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Structure

Two main segments

Eight segments

Divided by hepatic veins

Segments have independent circulation and innervation resection of one does not affect the others

Blood Supply

Two main vessels

Hepatic artery

A branch of the coeliac axis

supplies 25% of the hepatic blood flow

the hepatic artery autoregulates flow ensuring a constant total blood flow

Portal vein

Drains most of the gastrointestinal tract and the spleen.

It supplies 75% of hepatic blood flow.

The normal portal pressure is 5–8 mmHg; flow increases after meals.

Blood distribution

Pathway from vessels to inferior vena cava

Blood flows from vessels into sinusoids in segments

Runs out through the veins, all returns back to vena cava

Supply of the caudate lobe

Caudate lobe receives independent blood supply

Circulation of lymph

Hepatic Units

Acinus

The acinus is the functional hepatic unit.

This consists of parenchyma supplied by the smallest portal tracts containing portal vein radicles, hepatic arterioles and bile ductules.

The hepatocytes near this triad (zone 1) are well supplied with oxygenated blood and are more resistant to damage than the cells nearer the terminal hepatic (central) veins (zone 3).

See fig 7.2

Sinusoids

The sinusoids lack a basement membrane and are loosely surrounded by specialist fenestrated endothelial cells and Kupffer cells (phagocytic cells).

Sinusoids are separated by plates of liver cells (hepatocytes).

The subendothelial space between the sinusoids and hepatocytes is the space of Disse, which contains a matrix of basement membrane constituents and stellate cells

Stellate cells

Stellate cells store retinoids in their resting state and contain the intermediate filament, desmin.

When activated (to myofibroblasts) they are contractile and probably regulate sinusoidal blood flow.

Endothelin and nitric oxide play a major role in modulating stellate cell contractility.

Activated stellate cells produce signal proteins for synthesis or inhibition of degradation of extracellular matrix components, including collagen, as well as cytokines and chemotactic signal

Billiary System

- Bile cannuli -> bile ductules -> l/r hepatic duct -> porta hepatis -> common portal duct -> common bile duct w/ cystic duct -> ampulla of vater w/ sphincter of Oddi

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Blood tests

Liver function test

Serum albumin

This is a marker of synthetic function and is useful to gauge the severity of chronic liver disease: a falling serum albumin is a bad prognostic sign.

In acute liver disease initial albumin levels may be normal.

Prothrombin time

This is also a marker of synthetic function.

Because of its short half-life, it is a sensitive indicator of both acute and chronic liver disease.

Vitamin K deficiency should be excluded as the cause of a prolonged PT by giving an intravenous bolus (10 mg) of vitamin K.

Vitamin K deficiency commonly occurs in biliary obstruction, as the low intestinal concentration of bile salts results in poor absorption of vitamin K.

PT times differ greatly between labs depending on assay

Liver biochemistry

Bilirubin

serum levels indicate metabolism and bile excretion functions

aminotransferase - reflect hepatic damage

serum aspartate (AST) and alanine aminotransferases (ALT) - reflecting hepatocellular damage

These enzymes (often referred to as transaminases) are contained in hepatocytes and leak into the blood with liver cell damage.

Two enzymes are measured:

Aspartate aminotransferase (AST) is primarily a mitochondrial enzyme (80%; 20% in cytoplasm) and is also present in heart, muscle, kidney and brain.

High levels are seen in hepatic necrosis, myocardial infarction, muscle injury and congestive cardiac failure.

Alanine aminotransferase (ALT) is a cytosol enzyme, more specific to the liver so that a rise only occurs with liver disease.

Alkaline phosphatase - reflect hepatic obstruction

This is present in hepatic canalicular and sinusoidal membranes, but also in bone, intestine and placenta.

In clinical practice, if the γ-GT is also abnormal the ALP is presumed to come from the liver

Serum ALP is raised in both intrahepatic and extrahepatic cholestatic disease of any cause, due to increased synthesis.

