What Is a Hepatic Coma?

Hepatic coma, also known as hepatic encephalopathy. Central nervous system syndrome caused by severe liver dysfunction, based on metabolic disorders. Its main clinical manifestations are disturbance of consciousness, behavioral disorders and coma. There are acute and chronic encephalopathy. Treatment should actively eliminate the incentives to avoid or block the occurrence and further development of hepatic encephalopathy is the most basic treatment strategy and the key to treatment. Pay attention to actively prevent gastrointestinal bleeding, control infections, correct water-electrolyte and acid-base balance disorders, ban liver damage drugs, prohibit a large amount of ascites, etc .; minimize the production of ammonia and promote oxygen metabolism. For the hepatic encephalopathy that has occurred, on the basis of removing the inducement, first select drug treatment to restore brain cell function as much as possible. If the patient is ineffective for all drugs and there is no contraindication to surgery, portal shunt embolization or liver transplantation can be selected according to the patient's condition and hospital conditions.

Basic Information

nickname

Hepatic encephalopathy

English name

hepatic coma

Visiting department

Gastroenterology, Neurology

Common causes

Severe viral hepatitis, severe toxic hepatitis, drug-induced liver disease, acute fatty liver during pregnancy, various types of cirrhosis, and primary liver cancer

Common symptoms

Disturbance of consciousness, behavioral disorders, coma

Causes of liver coma and common diseases

The primary causes of hepatic encephalopathy include severe viral hepatitis, severe toxic hepatitis, drug-induced liver disease, acute fatty liver during pregnancy, various types of liver cirrhosis, postoperative portal-systemic shunt, primary liver cancer, and other diffuse In the terminal stage of liver disease, hepatic encephalopathy is most common in patients with cirrhosis, accounting for about 70%. There are many factors that induce hepatic encephalopathy, such as upper gastrointestinal bleeding, high protein diet, large amount of potassium diuresis, ascites, use of sleeping, sedation, anesthesia, constipation, uremia, infection or surgical trauma. These factors are mainly caused by: increasing or increasing the toxicity of neurotoxic substances. Improve the sensitivity of brain tissue to various toxic substances. Increase the permeability of blood-cerebrospinal fluid barrier and induce encephalopathy.

Differential diagnosis of liver coma

Differential diagnosis should pay attention to the mental and neurological manifestations of patients with chronic liver disease can also be caused by other reasons. If there are signs of neurological localization, clinical manifestations of atypical hepatic encephalopathy such as high fever, epilepsy, hallucinations, other diseases such as intracranial hematoma, sepsis, encephalitis, meningitis, cerebrovascular accident, uremia, diabetic coma, low The possibility of blood sugar coma, sedation overdose, drunk reaction, etc. Some characteristic manifestations of hepatic encephalopathy can also be seen in other diseases, such as flutter tremor can be seen in uremia, hypokalemia coma, respiratory failure and severe heart failure. High amplitude slow wave EEG can also be seen in hypoglycemia, cerebral hypoxia and uremia. Sometimes hepatic encephalopathy is easy to be misdiagnosed or missed at an early stage, such as being misdiagnosed as a mental illness due to outstanding manifestations of insanity. Hepatic encephalopathy can be induced by several factors at the same time. It should be noted that these inducing factors can also cause coma and should be identified.

Liver coma

Blood ammonia

Most patients with chronic hepatic encephalopathy and liver coma have elevated blood ammonia. However, patients with acute hepatic encephalopathy may have normal blood ammonia.

2. EEG

The electrical activity emitted by brain cells when active, the EEG of a normal person is an alpha wave, 8 to 13 times per second. Electroencephalograms in patients with hepatic encephalopathy show slower rhythms. Stage - patients show delta waves or three-phase waves, 4 to 7 times per second; when in a coma, they show high delta waves, less than 4 times per second. The changes in EEG are not very specific. Similar changes can be seen in uremia, respiratory failure, and hypoglycemia. In addition, EEG has less diagnostic value for subclinical hepatic encephalopathy and early hepatic encephalopathy.

3. Evoked potential

It is the potential generated by the cerebral cortex or subcortex after receiving information from various sensory organs, which is different from the spontaneous electrical activity of the brain recorded by EEG. Evoked potentials can be divided into visual evoked potentials (VEP), brainstem auditory evoked potentials (BAEP), and somatosensory evoked potentials (SEP) according to the different parts of the stimulated sensation. Evoked potential tests are mostly used for the diagnosis and research of mild hepatic encephalopathy. . There is still a p300 event-related potential that is not affected by the physiological characteristics of the stimulation site compared to traditional evoked potentials. Patients with mild hepatic encephalopathy have a prolonged incubation period for p300.

4. Mental Intelligence Test

It is suitable for the diagnosis of hepatic encephalopathy and the screening of mild hepatic encephalopathy. Its disadvantage is affected by age and education. Older people and people with lower education levels are slower in testing and affect results. Other methods that can be used to detect mild hepatic encephalopathy include streaking and a series of dot tests.

5. Imaging examination

Brain edema can be found in patients with acute hepatic encephalopathy by CT or MRI of the head. Patients with chronic hepatic encephalopathy can find different degrees of brain atrophy. In addition, an MRI examination revealed an increase in T1-weighted signal in the basal ganglia, which was related to the deposition of manganese there. The developed magnetic resonance spectroscopy (MRS) is a method to determine the content of metabolites in some parts of a living body on a high magnetic field (more than 1.5t) magnetic resonance scanner. Hepatic encephalopathy, mild hepatic encephalopathy, and even general liver cirrhosis patients have some changes.

6. Critical visual flicker frequency detection

Mild stellate cell swelling is an early pathological change, while stellate cell swelling (alztrimer type II) will change the glial-neuronal signal transmission. The morphological changes of retinal glial cells are similar to aiztrimier type astrocytic cells, so Retinal glial cell disease can be used as a marker of glial astrocytic lesions in the brain. It can be quantitatively diagnosed by measuring the critical visual flash frequency. The method is sensitive, simple and reliable, and can be used to find and detect mild hepatic encephalopathy.

Liver coma treatment principles

The basic principle of general treatment is to remove the cause of hepatic encephalopathy. Pay attention to adjusting the diet structure, use sedatives with caution, correct electrolyte and acid-base balance disorders, stop bleeding and clear intestinal hemorrhage; reduce intestinal ammonia production and absorption, promote ammonia metabolism in the body, GABA / BZ complex receptor antagonist fluoride Massini, the application of reducing or antagonizing the preparation of pseudo neurotransmitter branched chain amino acid (BCAA). Other treatments include; interventional therapy, artificial liver, liver cell transplantation, etc.