis(呕血 )/melena(黑粪 ),
Esophageal/ gastric variceal bleeding (食
管 /胃静脉出血 );
portal hypertensive gastropathy (门脉高压
性胃病 );
peptic ulcer(消化性溃疡 )
Infections,
spontaneous bacterial peritonitis(自发性细菌
性腹膜炎 ) (4-8%),Fever,worsening jaundice
or renal dysfunction,abdominal pain (occurring
only in 50% of patients),and encephalopathy
are the most common clinical findings in SBP,
However,the patient is frequently
asymptomatic,Because culture of ascites fluid
is negative in a large number of patients with
SBP,diagnosis should be based on the presence
of >250 neutrophils/mm3,
Complications[II]
?Hepatocellular carcinoma(肝细
胞肝癌 )
? Hepatic encephalopathy (肝性
脑病 )
Asterixis(扑翼样振颤 )
Disoriented(定向障碍 )
Coma(昏迷 )
Complications[III]
?Hepatorenal syndrome(HRS),
Oliguria(少尿 ),azotemia(氮质血
症 ),hypotension(低血压 ),dilutional
hyponatremia(稀释性低钠血症 ),low
urinary sodium(低钠尿 )
Complications[IV]
Electrolyte and acid-base
imbalance(电介质酸硷平衡失调 )
hyponatremia,hypokalemia
And hypochloremic alkalosis
Laboratory findings[I]
?Blood and urine routines
?Liver function tests
---to estimate the severity of liver
dysfunction,ALT,AST,AKP,GGT,
serum total bilirubin,serum albumin,
prothrombin time,globulin,cholesterol,
--- to differential diagnosis,
Alcoholic,AST/ALT>=2;
PBC,AKP,GGT>>ALT,AST
---to refect hepatic fibrosis,PIIIP,HA、
laminin
---to quanlity liver function
Immunology
?Cellular immune?,hormonal
?immune?autoimmune liver disease,
IgG?,globulin? ANA(+),SMA(+)
?PBC,IgM?,AMA(+)
?Marker of virus
?AFP
Laboratory findings[II]
? Ascites paracentesis,
routine,culture,ADA,LDH,
SAAG (serum ascites albumin gradient)
(血清腹水白蛋白梯度 ) > 11g/L
? Ultrasonography,CT scanning,
biliary obstruction,liver masses,
splenomegaly,ascites,
? Endoscopy,
the number,appearance,and size of any
esophageal/gastric varix,
portal hypertensive gastropathy (PHG)
Laboratory findings[III]
? Radionuclide,99m TC-MIBI,H/L
? liver biopsy,to confirm the diagnosis
? Laparoscopy
? HVPG (hepatic vein pressure gradient)(肝静脉
压力梯度 ) (wedged - free )hepatic venous
pressure
Normal,5-6mmHg,
>10mmHg,varices;
>12mmHg:rupture
Diagnosis [I]
? Etiology of cirrhosis
? Pathology of cirrhosis
? Evaluating of liver function,Child-Pugh
classification
? Searching for complications
Diagnosis[II]
? the history of disease contributes to identifying the cause
of cirrhosis,
history of viral hepatitis,blood transfusions,medication
use,alcohol use,sexual practices should be carefully
reviewed,
? signs and symptoms confirm to existence of portal
hypertension and impared liver function,
? liver function tests,hypoalbuminemia,hyperbilirubinemia，
the prolonged prothrombin time suggest hepatic
decompensation,
? Imaging study,Ultrasound and CT readily identify the
lesion,but have no characteristic findings,
Child-Pugh classification
Scorea
variable 1 2 3
Encephalopathy(degree) Nil Slight-Moderate Moderate-Severe
Ascites(degree) Nil Slight Moderate-Severe
Bilirubin(umol/L) <34 34-51 >51
Albumin(g/L) ?35 28-34 <28
Prothrombin Index(%) >70 40-70 <40
Prothrombin Time(s) <14 15-17 >18
Prothrombin Time(INR) <1.3 1.3～ 1.5 >1.5
* PBC,SB(μ mol/L) 17～ 68 68～ 170 >170
aScores are summed to determine Child’s class,
class A=5-6 class B= 7-9 class C= 10-15
Diagnosis[III]
Differential Diagnosis
?Other condition of hepatomegaly or
splenomegaly,
chronic virus hepatitis,Gaucher’s disease,
lymphomas and leukaemias,congestive splenomegaly
?Differebtial diagnosis of cirrhotic ascites
and other types of ascites,
malignant ascites,constrictive pericarditis,tuberculous
peritonitis,et al,
?Portal hypertension,
Treatment of cirrhosis[I]
?specific treatment for the underlying
etiology of the liver disease
