Imminent coma

Introduction Hepatoencephalopathy (hepatoencephalopathy) used to be called hepatic coma. It is a comprehensive symptom of central nervous system dysfunction caused by severe liver disease and is caused by metabolic disorders. It is one of the manifestations of severe liver cell function failure. The main symptoms are conscious disturbance, behavioral disorder and coma, while subclinical or recessive hepatic encephalopathy has no obvious clinical manifestations and biochemical abnormalities. Only a fine intelligence test and/or electrophysiological test can be used to make a diagnosis. Portal shunt encephalopathy is the most common, the main mechanism of occurrence is portal hypertension, there is a collateral circulation between the portal vein and the vena cava, so that a large number of portal vein blood bypasses the liver and the human body circulates. The clinical manifestations of major encephalopathy include: onset can be urgent and slow; personality changes, the original extroverted personality is depressed, the original introverted personality is euphoric; behavioral changes, such as scribbling, sprinkling, Spitting, throwing confetti, cigarette butts, chaos, and squatting; sleep habits change, often manifested as sleep inversion, also known as impending coma, often predicting the onset of hepatic encephalopathy; The appearance of liver odor is due to liver failure. This smell is known by rotten apple flavor, garlic flavor, fishy smell, etc.; flapping tremor is the most characteristic neurological sign of hepatic encephalopathy, with early diagnosis. ; visual impairment; is also a simple and reliable method for early identification of hepatic encephalopathy; consciousness disorder, after the mental retardation, there is a more obvious disturbance of consciousness. The main clinical manifestations of hepatic degenerative hepatic encephalopathy are: mental retardation, dysarthria, memory loss, slow thinking, ataxia, tremor, and paraplegia (hepatic myelopathy). But there is no obvious disturbance of consciousness.

Cause

1. Causes: The primary diseases causing hepatic encephalopathy include severe viral hepatitis, severe toxic hepatitis, drug-induced liver disease, acute fatty liver during pregnancy, various types of cirrhosis, portal-to-body venous shunt, and primary liver cancer. As well as the end stage of other diffuse liver diseases, hepatic encephalopathy is most common in patients with cirrhosis, accounting for about 70%. There are many factors that induce hepatic encephalopathy, such as gastrointestinal bleeding, high protein diet, massive potassium diuresis, ascites, use of sleep, sedation, anesthetics, constipation, uremia, infection or surgical trauma. These factors are generally passed:

1 Increase the production of neurotoxicity or increase the toxic effects of neurotoxicity.

2 Improve the sensitivity of brain tissue to various toxic substances.

3 Increase the permeability of the blood-cerebrospinal fluid barrier to induce encephalopathy.

2. Pathogenesis: The pathogenesis of hepatic encephalopathy has not been fully elucidated so far. In the long-term basic research and clinical practice, it has been found that due to the failure of hepatocyte function, metabolic disorders such as proteins, amino acids, sugars and fats are produced. The accumulation of toxic substances in the body, as well as the detoxification effect of the liver on toxic substances, causes the toxic substances in the body to pass through the blood-cerebrospinal fluid barrier, affecting the central nervous system function, and severely inhibiting the normal physiological activities of the brain tissue, and the signs of encephalopathy occur. The main pathogenesis of the disease is as follows:

(1) Ammonia poisoning theory: However, hepatic encephalopathy cannot be completely explained by the ammonia poisoning theory. Some patients with hepatic encephalopathy have low blood ammonia. The authors have also found that some patients have normal blood ammonia, and treatment with branched-chain amino acids can make some patients Hepatic encephalopathy improved, confirming this phenomenon. And the degree of elevated blood ammonia is not related to the extent of hepatic encephalopathy. Treatment with reduced blood ammonia is not necessarily effective. In patients with fulminant hepatic failure, most of the blood ammonia is not high, and patients with cirrhosis have no abnormal neurological abnormalities. The determination of serum ammonia does not represent the concentration of ammonia in the cells, and in particular does not represent the concentration of ammonia in the brain's nerve cells. Therefore, most scholars believe that elevated blood ammonia is not the only cause of hepatic encephalopathy. However, in recent years, positron emission tomography (PET) studies have found that patients with chronic portal shunt encephalopathy have elevated brain ammonia metabolism, and ammonia is easily transferred from the blood to the brain. Therefore, even if blood ammonia is normal, it will occur. Brain dysfunction.

(2) Pseudo-neurotransmitter theory: In the early 1970s, American scholar Fischer proposed this theory, which is believed to be due to the involvement of pseudo-neurotransmitters in the conduction process of interneuronal nerve fibers in the central nervous system, which interferes with normal neural mediators. , so that the excitability of the nerve can not be transmitted to the next neuron, resulting in disturbance of consciousness, that is, the disorder of the amine transmitter.

