Cirrhosis Complications: Swelling, Confusion or Bleeding and Why They Need Urgent Care

The belt notch moved first. A man who had lost weight everywhere else found his trousers straining at the waist, and his ankles left deep sock lines by evening. His partner noticed something different: he was dozing through afternoons and had started reversing the order of words. Neither of them connected the two.

Cirrhosis is scarring of the liver so extensive that the organ can no longer do its ordinary jobs. It can stay quiet for years, which is precisely why the cirrhosis complications warning signs matter so much. Swelling, confusion and bleeding are not three unrelated nuisances. They are three signals from one failing system, and they tend to arrive at the point where the liver has run out of reserve.

This explainer walks through what each sign means inside the body, what a hospital team actually does about it, and how to tell the difference between something to mention at the next appointment and something that should not wait until morning.

Why cirrhosis complications warning signs so often arrive late

The liver has an unusual talent for hiding damage. It performs hundreds of tasks, from filtering blood to making clotting proteins, and it keeps performing most of them with a fraction of its healthy tissue. Doctors describe this quiet phase as compensated cirrhosis: the scarring is present, blood tests may be only mildly abnormal, and the person often feels well.

Scar tissue does more than replace working cells. It stiffens the liver and squeezes the vessels running through it. Blood arriving from the gut through the portal vein meets resistance and backs up, a state called portal hypertension (high pressure in the veins that drain the intestines into the liver). The NHS notes that cirrhosis frequently causes no symptoms until the damage is advanced, and portal hypertension is the engine behind much of what happens next.

At some point the balance tips. Pressure forces fluid out of vessels into the abdomen. Toxins that a healthy liver would clear slip through to the brain. Swollen veins in the food pipe stretch until they tear. The moment any of these happens, the label changes to decompensated cirrhosis, and the medical urgency changes with it.

This is why the first obvious sign is often not an early sign at all. Someone can move from feeling fine to needing hospital care within days, not because the liver failed suddenly but because it finally stopped covering for years of gradual loss. Recognizing the signals quickly does not undo the scarring, yet it does change what the care team can do, and how safely.

What actually happens inside a scarred liver

Picture the liver as a dense sponge with blood flowing through millions of tiny channels. Cirrhosis replaces soft, working tissue with fibrous bands and hard nodules, and the channels narrow. Three consequences follow, and each maps onto one of the warning signs.

First, pressure. When blood cannot pass easily through the liver, it seeks other routes. Veins in the esophagus (the food pipe) and stomach enlarge into varices, which are thin-walled, swollen vessels under high pressure. The Mayo Clinic describes esophageal varices as one of the more dangerous consequences of portal hypertension because they can rupture with little warning.

Second, protein. Healthy liver cells manufacture albumin, a blood protein that acts like a sponge holding water inside blood vessels. As production falls, fluid leaks into tissues and the abdominal cavity. The same cells also make most clotting factors, so bleeding, once it starts, is harder to stop and bruises appear from minor knocks.

Third, filtering. Gut bacteria produce ammonia and other by-products as they digest protein. A healthy liver clears these before they reach general circulation. In cirrhosis they pass through, or bypass the liver entirely via those new vessel routes, and reach the brain, where they disturb thinking, sleep and coordination. Cleveland Clinic explains this process as the basis of hepatic encephalopathy.

Kidneys are drawn in too. Sensing lower effective blood volume, they hold onto salt and water, which worsens swelling, and in advanced disease they may shut down in a pattern called hepatorenal syndrome (kidney failure driven by liver failure rather than kidney damage). One organ, several failing systems: that interdependence is why a single warning sign prompts a whole-body assessment.

Swelling: what ascites and leg edema are telling you

Ascites (pronounced a-SY-teez) is fluid collecting in the abdominal cavity, the space around the intestines and other organs. Cleveland Clinic lists cirrhosis as its leading cause. People often notice it as a waistband that no longer fits, a belly that feels tight or heavy, or early fullness after small meals. Breathing can feel effortful when lying flat because the fluid presses upward on the diaphragm.

Leg swelling, called edema, usually appears alongside it. Gravity pulls leaked fluid downward, so ankles and shins puff up during the day and may improve overnight. Pressing a thumb into the skin can leave a dent that lingers.