antivirus therapy --viral hepatitis
abstinence from alcohol--alcoholic
Ursodeoxycholic acid(UDCA)(熊去氧胆酸 )--
PBC
Penicillamine(青霉胺 )— Wilson’s disease
?General Treatments,
High calories (40 kcal/kg· d),adequate protein
(1-1.5g/kg· d), vitamin,Herbal compounds,
Treatment of Ascites
a,Bed rest,sodium and water restriction,
1,Fluid intake,800-1000ml/d (hyponatremia,
serum sodium<130meq/L)
2,Dietary sodium intake, 88mmol/d
(2.0gNacl)
Mild patients,rest on bed, with dietary salt
restriction,loss of ascites occurs in 10% to
15% of patients,
Treatment of Ascites[II]
b,Increasing renal sodium and water
excretion,
--Diuretics,urinary sodium /urinary
potassium >1 Spironolactone(安体舒通 )
+furosemide(速尿 )
urinary sodium / urinary potassium <1
higher doses spironolactone,
Treatment of Ascites(III)
c,Large-volume paracentesis associated with
plasma volume expansion
d,Ascites ultrafiltration and re-infusion
e,Peritoneo-venous (LeVeen) shunts
f,TIPS(transjugular intrahepatic porto-systemic
stent)(经颈静脉门体分流术 )
g,Liver transplantation(肝移植 )
TIPS---stent positioned between the hepatic and portal veins
Treatment of cirrhosis[IV]
?surgical treatment of portal hypertension
portacaval shunt surgery,
portacaval
mesocaval
distal splenorenal shunts
Choice of patients,
Child-Pugh,A,B
bleeding from gastroesophageal varices,
hypersplenism,
Treatment of cirrhosis[V]
?Treatment complations
? Treatment of acute variceal haemorrhage,
----General management,abstain food,intensive
care,volume and blood replacement,specific
measures to stop the bleeding
---- Pharmacological therapy,
vasopressin(垂体后叶素 )
somatostatin(生长抑素 )
Octreotide(奥曲肽 )
Treatment of acute variceal
haemorrhage,
___Emergent endoscopy,after Patient’s hemodynamic status stabilized(usually within
2-12 hours)
----Balloon tube tamponade( if bleeding
continues)
----Endoscopic variceal sclerotherapy and band
ligation
----Prophylactic therapy to prevent rebleeding,
Beta-adrenergic antagonists(普奈 洛 尔 ),
endoscopic sclerotherapy(硬化剂 )/banding(套
扎 ) (usually 3-6 sessions),portacaval shunting,
TIPS
TIPS---stent positioned between the hepatic and portal veins
Treatment
portal hypertension
(<12mmHg)
Eradicate varices
Liver transplantation
Shunt
Surgical shunts
TIPS
Pharmacotherapy Q
Endoscopy,EVS,EVL
Devascularization
R
Treatment of SBP
1,Ascites PMN>250/mm3, antibiotic therapy should be
initiated,
2,Ascites PMN<250/mm3 and ascitic fluid culture
continues to be positive,initiation of antibiotic treatment,
3,Follow-up diagnostic paracentesis performed 48 hours
after starting therapy allows assessment of response to
treatment and the need to modify antibiotic coverage,
4,Long-term prophylaxis ---Patients who have recovered
from an episode of SBP are at a high risk of developing
SBP recurrence,
Therapies for HRS[I]
? Avoid use of nephrotoxic drugs,
（ 1） Antibiotics, aminoglycosides
（ 2） NSAIDs,inhibit formation intrarenal
prostaglandins
---marked decline in renal function
? Avoid and treat factors to hypovolaemia,
（ 1） active treatments of upper gastrointestinal
bleeding
（ 2） Judicious use of diuretics（ weight loss<0.5Kg/d）
? Rectify electrolyte and metabolic
imbalance,Fluid intake restriction
Therapies for HRS[II]
? Volume expansion,with IV dextrose,plasma,albumin
or Concomitant plasma volume expansion with
albumin has been used with LVP to correct decreased
effective arterial volume that leads to sodium retention,
TIPS
? Vasoactive drugs,terlipressin(可利新 ),
ornipressin,dopamine,---increasing renal plasma flow
? Elimination of endotoxaemia and control
infections
? Liver transplantation,the most effective
treatment for patients with HRS