(3) Amino acid ratio imbalance theory: The liver is an important organ for the decomposition and transformation of various amino acids in the body, except for branched chain amino acids (BCAA, including leucine, isoleucine and valine) from skeletal muscle and fat. In addition to tissue metabolism, almost all essential amino acids are metabolized by the liver. The ratio of plasma branched/aromatic amino acids under normal conditions is from 3 to 3.5:1.

(4) -aminobutyric acid theory: Since 1982, Schafer and Jones and other scholars, according to hepatic encephalopathy, increased blood gamma-aminobutyric acid (GABA) concentration, increased blood-cerebrospinal fluid barrier, and neuronal cell membrane surface receptors. The changes made this doctrine.

(5) Other factors:

1 Mercaptans: Sulfur-containing amino acids (methionine, cystine, etc.) are deaminated and decarboxylated by bacteria in the colon to form mercaptans, methyl mercaptans, dimethyl sulfides, ethanethiols, and the like. When the liver is depleted or shunted through the portal, it is retained in the systemic blood.

2 short-chain fatty acids: fatty acids are mostly from the intestines, which are decomposed by fats in foods (such as triacylglycerols), or by the action of bacteria by amino acids and sugars, and enter the blood through the portal vein.

3 Glutamine and -ketoglutaric acid: Glutamate is the most abundant neurotransmitter in the brain. It is present in the cytoplasm of neuronal cells and is the main excitatory transmitter of nerve cells.

4 other: hypoglycemia; microcirculatory disorders; water, electrolytes and acid-base balance disorders; endotoxin, IL-1, IL-6 and TNF.

(6) Synergistic theory of neurotoxins: In summary, the exact pathogenesis of hepatic encephalopathy has not yet been fully elucidated. Although many of the above factors have been found to be associated with the occurrence of hepatic encephalopathy, none of the doctrines or factors can fully explain hepatic encephalopathy. The pathogenesis and clinical manifestations, therefore, Zieve proposed that the occurrence of hepatic encephalopathy is the result of the interaction and comprehensive balance of two kinds of substances or factors in the human body, that is, the synergistic theory of neurotoxicants.

In addition, the GABA/BZ inhibitory neurotransmitter activation theory suggests that inhibitory neurotransmitters interact and interact with each other to aggravate coma.

an examination

Related inspection

EEG examination of blood ammonia liver function test

1. Symptoms and signs: There are differences depending on the type of liver disease, the degree of hepatocyte damage, the onset of illness, and the cause of the cause. Due to the different underlying diseases leading to hepatic encephalopathy, its clinical manifestations are also complex and variable, and the variability of early symptoms is characteristic of this disease. But there are also their common manifestations: that is, reflected as neuropsychiatric symptoms and signs. Both the performance of primary liver disease and its unique clinical manifestations are generally characterized by personality, behavior, intellectual change and disturbance of consciousness. The classification of clinical manifestations of encephalopathy is mainly described as follows:

(1) Onset: It can be urgent or slow. Acute hepatic encephalopathy has a rapid onset, and the prodromal period is extremely short. It can quickly enter a coma. Most of the coma occurs after the appearance of jaundice. There are also people who have been diagnosed as mentally ill before the onset of jaundice. Chronic hepatic onset of the brain is insidious or gradual, and it is often difficult to find misdiagnosis and missed diagnosis at first.

(2) Personality change: It is often the earliest symptom of this disease, mainly because the original extroverted personality showed depression, while the original introverted personality showed euphoric multilingual.

(3) Behavioral changes: Initially it may be limited to some disregarding behaviors, such as scribbling, sprinkling water, spitting, throwing confetti, cigarette butts, chaos, and casually, the tables and chairs in the room are free. Indiscriminate and unreasonable movements.

(4) changes in sleep habits: often manifested as sleep inversion, also known as impending coma (impending coma), this phenomenon has been found to be related to the patient's serum melatonin secretion disorder, suggesting that the patient's central nervous system is excited and inhibited Disorders often indicate that hepatic encephalopathy is imminent.

(5) The appearance of liver odor: due to liver failure, a characteristic odor of exhaled or exuded through the lungs by intermediates of sulfur-containing amino acid metabolism (such as methyl mercaptan, ethanethiol, and dimethyl sulfide) in the body. . This smell is known by scholars as rotten apple flavor, garlic flavor, fishy smell and so on.