In cholestatic jaundice, levels may be four to six times the normal limit.

Raised levels also occur with hepatic infiltrations (e.g. metastases), and in cirrhosis, frequently in the absence of jaundice.

The highest serum levels due to liver disease (>1000 IU/L) are seen with hepatic metastases and primary biliary cirrhosis.

gamma glutamyl transpeptidase

This is a microsomal enzyme present in liver, but also in many tissues.

Its activity can be induced by drugs such as phenytoin and by alcohol.

If the ALP is normal, a raised serum γ-GT can be a useful guide to alcohol intake.

However, mild elevations of γ-GT are common, even with a small alcohol consumption and is also raised with fatty liver disease.

It does not necessarily indicate liver disease if the other liver biochemical tests are normal

In cholestasis the γ-GT rises in parallel with the ALP as it has a similar pathway of excretion.

total protein and globulin function.

This measurement is of little value.

Serum albumin is discussed above.

The proteins in the globulin fraction, raised in liver disease, can be separated by electrophoresis and is usually due to increased circulating immunoglobulins; it is polyclonal (see below).

Viral markers

Viruses are a major cause of liver disease.

Additional: haematological, biochemical, immunological, genetic

Urine tests

Dipstick tests are available for bilirubin and urobilinogen.

Bilirubinuria is due to the presence of conjugated (soluble) bilirubin, is found in patients with jaundice due to hepatobiliary disease, but is absent if unconjugated bilirubin is the major cause of jaundice.

Imaging techniques

Ultrasound

Can show liver and related structure

Show presence of stones (white w/ black shadow)

Endoscopic ultrasound

CT

MRI

Magnetic resonance cholangiopancreatography (MRCP)

Plain x-rays of the abdomen

Radionuclide imaging - scintiscanning

Endoscopy

Endoscopic retrograde cholangiopancreatography (ERCP)

Percutaneous transhepatic cholangiography (PTC)

Angiography

Liver Biopsy

Histological examination of the liver is valuable in the differential diagnosis of diffuse or localized parenchymal disease.

Liver biopsy can be performed on a day-case basis

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Protein metabolism

The liver is the principal site of synthesis of all circulating proteins apart from γ-globulins

Albumin

Controls plasma levels by controlling gluconeogensis and transamination

Transport of carrier proteins

Synthesises coagulation factors

Storage of vitamins and minerals

Degradation of amino acids produces ammonia -> urea

Carbohydrate metabolism

Glucose homeostasis and the maintenance of the blood sugar is a major function of the liver.

In the immediate fasting state, blood glucose is maintained either by glucose release from breaking down glycogen (glycogenolysis) or by synthesizing new glucose (gluconeogenesis).

In prolonged starvation, ketone bodies and fatty acids are used as alternative sources of fuel as the body tissues adapt to a lower glucose requirement

Lipid metabolism

It synthesizes very-low-density lipoproteins (VLDLs) and high-density lipoproteins (HDLs)

HDLs are the substrate for lecithin-cholesterol acyltransferase (LCAT), which catalyzes the conversion of free cholesterol to cholesteryl ester

MDLs remove triglycerides

Cholesterol may be of dietary origin but most is synthesized from acetyl-CoA mainly in the liver, intestine, adrenal cortex and skin.

Bile formation

Bile secretion & metabolism

Bile formation requires uptake of bile acids and other organic and inorganic ions across the basolateral (sinusoidal) membranes by multiple transport proteins; NTCP and sodium independent OATP2,

Two processes are involved in bile secretion across the canalicular membrane of the hepatocyte – bile salt-dependent and bile salt independent processes – each contributing about 230 mL/ day.

Bile salt-dependent process:

the bile acid receptor, farnesoid X, blocks bile acid formation from cholesterol and also regulates the transport proteins (NTCP, OATP2) that increase bile acid uptake by the liver Na+ and water follow the passage of bile salts by diffusion across the tight junction between hepatocytes.