Indications for Liver transplantation
(irreversible,progressive chronic liver diseases)
? Primary biliary cirrhosis
? Sclerosing cholangitis
? Fulminant liver failure
? Metabolic liver diseases
? Alcoholic cirrhosis
? Postnecrotic cirrhosis
? Autoimmune liver disease
? Budd-Chiari syndrome
? Hepatocellular carcinoma
Indications for Liver transplantation
(cirrhosis)
? Refractory ascites
? Recurrent variceal bleeding
? Hepatic encephalopathy
? spontaneous bacterial peritonitis
? Worsening functional status,rising
bilirubin,decreasing albumin,worsening
coagulopathy (Child-Pugh C)
Professor Wang Ji-yao
Department of Internal Medicine
Division of Gastroenterology,
Zhongshan hospital,Fu Dan university,
Cirrhosis---definition
chronic,progressed,diffuse
hepatocellular injury
fibrosis
nodular regeneration
Incidence,17/100000/y
Age,20-50 yr,
Hepatic cirrhosis
,
Etiology
Liver function Injury,Portal hypertension
Diffuse,chronic liver injury
Hepato-cellular
necrosis,collapse of
hepatic lobules
regenerative
nodules formation
Formation of
diffuse
fibrous septa
Complations,Upper GI Bleeding,
Hepatic coma,infections,primary liver cancer,
Functional renal failure
1.Chronic viral hepatitis (慢性病毒性肝炎 ),
[HBV,HCV,HBV+HDV]
2,Long-term alcoholism(慢性酒精中毒 )
[80g/d,10 yr.]
3,Prolonged cholestasis(长期胆汁郁积 ),intra-and
extra-hepatic,[primary biliary cirrhosis,PBC]
/[secondary biliary cirrhosis]
4,Drugs and toxins(药物和毒物 )
[toxic hepatitis---chronic active hepatitis---
cirrhosis]
5,Nonalcoholic steatohepatitis (NASH)(非酒精性
脂肪性肝炎 )
Etiology of cirrhosis(I)
Etiology of cirrhosis(II)
6,Hepatic venous outflow obstruction(肝血液循环
障碍 )
veno-occlusive disease,Budd-Chiari syndrome,constrictive
pericarditis
7,Metabolic disorders (遗传代谢性疾病 )
hemochromatosis(血色病 ); Wilson‘s disease(肝豆状核变性 );
8,Autoimmune hepatitis (AIH)(自身免疫性肝炎 )
9,Schistosomiasis (血吸虫病 )
10,Cryptogenic (隐原性 )
11,Mixed,alcohol+virus,HBV+HCV,HBV+schistosomiasis
Hepatic stellate cell activation
Liver fibrosis
accumulation of
extracellular
matrix in liver
synthesis
of matrix
proteins
degradation
of matrix
proteins
Collagens type I and III
constitute more than
95% of the total content
of increased collagen in
fibrotic liver
Pathogenesis,chronic,progressed,
diffuse
? Hepatocyte injury leading to necrosis,
? Chronic inflammation - (hepatitis),
? Capillarization (肝窦毛细血管化 ) of the space of
Disse is a key event,
? Bridging fibrosis,
? Regeneration of remaining hepatocytes
proliferate as round nodules surrounded by
fibrous septa,
? Loss of vascular arrangement results in
regenerating hepatocytes ineffective,
? Cirrhosis may lead to liver failure,portal
hypertension,or development of hepatocellular
carcinoma
Histopathologic classification
? micronodular
uniformly small nodules (< 3 mm in diameter) and
regular bands of connective tissue
? macronodular
nodules that vary in size (3 mm to 5 cm in diameter)
? mixed macro and micronodular
(incomplete septal cirrhosis) combines elements
of micronodular and macronodular cirrhosis,
Consequences of portal hypertension[I]
1.Splenomegaly (脾肿大 )
2.Formation and open of portal-
systemic collateral’s (门体侧支循环
开放 )
--Esophageal/gastric varices (食管 /胃静脉曲张 )
(short gastric/coronary veins)
--Rectal collateral‘s(痔静脉丛 )
(Suphemorrhoidal/middle & inf,hemorrhoidal)
--Caput medusae(水母头 )( umbilical/epigastric)
--abdominal wall varices (腹壁静脉曲张 )
--Portal system and left renal
Consequences of portal hypertension[II]
3,Ascites (腹水 )
Theories of ascites formation
? Underfilling theory (灌注不足假说）
? Overflow theory (泛溢假说 )
? Arterial vasodilation theory (动脉扩张假说 )
Ascites
? Sodium retention
---Renin angiotension aldosterone system(RAAS)?