Why urgent rather than simply uncomfortable? Ascitic fluid is an ideal place for bacteria to grow. Spontaneous bacterial peritonitis, an infection of that fluid without any obvious puncture or leak, can develop quietly and become life-threatening quickly. Fever, new abdominal pain or tenderness, or a sudden worsening of confusion in someone with known ascites is treated as an emergency until proven otherwise.

In hospital, the usual first step is paracentesis, a procedure in which a thin needle drains fluid from the abdomen under local anesthetic, both to relieve pressure and to test the fluid for infection and protein content. Medical management centers on limiting salt, since salt drives water retention, and on diuretics, a class of medicines that prompt the kidneys to release sodium and water. The prescribing team sets any restrictions and adjusts treatment based on weight trends, blood tests and kidney function, because over-vigorous fluid removal can itself harm the kidneys. Rapid weight gain over a few days, or swelling that returns faster than before, is worth reporting rather than waiting out.

Confusion: hepatic encephalopathy signs, from subtle to severe

Hepatic encephalopathy is a decline in brain function caused by toxins the liver can no longer remove. Families often spot it before the person does. The earliest changes are easy to dismiss: sleeping during the day and waking at night, a shorter fuse, forgetting the thread of a conversation, or handwriting that suddenly looks unfamiliar. Cleveland Clinic notes that even mild encephalopathy can affect concentration and reaction time enough to make driving unsafe.

Clinicians grade severity on a scale from 1 to 4. Grade 1 is subtle mood and sleep change; grade 2 brings obvious disorientation, slurred speech and a characteristic flapping tremor of the outstretched hands; grade 3 is marked confusion with drowsiness; grade 4 is coma. Someone can move between grades within hours.

Triggers matter, because encephalopathy is often a reaction to something else. Common precipitants include infection, bleeding into the gut (digested blood is a large protein load), constipation, dehydration from vomiting or excess diuretic effect, low potassium, and sedating medicines. Finding and correcting the trigger is as central to treatment as clearing the toxins.

The mainstay of treatment is lactulose, a non-absorbable sugar that draws water into the bowel, speeds transit and reduces ammonia production by gut bacteria. A gut-targeted antibiotic may be added to reduce the bacteria responsible. How these are used, and for how long, is a decision for the liver team, who balance benefit against dehydration risk. The practical message for households is blunt: new confusion in someone with cirrhosis is not a bad day or a sign of aging. It is a medical event, and the earlier it is assessed, the smaller the trigger tends to be.

Bleeding: varices, bruising and why blood loss escalates fast

Two very different kinds of bleeding occur in cirrhosis, and they carry different levels of urgency.

The first is the everyday kind: bruises from minor bumps, gums that bleed on brushing, nosebleeds that take longer to stop. These reflect fewer clotting factors and a low platelet count, since the enlarged spleen traps platelets as blood backs up behind the liver. Worth mentioning at appointments, rarely an emergency on their own.

The second is variceal hemorrhage, and it is one of the most dangerous events in liver disease. Varices are swollen veins in the esophagus or stomach that have taken on blood diverted around the scarred liver. Their walls are thin and the pressure inside is high. When one tears, the result can be vomiting of bright red blood or material resembling coffee grounds, or the passage of black, tarry, foul-smelling stools, which is digested blood. The Mayo Clinic describes bleeding varices as a life-threatening emergency requiring immediate care.

Blood loss compounds every other problem. Reduced blood pressure starves the kidneys. The protein load in the gut tips the brain into encephalopathy. Infection risk climbs. That cascade is why hospitals treat suspected variceal bleeding with a bundle of measures at once: fluid and blood replacement, medicines that lower portal pressure, antibiotics to prevent the infections that commonly follow, and an urgent endoscopy, a camera examination of the esophagus during which bleeding veins can be tied off with small bands.

Where varices are found before they bleed, teams often use non-selective beta-blockers, a class of medicine that lowers pressure in the portal system, or scheduled banding sessions, to reduce the chance of a first bleed. Which route suits a given person, and whether either is appropriate, depends on the size of the varices and the rest of their health, and rests with the treating specialist.

The three warning signs at a glance

Placing the three signals side by side shows how differently they present and how similarly they should be handled: assessment on the same day, and emergency care for the severe forms.

