Complications of liver cirrhosis: what are they?

Usually, cirrhosis of the liver shows no obvious signs and may be asymptomatic for several years. As the fibrosis process progresses, the disease can lead to a number of complications. These are

The main complications of liver cirrhosis are:

  • digestive haemorrhage due to ruptured venous dilations (varices) of the oesophagus or stomach or diffuse bleeding from the stomach lining (congestive gastropathy);
  • the accumulation of liquids in the body (water-saline retention), mainly located in the lower extremities (ankle oedema) and inside the abdomen (ascites);
  • hepatic encephalopathy (which, through varying degrees, can progress to hepatic coma).
  • cancer (hepatocarcinoma) of the liver.

Digestive haemorrhage is manifested by vomiting of bright red or dark blood (‘coffee-break’) and, more frequently, by the emission of black-coloured stools (melena).

An important contributory cause in triggering digestive haemorrhage is the use of anti-inflammatory drugs (aspirin, anti-rheumatics), which should therefore be prohibited in patients suffering from cirrhosis of the liver.

Hepatic encephalopathy manifests itself in the early stages with behavioural changes (night-time insomnia and daytime sleepiness, easy irritability, changes in handwriting, inability to perform simple gestures or irrational behaviour) and a peculiar tremor in the hands with broad tremors (‘flapping tremor’).

A sign used by former clinicians is the garlicky smell of breath (foetor hepaticus)

The progression of hepatic encephalopathy may then lead to profound drowsiness, states of great agitation and finally to unrelievable coma.

Urgent hospitalisation when one or more of these complications occur is mandatory in almost all cases.

Admission is always necessary in cases of digestive haemorrhage.

Admission is also necessary at the first appearance of ascites in order to make an accurate diagnosis and evaluation for possible inclusion on the waiting list for liver transplant if the liver failure is considered to be severe.

Obviously, even short hospitalisation (day hospital) is useful in cases of ascites that poorly respond to therapy.

Finally, it is important to refer to a specialist centre at the first appearance of premonitory signs of encephalopathy in order to assess the need for hospitalisation.

Digestive haemorrhage in patients with liver cirrhosis

Among the possible complications of cirrhosis of the liver, digestive haemorrhage (ED) is undoubtedly the most dramatic event, both because of the acute way in which it presents itself and because each episode is potentially burdened with a discrete mortality rate.

The key event in determining the major complications of liver cirrhosis is the development of so-called portal hypertension, i.e. excessively high pressure in the portal vein.

When, in the course of the disease, portal hypertension reaches and exceeds a certain level (12 mmHg), there is a serious possibility of a sudden episode of digestive haemorrhage due to rupture of oesophageal or gastric varices (dilatation of the veins of the oesophagus or the bottom of the stomach) or congestive gastropathy (imbibition of the stomach wall).

The haemorrhagic event may be manifest, presenting with haematemesis (haematic vomiting) and/or melena (emission of dark, ‘pice-like’ stools due to the presence of digested blood), or, alternatively, it may be strongly suspected when there is more or less acute anaemia in a cirrhotic patient.

In Italy (ISTAT data referring to 2014) about 21,000 patients a year still die from complications of cirrhosis of the liver

Of these, about one fifth (three thousand patients) die as a result of an episode of digestive haemorrhage.

Thanks to recent therapeutic advances, a significant reduction in mortality per episode of haemorrhage has been achieved in recent years. Mortality is currently around 20-25% within six weeks (8% in the first 24 hours).

In the five years following the diagnosis of cirrhosis, 40% of patients develop varices, but only one third of these will have an episode of digestive haemorrhage during their lifetime.

The causes of digestive haemorrhage in cirrhotic patients in 60-70% of cases are caused by the rupture of an oesophageal varice, in 20% by congestive gastropathy, in 5% by the rupture of a gastric varice and in 5-10% by other causes (in particular gastric or duodenal ulcers).

Overall, therefore, portal hypertension causes more than 90% of digestive haemorrhages in cirrhotic patients.

Currently, two categories of drugs are used to prevent digestive haemorrhage in patients with marked portal hypertension, which act by reducing the pressure in the portal vein: beta-blockers or, alternatively, nitroderivatives.

Both drugs, taken daily, have proven to be effective, reducing the chance of a haemorrhagic event by 20-30%.

The very fact that only a fraction of patients with more or less large varices present sooner or later with a haemorrhagic episode makes it clear why there is no indication for sclerosing therapy or surgical shunts in preventing the first episode of digestive haemorrhage.

From the therapeutic point of view, the dramatic nature and the impossibility of predicting the duration and extent of the digestive haemorrhage always impose the hospitalisation of the patient, as home treatment is not absolutely feasible.