---sympathetic nerve system ?,norepinephrine?
--- Intrarenal factors,Kallikrein-kinin system,
Adenosine,
? Water retention
---Antidiuretic hormone(ADH)?
---Impaired renal synthesis of PGs (PGE2?)
? Renal vasoconstriction
--- RAAS,AngiotensionII?
---SNS
---ADH?
---ET?
Endocrine system
?gynecomastia(男性乳房发育 ),
telangiectases (毛细血管扩张症 ),
spider nevi(蜘蛛痣 ),
palmar erythema(肝掌 )
testicular atrophy(睾丸萎缩 )
menstrual irregularities (月经失调 )
Pulmonary manifestations
?Hepatic hydrothorax (肝性胸水 )
?Hepatopulmonary syndrome
(HPS,肝肺综合征 )
HRS is characterized clinically by the triad of
pulmonary vascular dilatation causing arterial
hypoxemia in the setting of advanced liver
disease,
HRS(Hepatorenal syndrome,肝肾综合征 )
? Occurred in the setting of,
---chronic liver disease
---advanced hepatic failure
---portal hypertension
? characterized by,
---impaired renal function
---marked abnormalities in arterial circulation
---activation of endogenous vasoactive system
? Classified into 2 different types,
---Type I,Rapidly progressive
---Type II,Not rapidly progressive,Often results in
mild renal insufficiency causing diuretic resistant ascites
Mechanisms of HRS[II]
Clinical features[I]
Compensated cirrhosis (代偿期 )
Many people experience few symptoms at the onset of
cirrhosis,symptoms are typically vague and nonspecific,
---Fatigue and loss of energy,
---Loss of appetite and nausea,
---Spider angiomas
---liver function is normal
Decompensated cirrhosis (失代偿 )
? Symptoms caused by loss of functioning
liver cells
--- System,fatigue,weakness,weight loss,malnutrition
--- Digestive System:Loss of appetite,nausea,diarrhea,
Clinical features[II]
---Tendency to hemorrhage(出血倾向 ) and
anaemia(贫血 ),Due to reduced synthesis of
coagulation factors (II,V,VII,IX,X),
hypersplenism(脾亢 ),low platelet count,poor
absorption,gastrointestinal bleeding,
---Hormonal abnormalities
gynecomastia(男性乳房发育 ),telangiectases
(毛细血管扩张症 ),spider nevi(蜘蛛痣 ),palmar
erythema(肝掌 )
---Jaundice(黄疸 )
Clinical features[III]
Portal hypertension (门静脉高压 )
1,Splenomegaly,anemia,leukopenia,
thrombocytopenia due to hypersplenism
2,development and open of collateral vessels in
portal hypertension
a,Esophageal varices
b,Rectal collateral's
c,Caput medusae
d,Abdominal wall varices
e,Portal system and left renal
3,Ascites,hepatic hydrothorax
Clinical features[IV]
? Palpation of liver
firm,hard,irregular,enlargement
rounded or sharp edge
below the right lower ribs,
? The spleen is often palpable,and
may be very large,
The clinical
manifestations
found in
cirrhosis
,
Complications[I]
?Upper gastrointestinal bleeding(上消
化道出血 ),
Hematemesis(呕血 )/melena(黑粪 ),
Esophageal/ gastric variceal bleeding (食
管 /胃静脉出血 );
portal hypertensive gastropathy (门脉高压
性胃病 );
peptic ulcer(消化性溃疡 )
Infections,
spontaneous bacterial peritonitis(自发性细菌
性腹膜炎 ) (4-8%),Fever,worsening jaundice
or renal dysfunction,abdominal pain (occurring
only in 50% of patients),and encephalopathy
are the most common clinical findings in SBP,
However,the patient is frequently
asymptomatic,Because culture of ascites fluid
is negative in a large number of patients with
SBP,diagnosis should be based on the presence
of >250 neutrophils/mm3,
Complications[II]
?Hepatocellular carcinoma(肝细
胞肝癌 )
? Hepatic encephalopathy (肝性
脑病 )
Asterixis(扑翼样振颤 )
Disoriented(定向障碍 )
Coma(昏迷 )
Complications[III]
?Hepatorenal syndrome(HRS),
Oliguria(少尿 ),azotemia(氮质血
症 ),hypotension(低血压 ),dilutional
hyponatremia(稀释性低钠血症 ),low
urinary sodium(低钠尿 )
Complications[IV]
