Cirrhosis of the liver in the elderly

Introduction to cirrhosis in the elderly Cirrhosis is a chronic liver disease characterized by diffuse fibrosis of liver tissue, pseudolobules and regenerative nodules. It is clinically involved in multiple systems, with liver function damage and portal hypertension as the main manifestations. Serious complications such as hepatic encephalopathy and secondary infection. basic knowledge Sickness ratio: 0.05%-0.08% Susceptible people: the elderly Mode of infection: blood transmission, sexual contact transmission, close contact transmission, body fluid transmission Complications: upper gastrointestinal bleeding, shock, hepatic encephalopathy, sepsis, peritonitis, hepatorenal syndrome, primary liver cancer

Causes of cirrhosis in the elderly

(1) Causes of the disease

There are many causes of liver cirrhosis. In China, viral hepatitis is the main cause of cirrhosis, and alcoholism is common in foreign countries. Common causes are:

1 Viral hepatitis: mainly type B, C and D viruses overlap infection.

2 Alcoholism: Long-term heavy drinking, cirrhosis can occur when 80g of ethanol is taken every day for more than 10 years.

3 cholestasis.

4 circulation obstacles.

5 industrial poisons or drugs: long-term exposure to carbon tetrachloride, phosphorus, arsenic, etc. or taking methyldopa, tetracycline and so on.

6 metabolic disorders, hepatolenticular degeneration, hemochromatosis, 1-antitrypsin deficiency and galactose disease.

7 nutritional disorders.

8 immune disorders.

9 schistosomiasis infection.

10 Unexplained reasons are called cryptogenic cirrhosis.

(two) pathogenesis

1. Extensive hepatocyte degeneration and necrosis, hepatic lobular fiber scaffold collapse.

2. Residual hepatocytes do not regenerate along the original scaffold, forming irregular knotted hepatocytes.

3. The sub-tuberculosis area and the liver cell membrane have a large number of fibrous connective tissue hyperplasia, forming pseudo-lobules.

4. Due to the above changes, the disorder of intrahepatic blood circulation is caused by the reduction of the vascular bed, occlusion or distortion, and the blood vessels are squeezed by the regenerative nodules; the hepatic veins of the hepatic portal vein and the hepatic arteries have lost normal relations and mutual There is an alternating anastomosis, which forms a serious hepatic circulatory disorder, aggravates the nutritional disorders of liver cells, and promotes the further development of cirrhosis.

Elderly cirrhosis prevention

Three-stage preventive measures should be strengthened for cirrhosis in the elderly.

Primary prevention: Health education should be taken to prevent the cause of disease-free prevention. Active prevention of viral hepatitis, increase of living standards, rational nutrition, adjustment of drugs affecting liver function, and less drinking.

Secondary prevention: that is, early diagnosis and early treatment, active elderly patients should be actively organized for effective physical examination, timely detection of asymptomatic cirrhosis patients, monitoring of liver structure and functional status, prevention of serious complications, and appropriate health care Measures to delay the aging of the body.

Tertiary prevention: to establish a diagnosis and through reasonable treatment, reduce the damage of liver cirrhosis to the body, reduce the harm of complications to the body, and establish contact with the second and third-level hospitals through community services, improve the health status and quality of life of the elderly. .

Elderly cirrhosis complications Complications upper gastrointestinal hemorrhagic shock hepatic encephalopathy sepsis peritonitis hepatorenal syndrome primary liver cancer

Upper gastrointestinal bleeding

It is the most common complication. It is characterized by sudden hematemesis, melena, hemorrhagic shock or hepatic encephalopathy. The mortality rate is high. The cause is acute hemorrhagic gastritis and digestive tract except for rupture of gastric varices. ulcer.

2. Hepatic encephalopathy

Also known as hepatic coma, is caused by severe liver disease, central nervous system dysfunction syndrome based on metabolic disorders, often have obvious incentives, such as infection, upper gastrointestinal bleeding, diuresis, massive potassium excretion, ascites, high Protein diet, etc., the pathogenesis of hepatic encephalopathy is not fully understood. It is generally believed that the pathophysiological basis of hepatic encephalopathy is hepatic cell failure and surgically or naturally formed collateral shunts between the portal veins, mainly from Many toxic metabolites in the intestines are not detoxified or cleared by the liver, enter the systemic circulation through the collaterals, and pass through the blood-brain barrier to the brain, causing brain dysfunction.

The current theory of hepatic encephalopathy includes:

1 ammonia poisoning theory.

2r-aminobutyric acid/benzodiazepine complex theory.

Synergistic toxic effects of 3 amines, thiols and short chain fatty acids.

4 pseudo neurotransmitter theory.

5 amino acid metabolism imbalance theory.