Sign	What is happening	Usual first tests	Treat as emergency when
Abdominal or leg swelling	Fluid leaking into tissues and abdominal cavity because of portal pressure and low albumin	Examination, ultrasound, blood tests for kidney function and albumin, paracentesis with fluid analysis	Fever, abdominal pain or tenderness, rapid enlargement, breathlessness, new confusion
Confusion or drowsiness	Ammonia and other gut-derived toxins reaching the brain; often set off by infection, bleeding, constipation or dehydration	Clinical grading, blood tests, search for a trigger including infection screen and stool history	Unable to stay awake, disoriented to place or people, cannot safely swallow, any fall
Bleeding	Ruptured varices under high pressure, worsened by low clotting factors and platelets	Blood count and clotting, urgent endoscopy, blood grouping	Vomiting blood or coffee-ground material, black tarry stools, fainting, racing pulse

Several patterns emerge. Infection appears in more than one column because it is the most common trigger of decompensation and the most treatable. Confusion shows up as both a sign in its own right and a red flag for the other two, since bleeding and infected ascites both drive encephalopathy. The tests overlap heavily, which is why a person arriving with one complaint is routinely screened for all three.

MedlinePlus and the NHS both emphasize that these complications can develop in any type of cirrhosis, whatever its original cause. Alcohol-related disease, metabolic fatty liver disease, viral hepatitis and autoimmune conditions all reach the same final pathway of scarring and pressure, so the warning signs are the same for everyone living with the condition.

What is stage 4 cirrhosis of the liver?

People search this phrase constantly, and the honest answer is that the word stage is used in two overlapping ways.

In the language of liver fibrosis, scarring is scored from 0 to 4 on biopsy or imaging. Stage 4 fibrosis is cirrhosis itself: scar tissue has bridged across the liver and formed nodules. By this definition, everyone with cirrhosis has stage 4 liver disease, including people who feel entirely well.

In everyday and some clinical use, stage 4 means advanced or end-stage disease, the point at which complications have appeared and the liver is failing. This is what most people picture when they hear the term, and it corresponds more closely to decompensated cirrhosis.

Because of that ambiguity, specialists lean on scoring systems rather than the word stage. The Child-Pugh score combines bilirubin (a yellow pigment that rises when the liver cannot process it), albumin, clotting time, and the presence and severity of ascites and encephalopathy into classes A, B and C. The MELD score, short for Model for End-Stage Liver Disease, uses blood results alone and is widely used to rank urgency for transplantation. Both are tools for the care team and neither is a countdown. They shift with treatment, infection and hydration, sometimes considerably.

What a stage 4 label should prompt is a conversation, not a conclusion. Useful questions include which definition is being used, whether the disease is currently compensated or decompensated, what the driving cause is and whether it is being treated, and whether a transplant assessment has been considered. Johns Hopkins Medicine notes that removing the cause, such as treating viral hepatitis or stopping alcohol, can slow or halt progression even when scarring is established. That fact alone makes the stage label less final than it sounds.

What are the early signs of cirrhosis, honestly?

The uncomfortable truth is that there often are none, or none specific enough to act on. The Mayo Clinic lists fatigue, loss of appetite, nausea, mild upper-abdominal discomfort and unexplained weight loss among the earliest complaints, and every one of them overlaps with dozens of ordinary conditions. Nobody should diagnose cirrhosis from a list, and this article deliberately does not offer one.

What does help is knowing who is at risk and asking for the right tests. Long-term heavy alcohol use, chronic hepatitis B or C infection, type 2 diabetes with fatty liver, marked obesity, autoimmune liver disease and certain inherited conditions all raise the odds. In those groups, a simple blood panel and an ultrasound or elastography scan (a painless test that measures liver stiffness) can identify scarring years before symptoms would.

Some slightly more specific early changes do exist. Small red spider-like vessels on the chest, reddened palms, loss of body hair, breast tissue growth in men, itching without a rash and irregular periods in women can reflect the hormonal shifts of a struggling liver. Jaundice, a yellow tinge to the skin and whites of the eyes, is a later change but sometimes the first one noticed.

The single most valuable early sign may be the one on paper: a routine liver enzyme result flagged as abnormal and then never followed up. If that has happened, asking for a review is reasonable. The NHS is clear that cirrhosis cannot be reversed once established, but that treating the underlying cause can stop it worsening, and the earlier that happens the more liver there is left to protect.

Decompensated cirrhosis symptoms and the question of how long

Decompensated cirrhosis is the term for liver disease that has produced at least one major complication: ascites, encephalopathy, variceal bleeding or jaundice. It marks a real change in outlook, and people naturally want to know what it means for time.

