cirrhosis n.
Skip this Video
Download Presentation

Loading in 2 Seconds...

play fullscreen
1 / 111

cirrhosis - PowerPoint PPT Presentation

  • Uploaded on

cirrhosis. Dr akhondei. cirrhosis. Cirrhosis is a pathologically defined entity that is associated with a spectrum of characteristic clininical manifestation 1-Irreversible chronic injury of the hepatic parenchyma 2-Extensive fibrosis 3-formation of regenerative nodules.

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'cirrhosis' - isaac-cox

Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript


Dr akhondei

  • Cirrhosis is a pathologically defined entity that is associated with a spectrum of characteristic clininical manifestation

1-Irreversible chronic injury of the hepatic parenchyma

2-Extensive fibrosis

3-formation of regenerative nodules


Cirrhosis of the liver is the third leading cause of death in people between the ages of 25 and 65 years, exceeded only by cardiovascular disease and cancer.


The cost of cirrhosis in terms of human suffering, financial burden, and loss of productive life is devastating.

patients with cirrhosis may present in a variety of ways
Patients with cirrhosis may present in a variety of ways.
  • Variceal bleeding
  • New onset of ascites
  • Hepatomegaly and/or
  • splenomegaly
patients with cirrhosis may present in a variety of ways1
Patients with cirrhosis may present in a variety of ways.
  • Incidental Discovery Of Abnormal Laboratory Tests
  • Serum Aminotransferases,
  • Hypoalbuminemia,
  • Prolonged Prothrombin Time,
  • Hrombocytopenia)
patients with cirrhosis may present in a variety of ways2
Patients with cirrhosis may present in a variety of ways.

Detection of the peripheral stigmata ofchronic liver disease such as

  • Jaundice,
  • Dupuytren's contracture,
  • Manifestations related to hyperestrogenemia such as
  • Spider angiomata,
  • Palmar erythema,
  • Gynecomastia, and testicular atrophy which may also be related to low testosterone concentrations
patients with cirrhosis may present in a variety of ways3
Patients with cirrhosis may present in a variety of ways.

hepatic encephalopathy or one or more complications or systemic manifestations of hepatocellular carcinoma

  • Some patients never come to clinical attention. In older reviews, cirrhosis was diagnosed at autopsy in up to 30 to 40 percent of patients
Cirrhosis represents the terminal stage of a number of chronic liver diseases including those caused by
  • excessive ethanol consumption
  • Viral hepatitis
  • Drugs and toxins,
  • Vascular
  • Autoimmune
  • Metabolic disorders
  • Cryptogenic.

In some cases, no cause can be determined and the cirrhosis is


Early cirrhosis may be asymptomatic and undetectable except by biopsy.

  • However, by the time cirrhosis becomes clinically apparent, hepatic functional reserve is markedly impaired.
  • If liver injury cannot be arrested, the prognosis without intervention is poor

