Hepatic encephalopathy in the elderly
Introduction
Introduction to hepatic encephalopathy in the elderly Hepatic encephalopathy (HE) is a syndrome of central nervous system dysfunction based on metabolic disorders caused by severe liver disease or extensive portal-to-venal shunt. Its main clinical manifestations are disturbance of consciousness, behavioral disorders and coma. basic knowledge The proportion of illness: 0.075%, more common in patients with hepatitis B cirrhosis Susceptible people: the elderly Mode of infection: non-infectious Complications: cerebral edema, hepatorenal syndrome
Cause
The cause of hepatic encephalopathy in the elderly
Liver disease complications (55%):
Hepatic encephalopathy is mainly seen in various types of cirrhosis (the most common cirrhosis after hepatitis), and can also be caused by portal-to-venous shunt surgery, acute or fulminant liver failure in severe viral hepatitis, toxic hepatitis and drug-induced liver disease. Primary liver cancer, acute fatty liver during pregnancy, severe biliary infection can also cause hepatic encephalopathy.
Other diseases (35%):
Hepatic encephalopathy, especially portal-body shunt encephalopathy, often has obvious incentives, such as gastrointestinal bleeding, massive potassium diuresis, ascites, high protein diet, sleeping sedatives, anesthetics, constipation, uremia, surgery, infection Wait.
Pathogenesis
The pathogenesis of hepatic encephalopathy has not been fully understood. It is generally believed that the pathophysiological basis of hepatic encephalopathy is hepatic cell failure and surgically occurring or naturally formed collateral shunts between the portal veins. Many toxicity from the intestines. Metabolites, which are not detoxified and cleared by the liver, enter the systemic circulation through the collaterals, and pass through the blood-brain barrier to the brain, causing brain dysfunction. There are many theories about the pathogenesis of hepatic encephalopathy, among which the study of ammonia poisoning theory is the longest. ,most.
Ammonia poisoning theory
Ammonia poisoning caused by ammonia metabolism disorder is an important pathogenesis of hepatic encephalopathy, especially portal shunt encephalopathy. The ammonia in the human blood circulation is mainly derived from the intestinal, renal and skeletal muscle ammonia, in which the intestinal ammonia is produced. Main (4g / d), the ammonia in the blood is mainly converted into urea and glutamine through the ornithine metabolic cycle in the liver, and a small part is metabolized or excreted through the brain, kidney, lung and other tissues, so the formation of blood ammonia in normal people Clearance is always in dynamic balance. When liver function is depleted and/or the portal is shunted, the liver's ability to synthesize urea into the liver is reduced. The ammonia in the intestine is directly detoxified by the liver and enters the systemic circulation, so that the blood ammonia is increased. Excessive nitrogen-containing foods or drugs, blood ammonia will be further increased, in addition, constipation, infection, etc. can also increase the amount of ammonia into the body, brain cells are extremely sensitive to ammonia, when a large amount of ammonia into the brain tissue, can interfere with the brain Energy metabolism, causing a decrease in the concentration of high-energy phosphate compounds, and high blood ammonia may inhibit pyruvate dehydrogenase activity, thereby affecting the production of acetyl-CoA, interfering with the tricarboxylic acid cycle in the brain, and on the other hand, ammonia is large. In the process of detoxification, it combines with -ketoglutaric acid to form glutamic acid, and glutamic acid combines with ammonia to form glutamine. Glutamine is an organic osmotic substance, and excessive synthesis can cause swelling of stellate cells, resulting in swelling. Cerebral edema, -ketoglutaric acid is an important intermediate in the tricarboxylic acid cycle. In the absence of it, the energy supply of brain cells is insufficient to maintain normal function. Glutamate is an important excitatory neurotransmitter in the brain. In the absence of brain inhibition increases.
2. Synergistic toxicity of ammonia, thiol and short-chain fatty acids
Methyl mercaptan is a product of methionine metabolized by bacteria in the gastrointestinal tract, methyl mercaptan and its derived dimethyl sulfoxide, both of which can cause confusion, loss of orientation, lethargy and coma in experimental animals. The mechanism of hepatic encephalopathy after sclerosing in patients with sclerosing may be related to these two metabolites. Liver odor may be the odor of methyl mercaptan and dimethyl disulfide. In patients with severe liver disease, blood of methyl mercaptan The concentration is increased, and the increase in brain disease is more obvious. Short-chain fatty acids (mainly valeric acid, caproic acid and caprylic acid) are formed by decomposition of long-chain fatty acids by bacteria, which can induce experimental hepatic encephalopathy in the plasma of patients with hepatic encephalopathy. And the cerebrospinal fluid is also significantly increased.