The candid answer is that no responsible clinician can give a single figure from a description alone, and this article will not invent one. Outcomes vary enormously depending on which complication occurred, whether it was triggered by something reversible such as infection, whether the underlying cause of the cirrhosis is still active, how the kidneys are functioning, and whether transplantation is an option. Two people with the same diagnosis can follow very different paths.

What guidelines and major centers agree on is direction. Decompensation is associated with substantially higher risk than the compensated phase, and each additional complication adds to that risk. Tools such as the MELD score exist because clinicians needed a structured way to estimate urgency for transplant listing, not because the future is fixed. Scores rise during acute illness and can fall again once infection is treated and fluid is controlled.

Several things move the needle in a favorable direction. Stopping alcohol completely, in alcohol-related disease, is the single most powerful step and can allow some recovery of function even in decompensated cirrhosis. Treating hepatitis C or suppressing hepatitis B removes the ongoing injury. Managing complications promptly reduces the chance of one tipping into another. Referral for transplant assessment, where appropriate, opens a path that did not exist a generation ago.

Ask the treating team directly what the numbers mean for you, what would change them, and what they are watching for. Those are answerable questions. A generic prognosis found online is not.

How complications are treated, who is usually treated and who is asked to wait

Treatment in decompensated cirrhosis works on two levels: settling the immediate crisis and lowering the pressure that caused it.

For ascites, the sequence is usually salt restriction and diuretics, escalating to repeated paracentesis when medicines cannot keep pace. A procedure called TIPS, short for transjugular intrahepatic portosystemic shunt, creates a channel through the liver so blood can bypass the scarred tissue and portal pressure falls. It can dramatically reduce ascites and variceal bleeding, but it diverts blood the liver would otherwise filter, so encephalopathy can worsen afterward. Teams therefore reserve it for people whose ascites or bleeding is uncontrolled by other means and whose brain function and heart are robust enough to tolerate it. Those with frequent encephalopathy or advanced age are often asked to wait or offered alternatives.

For encephalopathy, treatment targets the gut and the trigger, as described earlier. Long-term preventive medicine is usually offered after a second episode, and a first episode is often managed by finding and removing the precipitant.

For varices, banding and portal-pressure-lowering medicines are the pillars. People with very small varices and well-compensated disease may be monitored with repeat endoscopy rather than treated, because the risk of the treatment can outweigh the risk of a bleed in that group.

Transplantation is the one treatment that addresses the scarring itself. Assessment considers the severity of liver failure, other medical conditions, the ability to manage the demanding aftercare, and, in alcohol-related disease, a sustained period without drinking. Some people are listed promptly. Others are asked to work on fitness, nutrition or abstinence first, and some are not candidates. None of these decisions belong to a search engine or a magazine; every one of them sits with the treating team, who weigh risks and alternatives for that particular person.

What the days and weeks after an admission usually look like

A first hospital stay for decompensation tends to follow a recognizable arc, though the length varies with the complication and how quickly a trigger is found.

The first day or two are about stabilizing: draining fluid, controlling bleeding, starting antibiotics if infection is suspected, and correcting salt and potassium levels. Encephalopathy commonly improves within a few days once the trigger is addressed and bowel transit is restored, though thinking may feel foggy for longer. Ascites relieved by paracentesis begins to return almost immediately in most people, which is why medicines and salt limits start before discharge.

Going home usually comes with a package rather than a single prescription: daily weight checks to catch fluid returning early, a written plan for what to do if confusion recurs, a follow-up endoscopy if varices were banded, and blood tests within a week or two to watch kidney function under diuretic treatment. Many teams also arrange a dietitian review, because muscle loss is common in cirrhosis and adequate protein, spread across the day with a late-evening snack, supports both strength and brain function.

The weeks that follow are often the period of highest vulnerability for a second event. Infection, missed medicines, dehydration during a stomach bug, or a return to drinking are the usual culprits. Families frequently describe this as the time they learned to read the small signs: the slightly slower speech, the sock lines that appeared earlier in the day.

Recovery of energy is slow and non-linear. The NHS advises people with cirrhosis to avoid alcohol entirely, to check with a pharmacist or doctor before taking any new medicine including over-the-counter painkillers, and to keep vaccinations current, because a body with a scarred liver handles infection poorly. Those unglamorous habits do more to prevent the next admission than anything found in a supplement aisle.