(6) flapping tremor: it is the most characteristic neurological sign of hepatic encephalopathy, with early diagnosis. Unfortunately, not all patients have flapping tremors. The method is: when the patient protrudes from the forearm, expands the five fingers, or the wrist is overstretched and fixed, the patient's palm-finger and wrist joints may exhibit rapid flexion and stretching, which may often occur 1 or 2 times per second. There are also 5 to 9 times per second, and often accompanied by lateral movements of the fingers. At this time, the patient can be accompanied by subtle tremors of the entire upper limb, tongue, chin, jaw, and gait ataxia. Or on one side, it can also appear on both sides. This tremor is not characteristic, but can also be seen in patients with heart failure, renal failure, and lung failure. Tremors often disappear after the patient's sleep and coma, and can still appear after waking up.

(7) Visual impairment: not common. However, in recent years, the literature reports at home and abroad have gradually increased. When hepatic encephalopathy occurs, the patient may have visual impairment and blindness as the main clinical manifestations. This visual impairment is transient and functional, which may be aggravated with the deepening of hepatic encephalopathy. It can also be recovered as the hepatic encephalopathy recovers. The pathogenesis is unknown, and most of them are considered to be as complex as hepatic encephalopathy, which is the result of a combination of multiple factors. This phenomenon of visual impairment, the current naming has not been completely unified. To fully reflect this relationship between the liver, brain, and eyes, the authors referred to this type of performance as "liver-brain-eye syndrome."

(8) Intelligent obstacles: As the disease progresses, the patient's intelligence changes, showing that the concept of time and space is unclear, the concept of the characters is vague, the words are unclear, and the writing is difficult, the writing and calculation skills are difficult, the calculation and counting ability are declining, and the digital connection is wrong. A simple and reliable method for early identification of hepatic encephalopathy.

(9) Disorder of consciousness: Following the mental retardation, there is a relatively obvious disturbance of consciousness. From lethargy and lethargy, it gradually enters a coma, and various reactions and reflexes disappear. There are also people who gradually enter the coma from the manic state. The main clinical manifestations of hepatic degenerative hepatic encephalopathy are: mental retardation, difficulty in articulation, memory loss, slow thinking, ataxia, tremor, and paraplegia (hepatic myelopathy). But there is no obvious disturbance of consciousness.

2. Clinical staging: In order to facilitate early diagnosis and guide treatment, clinical stage of hepatic encephalopathy is often staged according to the patient's clinical manifestations. However, the clinical stages of each report are inconsistent, and some are divided into three, four, five, or even six. At present, most scholars agree that Davidson divides hepatic encephalopathy into prodromal phase, pre-coma, slumber, and coma according to its clinical manifestations. However, there is no clear boundary between the periods.

(1) Stage I (progenitor period): mild personality changes and behavioral disorders. The performance is: depression or euphoria in personality changes, unconscious movements in behavioral changes, and sleep inversion when sleep time changes. Flapping tremor (-), normal reflex exists, pathological reflex (-), EEG is more normal.

(2) Phase II (pre-coma): mainly characterized by confusion, sleep disorders, and behavioral disorders, manifested as disorientation, timing disorders, decreased computational power, written confusion, unclear language, blurred concept of characters, flapping tremors, The presence of normal reflexes, pathological reflexes, common knee reflexes, and sputum (-), muscle tension can be enhanced. Involuntary movements and movement disorders may occur, and EE waves appear in the EEG (4 to 7 times per second).

(3) Stage III (sleeping period): Mainly due to lethargy and mental disorder, the patient is in a state of lethargy most of the time, the reaction exists (can be awakened), or violent disturbance, flapping tremor (-), muscle tension is significantly enhanced. EEG is the same as phase II.

(4) Stage IV (coma): During this period, the patient's mind is completely lost and cannot be awakened. In the case of light coma, there is still a reaction to pain stimuli (such as positive pressure reflex) and discomfort position, sputum reflex and muscle tension are still hyperthyroidism, and flapping tremor cannot be elicited because the patient's physical examination cannot cooperate. In deep coma, all kinds of reflexes disappear, muscle tension is reduced, pupils are often scattered, and can be expressed as paroxysmal convulsions, convulsions (-), hyperventilation, extremely slow waves on the EEG (1.5 to 3) Times/second).

3. Clinical classification

(1) Clinically, according to the rapid development of hepatic encephalopathy, it is often divided into acute type and chronic type.

1 acute type: hepatic encephalopathy caused by fulminant hepatic failure caused by acute or subacute severe viral hepatitis or drugs or poisons. Due to massive or large necrosis of hepatocytes, the remaining hepatocytes cannot maintain the normal metabolism of the body, causing metabolic imbalance, and the metabolic poisons in the body cannot be effectively cleared and accumulated, resulting in central nervous system dysfunction. Also known as endogenous hepatic encephalopathy or non-ammonotic hepatic encephalopathy.

