Fatty liver disease affects approximately one in three UK adults, often discovered incidentally during routine health checks. Whilst simple fatty liver (steatosis) typically causes no immediate harm, many patients wonder whether it can progress to serious complications such as hepatic encephalopathy—a neuropsychiatric syndrome characterised by confusion and altered consciousness. Understanding the relationship between fatty liver and hepatic encephalopathy is crucial for patients diagnosed with hepatic steatosis. This article explains how fatty liver disease can lead to hepatic encephalopathy, the warning signs to watch for, and the NHS treatment pathways available to prevent progression and manage complications effectively.

Understanding Fatty Liver Disease and Hepatic Encephalopathy

Fatty liver disease, medically termed hepatic steatosis, occurs when excess fat accumulates in liver cells. The two main types are non-alcoholic fatty liver disease (NAFLD) and alcohol-related fatty liver disease (ARLD). NAFLD affects approximately one in three adults in the UK and is strongly associated with obesity, type 2 diabetes, and metabolic syndrome (NHS). In its early stages, fatty liver typically causes no symptoms and is often discovered incidentally during routine blood tests or imaging for other conditions.

Most people with simple fatty liver (steatosis) will not develop serious complications. However, in some individuals, the condition can progress to non-alcoholic steatohepatitis (NASH), where inflammation and liver cell damage occur alongside fat accumulation. Around 10–20% of people with NAFLD have NASH; a smaller proportion of these progress to advanced fibrosis and cirrhosis over time (NICE NG49). This progression typically occurs over many years or decades.

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that develops when the liver can no longer effectively remove toxins—particularly ammonia—from the bloodstream. These toxins cross the blood-brain barrier and interfere with normal brain function, causing symptoms ranging from mild confusion and personality changes to severe disorientation, drowsiness, and coma. Hepatic encephalopathy is a serious complication that indicates significant liver dysfunction and typically occurs in the context of advanced liver disease (decompensated cirrhosis) or acute liver failure.

Understanding the relationship between these two conditions is essential for patients with fatty liver disease, as early intervention and lifestyle modifications can significantly reduce the risk of progression to cirrhosis and its associated complications, including hepatic encephalopathy.

Can Fatty Liver Lead to Hepatic Encephalopathy?

Simple fatty liver disease alone does not cause hepatic encephalopathy. The liver retains normal or near-normal function in uncomplicated steatosis, maintaining its ability to metabolise toxins, synthesise proteins, and perform other vital functions. Hepatic encephalopathy only develops when liver function becomes severely impaired, which occurs in advanced stages of liver disease.

The critical link between fatty liver and hepatic encephalopathy is disease progression. When NAFLD or ARLD advances through the stages of inflammation (steatohepatitis), fibrosis, and ultimately cirrhosis, the liver's functional capacity gradually diminishes. Cirrhosis—characterised by extensive scarring and architectural distortion of liver tissue—represents the point at which complications such as hepatic encephalopathy become possible. In cirrhotic patients, the damaged liver cannot adequately clear ammonia and other neurotoxic substances, and abnormal blood flow patterns (portosystemic shunting) allow these toxins to bypass the liver entirely. Large spontaneous portosystemic shunts and transjugular intrahepatic portosystemic shunt (TIPS) procedures further increase the risk of hepatic encephalopathy.

Approximately 30–45% of patients with cirrhosis will experience at least one episode of overt hepatic encephalopathy during their illness (EASL 2022). The risk is particularly elevated in those with decompensated cirrhosis—when complications such as ascites (fluid accumulation), variceal bleeding, or jaundice develop. Additional precipitating factors include infections, gastrointestinal bleeding, constipation, dehydration, certain medications (particularly sedatives and opioids), and electrolyte imbalances. Suspected hepatic encephalopathy in a person with cirrhosis warrants urgent same-day medical assessment.

It is important to emphasise that progression from fatty liver to cirrhosis typically takes many years or decades and does not occur in the majority of patients. Regular monitoring, lifestyle interventions, and management of metabolic risk factors can substantially reduce the likelihood of progression. Patients diagnosed with fatty liver disease should work closely with their GP or hepatology team to assess their individual risk and implement appropriate preventive strategies.

Recognising Early Warning Signs and Symptoms

Early-stage fatty liver disease and even early cirrhosis are often asymptomatic, which underscores the importance of case-finding and risk stratification in at-risk people (for example, using the FIB-4 or NAFLD Fibrosis Score in primary care). However, as liver disease progresses, several warning signs may emerge that warrant medical attention. Patients should be aware of symptoms that might indicate advancing liver dysfunction or the development of complications.

