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Liver cirrhosis is not a sudden event but the end point of damage that has gone on for years. When liver tissue is injured over a long period — by alcohol, fat, viruses or an autoimmune reaction — the body repairs it with connective tissue. Bit by bit, working liver cells become scar tissue.¹
Almost every complaint follows from that. The loss of function means that proteins and clotting factors are missing and breakdown products such as bilirubin or ammonia build up. The backed-up blood flow (portal hypertension) drives blood into bypass routes through thin-walled veins, among them those in the oesophagus; fluid leaks into the abdominal cavity.¹,²
Knowing the cause is not an academic exercise — almost the whole of the treatment follows from it.
Often more than one cause comes together — alcohol plus fatty liver plus excess weight, say. The factors do not merely add up, they reinforce one another.
This distinction is the most important one in the whole subject, because it determines the outlook, the treatment and the urgency.¹,³
| Stage | What is happening | How it feels | What matters most |
|---|---|---|---|
| Compensated | The liver is scarred, the remaining cells keep function going | Often nothing at all — or a tiredness that nobody connects with the liver | Remove the cause, prevent, monitor |
| Decompensated | The reserves no longer suffice; the loss of function and the backed-up blood become visible | Fluid in the abdomen, jaundice, confusion, bleeding | Treat the complications, weigh up the options at a liver centre |
The compensated phase can last many years — and that is exactly where the trap lies: because nothing hurts, cirrhosis is often picked up as an incidental finding, on an ultrasound done for another reason or in a routine blood test. Anyone caught at this stage has the greatest leverage: every measure that delays the move into decompensation buys time. Scoring systems such as Child-Pugh and the MELD score are used to judge how severe the disease is.
The early signs are so non-specific that they are almost always put down to something else: persistent tiredness, a drop in performance, loss of appetite, pressure in the upper right abdomen, itching. Later, visible clues are added — reddened palms, spidery markings of the vessels, bruises for no reason.²,³
With encephalopathy there is one point that relatives often notice first: the early stages do not show themselves as obvious confusion but as slowed thinking, trouble finding words, a reversed sleep rhythm or mistakes at the wheel. That belongs on the table — it can be treated.
There is no medicine that dissolves scar tissue. What works is a sober bundle: remove the cause, treat complications early and avoid everything that puts extra strain on the liver. The decisions are made by your treating practice together with you.¹
The liver is the central organ for breaking down most drugs. Once it is scarred, medicines are broken down more slowly, work more strongly and for longer, and part of the blood bypasses the liver altogether. At the same time clotting, the kidneys and the brain's metabolism are more sensitive. The very tablet that was unproblematic before can now be a real risk.¹,⁴
| Substance / group | Where it stands in cirrhosis | What that means in practice |
|---|---|---|
| Paracetamol | At a reduced daily dose usually better than an NSAID | At a lowered maximum dose and without alcohol it counts as an acceptable painkiller. The upper limit is set by your practice — cold remedies often contain paracetamol as well |
| Ibuprofen, diclofenac (NSAIDs) | Unfavourable — they raise the risk of bleeding and of kidney damage | They inhibit the platelets (risky when clotting is already disturbed), encourage stomach bleeding, worsen the blood supply to the kidneys and increase fluid in the abdomen — avoid where possible |
| Lorazepam, other benzodiazepines, Z-drugs | Critical — they can trigger encephalopathy | In cirrhosis they work more strongly and for longer — only after a medical weighing-up, never on your own and never on top of alcohol |
| Non-selective beta blockers | Therapeutically wanted — they lower the pressure in the portal vein | Propranolol or carvedilol prevent bleeding from varicose veins in the oesophagus. A cardioselective beta blocker such as metoprolol is not suitable for this |
| Lactulose, alternatively macrogol | Standard in hepatic encephalopathy | Speeds up the removal of ammonia-forming substances from the bowel. The aim: several soft stools a day — too little has no effect, too much costs fluid and salts |
| Spironolactone, with furosemide added | Effective against fluid in the abdomen, but needs monitoring | They call for regular checks of weight, kidney values, sodium and potassium. Losing fluid too quickly worsens kidney function and encephalopathy |
| Over-the-counter and herbal products | Not automatically harmless | High-dose vitamin A, some herbal remedies and combination products put extra strain on the liver. Everything belongs on the medication list — including what comes from the drugstore |
The most important rule behind all this is banal, and it is broken all the time: say at every contact with a doctor or a pharmacy that you have liver cirrhosis. Many doses are then adjusted, and some substances avoided altogether. Anyone who does not mention it gets standard doses — and those can be too high. More in medications in kidney and liver impairment.
Substances, doses and check-up dates — for the emergency department too.
The pressure in the portal system widens thin-walled veins in the oesophagus. If they tear, massive bleeding follows — which is why a gastroscopy is done to look for them once cirrhosis is confirmed. Where the varices are relevant, non-selective beta blockers or band ligation come into question. Vomiting blood or tarry stools are always an emergency, with a call to 112.¹
Fluid collects in the abdominal cavity, often together with oedema in the legs. Treatment is with less salt and with water tablets; where the amounts are large, the fluid is drained with a needle. Weighing yourself daily at the same time is the most telling thing you can do yourself — the weight curve shows faster than any feeling whether the dose is right. A fever and abdominal pain with ascites need assessing immediately.
If the liver no longer detoxifies ammonia sufficiently, brain function suffers — from mild slowing to coma. Treatment is with lactulose, often with a poorly absorbed antibiotic added; triggers such as infections, constipation, bleeding or sedating medicines are removed. Important: during this phase you must not drive.
The liver and the kidneys are closely linked — a drop in blood pressure, fluid loss and infections worsen kidney function quickly. That is why kidney values belong among the checks, and why NSAIDs are particularly unfavourable here; the parallels are described in the article on chronic kidney disease. Infections are at the same time a frequent trigger of decompensation. For chronic liver disease, Germany's standing committee on vaccination (STIKO) therefore recommends consistent vaccination cover, above all against hepatitis A and B, flu, pneumococci and COVID-19 — see vaccinations for adults.⁵
One outdated piece of advice holds on stubbornly here: "with liver damage you have to cut down on protein". That used to be the standard in encephalopathy — and on current knowledge it is wrong, and even harmful. People with cirrhosis often have a raised protein requirement and lose muscle mass quickly; and it is precisely the loss of muscle that worsens the outlook and the encephalopathy, because muscles help to break ammonia down.¹,⁴
To put it in perspective, without glossing over it and without painting it black: liver cirrhosis is a serious, chronic illness. How it runs depends strongly on whether the cause is removed and whether complications are treated early. You have more influence over that in everyday life than it feels like at first.
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