In the bile salt-independent process, water flow is due to other osmotically active solutes such as glutathione and bicarbonate.

The bile acids are excreted into bile and then pass via the common bile duct into the duodenum

Bilirubin metabolism

Bilirubin is produced from breakdown of mature red cells by Kupffer cells in the liver and reticuloendothelial system; 15% of bilirubin is formed from catabolism of other haem-containing proteins

Normally, 250–300 mg daily.

unconjugated bilirubin is water-insoluble, due to internal hydrogen bonding, and is transported to the liver attached to albumin.

Bilirubin dissociates from albumin and is taken up by hepatic cell membranes and transported to the endoplasmic reticulum by cytoplasmic proteins, where it is conjugated with glucuronic acid and excreted into bile.

conjugated bilirubin is water-soluble and is actively secreted into biliary canaliculi and excreted into the intestine within bile

not absorbed from the small intestine because of its large molecular size

In the terminal ileum, bacterial enzymes hydrolyse the molecule, releasing free bilirubin which is then reduced to urobilinogen, some of which is excreted in the stools as stercobilinogen.

The remainder is absorbed by the terminal ileum, passes to the liver via the enterohepatic circulation, and is re-excreted into bile. Then excreted kidneys

= When hepatic excretion of conjugated bilirubin is impaired, a small amount is strongly bound to serum albumin and is not excreted by the kidneys; it accounts for the persistent hyperbilirubinemia

Hormone and drug activation

The liver catabolizes hormones such as insulin, glucagon, oestrogens, growth hormone, glucocorticoids and parathyroid hormone.

It is also the prime target organ for many hormones (e.g. insulin).

It is the major site for the metabolism of drugs and alcohol.

Fat-soluble drugs are converted to water-soluble substances that facilitate their excretion in the bile or urine.

Cholecalciferol is converted to 25-hydroxycholecalciferol.

Immunological function

The hepatic reticuloendothelial system contains many immunologically active cells.

The liver acts as a ‘sieve’ for bacterial and other antigens carried to it by the portal vein from the gastrointestinal tract.

These antigens are phagocytosed and degraded by the Kupffer cells, which have specific membrane receptors for ligands and are activated by several factors, such as infection.

They are part of the innate immune system and secrete interleukins, tumour necrosis factor (TNF), collagenase and lysosomal hydrolases

The cytokines stimulate sinusoidal, stellate, and natural killer cells to release pro-inflammatory cytokines

Antigens are degraded without the production of antibody, as there is very little lymphoid tissue and thus, they are prevented from reaching antibody-producing sites and thereby prevent generalized adverse immunological reactions

Cytokines also stimulate hepatic apoptosis.

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Liver CT (contrast-enhancement shows irregular mass)

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Liver CT (contrast-enhancement shows irregular mass)

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Symptoms

Acute liver disease

This may be asymptomatic and anicteric.

Symptomatic disease, which is often viral, produces generalized symptoms of malaise, anorexia and fever.

Jaundice may appear as the illness progresses.

Chronic liver disease

Patients may be asymptomatic or complain of nonspecific symptoms, particularly fatigue.

Specific symptoms include:

Right hypochondrial pain due to liver distension

Abdominal distension due to ascites

Ankle swelling due to fluid retention

Jaundice

Haematemesis and melaena from gastrointestinal haemorrhage

Pruritus due to cholestasis – this is often an early symptom of primary biliary cirrhosis

Breast swelling (gynaecomastia), loss of libido and amenorrhoea due to endocrine dysfunction

Confusion and drowsiness due to neuropsychiatric complications (portosystemic encephalopathy).

Signs

Acute liver disease

There may be few signs apart from jaundice and an enlarged liver.

Jaundice is a yellow coloration of the skin and mucous membranes and is best seen in the conjunctivae and sclerae.

In the cholestatic phase of the illness, pale stools and dark urine are present.

