Graphic Liver Transplantion Photos

***WARNING*** Graphic Surgery Photos

Cirrhosis Surgery

Liver Transplantaion in Progress

More Photos

Liver Anatomy

Living-Donor Liver Transplantaion Detailed

The Liver - In Detail
Pitting Oedema


Caput Medusae

Portal hypertension results from the abnormal blood flow pattern in liver created by cirrhosis. The increased pressure is transmitted to collateral venous channels. Sometimes these venous collaterals are dilated. Seen here is "caput medusae" which consists of dilated veins seen on the abdomen of a patient with cirrhosis of the liver


Photo Gallery 2

The Progression of Liver Damage

Happy Liver

Effects of Cirrhosis

Person without A1ATD (Healthy)

Patient with A1ATD

Liver Biopsy Results

Prevalence of A1ATD in Europe

Links & PDF's

Hereditary alpha-1-antitrypsin deficiency and its clinical consequences (A1ATD Fully Explained with Diagrams)

A1ATD - Pulmonary Genetic Disorder (A1ATD Lung Disease Explained)

A1ATD and the Liver 

A Fully Detailed Look into Liver Disease in the UK (NHS)

Liver Cirrhosis

Liver Cirrhosis

What is it?

Cirrhosis is a condition where normal liver tissue is replaced by scar tissue (fibrosis). 

The scarring tends to be a gradual process. The scar tissue affects the normal structure and regrowth of liver cells. Liver cells become damaged and die as scar tissue gradually develops. Therefore, the liver gradually loses its ability to function well. The scar tissue can also affect the blood flow through the liver which can cause back pressure in the blood vessels which bring blood to the liver. This back pressure is called portal hypertension.

The Symptoms/Complications:

  • Tiredness and weakness.
  • Fluid which leaks from the bloodstream and builds up in the legs (oedema) and abdomen (ascites).
  • Loss of appetite, feeling sick, and vomiting.
  • Weight loss (although you may put on weight if you retain a lot of fluid).
  • A tendency to bleed and bruise more easily.
  • Jaundice (going yellow) due to a build-up of bilirubin.
  • Itch due to a build-up of toxins.
  • Mental health changes can develop in severe cases as toxins build up in the bloodstream and affect the brain. This can cause changes to your personality and behaviour, confusion, forgetfulness and difficulty concentrating. Eventually it can lead to loss of consciousness and hepatic coma. These changes are known as hepatic encephalopathy.
  • Oesophageal Varices (enlarged dilated viens in the oesophagus, which are prone to rupturing)
Complications Explained:

  • Ascites - is the result of poor liver function, as the liver is unable to produce albumin this allows fluid to leak out from the interstitial spaces into the peritoneal cavity.

Patient with massive ascites caused by portal hypertension due to cirrhosis.

Real Liver 1

Living-donor Liver Transplantation

What is the Child-Pugh score?

II. Criteria

  1. Total Serum Bilirubin
    1. Bilirubin <2 mg/dl: 1 point
    2. Bilirubin 2-3 mg/dl: 2 points
    3. Bilirubin >3 mg/dl: 3 points
  2. Serum Albumin
    1. Albumin >3.5 g/dl: 1 point
    2. Albumin 2.8 to 3.5 g/dl: 2 point
    3. Albumin <2.8 g/dl: 3 point
  3. INR
    1. INR <1.70: 1 point
    2. INR 1.71 to 2.20: 2 point
    3. INR >2.20: 3 point
  4. Ascites
    1. No Ascites: 1 point
    2. Ascites controlled medically: 2 point
    3. Ascites poorly controlled: 3 point
  5. Encephalopathy
    1. No Encephalopathy: 1 point
    2. Encephalopathy controlled medically: 2 point
    3. Encephalopathy poorly controlled: 3 point

III. Interpretation

  1. Child Class A: 5 to 6 points
    1. Life expectancy: 15 to 20 years
    2. Abdominal surgery peri-operative mortality: 10%
  2. Child Class B: 7 to 9 points
    1. Indicated for liver transplantation evaluation
    2. Abdominal surgery peri-operative mortality: 30%
  3. Child Class C: 10 to 15 points
    1. Life expectancy: 1 to 3 years
    2. Abdominal surgery peri-operative mortality: 82%


The Child-Pugh score, or the Child-Pugh grade, can be used in patients with liver cirrhosis to assess the severity of the clinical condition. Five variables are considered (severity of ascites and of encephalopathy, abnormality in the serum bilirubin, serum albumin and clotting times), and a score (of between 1 and 3) is accordingly assigned to each of these factors. The sum of the scores provides the Child-Pugh score, which corresponds to a Child-Pugh grade (or Child’s grade) of A, B or C. 

This grade is used as a general means to verify the prognosis of the patient. For example, it can be used to determine the risk to a patient with regard to possible surgery, and also, to suggest the perceived survival of the patient over a period of time. Pharmaceutical manufacturers may use the Child-Pugh grade to suggest dose reductions, or to contraindicate the use of the drug, dependent on the degree of dysfunction of the cirrhotic liver. 

Photo Gallery 1

Pitting Oedema (Water retention in the ankles/legs)


Cirrhosis - The Complications Explained

Cirrhosis - The Complications Explained

Lets take a closer look into the complications of cirrhosis, why and how they happen:

  • Portal Hypertension - in the cirrhotic liver, blood flow through the liver is impaired, this causes the blood to back-up into the portal vein, this in turn causes high blood pressure to occur within the portal venous system. (Link provides more detailed info) 
Portal Hypertension is the cause for the most severe cirrhosis complications, such as the following:

  •   Oesophageal Varices - is the direct result of portal hypertension, they are extremley dilated veins in the oesophagus, these veins are extremley thin and have to withstand high portal venous system blood pressure. Therefore the veins are likey to rupture (burst), the likleyhood of repturing depends on the grading of the varices, which I will not go into here, but you can Google it.
            When veins rupture this is called a Variceal Haemorrhage, a variceal haemorrage is a               medical emergency, and can be potentially life threatening. Signs of a bleed are:
  • Haematemesis (vomiting blood)
  • Melaena (black tarry stools/poo)
  • Abdominal pain (mild to severe stomach pain)
  • Pallor (pale skin due to shock and blood loss)

  • Ascites - is the accumulation of fluid in the abdominal cavity, ascites has 3 grades, ascites happens because the cirrhotic liver cannot produce enough of the protein albumin, the protein keeps fluid from leaking out from the bloodstream, as the cirrhotic cannot produce ennough of it the fluid leaks into abdominal cavity. (Grades and lots more info on link)

  • Hepatic Encephalopathy - occurs in liver failure and advanced cirrhosis, it can also present after a variceal haemorrhage, the link provies all detailed info including the grades.

Brief Overview

In the unaffected individual the alpha-1 antitrypsin (a1at) protein is produced normally and secreted into the bloodstream. In the A1ATD affected person, the Z gene produces mutated forms of alpha-1, all of the mutated alpha-1 protein cannot be misfolded and secreted into the bloodstream. This causes the mutated alpha-1 to get trapped in liver cells and clump together, in turn causing toxic effects, this ongoing damage leads to further liver damage.


Notice the red globules on FIG. 1A. With are periodic acid-Schiff (PAS) stain, they are characteristic for alpha-1-antitrypsin (AAT) deficiency. More persons with AAT deficiency are likely to develop chronic obstructive pulmonary disease with panlobular emphysema. 

The globules are collections of alpha-1-antitrypsin not being excreted from hepatocytes. This may eventually lead to chronic hepatitis and cirrhosis. Liver disease is more likely to occur in children with AAT deficiency, while lung disease occurs in adults