2 Chronic type: caused by chronic liver disease, cirrhosis or portal shunt after various reasons, often hepatocyte degeneration and necrosis, and hepatocyte regeneration and repair, but the regenerative hepatocyte insufficiency, resulting in metabolic imbalance The toxic substances in the body cannot be effectively removed, or the toxic substances in the portal body directly enter the systemic circulation and cause central nervous system dysfunction. The brain tissue of this type of patient often has pathological changes such as stellate cell hypertrophy, increase, cerebral cortex thinning, and focal necrosis. This type belongs to exogenous hepatic encephalopathy, also known as ammoniatic or portal shunt encephalopathy.

(2) Hepatic encephalopathy In addition to the above-mentioned acute and chronic types, there are other special types.

1 hepatic degeneration type: due to spontaneous or portal shunt patients, intestinal toxic substances are continuously shunted to the systemic circulation, repeatedly acting on the central nervous system, causing neuronal degeneration, clinically slow thinking, memory loss, consciousness Abnormal, dull or ataxia, but unconscious. Also known as acquired hepatic brain degeneration.

2 Hepatic encephalomyelopathy: In addition to extensive degeneration of brain cells, patients with advanced cirrhosis may also have demyelinating lesions of corticospinal tract, cortical cerebellar tract, and spinal cord posterior cord. Clinically, lower extremity weakness, gait instability, and fine limbs Tremors, hyperreflexia, and EEG showed extensive changes in damage. Among them, the brain and spinal cord have clinical manifestations called hepatic encephalomyelopathy; the prominent spinal cord lesions are called hepatic myelopathy.

3 Subclinical hepatic encephalopathy: This study has been proposed in recent years. This type of patient often has no hepatic encephalopathy in clinical practice, and is qualified for general work. There is no obvious abnormality in routine examination, only after completing routine mental exercise tests (such as drawing or Digital connectivity) is impaired in its ability. Due to the atrophy of the brain and the decrease of cerebral blood flow, the intelligence detection (especially the ability to operate) and the abnormality of the brain evoked potential, such as high-altitude, mechanical, driving and other types of work are prone to accidents or car accidents. For early diagnosis or replacement work, potential accidents or further development of clinical hepatic encephalopathy can be avoided. This type may also be a subclinical stage of hepatic encephalopathy, which may develop into chronic hepatic encephalopathy as liver disease worsens. Rikker et al. followed up on 9 patients with subclinical hepatic encephalopathy for 1 year and found that there were no changes in blood ammonia and intelligence tests in 6 patients. Only 3 patients with elevated blood ammonia had mental retardation and developed clinical hepatic encephalopathy.

4. Complications

(1) cerebral edema: cerebral edema has been confirmed as a complication of fulminant hepatic failure, the incidence rate can reach more than 80%. There is no consensus on whether there is cerebral edema in chronic liver disease, but most scholars believe that chronic hepatic encephalopathy can be concurrent Cerebral edema, the incidence of each report is also inconsistent, most believe that 21% to 58%, but recently through the autopsy found that cirrhosis cerebral edema detection rate as high as 89.5%, of which mild edema was 23.7%, severe edema accounted for 65.8 %, 21% have clear brain disease. It indicates that the incidence of cerebral edema in chronic liver failure is also high. It is also one of the main causes of death.

(2) Gastrointestinal bleeding: See gastrointestinal bleeding.

(3) renal insufficiency: see liver and kidney syndrome.

(4) Water and acid acid-base balance imbalance.

Third, medical technology inspection

Laboratory examination

(1) Abnormal liver function and abnormal blood coagulation: often only reflect the functional status of liver cells. Such as the separation of enzymes, high bilirubin, hypoproteinemia, decreased cholinesterase activity and decreased serum cholesterol, can not explain the severity of hepatic encephalopathy. Blood biochemical tests such as water, electrolytes and acid-base balance disorders can promote and aggravate hepatic encephalopathy. Renal function (creatinine, urea nitrogen) examination, such as abnormalities, only indicates that kidney failure is about to occur or has occurred. In recent years, it has been suggested that the dynamic observation of serum melatonin levels has important reference value for predicting and diagnosing the occurrence of hepatic encephalopathy and judging the changes of the condition.

(2) Determination of blood ammonia: The blood ammonia concentration of patients with HE increased by about 75% in different degrees, and the increase in chronic patients was more, and the increase in acute patients was less. However, elevated blood ammonia does not necessarily cause hepatic encephalopathy, so elevated blood ammonia concentration has certain reference significance for diagnosis, and it also has reference significance for guiding treatment. For example, it is more meaningful to determine the increase in arterial blood ammonia concentration than venous blood ammonia.

(3) Determination of plasma amino acid: If the concentration of branched chain amino acids is lowered, the concentration of aromatic amino acids (especially tryptophan) is increased, and the ratio of the two is inverted.