The clinical manifestations of hepatic encephalopathy are mainly summarized into five aspects: neuropsychiatric changes, personality and behavioral changes, intellectual function changes, neuromuscular abnormalities, flapping tremors, according to the degree of disturbance of consciousness, nervous system performance and EEG changes in the liver Sexual encephalopathy causes a deep coma due to mild mental changes. It is divided into 4 phases: Phase I (precursor period): mild personality and behavioral abnormalities, euphoric or apathetic, or behavioral abnormality, such as a disordered dress, casual notes The response time is unclear and slow, there may be stun-like tremor, EEG is normal, lasts for several days or weeks or longer, and second phase (pre-coma): mental disorder, sleep disorder, behavior Disordered, orientation and understanding are declining. The concept of time, place, people is confusing, writing is difficult, speech is unclear, and there are many sleep time reversals, day and night inversion, and even hallucinations, fear, arrogance, and being seen. In general mental illness, there may also be involuntary movements and movement disorders. In this period, neurological signs such as hyperreflexia, increased muscle tone, convulsions and positive Babinsky signs, etc. Both tremor and EEG abnormalities are obvious and have certain characteristics. Phase III (sleeping period): Mainly due to lethargy and severe mental confusion, various neurological signs continue to increase, and the patient becomes drowsy most of the time, but can wake up. Wake up fashion can answer questions, but often have unconsciousness or hallucinations, stun tremor can still be induced, muscle tension is enhanced, passive movements of limbs are often resistant, pyramidal tract signs are positive, EEG is also abnormally found, Phase IV (Contemplative period): The patient completely loses consciousness and can't wake up. When the coma is in front of the coma, it still reflects the painful stimulation and discomfort. The tendon reflex and muscle tension are still hyperthyroidism. Sometimes it is gaze-like, because the patient can't cooperate, the smear-like Tremor can not be induced, when the deep coma, the various reflexes disappear, the muscle tension is reduced, the pupils are often scattered, and there may be convulsions, convulsions and excessive ventilation.

3. Infection

Patients with cirrhosis have low resistance, often with bacterial infections such as pneumonia, intestinal infections, Escherichia coli sepsis and spontaneous peritonitis.

4. Hepatorenal syndrome

When there is a large amount of ascites in decompensated cirrhosis, hepatorenal syndrome, also known as functional renal failure, may occur due to insufficient circulating blood volume and redistribution of blood in the kidney. It is characterized by spontaneous oliguria or anuria. Nitrogenemia and low urinary sodium, but the kidney has no important pathological changes, the reasons for which are as follows:

(1) abnormal renal blood flow: patients with cirrhosis and ascites with oliguria and azotemia, renal blood flow and glomerular filtration rate are severely low, and renal vascular resistance is significantly increased.

(2) renal vasoconstriction:

1 Increased renal sympathetic tone: In the case of severely impaired liver function, the following factors can increase the renal sympathetic tone, whether it is a decrease in blood volume or a change in splanchnic hemodynamics, causing massive blood stasis in the portal system. , resulting in a reduction in effective circulating blood volume, and thus reflex causes sympathetic - excitatory enhancement of the adrenal medullary system, renal vasoconstriction.

2 renin-angiotensin system activity enhancement: in the late stage of liver disease, there is generally an obvious increase in renin-angiotensin.

3 kallikrein-kinin system activity abnormalities: plasma kallikrein and bradykinin decreased in patients with severe cirrhosis, and plasma renin angiotensin II activity increased, these comprehensive changes, namely vasodilators (slow stimulation) The activity of the peptide) is decreased and the activity of the vasoconstrictor (angiotensin II) is enhanced, which is particularly remarkable in the case of functional renal failure in patients with cirrhosis.

4 prostaglandin synthesis is insufficient: In recent years, it has been found that patients with hepatic functional renal failure have reduced PCE2 in the urine while TXA2 level is significantly increased, but patients with cirrhosis without ascites with functional renal failure have no such changes, presumably TXA2 is onset. Has an important role.

5 Endotoxemia: The presence of endotoxemia was examined by LLT ( test) method. It was found that the LLT test was almost positive in patients with hepatic functional renal failure, and the patients with normal renal function were negative and survived. The fact that endotoxemia disappears and renal function improves, these facts indicate the important role of endotoxemia in the pathogenesis of functional renal failure.

6 pseudo-neurotransmitter accumulation: in liver failure, due to the lack of normal neurotransmitter-norepinephrine in the peripheral nerve endings or replaced by pseudo-neurotransmitters, causing arteriolar dilatation, due to decreased renal blood flow, The renin-angiotensin system is activated to maintain its blood perfusion, resulting in increased local renal vascular resistance, and finally, renal cortical blood flow is reduced to cause functional renal failure.

5. Primary liver cancer

Patients with complicated primary liver cancer often occur on the basis of large nodular or large-sized nodular mixed cirrhosis. For example, patients with rapid liver enlargement in the short term, persistent liver pain, liver mass on the surface or ascites should be bloody. Suspected primary liver cancer and further examination.

6. Electrolyte acid-base balance disorder

Common ones are:

1 hyponatremia.

2 low potassium hypochloremia and metabolic alkalosis.