What people often get wrong about cirrhosis complications

Myths cluster thickly around liver disease, and several of them delay care.

Only heavy drinkers get cirrhosis. Alcohol is a major cause, but so are chronic viral hepatitis, metabolic fatty liver disease linked to diabetes and excess weight, autoimmune conditions and inherited disorders. The NHS and Mayo Clinic both list these causes side by side. Assuming a non-drinker cannot have cirrhosis means warning signs get attributed to something else.

If it does not hurt, it is not serious. The liver has few pain fibers. Variceal bleeding and encephalopathy are typically painless until very advanced. Pain is a poor guide here.

Confusion is just aging or stress. In someone with cirrhosis, new confusion has a medical cause until proven otherwise, and that cause is usually treatable. Waiting a few days to see if it passes allows a trigger such as infection to progress.

Liver cleanses and supplements repair scarring. No supplement has been shown in mainstream evidence to reverse cirrhosis, and several herbal products are themselves associated with liver injury. NIH resources on dietary supplements caution that natural does not mean safe for the liver. Money spent there is better spent on the dietitian.

Drinking less is enough. For alcohol-related cirrhosis, guidelines are consistent that complete abstinence is the goal, because a scarred liver has no margin.

Once decompensated, nothing can be done. This is perhaps the most harmful belief. Complications are managed every day; some people return to a compensated state once a trigger is removed and the cause is treated; and transplantation exists. The outlook is serious, and honesty about that matters, but resignation is not evidence-based.

Questions to ask your care team

Appointments after a diagnosis of cirrhosis, and especially after a first complication, can feel rushed. Arriving with specific questions changes the quality of the conversation. These are ones that patients and families consistently find useful.

• Is my cirrhosis currently compensated or decompensated, and what would move it from one to the other?
• What is causing my liver disease, and is that cause being fully treated?
• Have I been checked for varices, and if so, what is the plan: monitoring, medicine or banding?
• What is my current Child-Pugh class or MELD score, and what do those numbers mean for me specifically?
• Which of my medicines, including over-the-counter and herbal products, should I stop or avoid because of my liver?
• What exactly should I do at home if I notice swelling, confusion or bleeding, and who do I call out of hours?
• Should I be weighing myself daily, and what change in weight should prompt a call?
• Do I need a dietitian, and how much protein and salt is right for me?
• Which vaccines do you recommend for me given my liver disease?
• Am I a candidate for transplant assessment, and if not now, what would need to change?
• How often will I have scans to check for liver cancer, which is more common in cirrhosis?
• Is it safe for me to drive, work or travel, and what would change that advice?

Bringing a family member or friend helps, particularly where encephalopathy is a concern, because they may notice changes the person cannot. Writing down answers, or asking whether the clinic provides a written care plan, turns a one-off conversation into something the household can refer to at two in the morning, when the questions tend to feel most urgent.

When to call your doctor: cirrhosis complications warning signs that cannot wait

For anyone living with cirrhosis, the threshold for seeking help should be lower than for the general population, because complications compound each other and infection can escalate within hours.

Call emergency services or go to an emergency department immediately for:

• Vomiting blood, or material that looks like coffee grounds
• Black, tarry or maroon stools, or large amounts of fresh blood from the back passage
• Confusion severe enough that the person cannot say where they are, cannot be kept awake, or cannot swallow safely
• A tense, painful abdomen with fever, chills or vomiting, especially in someone known to have ascites
• Fainting, a racing heartbeat or cold, clammy skin, which can signal serious blood loss
• Sudden severe breathlessness

Contact your liver team or doctor the same day for:

• New or rapidly increasing swelling of the abdomen or legs, or a weight gain of several pounds over a few days
• New drowsiness, sleep reversal, irritability, slurred speech, tremor or handwriting changes
• Fever or feeling generally unwell without an obvious cause
• Yellowing of the skin or eyes that is new or deepening
• Passing much less urine than usual
• Bruising or bleeding that is more frequent or harder to stop than before
• Vomiting or diarrhea lasting more than a day, since dehydration can trigger both kidney trouble and encephalopathy

When in doubt, call. Liver teams would far rather hear about a change that turns out to be minor than see someone arrive a day later with an infection that has spread. Every one of these signs has a management pathway, and the decisions about which to follow rest with the clinicians who know the person’s history. The job of the household is simply to notice, and to pick up the phone.