In experimental animals with liver failure, any of the three toxic substances, ammonia, thiol and short-chain fat, if used in a small amount, is not sufficient to induce hepatic encephalopathy. If used in combination, even if the dose is unchanged. It can cause brain symptoms. For this reason, some scholars have proposed that the synergistic toxicity of ammonia, thiol and short-chain fatty acids to the central nervous system may play an important role in the pathogenesis of hepatic encephalopathy.
3. Pseudo-neurotransmitter theory
In 1971, Fischer proposed the pseudo-neurotransmitter theory on hepatic encephalopathy. The main contents of this theory are as follows: aromatic amino acids in food, such as tyrosine, phenylalanine, etc., by the action of enterobacterial decarboxylase It is converted into tyramine and phenethylamine. When normal, these two amines are decomposed and eliminated by monoamine oxidase in the liver. When liver function fails, the clearance is cleared. These two amines can enter the brain tissue and act as p-hydroxylase in the brain. Forming the amines (-hydroxytyramine) and phenylethanolamine, respectively, the chemical structure of the latter two is similar to the normal neurotransmitter norepinephrine, but can not transmit nerve impulses or weak, so it is called pseudo-neurotransmitter. When the pseudo-neurotransmitter is taken up by the brain cells and replaces the normal transmitter in the synapse, the nerve conduction is impaired, and the excitatory impulse cannot be normally transmitted to the cerebral cortex to cause abnormal inhibition, and there is a disturbance of consciousness and coma.
4. Amino acid metabolism imbalance theory
Plasma amino acid determination found that patients with cirrhotic decompensation increased plasma aromatic amino acids (such as phenylalanine, tyrosine, tryptophan), while branched chain amino acids (such as valine, leucine, isoleucine) ), the amino acid metabolism of the two groups is unbalanced, the concentration of branched chain amino acids decreases, and the concentration of aromatic amino acids increases significantly. The ratio of the number of moles of branched chain amino acids to aromatic amino acids decreases from normal 3 to 3.5 to 1 or lower. The above two groups of amino acids are exchanged with the glutamine through the blood-brain barrier in competition and rejection, and the branched-chain amino acids are reduced, and the aromatic amino acids entering the brain are increased, and the latter further forms pseudo-neurotransmitters such as the above, liver In patients with sclerotherapy, due to hepatic metabolic disorders and decreased plasma albumin levels, serum free tryptophan increases, and increased tryptophan in the brain can produce serotonin, which is an inhibitory neurotransmitter of certain neurons in the central nervous system. The role of antagonizing norepinephrine may also be related to coma. The input of mixed amino acids mainly composed of branched chain amino acids has a wake-up effect on patients with cirrhosis and coma.
Prevention
Elderly patients with hepatic encephalopathy prevention
Active prevention and treatment of liver disease, patients with liver disease should avoid all factors that induce hepatic encephalopathy, closely observe patients with liver disease, timely detect the manifestations of hepatic encephalopathy and pre-coma and perform appropriate treatment.
Complication
Elderly patients with hepatic encephalopathy complications Complications, brain edema, hepatorenal syndrome
There are bleeding, secondary infection, accompanied by cerebral edema, liver and kidney syndrome.
Symptom
Symptoms of hepatic encephalopathy in the elderly Common symptoms Hepatocyte necrosis Ascites Liver failure Unconscious fainting Illusion conscious disorder Deep coma Unconscious edema
The clinical manifestations of hepatic encephalopathy are often inconsistent due to the nature of the original liver disease, the severity of hepatocyte damage and the cause of the injury. Acute hepatic encephalopathy is common in acute severe hepatitis, with massive hepatocyte necrosis and acute liver failure. The cause is not obvious. The patient enters a coma to death within a few days of onset, and there is no prodromal symptoms before coma. Chronic hepatic encephalopathy is more common in patients with cirrhosis and/or after portal-cavary shunt surgery, with chronic recurrent stupor and coma. In order to highlight the performance, it is often induced by a large amount of protein food, upper gastrointestinal bleeding, infection, ascites, and a large amount of potassium diuresis.
Clinically, according to the degree of disturbance of consciousness, nervous system performance and EEG changes, hepatic encephalopathy is divided into four phases.
1. Phase I (predecessor period)
Patients have only mild personality changes and behavioral disorders, such as euphoric or indifferent, lack of dress or casual stools, anxiety, inattention, and accurate response, but the words are unclear and slow, but there are Wing tremor or asterixis, most of the EEG is normal, this period lasts for several days or weeks, sometimes the symptoms are not obvious, easy to be ignored.