Spider naevi and palmar erythema usually indicate chronic disease but they can occur in severe acute disease

Chronic liver disease - see figure 7.9

The skin

The abdomen

The endocrine system

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Acute hepatitis

Can be caused by infection, drugs, alcohol, or poison

Chronic hepatitis

Can be caused by infection, autoimmune

Hep A is fine, we do not want any other forms of hepatitis

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Epidemiology

Hep A virus

Clinical features

Investigations

Liver biochemistry

Haematological tests

Viral biomarkers: HAV antibodies

Other tests

Course and prognosis

Treatment

Prevention and prophylaxis

Active immunisation

Vaccine leading to body's immune system being activated

Passive immunisation

Given active antibodies, not produced in own body

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Effects of alcohol

Pathology

Fatty change

Alcoholic hepatitis

Alcoholic cirrhosis

Clinical features

Fatty change

Alcoholic hepatitis

Alcoholic cirrhosis

Investigations

Fatty change

Alcoholic hepatitis

Alcoholic cirrhosis

Management and prognosis

Fatty change

Alcoholic hepatitis

Alcoholic cirrhosis

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Non-alcoholic Fatty Liver Disease (NAFLD)

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Non-alcoholic Fatty Liver Disease (NAFLD)

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Definition and epidemiology

Incidence: 3-6% of US pop, 1-2% of these NASH

Estimated prevalence of 25%

Risk factors:

Obesity

Diabetes

Hispanic

Histological changes

Spectrum from simple fatty change to inflammation to cirrhosis

Diagnosis

Fatty liver on ultrasound

Exclusion of other cause

Management

Dietary changes

exercise

extreme cases might need transplant

can progress into cirrhosis

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Stellate cells affected by many cytokines (e.g. TGF-beta) -> become swollen and lose retinoids -> favours fibrosis

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Pathogenesis

Sodium and water retention

Portal hypertension

Low serum albumin

Causes

Clinical features

Swelling

Investigations

Management

Drain - multiple litres

Give fluids

Course and prognosis

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Aetiology

Alcohol

Viral infections

NASH

Autoimmune disorders

Cholestatic disorders

Metabolic diseases

Pathogenesis

Injury -> cirrhosis can take 5-50 years, affected by risk factors

Injury -> fibrosis (resolvable!)

Inflammatory damage

Matrix deposition

Parenchymal necrosis

Angiogenesis

Fibrosis -> Cirrhosis (can regress)

Disrupted architecture

Loss of function

Aberrant hepatocyte regeneration

Pathology

Destruction of extracellular matrix

formation of micro and macro nodules

Micronodular

Macronodular

aggregated cells, clumps

Redistribution of blood supply in liver

Investigations - to check prognosis & liver function

Severity

Type

Imaging

Biopsy

Management

Transplant

Reversing damage by removing underlying cause

Course and prognosis

5 year survival rate of 50%

Depends on influencing factors

Genetic

Environment

Liver transplantation

Indications

Mainly: cirrhosis or conditions which result in this

Contraindication

sepsis

rate of recurrence of carcinoma is high

Preparation

Rejection

Prognosis

90% 1 year, 70-85% 5 year survival

Carcinoma's can recur

Complications and effects

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Secondary liver tumours

Clinical features

variable

weight loss

malaise

upper abdominal pain

hepatomegaly w/ or w/o jaundice

Diagnosis

serum

Treatment

depends on site

removal/resection

Primary malignant tumours

Hepatocellular carcinoma

most common

90% are positive with Hep B

80% develop cirrhosis

Occurrence in multiple nodules

can metastasise

treated w HBV vax - prevention

Cholangiocarcinoma

arise from bile ducts

not related to cirrhosis

cholangitis more frequent

rarely able to resect

mortality within 6 months

Benign tumours

mostly haemangiomas

hepatic adenomas

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Classification

Prehepatic

blockage of portal vein before liver

Intrahepatic

distortion of liver itself (pre or post sinusoidal)