The onset of complications

  • (eg, ascites, encephalopathy, variceal hemorrhage) indicates a more advanced stage of disease and a poorer prognosis, with median survival of about 5 years or less.
  • Term was 1st coined by Laennec in 1826
  • Many definitions but common theme is injury, repair, regeneration and scarring
  • NOT a localized process; involves entire liver
  • Primary histologic features:
    • Marked fibrosis
    • Destruction of vascular & biliary elements
    • Regeneration
    • Nodule formation
cirrhosis pathophysiology
Cirrhosis: Pathophysiology
  • Primary event is injury to hepatocellular elements
  • Initiates inflammatory response with cytokine release->toxic substances
  • Destruction of hepatocytes, bile duct cells, vascular endothelial cells
  • Repair thru cellular proliferation and regeneration
  • Formation of fibrous scar
cirrhosis pathophysiology1
Cirrhosis: Pathophysiology
  • Primary cell responsible for fibrosis is stellate cell
  • Become activated in response to injury and lead to ed expression of fibril-forming collagen
  • Above process is influenced by Kupffer cells which activate stellate cells by eliciting production of cytokines
  • Sinusoidal fenestrations are obliterated because of ed collagen and EC matrix synthesis
cirrhosis pathophysiology2
Cirrhosis: Pathophysiology
  • Prevents normal flow of nutrients to hepatocytes and increases vascular resistance
  • Initially, fibrosis may be reversible if inciting events are removed
  • With sustained injury, process of fibrosis becomes irreversible and leads to cirrhosis
causes of cirrhosis
Causes of Cirrhosis
  • Alcohol
  • Viral hepatitis
  • Biliary obstruction
  • Veno-occlusive disease
  • Hemochromatosis
  • Wilson’s disease
  • Autommune
  • Drugs and toxins
  • Metabolic diseases
  • Idiopathic
classification of cirrhosis
Classification of Cirrhosis
  • WHO divided cirrhosis into 3 categories based on morphological characteristics of the hepatic nodules
    • Micronodular
    • Macronodular
    • Mixed
micronodular cirrhosis
Micronodular Cirrhosis
  • Nodules are <3 mm in diameter
  • Relatively uniform in size
  • Distributed throughout the liver
  • Rarely contain portal tracts or efferent veins
  • Liver is of uniform size or mildly enlarged
  • Reflect relatively early disease
macronodular mixed cirrhosis
Macronodular & Mixed Cirrhosis
  • Nodules are >3 mm in diameter and vary considerably in size
  • Usually contain portal tracts and efferent veins
  • Liver is usually normal or reduced in size
  • Mixed pattern if both type of nodules are present in equal proportions
cirrhosis alcohol
Cirrhosis - Alcohol
  • Also known as Laennec’s cirrhosis
  • >50% of pts. with alcoholic cirrhosis die within 4 yrs of diagnosis
  • Develops in only 10% to 30% of heavy drinkers
  • Morphologically, micronodular pattern
  • Multifactorial - genetic, nutritional, drug use and viral
cirrhosis alcohol1
Cirrhosis - Alcohol
  • Fatty liver, alcoholic hepatitis
  • Histology - megamitochondria, Mallory bodies, inflammation, necrosis, fibrosis
  • Key mediator is acetaldehyde (ADH), the product of alcohol metabolism by alcohol dehydrogenase
  • ADH directly activates stellate cells, inhibits DNA repair and damage microtubules
nafld nash
  • Nonalcoholic Fatty Liver Disease and Steatohepatitis
  • Becoming more common
  • Infiltration of the liver with fat ± inflammation
  • Pathologically similar to alcoholic liver but in absence of alcohol
  • Associated with obesity, hyperlipidemia, NIDDM,
viral hepatitis
Viral Hepatitis
  • Most common cause of cirrhosis worldwide (>50% of cases)
  • Incidence of cirrhosis in Hepatitis B pts. is 1% and 10% in Hepatitis C pts.
  • Incidence increases to 70-80% in HBV +ve pts. who are superinfected with HDV
  • Can be asymptomatic for decades
  • History
  • Physical findings: Hepatomegaly, jaundice, ascites, spider angioma, splenomegaly, palmar erythema, fetor hepaticus, purpura etc.
  • Elevated LFTs, thrombocytopenia,
  • Definitive diagnosis is by biopsy or gross inspection of liver
  • Noninvasive methods include US, CT scan, MRI
  • Indirect evidence - esophageal varices seen during endoscopy
manifestations of cirrhosis
Manifestations of Cirrhosis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Portal hypertension
  • Water retention
  • Hematologic
  • Hepatocellular carcinoma
portal hypertension ph
Portal Hypertension (PH)
  • Portal vein pressure above the normal range of 5 to 8 mm Hg
  • Portal vein - Hepatic vein pressure gradient greater than 5 mm Hg (>12 clinically significant)
  • Represents an increase of the hydrostatic pressure within the portal vein or its tributaries
pathophysiology of ph
Pathophysiology of PH
  • Cirrhosis results in scarring (perisinusoidal deposition of collagen)
  • Scarring narrows and compresses hepatic sinusoids (fibrosis)
  • Progressive increase in resistance to portal venous blood flow results in PH