(4) Cerebrospinal fluid examination: routine, pressure and biochemistry can be normal, such as the simultaneous determination of ammonia, glutamic acid, tryptophan, glutamine concentration can be increased. In the case of concurrent cerebral edema, the pressure can be increased.

2. EEG examination: EEG changes have a certain significance for the diagnosis and prognosis of this disease. The normal EEG has a low amplitude and a fast frequency, and the waveform is an alpha wave. As the condition changes and develops, the frequency slows down and the amplitude gradually increases. The wave shape changes from wave to 4 to 7 times per second, which indicates that it is coma, such as symmetrical, high amplitude, 1.5 per second. The wave of ~3 times is a coma. Suspected EEG changes can be made clear by changes in EEG after eating high-protein and intramuscular low-dose morphine. EEG changes in hepatic encephalopathy can also be seen in uremia, pulmonary failure, and hypoglycemia, and should be distinguished.

3. Visual-evoked potential (VEP) can stimulate the cortex of the occipital lobe to stimulate the response, which produces a synchronous discharge effect, causing potential changes, ie, VEPs. It represents the sum of post-synaptic excitatory and inhibitory potentials in the cortical and subcortical neural cell populations. It is specific for the assessment of brain dysfunction in hepatic encephalopathy and can be quantitatively analyzed. Compared with general EEG, it can accurately reflect brain potential activity and can be used to detect hepatic encephalopathy before symptoms (such as subclinical hepatic encephalopathy). In addition, people have used auditory event-related potential P 300 and somatosensory evoked potential to diagnose subclinical hepatic encephalopathy. It is considered that the diagnostic value of auditory event-related potential P 300 is more sensitive and specific than somatosensory evoked potential.

4. Brain magnetic stimulation test: Nolano et al. used brain magnetic stimulation to measure the cerebral cortical motor function of patients with liver cirrhosis, and found that the central motor nerve conduction time prolonged, the threshold of motor arousal during sleep increased, the central non-recording period was shortened, and the peripheral circumference was normal, indicating The corticospinal pathway has been damaged and can be considered as a pre-existing manifestation of hepatic encephalopathy in cirrhosis.

Fourth, the basis of diagnosis

1. Meet the diagnostic criteria for mental disorders caused by physical illness.

2. There is sufficient evidence to prove that there is a serious liver disease, and the occurrence and duration of mental symptoms are closely related to liver diseases.

3. Mental disorders of acute hepatic encephalopathy:

1 inhibition state, the early manifestations of the disease are mostly dull, less moving, ignoring, etc.;

2 excited state (such as swaying, screaming, screaming or snoring);

3 different levels of disturbance of consciousness such as lethargy, lethargy, paralysis or confusion, and coma;

4 pieces of illusion or delusion; 5 after mental disorders or coma aura, there are unclear pronunciation, flapping tremor, nystagmus, and may have seizures, myoclonus, increased muscle tone, pathological reflexes.

4. Mental disorders of hepatic encephalopathy:

1 disturbance of consciousness is one of the main symptoms;

2 mental retardation or dementia status;

3 personality changes, emotional instability, impatience, irritability, lack of courtesy, etc.;

4 In the same period, there may be flapping tremor, hand and foot dyskinesia, myoclonus, dysarthria, pyramidal tract sign, cerebellar symptoms.

5. EEG showed more diffuse bilateral high-amplitude waves and synchronous high-amplitude waves. Characteristic three-phase waves can occur in coma, mostly in the frontal lobe, and bilaterally symmetric.

6. Encephalopathy caused by other causes.

Differential diagnosis

1. Symptoms and signs: There are differences depending on the type of liver disease, the degree of hepatocyte damage, the onset of illness, and the cause of the cause. Due to the different underlying diseases leading to hepatic encephalopathy, its clinical manifestations are also complex and variable, and the variability of early symptoms is characteristic of this disease. But there are also their common manifestations: that is, reflected as neuropsychiatric symptoms and signs. Both the performance of primary liver disease and its unique clinical manifestations are generally characterized by personality, behavior, intellectual change and disturbance of consciousness. The classification of clinical manifestations of encephalopathy is mainly described as follows:

(1) Onset: It can be urgent or slow. Acute hepatic encephalopathy has a rapid onset, and the prodromal period is extremely short. It can quickly enter a coma. Most of the coma occurs after the appearance of jaundice. There are also people who have been diagnosed as mentally ill before the onset of jaundice. Chronic hepatic onset of the brain is insidious or gradual, and it is often difficult to find misdiagnosis and missed diagnosis at first.

(2) Personality change: It is often the earliest symptom of this disease, mainly because the original extroverted personality showed depression, while the original introverted personality showed euphoric multilingual.