Post-hepatic

blockage of passage out of the liver

Pathophysiology

Stellate cells:

hyperactivated, leading to constant inflammation

destroys hepatocytes, extracellular matrix

increased sodium retention, increased BP in portal vessels

Causes

Dependent on type

pre: thrombosis

intra: schistosomiasis

post: budd-chiari syndrome

Clinical Features
-> see figure of signs/symptoms under section 1

-> this is what causes splenomegaly

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Alcoholic cirrhosis

Cause

Heavy use of alcohol

Types

Fatty liver

alcoholic hepatitis - acute inflamation, necrosis

alcoholic cirrhosis - destruction of normal tissue, leave scar tissue

Clinical features

Abdominal pain

weight loss

appetite loss

weakness

intestinal bleeding

liver cancer

Primary biliary cirrhosis

Primary sclerosing cholangitis

Secondary biliary cirrhosis

Hereditary haemochromatosis

Wilsons disease (progressive hepatolenticular degeneration)

Alpha antitrypsin deficiency

Clinical features

Investigations

Treatment

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Pathogenesis

Clinical features

Management

Course and prognosis

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Cause

Mechanism
Hypertension -> RAAS

Relation to ascites
Ascites leads to RAAS system -> renal failure

Treatment

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Management

Initial management of acute variceal bleeding

Resuscitation

Urgent endoscopy

Variceal banding or injection sclerotherapy

Other available measures

Additional management of acute episode

Management of an acute rebleed

Prevention of recurrent variceal bleeding

Long term measures

Surgical procedures

Prophylactic measures

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Dilation of vessels in lungs due to liver hypertension

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pulmonary arterial hypertension that is associated with portal hypertension

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Epidemiology

Vertical transmission

i.e. Mother to child

Horizontal transmission

to other adult individuals

Hepatitis B virus

Pathogenesis

Acute HBV

Clinical features

Investigations

Course

Treatment

Prevention & prophylaxis

Chronic HBV

Types

Immune tolerant chronic HBV infection

Inactive carrier with chronic HBV infection

Active chronic infection

Clinical features and investigations of active chronic hepatitis B infection

Investigations

Histological changes

Treatment

Classifications:

Moderate to severe active necroinflammation

Presence of cirrhosis

Immunotolerant patients

Antiviral agents

Oral therapy

Prognosis

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Epidemiology

Hepatitis C Virus

Clinical features

Diagnosis

Treatment

Course

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Cytomegaly virus
Epstein-Barr
HIV

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Acute hepatitis due to other infectious agents

Causes

Drug induced chronic hepatitis

Chronic hepatitis of unknown cause

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Definition

Clinical features

Investigations

Treatment

Course & Prognosis

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Pathogenesis

Clinical features

Investigations

Treatment

Course and prognosis

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Types of infection

Co-infection

occurs simultaneously with HBV

no distinguishable acute phase

Super infection

HBV infection causing flareup in HDV

Chronic hepatitis D

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Investigations

Differential diagnosis

Treatment

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aka veno-occlusive disease

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Polycystic disease of the liver

Solitary cysts

Congenital hepatic fibrosis

Congenital intrahepatic biliary diation (Caroli's disease)

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Schistosomiasis

Hydatid disease

Acquired immunodeficiency syndrome

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Pyogenic abscesses

Clinical features

Investigations

Management

Prognosis

Amoebic abscesses

Investigations

Treatment

Complications

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Hepatic mitochondrial injury syndromes