Frequently asked questions

What are the end stage liver disease symptoms families usually notice?

The most common features are a swollen abdomen from ascites, deepening yellow skin and eyes, marked drowsiness or confusion from hepatic encephalopathy, easy bruising or bleeding, muscle wasting and profound fatigue. Kidney function often declines and urine output falls. These signs reflect a liver that can no longer compensate, and each has a management plan; the treating team can explain which apply and what comfort and treatment options exist.

What are the early signs and symptoms of liver cirrhosis?

Frequently there are none, which is why the condition is often found on routine blood tests or scans. When early symptoms occur they are vague: tiredness, poor appetite, nausea, mild upper-abdominal discomfort or weight loss, according to the Mayo Clinic. Because these overlap with many conditions, people with risk factors such as heavy alcohol use, viral hepatitis or fatty liver should ask for liver tests rather than rely on symptoms.

What is stage 4 cirrhosis of the liver?

It depends who is using the term. On fibrosis scoring, stage 4 simply means cirrhosis is present, whether or not symptoms have appeared. In everyday use it often means end-stage or decompensated disease with complications such as ascites or encephalopathy. Specialists usually prefer Child-Pugh class or MELD score because these track severity more precisely. Asking your team which definition they mean clears up most of the confusion.

How long can someone live with decompensated cirrhosis?

There is no single honest figure. Outlook depends on which complication occurred, whether a reversible trigger such as infection caused it, whether the underlying cause is still active, kidney function, and eligibility for transplant. Decompensation carries substantially higher risk than compensated disease, but stopping alcohol, treating viral hepatitis and prompt management of complications can change the course. Your liver team can discuss your own scores and what would improve them.

What are the decompensated cirrhosis symptoms that mean an emergency?

Vomiting blood or coffee-ground material, black tarry stools, confusion severe enough that the person cannot stay awake or say where they are, a tense painful abdomen with fever, fainting or a racing pulse, and sudden severe breathlessness all need emergency care. Less dramatic changes such as new swelling, drowsiness, fever or reduced urine should still be reported to the liver team the same day.

What are the first hepatic encephalopathy signs?

Early signs are subtle and often noticed by family first: sleeping in the day and waking at night, irritability or personality change, trouble concentrating, forgetting recent conversations and changes in handwriting. As it progresses, slurred speech, disorientation and a flapping tremor of the outstretched hands appear. Cleveland Clinic notes even mild encephalopathy can impair driving. Any new confusion in someone with cirrhosis warrants same-day medical assessment.

Can cirrhosis swelling go down on its own?

Rarely without treatment, because the fluid reflects ongoing portal pressure and low albumin. Ascites and leg edema are usually managed with salt restriction and diuretics set by the care team, and by paracentesis when fluid builds faster than medicines can clear it. Swelling that appears suddenly, returns quickly after drainage, or comes with fever or pain needs prompt review, since infected ascites is a medical emergency.

Why does cirrhosis cause bleeding and bruising?

A scarred liver makes fewer clotting proteins, and the enlarged spleen that develops behind a congested liver traps platelets, so minor knocks bruise and cuts bleed longer. Separately, high portal pressure swells veins in the esophagus and stomach into varices, which can rupture and bleed heavily. Everyday bruising should be mentioned at appointments; vomiting blood or black stools is an emergency.

Does stopping alcohol help once cirrhosis is decompensated?

Yes, in alcohol-related disease it is the most powerful single step. The NHS and Johns Hopkins Medicine both note that removing the cause can slow or halt progression even when scarring is established, and some people regain enough function to return to a compensated state. Abstinence is also generally required before transplant listing. Support for stopping safely is available through the care team, since abrupt withdrawal can itself need medical supervision.

Do liver cleanses or supplements help cirrhosis complications?

No mainstream evidence shows that any cleanse or supplement reverses scarring or prevents complications, and several herbal products are associated with liver injury. NIH resources on dietary supplements advise caution for anyone with liver disease. Because a scarred liver processes many substances poorly, people with cirrhosis should check with a pharmacist or their doctor before taking any new product, including over-the-counter painkillers.

References

• NHS: Cirrhosis
• Cleveland Clinic: Hepatic encephalopathy
• MedlinePlus: Cirrhosis

This article is for general information only and is not a substitute for professional medical advice. Please consult a qualified doctor about your individual situation.