Hepatic Encephalopathy

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Hepatic Encephalopathy
Hepatic Encephalopathy

Video: Hepatic Encephalopathy

Video: Hepatic Encephalopathy
Video: Hepatic Encephalopathy 2023, March

Hepatic encephalopathy

Hepatic encephalopathy (HE) is a potentially reversible (reversible) functional disorder of the brain that results from an inadequate detoxification function of the liver. This is the result of acute liver failure or chronic liver disease (e.g. liver cirrhosis). This leads to increasing concentrations of various mainly neurotoxic, i.e. nerve-damaging substances in the body. Ammonia in particular plays an important role here. This can lead to various forms of impaired consciousness.

With minimal hepatic encephalopathy (MHE), no symptoms are noticeable at first glance. However, neuropsychological tests can already detect disorders of perception and thinking. In severe cases, hepatic encephalopathy can be fatal.


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  • What are the causes of hepatic encephalopathy?
  • What are the symptoms?
  • How is the diagnosis made?
  • How is hepatic encephalopathy treated?
  • Whom can I ask?
  • How will the costs be reimbursed?

What are the causes of hepatic encephalopathy?

The hepatic encephalopathy is caused by nerve-damaging substances that cannot be broken down due to liver damage (e.g. liver cirrhosis, liver inflammation - hepatitis). In addition to ammonia, these substances include mercaptans, short-chain fatty acids and phenols. Even if blood from the abdominal organs enters the body's circulation via venous connections, bypassing the liver, neurotoxic substances can get into the brain. Such vein connections are called portosystemic shunts (short-circuit connections). They arise mainly in the case of portal hypertension (portal hypertension), mostly in liver diseases such as liver cirrhosis or in thrombosis of the portal vein. A therapeutic short-circuit connection (shunt) for treating portal hypertension can also be a cause.

The nerve-damaging substances lead to an imbalance of messenger substances in the brain (neurotransmitters). There are also changes in their binding sites (neurotransmitter receptors). In addition to liver disease, other factors usually lead to a deterioration in brain functions.

Favorable factors for the development of hepatic encephalopathy are:

  • Infections,
  • Gastrointestinal bleeding
  • certain sedative drugs such as sedatives or sleeping pills (e.g. benzodiazepines),
  • water medicines (diuretics),
  • Renal failure,
  • increased protein intake,
  • Constipation (opstipation),
  • Lack of fluid (hypovolaemia)
  • Hypokalaemia (low blood serum potassium)
  • metabolic alkalosis (predominance of basic substances - high pH value - in the blood),
  • Hypoxia (lack of oxygen) as well
  • Hypoglycaemia (low blood sugar).

Note In children up to the age of twelve, taking acetylsalicylic acid (ASA) in the event of a virus infection can lead to severe liver damage (Reye's syndrome). It is not uncommon for this to result in hepatic encephalopathy.

What are the symptoms?

Even in people with minimal hepatic encephalopathy, thinking difficulties and mental changes can occur, but these are often not yet recognized. However, they can, among other things, lead to difficulties in exercising the job or driving a car. Later on, there are mostly mild complaints such as lack of movement and facial expression, tremors, fluttering of the eyelids and other muscle twitching (myoclonus). In the advanced stage, an obsessive need to sleep, uncoordinated and jerky movements of the hands (asterixis; flapping tremor) and unsteady gait can also occur. Finally, there is increasing confusion, sleepiness (somnolence) and sweet breath (foetor hepaticus). The most severe form of hepatic encephalopathy is also known as hepatic coma (coma hepaticum).

How is the diagnosis made?

After taking the medical history and the physical examination, the doctor will make a suspected diagnosis. If the picture is not entirely clear, an imaging examination of the brain using computed tomography (CT) or magnetic resonance imaging (MRI) is often done. In this way, other diseases of the brain can be excluded.

Liver disease can be determined by doing a blood test. The extent of the disease and some of the causes of the hepatic encephalopathy can also be determined through blood tests. An important laboratory value in diagnosing hepatic encephalopathy is ammonia level.