  • Portal vein thrombosis, or hepatic venous obstruction also cause PH by increasing the resistance to portal blood flow
pathophysiology of ph1
Pathophysiology of PH
  • As pressure increases, blood flow decreases and the pressure in the portal system is transmitted to its branches
  • Results in dilation of venous tributaries
  • Increased blood flow through collaterals and subsequently increased venous return cause an increase in cardiac output and total blood volume and a decrease in systemic vascular resistance
  • With progression of disease, blood pressure usually falls
portal vein collaterals
PortalVein Collaterals
  • Coronary vein and short gastric veins -> veins of the lesser curve of the stomach and the esophagus, leading to the formation of varices
  • Inferior mesenteric vein -> rectal branches which, when distended, form hemorrhoids
  • Umbilical vein ->epigastric venous system around the umbilicus (caput medusae)
  • Retroperitoneal collaterals ->gastrointestinal veins through the bare areas of the liver
etiology of ph
Etiology of PH
  • Causes of PH can be divided into
    • Pre-hepatic
    • Intra-hepatic
    • Post-hepatic
pre hepatic ph
Pre-hepatic PH
  • Caused by obstruction to blood flow at the level of portal vein
  • Examples: congenital atresia, extrinsic compression, schistosomiasis, portal, superior mesenteric, or splenic vein thrombosis
post hepatic
  • Caused by obstruction to blood flow at the level of hepatic vein
  • Examples: Budd-Chiari syndrome, chronic heart failure, constrictive pericarditis, vena cava webs
budd chiari syndrome
Budd-Chiari Syndrome
  • Caused by hepatic venous obstruction
  • At the level of the inferior vena cava, the hepatic veins, or the central veins within the liver itself
  • result of congenital webs (in Africa and Asia), acute or chronic thrombosis (in the West), and malignancy
budd chiari syndrome1
Budd-Chiari Syndrome
  • Acute symptoms include hepatomegaly, RUQ abdominal pain, nausea, vomiting, ascites
  • Chronic form present with the sequelae of cirrhosis and portal hypertension, including variceal bleeding, ascites, spontaneous bacterial peritonitis, fatigue, and encephalopathy
  • Diagnosis is most often made by US evaluation of the liver and its vasculature
  • Cross-sectional imaging using contrast-enhanced CT or MRI
budd chiari syndrome2
Budd-Chiari Syndrome
  • Gold standard for the diagnosis has been angiography
  • Management has traditionally been surgical intervention (surgical decompression with a side-to-side portosystemic shunt)
  • Minimally invasive treatment using TIPS may be first-line therapy now
  • Response rates to medical therapy are poor
portal vein thrombosis
Portal Vein Thrombosis
  • Most common cause in children (fewer than 10% of adult pts.)
  • Normal liver function and not as susceptible to the development of complications, such as encephalopathy
  • Diagnosis by sonography, CT and MRI
  • Often, the initial manifestation of portal vein thrombosis is variceal bleeding in a noncirrhotic patient with normal liver function
portal vein thrombosis causes
Portal Vein Thrombosis - Causes
  • Umbilical vein infection (the most common cause in children)
  • Coagulopathies (protein C and antithrombin III deficiency),
  • Hepatic malignancy, myeloproliferative disorders
  • Inflammatory bowel disease
  • pancreatitis
  • trauma
  • Most cases in adults are idiopathic
portal vein thrombosis1
Portal Vein Thrombosis
  • Therapeutic options are esophageal variceal ligation and sclerotherapy
  • Distal splenorenal shunt
  • Rex shunt in patients whose intrahepatic portal vein is patent (most commonly children)
splenic vein thrombosis
Splenic Vein Thrombosis
  • Most often caused by disorders of the pancreas (acute and chronic pancreatitis, trauma, pancreatic malignancy, and pseudocysts)
  • Related to the location of the splenic vein
  • Gastric varices are present in 80% of patients
  • Occurs in the setting of normal liver function
  • Readily cured with splenectomy (variceal hemorrhage), although observation for asymptomatic patients is acceptable.
complications of ph
Complications of PH
  • GI bleeding due to gastric and esophageal varices
  • Ascites
  • Hepatic encephalopathy
  • Most life threatening complication is bleeding from esophageal varices
  • Distal 5 cm of esophagus
  • Usually the portal vein-hepatic vein pressure gradient >12 mm Hg
  • Bleeding occurs in 25-35% of pts. With varices and risk is highest in 1st yr.
prevention of varices
Prevention of Varices
  • Primary prophylaxis: prevent 1st episode of bleeding
  • Secondary prophylaxis: prevent recurrent episodes of bleeding
  • Include control of underlying cause of cirrhosis and pharmacological, surgical interventions to lower portal pressure
prevention of varices1
Prevention of Varices
  • Beta blockade: Beta blockade (Nadolol, Propranolol)
  • Nitrates:Organic nitrates
  • Surgery: No longer performed*
  • Endoscopy: Sclerotherapy (no longer used*) and variceal ligation

