Help the development of the site, sharing the article with friends!

Hepatic encephalopathy is a neurological disorder that occurs as a result of liver dysfunction. The cause of this problem is the harmful effect of an excessive amount of toxins in the blood on the nervous tissue. The course of hepatic encephalopathy varies: in the most severe cases, the disease leads to coma, but earlier it manifests itself as cognitive impairment and personality changes.

Hepatic encephalopathycan occur when the liver is unable to function properly. The liver is a special organ. Its functions include cleansing the blood of toxins, regulating metabolic management or the synthesis of various proteins (e.g. coagulation factors). Liver dysfunction results in symptoms affecting various body systems. One system in which disturbances can occur is the nervous system. When the liver is unable to function properly, various toxic substances can accumulate in the blood. Examples are ammonia, phenols, mercaptans and fatty acids. The amount of the so-called false neurotransmitters such as octopamine. If the substances mentioned are not removed from the body, they have a toxic effect on various tissues. One of them is the nervous tissue - the emerging disorders are called hepatic encephalopathy.

Hepatic encephalopathy: types

There are two main forms of hepatic encephalopathy. The first is the minimal form, in the course of which variations in patients are so small that they can only be detected with the help of specialized psychometric tests. On the other hand, overt hepatic encephalopathy is much richer in symptoms, with its episodic and permanent forms.

Hepatic encephalopathy: causes

Hepatic encephalopathy is most common in patients who have had some liver dysfunction for a long time. These can be caused by both hepatitis and Reye's syndrome or cirrhosis. In the course of these diseases, there may be a permanent form of hepatic encephalopathy (i.e. the one with symptomsgenerally constantly) or episodic (in this form, symptoms of encephalopathy appear from time to time).

There are a number of factors that may trigger an episode of hepatic encephalopathy in a patient with chronic hepatic impairment. Examples of such factors include:

  • dehydration
  • constipation
  • infections (e.g. pneumonia)
  • gastrointestinal bleeding
  • renal dysfunction
  • alcohol abuse
  • hypoxia
  • state after surgery of some organ
  • trauma experience
  • eating too much protein
  • taking drugs that depress the nervous system (e.g. benzodiazepines)
  • electrolyte disturbances (e.g. hypokalemia, i.e. too low blood potassium)

Hepatic encephalopathy: symptoms

The clinical course of hepatic encephalopathy can be very variable. Some patients may develop a full-blown disease, while in others the symptoms are initially sparse and gradually worsen. Sometimes hepatic encephalopathy begins with changes in the personality and behavior of patients - the family may even claim that the patient has changed beyond recognition. The patient may become extremely irritable, but also fall into extreme euphoria, his behavior may be completely inadequate to the given situation. The symptoms of hepatic encephalopathy include:

  • slowing down your thinking
  • personality changes
  • memory impairment
  • impaired concentration
  • speech disorders in the form of dysarthria
  • sleep disturbance
  • thick-wavy hand tremors
  • mood disorders
  • distinctive, musty, mouth odor (referred to asfoetor hepaticus )

These ailments do not occur in all patients with hepatic encephalopathy. The severity of the disorder depends both on the degree of hepatic impairment and on the length of time the nervous tissue is exposed to toxic metabolites. The clinical classification distinguishes five degrees of hepatic encephalopathy. In this classification, the following are assessed: the patient's state of consciousness, his intellectual functions and behavior, as well as possible neurological disorders. Grade 0, there are no disorders in any of the above-mentioned categories. In stage 1, slight drowsiness and disturbance of attention and concentration occur, patients become irritable and develop slight muscle tremors. Subsequent grades are recognized when the symptoms worsenhepatic encephalopathy, e.g. in stage 2, patients additionally lose their orientation in time, and in stage 3 there is, among others, delusions and dementia symptoms. Grade 4 is the most severe with hepatic coma.

Hepatic encephalopathy: diagnosis

In the diagnosis of hepatic encephalopathy, medical history and laboratory tests are of the greatest importance. The mere combination of symptoms of hepatic encephalopathy together with obtaining information that the patient has a chronic liver disease may allow the doctor to make a diagnosis. Laboratory tests that can be performed in the diagnosis of hepatic encephalopathy include the following signs:

  • blood ammonia concentration (blood ammonia standard is 15-45 micromol / liter)
  • liver enzymes
  • electrolyte concentrations (mainly sodium and potassium)

Patients may also undergo electroencephalography (EEG) because hepatic encephalopathy develops EEG abnormalities (e.g., paroxysmal discharges and three-phase waves). To assess the severity of hepatic encephalopathy, the patient can be assessed using the CHESS Score. This assessment is relatively simple, as it consists in answering 9 questions. Examples of them are: does the patient know the day of the week? Can he talk? Is the patient able (at the request of the examiner) to raise his arms? For each question, 0 or 1 point is awarded. A score of zero corresponds to no encephalopathy, while a score of nine suggests severe hepatic encephalopathy. Other tests performed in patients with suspected hepatic encephalopathy are designed to exclude alternative causes of the symptoms. For this purpose, for example, blood glucose tests (to exclude hypoglycaemia) or imaging tests (to exclude, for example, subarachnoid bleeding) may be performed.

Hepatic encephalopathy: treatment

The management of a patient with hepatic encephalopathy depends on the form of the disorders. In the case of episodic hepatic encephalopathy, first of all, one should look for the factor that could provoke symptoms (e.g. infection) and, after its detection, strive to eliminate it. Patients should be fed enterally for 24 to 48 hours, they should use nutritional mixtures with a limited supply of protein (it is this nutrient that is the source of toxic ammonia). Among pharmacological preparations, the following are used: lactulose (a laxative that acceleratesremoving toxins from the body) and antibiotics (e.g. rifaximin or neomycin, their administration is aimed at eliminating the bacteria that produce ammonia from the gastrointestinal tract). Ornithine aspartate (the drug accelerates the removal of ammonia from the body) is also useful in the treatment of hepatic encephalopathy. In the case of persistent hepatic encephalopathy, the aforementioned drugs are used chronically (lactulose, ornithine aspartate and antibiotics). Patients are also advised to constantly limit the amount of protein in their diet to 1-1.5 g / kg of body weight per day.

Hepatic encephalopathy: prognosis and prevention

A better prognosis is for those patients who develop slowly hepatic encephalopathy. Early implementation of therapeutic measures reduces the risk of the patient's symptoms worsening. In patients with chronic liver disease, they can reduce the risk of hepatic encephalopathy by following several recommendations. Such persons should take care of regular bowel movements and avoid alcohol. In the event of the appearance of symptoms of other diseases (e.g. fever, which may suggest the development of an infection), patients should see a doctor as soon as possible in order to start treatment promptly. In order to reduce the risk of hepatic encephalopathy, the advice on dietary protein restriction should also be followed. In patients at risk of hepatic encephalopathy, all medications should be given only when needed. Patients should be given diuretics with particular caution (they can lead to a drop in blood potassium levels, which can trigger hepatic encephalopathy) and drugs that depress the nervous system.

About the authorBow. Tomasz NęckiA graduate of medicine at the Medical University of Poznań. An admirer of the Polish sea (most willingly strolling along its shores with headphones in his ears), cats and books. In working with patients, he focuses on always listening to them and spending as much time as they need.

Help the development of the site, sharing the article with friends!

Category:

Neurology