Signs of progressive liver disease include:

• Persistent fatigue and weakness that interferes with daily activities

• Unexplained weight loss or loss of appetite

• Jaundice—yellowing of the skin and whites of the eyes

• Abdominal swelling or discomfort, particularly in the right upper quadrant

• Easy bruising or bleeding, indicating impaired clotting function

• Spider naevi (small, spider-like blood vessels on the skin) and palmar erythema (reddening of the palms)

• Ankle swelling (oedema) or abdominal distension from fluid accumulation (ascites)

Hepatic encephalopathy presents with neuropsychiatric symptoms that may be subtle initially but can progress rapidly. Early manifestations include:

• Mild confusion or difficulty concentrating

• Personality changes, irritability, or mood disturbances

• Sleep pattern disruption—excessive daytime sleepiness or insomnia

• Subtle tremor (asterixis or 'flapping tremor' of the hands)

• Slowed thinking or responses

As encephalopathy worsens, patients may develop marked disorientation, inappropriate behaviour, slurred speech, significant drowsiness, or loss of consciousness. These represent medical emergencies requiring immediate hospital assessment.

When to contact your GP, call 999, or attend A&E:

• Call 999 or go to A&E immediately if you or someone with liver disease experiences new confusion, altered consciousness, vomiting blood, or passing black, tarry stools

• Contact your GP urgently (same day) for new onset of jaundice, abdominal swelling or pain, or increasing fatigue with other symptoms of liver disease

• Call NHS 111 if you are unsure whether symptoms require urgent attention

Family members and carers should be particularly vigilant, as patients with early hepatic encephalopathy may lack insight into their cognitive changes. People with hepatic encephalopathy should not drive and may need to notify the DVLA, as the condition affects judgement and reaction times.

NHS Treatment and Management Options

Management of fatty liver disease focuses primarily on addressing underlying risk factors and preventing progression. NICE guidelines (NG49) recommend a comprehensive approach centred on lifestyle modification. For patients with NAFLD, weight loss of 7–10% of body weight has been shown to improve liver inflammation and may reverse fibrosis in some cases. This is best achieved through a combination of dietary changes—emphasising a Mediterranean-style diet rich in vegetables, whole grains, and healthy fats—and regular physical activity (at least 150 minutes of moderate-intensity exercise weekly).

Regarding alcohol, people with simple fatty liver should follow the UK Chief Medical Officers' low-risk drinking guidelines (no more than 14 units per week, spread over 3 or more days). If you have steatohepatitis, advanced fibrosis, or cirrhosis, you should abstain from alcohol completely, as any intake may accelerate liver damage.

Patients should also optimise management of associated conditions including type 2 diabetes, hypertension, and dyslipidaemia. Risk stratification in primary care typically uses the FIB-4 score or NAFLD Fibrosis Score; people at indeterminate or high risk may be offered the Enhanced Liver Fibrosis (ELF) blood test (NICE DG34) or transient elastography to refine their risk assessment. Those with advanced fibrosis, cirrhosis, or clinical decompensation should be referred to specialist hepatology services.

For established cirrhosis, management becomes more complex and typically involves specialist hepatology input. Patients require:

• Regular surveillance for hepatocellular carcinoma (ultrasound every 6 months with or without alpha-fetoprotein, NICE QS152)

• Endoscopic screening for oesophageal varices

• Monitoring for complications including ascites, spontaneous bacterial peritonitis, and hepatic encephalopathy

• Nutritional support, as malnutrition is common in advanced liver disease

• Vaccination against hepatitis A and hepatitis B where appropriate

Treatment of hepatic encephalopathy involves both acute management and prevention of recurrence. The mainstay of therapy is lactulose, a non-absorbable disaccharide that acidifies the colon, reduces ammonia production and absorption, and promotes its excretion. Typical dosing aims for 2–3 soft bowel movements daily. Rifaximin (550 mg twice daily), a non-absorbable antibiotic, may be added to lactulose for patients with recurrent episodes to prevent further recurrence (NICE TA337), as it reduces ammonia-producing gut bacteria.

Identifying and treating precipitating factors is crucial—this includes treating infections promptly, correcting electrolyte imbalances, managing constipation, avoiding sedative medications, and addressing gastrointestinal bleeding. Dietary protein restriction is no longer routinely recommended, as adequate nutrition is essential; instead, patients are advised to consume regular, small meals with an evening snack to prevent prolonged fasting.

For patients with decompensated cirrhosis or recurrent hepatic encephalopathy, referral to a specialist hepatology centre for consideration of liver transplantation may be appropriate. Transplantation offers the only definitive cure for end-stage liver disease and can provide excellent long-term outcomes when patients meet eligibility criteria.

The NHS provides comprehensive support through hepatology services, specialist nurses, dietitians, and alcohol liaison services where appropriate. Patients should maintain regular contact with their healthcare team and report any new symptoms promptly to enable early intervention and optimise outcomes. If you experience side effects from lactulose, rifaximin, or any other medicine, you can report them via the MHRA Yellow Card scheme at yellowcard.mhra.gov.uk or by searching for Yellow Card in the Google Play or Apple App Store.

Frequently Asked Questions