* Refers to primary prophylaxis

treatment of varices
Treatment of Varices
  • Initial Management:
    • Airway control
    • Hemodynamic monitoring
    • Placement of large bore IV lines
    • Full lab investigation (Hct, Coags, LFTs,)
    • Administration of blood products
    • ICU monitoring
pharmacologic treatment of varices
Pharmacologic Treatment of Varices
  • Decreases the rate of bleeding
  • Enhances the endoscopic ability to visualize the site of bleeding
  • Vasopressin - potent splanchnic vasoconstrictor; decreases portal venous blood flow and pressure
  • Somatostatin: decrease splanchnic blood flow indirectly; fewer side effects
  • Octreotide: Initial drug of choice for acute variceal bleeding
endoscopic therapy for varices
Endoscopic Therapy for Varices
  • Endoscopic Sclerotherapy: complications occur in 10-30% and include fever, retrosternal chest pain, dysphagia, perforation
  • Endoscopic variceal ligation: becoming the initial intervention of choice; success rates range from 80-100%
balloon tamponade
Balloon Tamponade
  • Sengstaken-Blakemore tube
  • Minnesota tube
  • Alternative therapy for pts. who fail pharmacologic or endoscopic therapy
  • Complications: aspiration, perforation, necrosis
  • Limited to 24 hrs; works in 70-80%
  • Transjugular inrahepatic portasystemic shunt
  • 1st line treatment for bleeding esophageal varices when earlier-mentioned methods fail
  • Performed in IR
  • Success rates 90-100%
  • Significant complication is hepatic encephalopathy
surgical intervention
Surgical Intervention
  • Liver transplantation: only definitive procedure for PH caused by cirrhosis
  • Shunts
    • Totally diverting (end-side portacaval)
    • Partially diverting (side-side portacaval)
    • Selective (distal splenorenal shunt)
  • Devascularization
severe complications
Severe complications
  • such as spontaneous bacterial peritonitis or ascites that is refractory to diuretic therapy, occur in the most advanced disease and are associated with a median life expectancy of less than 1 year.

Cirrhosis, even if early and stable, predisposes to development of primary hepatocellular carcinoma in as many as 3% of patients per year.


Until recently, little could be done to alter the prognosis of patients with cirrhosis and most died of complications. Today, the outlook has begun to change because of advances in orthotopic liver transplantation and development of therapies to prevent and treat complications.

biologic basis of hepatic fibrosis
Biologic Basis of hepatic fibrosis
  • Hepatic fibrosis is a wound-healing response
  • The same cell type produce hepatic fibrosis regardless of the underling cause.
  • hepatic fibrosis follows chronic,but not self-limited,injury.
  • Fibrosis occurs earliest in regions where injury is most severe.
antifibrotic therapies rationale and specific agent
Antifibrotic therapies :Rationale and specific Agent