2. Phase II (pre-coma)
With confusion, sleep disorders, and behavioral disorders, the symptoms of the previous period are aggravated, and the orientation and understanding are diminished. The concept of time, place, and people is confusing, and simple calculations and intellectual composition cannot be completed (such as building blocks, With a matchstick pendulum pendulum, etc.), speech is unclear, writing obstacles, abnormal behavior is also very common, more sleep time inversion, sleepy night, even illusion, fear, arrogance and is regarded as general mental illness, this period The patient has obvious neurological signs, such as hyperreflexia, increased muscle tone, sputum and positive Babinski sign. In this period, there are flapping tremors, EEG has characteristic abnormalities, and patients may experience involuntary movement and movement disorders.
3. Phase III (sleeping period)
Mainly due to lethargy and mental disorder, various neurological signs are aggravated, patients are in a state of lethargy most of the time, but can wake up, wake up fashion can answer questions, but often have unconsciousness and hallucinations, flapping tremor can still lead, muscle The tension is increased, the passive movement of the limbs is often resistant, the pyramidal tract sign is often positive, and the EEG has an abnormal waveform.
4. Phase IV (coma)
The mind is completely lost, can not wake up, when the light coma, there is still a reaction to painful stimulation and discomfort, the tendon reflex and muscle tension are still hyperthyroidism; flapping tremor can not be elicited, when the deep coma disappears, the various reflexes disappear, the muscle tension is reduced, the pupil Often scattered, there may be paroxysmal convulsions, convulsions and excessive ventilation, EEG is obviously abnormal.
There is no obvious demarcation in the above periods, and the clinical manifestations may overlap in the early and late stages. Recently, subclinical hepatic encephalopathy or recessive hepatic encephalopathy has received increasing attention. It is believed that patients with cirrhosis have clinical hepatic encephalopathy in the past. 60% to 70% of patients have subclinical hepatic encephalopathy. These patients are completely normal on the surface, and the general neuropsychiatric examination is not abnormal. However, special intelligence function tests and visual evoked potential tests can be found. These patients often have atrophy or edema in their brains, and their degree is consistent with the determination of intelligence. These people often have traffic accidents when performing special work, such as driving various vehicles. Therefore, it is recommended that they be clinically necessary. Subclinical hepatic encephalopathy was classified as stage 0.
Examine
Examination of hepatic encephalopathy in the elderly
Blood ammonia
Chronic hepatic encephalopathy, especially in patients with portal-body shunt encephalopathy, has more blood ammonia, and the blood ammonia caused by acute liver failure is more normal.
2. Abnormal liver function test
3. EEG examination
The prodromal period is normal, and the subsequent periods are abnormal. The typical change is that the rhythm is slow, and the wave is 4 to 7 times per second, and some waves are 1 to 3 times per second. Symmetrical high amplitude delta waves appear.
Evoked potential
It is a recordable potential in vitro. The synchronous discharge reaction generated by various external stimuli transmitted to the brain neuron network via the sensory sensor can be divided into visual evoked potential (VEP), auditory evoked potential (AEP) and Somatic evoked potential (SEP), which stimulates the evoked potentials recorded by hepatic encephalopathy model animals, has specific changes according to the depth of the disease. Later, this technique was used to study patients with hepatic encephalopathy, and VEP can be considered to have different degrees of hepatic encephalopathy. Including subclinical encephalopathy to make an objective and accurate diagnosis, its sensitivity is more than any other method. The current study indicates that VEP examination is too different in different people, different periods, lack of specificity and sensitivity, and is not as effective as simple intelligence test.
5. Simple intelligence test
It is currently considered that intelligence testing is most useful for diagnosing early hepatic encephalopathy, including subclinical encephalopathy. The test includes numerical numbers, digital connections, simple calculations, writing, word formation, drawing, building blocks, and five-pointed stars with matchsticks. The connection test is most commonly used, and the results are easy to measure and easy to follow up.
Diagnosis
Diagnosis and differential diagnosis of hepatic encephalopathy in the elderly
Diagnostic criteria
The main diagnostic basis for hepatic encephalopathy is:
1 severe liver disease and/or extensive portal-body collateral circulation.
2 mental disorders, lethargy or coma.
3 causes of hepatic encephalopathy.
4 obvious liver function damage or increased blood ammonia, stun-like tremor and typical EEG changes have important reference value.
Differential diagnosis
Hepatic encephalopathy with psychiatric symptoms as the only prominent manifestation should be differentiated from psychosis. Hepatic coma should be differentiated from diabetes, hypoglycemia, uremia, cerebrovascular accident, coma caused by brain infection and excessive sedatives. Questioning the history of liver disease, checking the size of liver and spleen, liver function, blood ammonia, EEG, blood sugar, kidney function and other items will help diagnosis and differential diagnosis.