Electroencephalography (EEG) is also performed. In addition, various neuropsychological tests can be used - even if minimal hepatic encephalopathy is suspected. With these tests, restricted sensory perception as well as mental disorders (cognitive abilities), psychological changes and disorders of the movement sequences (psychomotor abilities) can be detected.

To clarify the cause (s) of the hepatic encephalopathy, some further examinations (e.g. ultrasound, computed tomography of the abdominal cavity or liver biopsy) may be necessary.

How is hepatic encephalopathy treated?

Recommendations for patients with cirrhosis and hepatic encephalopathy include treatment of causative factors, drug therapies, and diet measures.

First and foremost are the treatment of the favorable factors and - if necessary - intensive medical treatment.

Intestinal bacteria can produce ammonia. Therefore, antibiotics reduce the number of bacteria in the intestine. For this purpose, antibiotics are used, which only work in the intestine and not in the entire body when they are taken orally (by mouth). These include rifaximin, neomycin, and metronidazole.

The laxatives lactulose or lactilol make bowel movements easier. In addition, taking these substances creates an acidic pH value in the intestine. As a result, less ammonia is formed and absorbed into the bloodstream through the intestines. They can also fix nitrogen, from which ammonia is formed. Douching and enemas can also be used to empty the bowel.

Flumazenil is a substance that acts on the central nervous system and, when administered via the vein, can lead to a short-term improvement in the condition of patients with hepatic encephalopathy.

A sufficient and regular intake of calories with a low intake of protein is particularly important. A light meal before bed is recommended. The intake of L-ornithine-L-aspartate or zinc in case of zinc deficiency may have positive effects.

A positive effect of the administration of branched-chain amino acids (e.g. leucine, isoleucine, valine etc.) could not yet be clearly demonstrated.

A liver transplant can often lead to a rapid improvement in the general condition of the person affected. Most of the time, however, changes in intellectual performance and emotional complaints do not completely regress. Which patients benefit from a liver transplant depends on many individual factors.

Prevention in at-risk patients and relapse prevention after an acute episode:

  • Refraining from alcohol and other substances that are harmful to the liver;
  • Avoidance of certain diuretic drugs (thiazide diuretics) or certain sleeping pills and sedatives (benzodiazepines);
  • Hepatitis A and B vaccination;
  • low protein diet;
  • Lactulose;
  • possibly rifaximin;
  • Zinc, folic acid and other vitamins and trace elements if there is a corresponding deficiency;
  • possibly probiotics and branched chain amino acids.

Whom can I ask?

The diagnosis and treatment of hepatic encephalopathy as a result of liver cirrhosis are possible in the following facilities:

  • Inpatient in a department for internal medicine or neurology (if necessary in a monitoring or intensive care unit),
  • special hospital outpatient department, e.g. hepatological outpatient department,
  • Cash outpatient clinics with special hepatology clinics,
  • In the private practice area: Specialist in internal medicine with in-depth hepatological knowledge.

Note In the event of unclear impaired consciousness, the ambulance (Tel.: 144 or 112) must be called immediately or a hospital visited.

How will the costs be reimbursed?

All necessary and appropriate diagnostic and therapeutic measures are taken over by the health insurance carriers. You can find more information under What does a hospital stay cost? Your resident doctor or outpatient clinic will generally settle accounts directly with your health insurance provider. With certain health insurance providers, however, you may have to pay a deductible (treatment contribution) (BVAEB, SVS, SVS, BVAEB). However, you can also use a doctor of your choice (ie doctor without a health insurance contract). For more information, see What does a hospital stay cost, a doctor's visit: Costs and deductibles.

For certain non-drug treatments (e.g. physical therapy) - in some cases only when a certain level has been reached - approval from the health insurance provider may be required.

For certain services (e.g. medical aids and medical aids) - depending on the health insurance provider - patient co-payments are provided. Most health insurance providers provide for a permit, sometimes depending on the type of medical aid. The prescription fee has to be paid for medication on a “prescription”. For more information about the respective provisions, please contact your health insurance provider, which you can find on the social security website, for example.

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