The paradigm of satellite cell activation provides an important framework to define potential sites of antifibrotic therapy follows

  • 1.Cure the primary disease to prevent injury.
  • 2.Reduce inflammation or the host response to avoid stimulating satellite cells.
  • 3.Directly down –regulate stellate cell activation
antifibrotic therapies rationale and specific agent1
Antifibrotic therapies :Rationale and specific Agent
  • 4.Neutralize the proliferative,fibrogenic,contractile,and proinflammatory responses of stellate cells.
  • 5.Stimulate apoptosis of stellate cells.
  • 6.Increase the degradation of scar martix,either by stimulating cells that produce matrix proteases,down-regulating their inhibitors ,or directly administering matrix proteases.
diagnostic approach
  • Unless the diagnosis is already established, specific serologic tests and often a liver biopsy are required to establish the cause of the cirrhosis .
diagnostic approach1
  • In addition, patients should undergo laboratory testing to document the severity of the disease and assessment of whether ascites or hepatic encephalopathy is present ..
diagnostic approach2
  • Obtaining this information helps to determine prognosis, the possibility of specific therapy, and the possible necessity for screening family members for inherited diseases or chronic viral hepatitis
specific therapy may be indicated
specific therapy may be indicated

Antiviral therapy for chronic hepatitis C and B,

Corticosteroids (with or without immunosuppressive therapy) for autoimmune hepatitis,

Phlebotomy for hereditary hemochromatosis,

Penicillamine for Wilson's disease.


In some cases, even hepatic fibrosis can be reversed; examples include abstinence from alcohol in alcoholic liver disease and immunosuppressive therapy in autoimmune hepatitis










30 - 50 Years

Progression of Hepatitis B Infection




initial testing should consist of the following
initial testing should consist of the following
  • Measurement of serum aminotransferases, bilirubin, alkaline phosphatase, albumin, creatinine, and sodium (otherwise unexplained hyponatremia is a marker of severe disease), the blood urea nitrogen, platelet count, and prothrombin time
  • .
initial testing should consist of the following1
initial testing should consist of the following
  • • Abdominal ultrasonography to assess the portal circulation. In one study, the severity of liver disease correlated with portal vein blood velocity as determined by ultrasound

Portal hypertension is the most common and lethal complication of chronic liver disease

  • Esophageal varices and hemorrhage ascites renal dysfunction hypersplenism portal-systemic encephalopathy
  • P H.. PPG>5mmHg
hepatocellular carcinoma
Hepatocellular carcinoma
  • The issue of periodic surveillance of such patients with serum alpha-fetoprotein (AFP) measurements (values above 20 µg/L being abnormal) and ultrasound examinations remains a contentious issue from the viewpoint of cost-effectiveness since an improvement in survival has not yet been demonstrate

All patients with cirrhosis should be evaluated for the presence of varices because of the beneficial effect of prophylaxis with propranolol or nadolol


Patients with most forms of cirrhosis, particularly due to hepatitis B and C, hereditary hemochromatosis, and alcoholic liver disease, are at high risk (1 to 6 percent per year) for the development of hepatocellular carcinoma

a cure the primary disease
A.Cure the primary disease

Clear chronic viral infection

Abstinence from alcohol,stop toxic drugs

Remove iron ,copper in overload disease

Eradicate schistosomiasis

Reverse biliary obstruction

Revers jejunoileal bypass

nonalcoholic steatohepatitis nash
Nonalcoholic steatohepatitis NASH
  • NASH is a disorder diagnosed by liver biopsy. The biopsy findings are indistinguishable from those of alcoholic hepatitis described above but the patient lacks a history of significant alcohol consumption. The liver disease is stable in most patients but a minority progress to cirrhosis
cirrhosis portal hypertension surgical complications