(3) Behavioral changes: Initially it may be limited to some disregarding behaviors, such as scribbling, sprinkling water, spitting, throwing confetti, cigarette butts, chaos, and casually, the tables and chairs in the room are free. Indiscriminate and unreasonable movements.

(4) changes in sleep habits: often manifested as sleep inversion, also known as impending coma (impending coma), this phenomenon has been found to be related to the patient's serum melatonin secretion disorder, suggesting that the patient's central nervous system is excited and inhibited Disorders often indicate that hepatic encephalopathy is imminent.

(5) The appearance of liver odor: due to liver failure, a characteristic odor of exhaled or exuded through the lungs by intermediates of sulfur-containing amino acid metabolism (such as methyl mercaptan, ethanethiol, and dimethyl sulfide) in the body. . This smell is known by scholars as rotten apple flavor, garlic flavor, fishy smell and so on.

(6) flapping tremor: it is the most characteristic neurological sign of hepatic encephalopathy, with early diagnosis. Unfortunately, not all patients have flapping tremors. The method is: when the patient protrudes from the forearm, expands the five fingers, or the wrist is overstretched and fixed, the patient's palm-finger and wrist joints may exhibit rapid flexion and stretching, which may often occur 1 or 2 times per second. There are also 5 to 9 times per second, and often accompanied by lateral movements of the fingers. At this time, the patient can be accompanied by subtle tremors of the entire upper limb, tongue, chin, jaw, and gait ataxia. Or on one side, it can also appear on both sides. This tremor is not characteristic, but can also be seen in patients with heart failure, renal failure, and lung failure. Tremors often disappear after the patient's sleep and coma, and can still appear after waking up.

(7) Visual impairment: not common. However, in recent years, the literature reports at home and abroad have gradually increased. When hepatic encephalopathy occurs, the patient may have visual impairment and blindness as the main clinical manifestations. This visual impairment is transient and functional, which may be aggravated with the deepening of hepatic encephalopathy. It can also be recovered as the hepatic encephalopathy recovers. The pathogenesis is unknown, and most of them are considered to be as complex as hepatic encephalopathy, which is the result of a combination of multiple factors. This phenomenon of visual impairment, the current naming has not been completely unified. To fully reflect this relationship between the liver, brain, and eyes, the authors referred to this type of performance as "liver-brain-eye syndrome."

(8) Intelligent obstacles: As the disease progresses, the patient's intelligence changes, showing that the concept of time and space is unclear, the concept of the characters is vague, the words are unclear, and the writing is difficult, the writing and calculation skills are difficult, the calculation and counting ability are declining, and the digital connection is wrong. A simple and reliable method for early identification of hepatic encephalopathy.

(9) Disorder of consciousness: Following the mental retardation, there is a relatively obvious disturbance of consciousness. From lethargy and lethargy, it gradually enters a coma, and various reactions and reflexes disappear. There are also people who gradually enter the coma from the manic state. The main clinical manifestations of hepatic degenerative hepatic encephalopathy are: mental retardation, difficulty in articulation, memory loss, slow thinking, ataxia, tremor, and paraplegia (hepatic myelopathy). But there is no obvious disturbance of consciousness.

2. Clinical staging: In order to facilitate early diagnosis and guide treatment, clinical stage of hepatic encephalopathy is often staged according to the patient's clinical manifestations. However, the clinical stages of each report are inconsistent, and some are divided into three, four, five, or even six. At present, most scholars agree that Davidson divides hepatic encephalopathy into prodromal phase, pre-coma, slumber, and coma according to its clinical manifestations. However, there is no clear boundary between the periods.

(1) Stage I (progenitor period): mild personality changes and behavioral disorders. The performance is: depression or euphoria in personality changes, unconscious movements in behavioral changes, and sleep inversion when sleep time changes. Flapping tremor (-), normal reflex exists, pathological reflex (-), EEG is more normal.

(2) Phase II (pre-coma): mainly characterized by confusion, sleep disorders, and behavioral disorders, manifested as disorientation, timing disorders, decreased computational power, written confusion, unclear language, blurred concept of characters, flapping tremors, The presence of normal reflexes, pathological reflexes, common knee reflexes, and sputum (-), muscle tension can be enhanced. Involuntary movements and movement disorders may occur, and EE waves appear in the EEG (4 to 7 times per second).

(3) Stage III (sleeping period): Mainly due to lethargy and mental disorder, the patient is in a state of lethargy most of the time, the reaction exists (can be awakened), or violent disturbance, flapping tremor (-), muscle tension is significantly enhanced. EEG is the same as phase II.

