Liver Cirrhosis Diagnosis and Management

Liver cirrhosis is permanent scarring of the liver after years of injury, most often from hepatitis B or C, alcohol or fatty liver disease. Early cirrhosis causes no symptoms and is best caught with a fibroscan. The diagnosis and management of liver cirrhosis then turn on controlling the cause, monitoring every six months, and referring for a liver transplant once complications such as ascites, bleeding or confusion appear.

That sequence framed the masterclass given to referring doctors by Dr. Sandeep K Jha, a liver transplant surgeon who was Consultant Liver Transplant at Manipal Hospital, New Delhi, India, at the time of the session. His message to physicians was practical: cirrhosis is silent for years, and the aim is to catch it early, before complications develop.

What is liver cirrhosis?

Cirrhosis is the end result of long-term damage to the liver from any cause. Healthy liver tissue is progressively replaced by scar tissue (fibrosis) and regenerating nodules, until the organ can no longer do its work. Dr. Jha put the number of functions the liver carries out at close to 400; when the liver is badly damaged, it can no longer carry them out.

He illustrated the process with photographs taken during operations, including one of a liver seen incidentally during gallbladder surgery. Set beside a picture of a normal liver, the images showed the stages of damage, ending in a liver that has shrunk and become, in his words, like a stone. At that last stage, blood can no longer flow through it.

That obstruction is the core of the disease. The portal vein carries blood from the intestines and spleen into the liver. When a hard, shrunken liver resists that flow, pressure builds up behind it (portal hypertension), and the familiar complications of cirrhosis follow: fluid in the abdomen, an enlarged spleen and bleeding into the gut.

The major causes of cirrhosis

Any injury that persists for long enough can end in cirrhosis. Dr. Jha named four causes that account for most cases:

• Hepatitis B, through prolonged infection.
• Hepatitis C, through prolonged infection.
• Alcohol, taken in excess over a long period; he cited 10 to 15 years.
• Non-alcoholic fatty liver disease (NAFLD), the fat-driven liver disease seen in people with diabetes, obesity and abnormal blood lipids.

The balance between them is shifting. Hepatitis B and C are the leading causes in the East, and hepatitis C and alcohol-related liver disease in the West. Because effective treatment now exists for both viruses, Dr. Jha expects cirrhosis from hepatitis B and C to decline over the next 10 to 15 years, while fatty liver disease, driven by sedentary lifestyles, obesity and diabetes, is rising very rapidly and is fast becoming the most important cause of cirrhosis and of liver transplantation. Each cause, its treatment and the role of early testing are covered in depth in liver cirrhosis causes, prevention and early diagnosis.

Stages of liver cirrhosis: a decade or more of silent progression

Dr. Jha described the natural history as a staircase. When risk factors such as hepatitis B, hepatitis C, diabetes, obesity or alcohol are present in the body for 10 to 15 years, a normal liver becomes inflamed or fatty, the damaged liver develops fibrosis, fibrosis becomes cirrhosis, cirrhosis becomes decompensated cirrhosis, and the patient eventually dies.

The clinical significance of that staircase is that the early steps are invisible. Early cirrhosis has no symptoms, and the physical signs doctors are taught to look for appear only late. The task for the referring physician is therefore to look for the disease in people at risk, rather than to wait for it to declare itself.

Compensated vs decompensated cirrhosis

Cirrhosis has two broad phases.

• Compensated cirrhosis: the liver is scarred but still copes. The patient may feel entirely well.
• Decompensated cirrhosis: the liver can no longer keep up, and complications appear: ascites (fluid in the abdomen), vomiting of blood, jaundice, confusion, kidney impairment. Dr. Jha equated this phase with liver failure and end-stage liver disease.

Not every patient crosses from the first phase to the second. According to the data Dr. Jha cited, about 5% of all patients with cirrhosis decompensate each year. When cirrhosis is diagnosed early and the causes are controlled (weight loss, control of diabetes, treatment of hepatitis B and C), there is, in his view, a very good chance that a patient can live out his or her life with the same liver.

What no one can do is predict how long a given cirrhotic liver will last. Dr. Jha was emphatic that no tool exists to answer that question. His answer is structured surveillance: patients with cirrhosis are tested every six months, and the moment those tests begin to deteriorate, or fluid starts to collect in the abdomen, the team knows the liver is failing. The complications of decompensation, the scores used to grade them and the point at which a transplant becomes necessary are set out in decompensated cirrhosis, MELD and Child-Pugh scoring.