Cirrhosis & Portal HypertensionSurgical Complications

Turner Lisle

Resident Teaching Conference

May 2008


End result of anything that causes hepatocellular


  • Toxins, viruses, prolonged cholestasis, autoimmunity, metabolic disorders

Pathologic response is uniform

  • Hepatocellular necrosis
  • Fibrosis
  • Nodular regeneration
cirrhosis why do we care
Cirrhosis - why do we care
  • Hepatic failure
  • Portal hypertension - variceal bleeding

Ischemia & autoimmune factors thought

to play a role, although mechanism is not


  • Dual blood supply
    • Hepatic arterial
    • Portal venous
  • Total hepatic blood flow ~1500 mL/min or 25% of cardiac output
  • Portal vein
    • 2/3 of total hepatic blood flow
  • Hepatic artery
    • >1/2 of O2
portal hypertension
Portal Hypertension
  • Usually due to increased portal venous resistance
  • Classification based on site of increased resistance
    • Prehepatic
    • Intrahepatic
prehepatic portal htn
Prehepatic Portal HTN
  • Portal vein thrombosis most common
  • Isolated splenic vein thrombosis
    • Usually caused by pancreatic inflammation or neoplasm
    • Results in gastrosplenic HTN with ensuing formation of gastric varices
    • Normal superior mesenteric & portal vein pressure
    • Easily reversed by splenectomy alone
intrahepatic portal htn
Intrahepatic Portal HTN
  • Often a combination of pre-, intra-, or post-sinusoidal


    • Schistosomiasis
    • Nonalcoholic cirrhosis


    • EtOH

Postsinusoidal - overall rare

    • EtOH
    • Budd-Chiari syndrome (hepatic vein thrombosis)
    • Constrictive pericarditis
    • Heart failure
portal hypertension1
Portal Hypertension
  • Portal pressure > 5 mmHg
  • Portal pressure > 8 mmHg needed for collateralization
evaluation of the cirrhotic
Evaluation of the Cirrhotic
  • Dx of underlying liver disease
  • Estimation of fxn hepatic reserve
  • Definition of portal venous anatomy
  • Hepatic hemodynamic evaluation
  • If present, identification of site of UGI bleeding
evaluation of the cirrhotic1
Evaluation of the Cirrhotic
  • Physical Exam
    • Jaundice
    • Ascites
    • Caput medusae
    • Asterixis
    • Spider angiomas
    • Palmer erythema
    • Testicular atrophy
    • Gynecomastia
    • +/- Palpable spleen (portal HTN)
  • Lab tests
    • Anemia
    • Thrombocytopenia
    • Coagulopathy
    • Hypoalbuminemia
    • AST/ALT
    • Bili
    • Alk Phos
    • GGT
    • Hepatitis serologies
    • -fetoprotein
liver biopsy
Liver biopsy
  • Cause of cirrhosis
  • Activity of liver disease
  • Approaches
    • Percutaneous (avoid with ascites or INR)
    • Transjugular venous
    • Laparoscopic
    • Open
hepatic functional reserve
Hepatic Functional Reserve


  • Encephalopathy grade
  • Amount of ascites
  • Bilirubin
  • Albumin
  • PT (INR)

Operative mortality

  • A (5%)
  • B (10-15%)
  • C (25%)



  • Bilirubin
  • INR
  • Creatinine
  • Cr Max = 4.0 mg/dL
  • On dialysis → calculate with CR = 4.0 mg/dL

Calculators on the web


MELD 5-20

1% increase in mortality with each integer rise in

MELD score

MELD >20

Additional 2% increase in mortality with each integer

rise in MELD score

diagnosis of bleeding
Diagnosis of bleeding
  • NGT decompression & lavage
  • Endoscopy - key procedure for UGIB
  • UGIB with portal HTN
    • 90% due to varices
    • 10% other causes (Mallory-Weiss tears, ulcers, etc)
  • Majority are esophagogastric varices
  • Isolated gastric varices
    • Likely splenic vein thrombosis
variceal hemmorrhage
Variceal Hemmorrhage
  • Single most life threatening complication of portal HTN
  • Risk of death is related to the underlying hepatic functional reserve
  • Pathogenesis of rupture incompletely understood
    • Multifactorial
    • Portal pressure >12mmHg