Genetics

Toxins

Drugs

Idiopathic

Idiopathic adult ductopenia

Indian Childhood cirrhosis

Hepatic Cirrhosis

Hepatic Porphyrias

Cystic fibrosis

Coeliac disease

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Drug metabolism

Drug hepatotoxicity

Hepatic damage

Individual drugs

Drug prescribing in patients with liver disease

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Changes during pregnancy

Hyperemesis gravidarum

Intrahepatic cholestasis of pregnancy

Pre-eclampsia and eclampsia

Acute fatty liver of pregnancy

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Aetiology

Alcohol abuse

Pathology

Fatty change

Alcoholic hepatitis

Alcoholic cirrhosis

Clinical features

Fatty liver

Alcoholic hepatitis

Alcoholic cirrhosis

Abdominal pain

weight loss

appetite loss

weakness

intestinal bleeding

liver cancer

Investigations

independent of cause, need to look at function of liver

Management & prognosis

General management

Fatty liver

Alcoholic hepatitis

Alcoholic cirrhosis

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Mechanisms of Hepatic circulatory disorders e.g cirrhosis

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Mechanisms of Hepatic circulatory disorders e.g cirrhosis

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Summary of pathophysiology of fatty liver disease

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Summary of pathophysiology of fatty liver disease

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Basically w HCV, put yourself on the transplant list

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Resolution of active infection or progression to chronic infection are both possible

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Summary of differences between hepatitis A - E

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Summary of differences between hepatitis A - E

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Investigation is same for all.
First comes from anamnesis, then testing serology for virus markers.

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Bilirubin metabolism and elimination - MEMORISE THIS

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Bilirubin metabolism and elimination - MEMORISE THIS

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https://www.webmd.com/hepatitis/digestive-diseases-liver-transplantation

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What Is a Liver Transplant?

A liver transplant is a surgical procedure that replaces someone's diseased liver with all or part of a healthy one from another person, who's called a donor.

When Is a Liver Transplant Needed?

The liver is your largest internal organ. An adult's weighs about 3 pounds. It's just below your diaphragm on the right side of your belly. Your liver does many important things, including making proteins and breaking down nutrients from food to help your body make energy.

You might need a transplant if your liver doesn't work the way it should. This is called liver failure.

Liver failure can happen suddenly as a result of viral hepatitis, drug-induced injury, or infection. This is called acute or fulminant hepatic failure.

It can also be the end result of a long-term problem (chronic). Conditions that can cause chronic liver failure include:

Chronic hepatitis with cirrhosis

Primary biliary cholangitis, a rare condition in which your immune system destroys your bile ducts

Sclerosing cholangitis, scarring and narrowing of the bile ducts inside and outside your liver, causing bile to back up

Biliary atresia, a rare liver disease that affects newborns

Alcohol overuse

Liver cancers such as hepatocellular carcinoma

Wilson's disease, which causes unusual levels of copper throughout your body, including in your liver

Hemochromatosis, in which your body has too much iron

Alpha-1 antitrypsin deficiency, an unusual buildup of a protein called alpha-1 antitrypsin in your liver, resulting in cirrhosis

How Do People Get Selected for Liver Transplants?

Your doctor may recommend a liver transplant if they've ruled out all other treatments for your condition and if they think you're healthy enough for surgery. They'll refer you to a transplant center. There, you'll talk with specialists and have tests to find out whether you can get a transplant.

Each center has different rules about who can have a transplant. You might not be able to get one if you have:

A severe infection

Problems with alcohol or drug use

Cancer outside your liver

Serious heart or lung disease

You or your caregivers will also need to understand and follow your doctor's directions after the surgery, including medications that you'll take for the rest of your life.

Your Liver Transplant Team

A team of specialists will help you every step of the way. They include:

A liver specialist (called a hepatologist)

A transplant surgeon

A transplant coordinator, usually a registered nurse who specializes in the care of liver transplant patients. This person will be your main contact with the transplant team.

A social worker to discuss your support network of family and friends, employment, and financial needs

A psychiatrist to help you deal with issues that might come along with a transplant, such as anxiety and depression

An anesthesiologist

A chemical dependency specialist to help if you have a history of alcohol or drug use

A financial counselor to act as a go-between for you and your insurance company

Which Tests Are Required Before Getting a Liver Transplant?