Liver cirrhosis diagnosis without a biopsy

A liver biopsy was once the reference test for cirrhosis. Dr. Jha's position is that a biopsy is not required in 99% of cases. A good fibroscan, an ultrasound-based test that measures the stiffness of the liver (transient elastography), can diagnose early cirrhosis, and blood tests with an abdominal ultrasound complete the picture. In advanced disease the diagnosis is often straightforward at the bedside: a swollen abdomen, vomiting of blood, deep jaundice or a very large spleen.

Cirrhosis in children: the 60-day window in biliary atresia

Cirrhosis is not confined to adults. Dr. Jha sees it frequently in children, and infants only a few months old can need a liver transplant because of it.

The most common cause in children is biliary atresia, a condition present from birth in which the bile ducts fail to form. The infant becomes jaundiced; bile cannot reach the gut, so stools turn pale and urine dark. Dr. Jha stressed one point above all: the child must be operated on before 60 days of life. If the infant reaches a surgeon within those first two months, a surgical procedure can be performed, and some children can be spared cirrhosis. The standard operation is the Kasai portoenterostomy, which connects the liver directly to a loop of bowel so that bile can drain. Once that window is missed, the child may go on to develop cirrhosis.

He showed the course of one such child, a six-month-old with biliary atresia whose abdomen was swollen with fluid, with prominent veins across the abdominal wall and an umbilical hernia. Photographs taken immediately after the transplant showed an infant surrounded by lines and monitoring wires, wrapped in plastic sheeting to keep warm. The last image, taken just before discharge, showed the same child smiling: a dramatic improvement over two to three weeks.

Acute liver failure is a different disease

Dr. Jha asked doctors to keep two terms distinct from cirrhosis: acute liver failure, in which a previously healthy liver fails suddenly, and acute-on-chronic liver failure, in which a patient with existing chronic liver disease deteriorates abruptly. Both are emergencies with very high short-term mortality; he noted that patients can die within 10 to 15 days, and that a liver transplant is the only way to save them. Some patients with acute liver failure, particularly after paracetamol poisoning treated early, do recover with intensive medical care alone, so transplant listing is decided case by case. Their triggers and place in transplant planning are discussed in the article on decompensated cirrhosis.

Liver cirrhosis management: control the cause, then transplant

Management of cirrhosis rests on three layers:

1. Treat or remove the cause. Antiviral therapy for hepatitis B and C, abstinence from alcohol, and control of weight, diabetes and blood lipids for fatty liver disease. Once cirrhosis has formed, however, the liver will not return to normal even if the virus is eliminated, which is why Dr. Jha placed so much weight on early detection.
2. Surveillance. Blood tests and imaging every six months to detect deterioration, decompensation and liver cancer, to which cirrhotic livers are particularly prone.
3. Liver transplantation once the liver decompensates. Dr. Jha's rule is direct: when any feature of decompensation appears in a patient with cirrhosis, that patient should be considered for a transplant.

There are two ways to transplant a liver. In a deceased donor liver transplant, the organ comes from a brain-dead donor. In a living donor liver transplant, a healthy living donor gives about 60% of his or her liver, and because the liver regrows, that same liver is enough for both donor and recipient. Dr. Jha was clear that the success rate for the patient is the same with either technique. Living donation dominates where deceased donation is limited, as in India and across South-East Asia. The techniques, donor safety and recovery are explored in Dr. Jha's separate masterclass, summarised in living donor liver transplant: a complete guide, and indicative costs are listed on the liver transplant cost page.

Supplements for liver health: none required

Asked whether any supplements are needed for a healthy liver, Dr. Jha's answer was an unequivocal no. A healthy lifestyle is what protects the liver:

• Keep weight under control, with a body mass index below 25.
• Control diabetes.
• Avoid alcohol.
• Exercise regularly.
• Have a check-up about once a year.
• Get tested for hepatitis B and C, and start treatment if either is found.

The remaining questions doctors raised during the session, from refractory ascites to the safety of liver donation, are collected on the Live Discussion page. Other liver specialists in the network are listed under hepatobiliary and liver transplant surgery.