    • Control the bleeding
    • Control the portal HTN
treatment of acute variceal bleeding
Treatment of acute variceal bleeding
  • Emergency tx should be non-operative
  • Resuscitation first
  • Endoscopy
    • Successful in >85%
  • Pharmacotherapy
    • Vasopressin +/- NTG
    • Somatostatin/Octreotide (fewer complications)
  • Balloon tamponade (rare)
  • TIPS
endoscopic treatment
Endoscopic treatment
  • Most common treatment modality for acute bleeding as well as prevention
  • Sclerosis
  • Ligation
  • Complications
    • Esophageal ulceration
    • Perforation
    • Worsening hemorrhage
    • Aspiration
  • Failure after two unsuccessful attempts
  • Equally efficacious (80-90%)

Sengstaken-Blakemore tube

  • as pharmacotherapy and endoscopy
  • Has been shown to be as effective
  • Potentially lethal complications
  • -esophageal perforation
  • -ischemic necrosis of esophagus
  • May be life saving
  • Deflation followed by
  • high re-bleeding rate
  • Portal decompression without surgery (nonselective shunt)
  • Not recommended as initial therapy for acute variceal bleeding
  • Preferred tx when pharmacotherapy and endoscopic means have failed
  • Best when used as a bridge to transplant
  • Problems include shunt stenosis/occlusion, encephalopathy (50% at 1-year)
  • Transjugular Intrahepatic Portosystemic Shunt
emergency surgery
Emergency surgery
  • Indications
    • Failure of acute endoscopic tx
    • Failure of TIPS placement
    • Hemorrhage from gastric varices
  • Esophageal transection rapid/simple
  • Portacaval shunt or splenorenal shunt
  • Operative mortality >25% in most series
prevention of recurrent hemorrhage
Prevention of recurrent hemorrhage
  • Likelihood of repeat episodes >70%
  • Goals
    • Prevention of recurrent bleeding
    • Maintenance of satisfactory hepatic function
  • Options
    • Pharmacotherapy (-blockers +/- nitrates)
    • Chronic endoscopy (successful in 2/3)
    • TIPS (less bleeding, more encephalopathy)
    • Operative shunts
    • Transplantation
portosystemic shunts
Portosystemic shunts
  • Most effective means of preventing recurrent bleeding in patients with portal hypertension
  • Problems
    • Encephalopathy
    • Accelerated hepatic failure
  • Types
    • Nonselective - End-to-end/side portocaval
    • Selective - Distal splenorenal
    • Partial - Small diameter PTFE
nonshunt procedures
Nonshunt procedures


  • Ablation of varices
  • Extensive interruption of collateral vessels


  • Transection and reanastamosis of the distal esophagus
  • Extensive esophagogastric devascularization + esophageal transection and splenectomy

Rebleeding rates similar to endoscopic


  • Usually an indicator of advanced cirrhosis
  • Initiated by altered hepatic and splanchnic hemodynamics
  • Intravascular volume deficit resulting in increased aldosterone…..
  • Central goal is to achieve a NEGATIVE sodium balance
ascites treatment
Ascites treatment
  • Dietary restriction
  • Dietary restriction + Diuretics
    • spironolactone +/- lasix
  • 5-10% are refractory
    • Intermittent paracentesis
    • TIPS
    • Peritoneovenous “Denver” shunt (rarely used)
  • SBP
    • PMN >250/mm3 or positive culture
  • Variety of manifestations
  • Pathogenesis - circulating cerebral toxins
    • Ammonia
    • Mercaptans
    • -aminobutyric acid
  • Precipitated by multiple factors
    • Shunts, hemorrhage, excessive diuresis, azotemia, infection, increased dietary protein, sedatives
  • Management
    • Eliminate/treat precipitating factors
    • Lactulose, neomycin (decrease absorption of intestinal ammonia)