Bring all medical records, X-rays, liver biopsy slides, and a record of your medications to your evaluation for a liver transplant. The team might do tests including:

CT, which uses X-rays and a computer to make pictures of your liver. CTs and chest X-rays will also check your heart and lungs.

Doppler ultrasound to find out whether the blood vessels to and from your liver are open

Echocardiogram to check your heart

Pulmonary function studies to look at how well your lungs exchange oxygen and carbon dioxide

Blood tests to learn more about your blood and to check how well your liver is working. You'll also be screened for HIV, other viruses (such as herpes and Epstein-Barr), and hepatitis.

How Does the Liver Transplant Waiting List Work?

If you meet the criteria for a transplant but don't have a donor lined up, the center will put you on a waiting list. It lists patients according to their blood type, body size, and medical condition (how ill they are). Each patient is given a priority score based on three blood tests ( creatinine, bilirubin, and INR). The score is known as MELD (model of end-stage liver disease) in adults and PELD (pediatric end-stage liver disease) in children.

Patients who have the highest scores and acute liver failure get top priority for a liver transplant. If their condition gets worse, their scores rise, and their priority for transplant goes up. This way, the transplants go to people who need them the most.

It's hard to say how long you might have to wait to get a liver. Your transplant coordinator is always available to discuss where you are on the waiting list.

Where Does a Liver for a Transplant Come From?

You might get a liver from a donor who's alive or one who's died.
Living donor
In a living donor liver transplant, your doctor will take part of a healthy person's liver and implant it in you. Both liver segments will grow back to their regular size in a few weeks.
Deceased donor
A donor who's died may have had an accident or head injury. Their heart is still beating, but they're legally dead because their brain has stopped working permanently. The donor is usually in an intensive-care unit. The team turns off life support in the operating room during the transplant.

The donor's identity and the details of their death are confidential.

Depending on your condition, you might have a "domino" liver transplant. This is when a young person who has a metabolic liver disease gets a liver from a healthy donor. But rather than destroying the young person's liver, doctors give it to an older patient who has a more diseased liver. It can take decades for the older person to have signs of the metabolic disease. Or they may never get it at all. Domino transplants help widen the pool of people who can donate organs.

Who Can Be a Liver Transplant Donor?

A living donor may be a relative, a spouse, a friend, or an unrelated "Good Samaritan." They'll have complete medical and psychological tests to keep risks as low as possible. Blood type and body size are crucial to finding a match. A donor younger than 60 years old is ideal.

Hospitals will check possible donors for liver problems or other things, including:

Liver disease

Overuse of alcohol or drugs

Cancer

Infections

Hepatitis

HIV

What Happens When They Find a Liver Transplant Match?

A transplant coordinator will contact you when they've found a possible donor liver. Don't eat or drink anything after they tell you to go to the hospital. When you get there, you'll probably have more blood tests, an electrocardiogram, and a chest X-ray. You also may meet with the anesthesiologist and a surgeon. If the donor liver is approved, the transplant will go ahead. If not, you'll go home.

What Happens During the Liver Transplant Operation?

Liver transplants usually take 6 to 12 hours. Your surgeons will take out your liver and replace it with the donor liver. Because a transplant is a major procedure, the surgeons will put several tubes in your body. These tubes are necessary to help your body do certain things during the operation and for a few days afterward.

What Complications Are Associated With Liver Transplant?

A liver transplant is a complex procedure that may have complications soon afterward or many years later.