(4) Stage IV (coma): During this period, the patient's mind is completely lost and cannot be awakened. In the case of light coma, there is still a reaction to pain stimuli (such as positive pressure reflex) and discomfort position, sputum reflex and muscle tension are still hyperthyroidism, and flapping tremor cannot be elicited because the patient's physical examination cannot cooperate. In deep coma, all kinds of reflexes disappear, muscle tension is reduced, pupils are often scattered, and can be expressed as paroxysmal convulsions, convulsions (-), hyperventilation, extremely slow waves on the EEG (1.5 to 3) Times/second).

3. Clinical classification

(1) Clinically, according to the rapid development of hepatic encephalopathy, it is often divided into acute type and chronic type.

1 acute type: hepatic encephalopathy caused by fulminant hepatic failure caused by acute or subacute severe viral hepatitis or drugs or poisons. Due to massive or large necrosis of hepatocytes, the remaining hepatocytes cannot maintain the normal metabolism of the body, causing metabolic imbalance, and the metabolic poisons in the body cannot be effectively cleared and accumulated, resulting in central nervous system dysfunction. Also known as endogenous hepatic encephalopathy or non-ammonotic hepatic encephalopathy.

2 Chronic type: caused by chronic liver disease, cirrhosis or portal shunt after various reasons, often hepatocyte degeneration and necrosis, and hepatocyte regeneration and repair, but the regenerative hepatocyte insufficiency, resulting in metabolic imbalance The toxic substances in the body cannot be effectively removed, or the toxic substances in the portal body directly enter the systemic circulation and cause central nervous system dysfunction. The brain tissue of this type of patient often has pathological changes such as stellate cell hypertrophy, increase, cerebral cortex thinning, and focal necrosis. This type belongs to exogenous hepatic encephalopathy, also known as ammoniatic or portal shunt encephalopathy.

(2) Hepatic encephalopathy In addition to the above-mentioned acute and chronic types, there are other special types.

1 hepatic degeneration type: due to spontaneous or portal shunt patients, intestinal toxic substances are continuously shunted to the systemic circulation, repeatedly acting on the central nervous system, causing neuronal degeneration, clinically slow thinking, memory loss, consciousness Abnormal, dull or ataxia, but unconscious. Also known as acquired hepatic brain degeneration.

2 Hepatic encephalomyelopathy: In addition to extensive degeneration of brain cells, patients with advanced cirrhosis may also have demyelinating lesions of corticospinal tract, cortical cerebellar tract, and spinal cord posterior cord. Clinically, lower extremity weakness, gait instability, and fine limbs Tremors, hyperreflexia, and EEG showed extensive changes in damage. Among them, the brain and spinal cord have clinical manifestations called hepatic encephalomyelopathy; the prominent spinal cord lesions are called hepatic myelopathy.

3 Subclinical hepatic encephalopathy: This study has been proposed in recent years. This type of patient often has no hepatic encephalopathy in clinical practice, and is qualified for general work. There is no obvious abnormality in routine examination, only after completing routine mental exercise tests (such as drawing or Digital connectivity) is impaired in its ability. Due to the atrophy of the brain and the decrease of cerebral blood flow, the intelligence detection (especially the ability to operate) and the abnormality of the brain evoked potential, such as high-altitude, mechanical, driving and other types of work are prone to accidents or car accidents. For early diagnosis or replacement work, potential accidents or further development of clinical hepatic encephalopathy can be avoided. This type may also be a subclinical stage of hepatic encephalopathy, which may develop into chronic hepatic encephalopathy as liver disease worsens. Rikker et al. followed up on 9 patients with subclinical hepatic encephalopathy for 1 year and found that there were no changes in blood ammonia and intelligence tests in 6 patients. Only 3 patients with elevated blood ammonia had mental retardation and developed clinical hepatic encephalopathy.

4. Complications

(1) cerebral edema: cerebral edema has been confirmed as a complication of fulminant hepatic failure, the incidence rate can reach more than 80%. There is no consensus on whether there is cerebral edema in chronic liver disease, but most scholars believe that chronic hepatic encephalopathy can be concurrent Cerebral edema, the incidence of each report is also inconsistent, most believe that 21% to 58%, but recently through the autopsy found that cirrhosis cerebral edema detection rate as high as 89.5%, of which mild edema was 23.7%, severe edema accounted for 65.8 %, 21% have clear brain disease. It indicates that the incidence of cerebral edema in chronic liver failure is also high. It is also one of the main causes of death.

(2) Gastrointestinal bleeding: See gastrointestinal bleeding.

(3) renal insufficiency: see liver and kidney syndrome.

(4) Water and acid acid-base balance imbalance.