Primary biliary cirrhosis

Primary biliary cirrhosis is a chronic disease affecting the small bile ducts (those that transport bile from the liver to the gallbladder and intestine) that mostly affects middle-aged women between 40 and 60 years of age.

It is an autoimmune-based disease, in which lymphocytes, which are cells responsible for the body’s defence against infection, mistakenly attack the cells of the bile ducts, causing their progressive inflammation and scarring.

Some patients develop the disease into cirrhosis, when the inflammation of the ducts extends to the liver, leading to scarring of the organ and permanent damage.

The mechanism causing the disease is not yet clearly known.

Probably due to a genetic defect, the T lymphocytes, which should only defend the organism against infections, act against the cells of the bile ducts as if they were foreign elements of the organism, triggering a chronic inflammatory process that in a variable percentage of cases leads to cirrhosis.

At an early stage, the disease does not give rise to symptoms, but as the inflammatory process progresses, characteristic symptoms such as itching, fatigue, diarrhoea with greasy stools, dry mouth, jaundice, swelling of the feet and ankles, and ascites appear.

In more advanced stages there are fatty deposits (lipids) in the skin, around the eyes and under the eyelids (xanthelasmas), in the hands and feet, at the elbows and knees (xanthomas) and then bacterial infections, liver failure, cirrhosis, portal hypertension, oesophageal varices with bleeding, malnutrition, osteoporosis, liver cancer, colon cancer.

Diagnosis is made by performing the following tests: blood tests for liver function, alkaline phosphatase, gammaGT, and for specific antibodies (anti-mitochondrial antibodies – AMA and certain subtypes of anti-nuclear antibodies – ANA).

In addition, abdominal ultrasound, MRI, abdominal CT scan, a liver biopsy, for laboratory evaluation of the state of cells and tissues.

At present, the only therapy recognised as active is ursodesoxycholic acid.

Other drugs are used with immunosuppressive activity (Cortisone, Cyclosporine, Methotrexate), others with antifibrotic properties (Colchicine) in combination with various treatments to alleviate symptoms, in particular itching, caused by the deposition of bile salts in the skin (Cholestyramine) and dietary supplementation of vitamin D, to prevent bone mineral density from being reduced due to liver disease.

In more advanced stages of the disease, liver transplantation is required.


The most serious and late complication of cirrhosis is hepatocarcinoma. It usually arises 20-30 years after viral disease, alcohol abuse or metabolic alterations (steatohepatitis).

Hepatocarcinoma accounts for about 2 per cent of all tumour types.

Its incidence at European level is 7 cases per 100,000 inhabitants per year among males and 2 per 100,000 among females.

Prevention from this tumour is achieved by reducing exposure to the disease’s risk factors (hepatitis B, C, biliary cirrhosis, alcohol and metabolic alterations).

Generally, this tumour has a slow growth rate and in most cases presents in an advanced stage.

Small tumours often give no symptoms and are usually detected as part of screening programmes or incidentally, during imaging examinations performed for other purposes.

Larger forms present with symptoms such as pain in the right upper abdominal quadrant, the presence of a palpable mass with weight loss often associated with fever, ascites and jaundice.

In more advanced stages splenomegaly, haemorrhage from oesophageal varices or gastropathy and encephalopathy also occur.

From a diagnostic point of view and in the staging of the tumour a central role is played by liver ultrasound, CT scan with contrast medium, MRI and finally liver biopsy.

As for treatment, this has a multidisciplinary approach and depends on the stage of the tumour, the degree of liver impairment and the patient’s general condition.

On the basis of these parameters, the most suitable treatment is chosen, such as surgical therapy, loco-regional therapy (transcutaneous ultrasound or laparoscopic thermo-ablation), chemo-embolisation by radiology, and finally liver transplantation.

If the disease is at an advanced stage, the treatment that can significantly prolong the patient’s survival is systemic therapy with Sorafenib.

Non-alcoholic steatohepatitis cirrhosis

Non-alcoholic steatohepatitis is a liver disease characterised by processes of inflammation, scarring and tissue death due to metabolic dysfunction and the excessive presence of fat within its cells, not due to alcohol consumption.

Fat can accumulate in internal organs (visceral fat) and is particularly dangerous to health.

When triglycerides are present in more than 5 per cent of liver cells, we speak of hepatic steatosis (fatty liver).

In a small percentage of individuals this condition evolves into non-alcoholic steatohepatitis, which carries a high risk of progression to major liver diseases such as fibrosis and liver carcinoma.

This condition affects at least 25% of Italians, (one in four has fatty liver) and this percentage increases with age and especially increases among overweight and diabetic people, reaching 50% (one in two) in obese people.

Even normal-weight people can be affected by this disease, as can children.

In fact, it is estimated that in 2030, around 30% of Italians will have fatty liver.

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