Electrolyte and acid-base
imbalance(电介质酸硷平衡失调 )
hyponatremia,hypokalemia
And hypochloremic alkalosis
Laboratory findings[I]
?Blood and urine routines
?Liver function tests
---to estimate the severity of liver
dysfunction,ALT,AST,AKP,GGT,
serum total bilirubin,serum albumin,
prothrombin time,globulin,cholesterol,
--- to differential diagnosis,
Alcoholic,AST/ALT>=2;
PBC,AKP,GGT>>ALT,AST
---to refect hepatic fibrosis,PIIIP,HA、
laminin
---to quanlity liver function
Immunology
?Cellular immune?,hormonal
?immune?autoimmune liver disease,
IgG?,globulin? ANA(+),SMA(+)
?PBC,IgM?,AMA(+)
?Marker of virus
?AFP
Laboratory findings[II]
? Ascites paracentesis,
routine,culture,ADA,LDH,
SAAG (serum ascites albumin gradient)
(血清腹水白蛋白梯度 ) > 11g/L
? Ultrasonography,CT scanning,
biliary obstruction,liver masses,
splenomegaly,ascites,
? Endoscopy,
the number,appearance,and size of any
esophageal/gastric varix,
portal hypertensive gastropathy (PHG)
Laboratory findings[III]
? Radionuclide,99m TC-MIBI,H/L
? liver biopsy,to confirm the diagnosis
? Laparoscopy
? HVPG (hepatic vein pressure gradient)(肝静脉
压力梯度 ) (wedged - free )hepatic venous
pressure
Normal,5-6mmHg,
>10mmHg,varices;
>12mmHg:rupture
Diagnosis [I]
? Etiology of cirrhosis
? Pathology of cirrhosis
? Evaluating of liver function,Child-Pugh
classification
? Searching for complications
Diagnosis[II]
? the history of disease contributes to identifying the cause
of cirrhosis,
history of viral hepatitis,blood transfusions,medication
use,alcohol use,sexual practices should be carefully
reviewed,
? signs and symptoms confirm to existence of portal
hypertension and impared liver function,
? liver function tests,hypoalbuminemia,hyperbilirubinemia，
the prolonged prothrombin time suggest hepatic
decompensation,
? Imaging study,Ultrasound and CT readily identify the
lesion,but have no characteristic findings,
Child-Pugh classification
Scorea
variable 1 2 3
Encephalopathy(degree) Nil Slight-Moderate Moderate-Severe
Ascites(degree) Nil Slight Moderate-Severe
Bilirubin(umol/L) <34 34-51 >51
Albumin(g/L) ?35 28-34 <28
Prothrombin Index(%) >70 40-70 <40
Prothrombin Time(s) <14 15-17 >18
Prothrombin Time(INR) <1.3 1.3～ 1.5 >1.5
* PBC,SB(μ mol/L) 17～ 68 68～ 170 >170
aScores are summed to determine Child’s class,
class A=5-6 class B= 7-9 class C= 10-15
Diagnosis[III]
Differential Diagnosis
?Other condition of hepatomegaly or
splenomegaly,
chronic virus hepatitis,Gaucher’s disease,
lymphomas and leukaemias,congestive splenomegaly
?Differebtial diagnosis of cirrhotic ascites
and other types of ascites,
malignant ascites,constrictive pericarditis,tuberculous
peritonitis,et al,
?Portal hypertension,
Treatment of cirrhosis[I]
?specific treatment for the underlying
etiology of the liver disease
antivirus therapy --viral hepatitis
abstinence from alcohol--alcoholic
Ursodeoxycholic acid(UDCA)(熊去氧胆酸 )--
PBC
Penicillamine(青霉胺 )— Wilson’s disease
?General Treatments,
High calories (40 kcal/kg· d),adequate protein
(1-1.5g/kg· d), vitamin,Herbal compounds,
Treatment of Ascites
a,Bed rest,sodium and water restriction,
1,Fluid intake,800-1000ml/d (hyponatremia,
serum sodium<130meq/L)
2,Dietary sodium intake, 88mmol/d
(2.0gNacl)
Mild patients,rest on bed, with dietary salt
restriction,loss of ascites occurs in 10% to
15% of patients,
Treatment of Ascites[II]
b,Increasing renal sodium and water
excretion,
--Diuretics,urinary sodium /urinary
potassium >1 Spironolactone(安体舒通 )
+furosemide(速尿 )
urinary sodium / urinary potassium <1