Rejection
Your immune system destroys things that invade your body. But it can't tell the difference between your transplanted liver and unwanted invaders, such as viruses and bacteria. So your immune system may attack your new liver. This is called a rejection episode. About 64% of liver transplant patients have some kind of organ rejection, most within the first 90 days. You'll get anti-rejection medications to prevent an immune attack.
Infection
The drugs that you take to keep your body from rejecting your new liver weaken your immune system. They're called immunosuppressants. They make you more likely to get an infection. This problem goes away over time.
Liver function problems
About 1% to 5% of new livers don't work as well as they should or don't work at all. If it doesn't get better quickly, you might need a second transplant.
Surgical risks
Complications related to the operation include:

Clots in the artery that takes blood from your heart to your liver (called hepatic artery thrombosis) or in the vein that takes blood from your intestines, pancreas, and spleen to your liver (portal vein thrombosis)

Bile leaking out of your bile ducts and into your belly

Narrowed bile ducts

Bleeding

Infection of the surgical wound

Return of disease
Some conditions that cause liver failure can still damage or destroy your new liver. These include:

Hepatitis C

Primary sclerosing cholangitis

Fatty liver disease

Cancer
People who have an organ transplant have a 25% higher chance of getting skin cancer than the rest of the population. Immunosuppressant drugs can also make you more likely to get other cancers, including a rare condition called post-transplant lymphoproliferative disorder (PTLD).

What Are Anti-Rejection Medications?

You'll need to take at least one immunosuppressant for the rest of your life. You might get a mix of a calcineurin inhibitor (CNI) such as cyclosporine ( Neoral) or tacrolimus ( Prograf); a glucocorticoid such as prednisone ( Medrol, Prelone, Sterapred DS); and a third agent such as azathioprine ( Imuran), everolimus (Afinitor, Zortress), mycophenolate mofetil (CellCept), or sirolimus ( Rapamune).

These drugs can have serious side effects. Along with a higher chance of infection, they can cause:

Bone loss

Diabetes

High blood pressure

High cholesterol

Kidney damage

Weight gain

Other drugs and supplements can affect how these medications work. Talk to your doctor before taking anything new or if you have concerns about side effects.

When Will I Be Able to Go Home After a Liver Transplant?

The average hospital stay after a liver transplant is 2 to 3 weeks. Some patients go home sooner, but others have to stay longer.

The nursing staff and your transplant coordinator will start to get you ready for discharge soon after you move from the intensive care unit (ICU) to the regular nursing floor. They'll give you a discharge manual, which reviews much of what you need to know before you go home.

You'll learn how to take new medications and how to check your blood pressure and pulse. You'll also learn the signs of rejection and infection, and you'll know when it's important to call your doctor.

Many people have to be admitted to the hospital again, especially within the first year after a transplant. This is usually for treatment of a rejection episode or infection.

After a Liver Transplant
Follow-up care
Your first return appointment will probably be about 1 to 2 weeks after you leave the hospital. You'll see your transplant surgeon and transplant coordinator. A social worker or a member of the psychiatric team may also be available. After that, you'll have follow-ups 3, 6, 9, and 12 months after the transplant and then once a year for the rest of your life.

Your primary care doctor should be notified when you have your transplant and when you're discharged. Though your transplant center will handle most problems related to the transplant, your primary care doctor will remain an important part of your medical care.

Self-care
Some lifestyle changes can protect your overall health after a liver transplant.

Eat a healthy, balanced diet. Limit salt, cholesterol, fat, and sugar. A dietitian or nutritionist can help you make a meal plan.

Don't eat grapefruit or drink grapefruit juice. They can affect how some immunosuppressants work.

Don't eat unpasteurized milk products or raw eggs, meat, or fish.

Don't drink alcohol or use it in food if you have a history of alcohol use disorder.

Get regular exercise.

Don't smoke.

Limit your contact with things that can carry germs, such as soil, mosquitoes, ticks, rodents, reptiles, birds, and water from lakes or rivers.

If you're planning to travel, especially to a developing country, talk to your care team about how to lower risks at least 2 months before you leave.

Liver Transplant Outlook

Your outlook after a liver transplant depends on several things, including the condition that caused your liver failure. About 88% of patients live at least a year after their transplant, and 73% live at least 5 years.

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You might need a liver transplant if your liver doesn't work the way it should. This is called liver failure. Learn more about liver transplantation, including when it may be needed, how candidates are picked, what to expect from the procedure, and what happens after surgery.