Third, medical technology inspection

Laboratory examination

(1) Abnormal liver function and abnormal blood coagulation: often only reflect the functional status of liver cells. Such as the separation of enzymes, high bilirubin, hypoproteinemia, decreased cholinesterase activity and decreased serum cholesterol, can not explain the severity of hepatic encephalopathy. Blood biochemical tests such as water, electrolytes and acid-base balance disorders can promote and aggravate hepatic encephalopathy. Renal function (creatinine, urea nitrogen) examination, such as abnormalities, only indicates that kidney failure is about to occur or has occurred. In recent years, it has been suggested that the dynamic observation of serum melatonin levels has important reference value for predicting and diagnosing the occurrence of hepatic encephalopathy and judging the changes of the condition.

(2) Determination of blood ammonia: The blood ammonia concentration of patients with HE increased by about 75% in different degrees, and the increase in chronic patients was more, and the increase in acute patients was less. However, elevated blood ammonia does not necessarily cause hepatic encephalopathy, so elevated blood ammonia concentration has certain reference significance for diagnosis, and it also has reference significance for guiding treatment. For example, it is more meaningful to determine the increase in arterial blood ammonia concentration than venous blood ammonia.

(3) Determination of plasma amino acids: If the concentration of branched-chain amino acids is decreased, the concentration of aromatic amino acids (especially tryptophan) is increased, and the ratio of the two is inverted. (4) Cerebrospinal fluid examination: normal, pressure and biochemistry can be normal, such as simultaneous determination of ammonia and glutamine. The concentration of acid, tryptophan and glutamine can be increased. In the case of concurrent cerebral edema, the pressure can be increased.

2. EEG examination: EEG changes have a certain significance for the diagnosis and prognosis of this disease. The normal EEG has a low amplitude and a fast frequency, and the waveform is an alpha wave. As the condition changes and develops, the frequency slows down and the amplitude gradually increases. The wave shape changes from wave to 4 to 7 times per second, which indicates that it is coma, such as symmetrical, high amplitude, 1.5 per second. The wave of ~3 times is a coma. Suspected EEG changes can be made clear by changes in EEG after eating high-protein and intramuscular low-dose morphine. EEG changes in hepatic encephalopathy can also be seen in uremia, pulmonary failure, and hypoglycemia, and should be distinguished.

3. Visual-evoked potential (VEP) can stimulate the cortex of the occipital lobe to stimulate the response, which produces a synchronous discharge effect, causing potential changes, ie, VEPs. It represents the sum of post-synaptic excitatory and inhibitory potentials in the cortical and subcortical neural cell populations. It is specific for the assessment of brain dysfunction in hepatic encephalopathy and can be quantitatively analyzed. Compared with general EEG, it can accurately reflect brain potential activity and can be used to detect hepatic encephalopathy before symptoms (such as subclinical hepatic encephalopathy). In addition, people have used auditory event-related potential P 300 and somatosensory evoked potential to diagnose subclinical hepatic encephalopathy. It is considered that the diagnostic value of auditory event-related potential P 300 is more sensitive and specific than somatosensory evoked potential.

4. Brain magnetic stimulation test: Nolano et al. used brain magnetic stimulation to measure the cerebral cortical motor function of patients with liver cirrhosis, and found that the central motor nerve conduction time prolonged, the threshold of motor arousal during sleep increased, the central non-recording period was shortened, and the peripheral circumference was normal, indicating The corticospinal pathway has been damaged and can be considered as a pre-existing manifestation of hepatic encephalopathy in cirrhosis.

Fourth, the basis of diagnosis

1. Meet the diagnostic criteria for mental disorders caused by physical illness.

2. There is sufficient evidence to prove that there is a serious liver disease, and the occurrence and duration of mental symptoms are closely related to liver diseases.

3. Mental disorders of acute hepatic encephalopathy:

1 inhibition state, the early manifestations of the disease are mostly dull, less moving, ignoring, etc.;

2 excited state (such as swaying, screaming, screaming or snoring);

3 different levels of disturbance of consciousness such as lethargy, lethargy, paralysis or confusion, and coma;

4 pieces of illusion or delusion; 5 after mental disorders or coma aura, there are unclear pronunciation, flapping tremor, nystagmus, and may have seizures, myoclonus, increased muscle tone, pathological reflexes.

4. Mental disorders of hepatic encephalopathy:

1 disturbance of consciousness is one of the main symptoms;

2 mental retardation or dementia status;

3 personality changes, emotional instability, impatience, irritability, lack of courtesy, etc.;

4 In the same period, there may be flapping tremor, hand and foot dyskinesia, myoclonus, dysarthria, pyramidal tract sign, cerebellar symptoms.

5. EEG showed more diffuse bilateral high-amplitude waves and synchronous high-amplitude waves. Characteristic three-phase waves can occur in coma, mostly in the frontal lobe, and bilaterally symmetric.

6. Encephalopathy caused by other causes.

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