higher doses spironolactone,
Treatment of Ascites(III)
c,Large-volume paracentesis associated with
plasma volume expansion
d,Ascites ultrafiltration and re-infusion
e,Peritoneo-venous (LeVeen) shunts
f,TIPS(transjugular intrahepatic porto-systemic
stent)(经颈静脉门体分流术 )
g,Liver transplantation(肝移植 )
TIPS---stent positioned between the hepatic and portal veins
Treatment of cirrhosis[IV]
?surgical treatment of portal hypertension
portacaval shunt surgery,
portacaval
mesocaval
distal splenorenal shunts
Choice of patients,
Child-Pugh,A,B
bleeding from gastroesophageal varices,
hypersplenism,
Treatment of cirrhosis[V]
?Treatment complations
? Treatment of acute variceal haemorrhage,
----General management,abstain food,intensive
care,volume and blood replacement,specific
measures to stop the bleeding
---- Pharmacological therapy,
vasopressin(垂体后叶素 )
somatostatin(生长抑素 )
Octreotide(奥曲肽 )
Treatment of acute variceal
haemorrhage,
___Emergent endoscopy,after Patient’s hemodynamic status stabilized(usually within
2-12 hours)
----Balloon tube tamponade( if bleeding
continues)
----Endoscopic variceal sclerotherapy and band
ligation
----Prophylactic therapy to prevent rebleeding,
Beta-adrenergic antagonists(普奈 洛 尔 ),
endoscopic sclerotherapy(硬化剂 )/banding(套
扎 ) (usually 3-6 sessions),portacaval shunting,
TIPS
TIPS---stent positioned between the hepatic and portal veins
Treatment
portal hypertension
(<12mmHg)
Eradicate varices
Liver transplantation
Shunt
Surgical shunts
TIPS
Pharmacotherapy Q
Endoscopy,EVS,EVL
Devascularization
R
Treatment of SBP
1,Ascites PMN>250/mm3, antibiotic therapy should be
initiated,
2,Ascites PMN<250/mm3 and ascitic fluid culture
continues to be positive,initiation of antibiotic treatment,
3,Follow-up diagnostic paracentesis performed 48 hours
after starting therapy allows assessment of response to
treatment and the need to modify antibiotic coverage,
4,Long-term prophylaxis ---Patients who have recovered
from an episode of SBP are at a high risk of developing
SBP recurrence,
Therapies for HRS[I]
? Avoid use of nephrotoxic drugs,
（ 1） Antibiotics, aminoglycosides
（ 2） NSAIDs,inhibit formation intrarenal
prostaglandins
---marked decline in renal function
? Avoid and treat factors to hypovolaemia,
（ 1） active treatments of upper gastrointestinal
bleeding
（ 2） Judicious use of diuretics（ weight loss<0.5Kg/d）
? Rectify electrolyte and metabolic
imbalance,Fluid intake restriction
Therapies for HRS[II]
? Volume expansion,with IV dextrose,plasma,albumin
or Concomitant plasma volume expansion with
albumin has been used with LVP to correct decreased
effective arterial volume that leads to sodium retention,
TIPS
? Vasoactive drugs,terlipressin(可利新 ),
ornipressin,dopamine,---increasing renal plasma flow
? Elimination of endotoxaemia and control
infections
? Liver transplantation,the most effective
treatment for patients with HRS
Indications for Liver transplantation
(irreversible,progressive chronic liver diseases)
? Primary biliary cirrhosis
? Sclerosing cholangitis
? Fulminant liver failure
? Metabolic liver diseases
? Alcoholic cirrhosis
? Postnecrotic cirrhosis
? Autoimmune liver disease
? Budd-Chiari syndrome
? Hepatocellular carcinoma
Indications for Liver transplantation
(cirrhosis)
? Refractory ascites
? Recurrent variceal bleeding
? Hepatic encephalopathy
? spontaneous bacterial peritonitis
? Worsening functional status,rising
bilirubin,decreasing albumin,worsening
coagulopathy (Child-Pugh C)