Symptoms of cirrhosis in the elderly Common symptoms Ascites lack of appetite, loss of appetite, loss of appetite, jaundice, pleural effusion, liver, liver and liver failure, upper gastrointestinal bleeding

Usually cirrhosis is insidious, the course of disease development is slow, the condition is mild, and it can be lurking for 3 to 5 years or more. A small number of liver necrosis due to short-term large-scale liver cirrhosis develops in 3 to 6 months, often divided into the following stages.

1 compensation period: can be asymptomatic or atypical symptoms, lack of specificity, fatigue, loss of appetite appear earlier, and more prominent, may be associated with abdominal distension, nausea, upper abdominal pain, mild diarrhea, etc. Intermittent, due to fatigue or associated disease, can be relieved by rest or treatment, the patient's nutritional status is general, the liver is mild, the texture is firm or hard, no or mild tenderness, mild or moderate spleen, liver function The result of the examination is normal or mild.

2 decompensation period: typical symptoms, mainly manifested as two major clinical manifestations of liver dysfunction or portal hypertension, and may have systemic multi-system symptoms.

1. Hepatic dysfunction

(1) Weakness and weakness: The reasons are:

1 Insufficient calories.

2 intermediate metabolism disorders such as carbohydrates, protein fats, and related to insufficient heat production.

3 When liver damage or bile excretion is not smooth, blood cholinesterase is reduced, affecting the normal physiological functions of neuromuscular.

4 The process of converting lactic acid into hepatic glycogen occurs, and lactic acid accumulates excessively after muscle activity.

(2) Weight loss: The main reason is loss of appetite, gastrointestinal tract malabsorption and decreased protein synthesis in the body.

(3) loss of appetite, accompanied by nausea, bloating, diarrhea and other symptoms: due to portal hypertension caused by gastrointestinal mucosal congestion.

(4) diarrhea: for the stool does not form, due to intestinal wall edema, malabsorption (fat-based), niacin deficiency.

(5) bloating: common symptoms, heavy in the afternoon and at night, may be due to indigestion, flatulence, hypokalemia, ascites and splenomegaly.

(6) double threatening pain or abdominal pain: progressive necrosis of hepatocytes, spleen and perihepatic inflammation can cause double flank pain, portal venous inflammation, portal vein thrombosis, cirrhosis patients with peptic ulcer, biliary infection, cholelithiasis Upper abdominal pain can occur.

(7) bleeding: bleeding tendency is more common, due to lack of coagulation factors and hypersplenism, thrombocytopenia and skin mucosal ecchymosis or bleeding, nose bleeding, bleeding gums, women may have menorrhagia, hematemesis and melena The cause is cirrhotic portal hypertension, collateral circulation, esophageal varices, varicose veins, duodenal varices and superior mesenteric vein can cause hemorrhage, esophageal varices bleeding more common, bleeding Large amount of rapid, often vomiting a lot of blood and blood in the stool, can quickly appear shock or even death, when the amount of bleeding is large, it can also be more red bloody stool, iliac vein bleeding is less common, for red bloody stool, portal hypertensive gastritis with erosion, Peptic ulcer, ascites, increased abdominal pressure, reflux reflux esophagitis, can cause upper gastrointestinal bleeding, but more than the esophageal varices bleeding.

(8) neuropsychiatric symptoms: excitement, orientation, abnormal computing power, lethargy, coma, should consider the possibility of hepatic encephalopathy.

(9) shortness of breath: obvious during activity, cleft lip, clubbing, seen in some patients, blood oxygen saturation decreased during blood gas analysis, oxygen partial pressure decreased, reported due to right branch left shunt, pulmonary venous fistula The portal vein to the pulmonary vein has collateral vessels.

(10) Low fever: About 1/3 of patients often have irregular hypothermia, which may be caused by the inability of the liver to inactivate pyrogenic hormones, such as reducing urinary testosterone. This kind of fever antibiotic treatment is ineffective. If persistent fever occurs, the potential should be excluded. Urinary tract, ascites, biliary tract infections, and should exclude malignant space-occupying lesions of the liver.

(11) Skin performance:

1 liver disease capacity: face color, black, dull, dull, may be secondary adrenal insufficiency and liver can not metabolize the melanocytes stimulated by the anterior pituitary gland, around the eyes, palm texture and skin wrinkles can have pigments calm.

2 spider mites and liver palm: the patient's face, neck, upper chest, shoulder and upper limbs and other upper vena cava drainage areas appear spider mites and / or telangiectasia, in the palm of the big fish, small fish and fingertips There are erythema in the ventral part, called the liver palm, which is thought to be related to the increase of estrogen.

3 Astragalus: indicates that the liver cells are damaged. If the liver cells have inflammation and necrosis, the jaundice is deepened.

(12) Endocrine performance:

1 female patients with irregular menstruation, amenorrhea, male libido, testicular atrophy and male breast hyperplasia.

2 aldosterone increased, the liver is the main site of aldosterone inactivation, aldilone patients often have aldosterone increase in the late stage, which plays an important role in the formation of ascites.

3 abnormal glucose metabolism, liver regulation of blood glucose disorders, can appear hyperglycemia or hypoglycemia.

2. Portal hypertension

Increased resistance of the portal system and increased portal blood flow are the mechanisms for the formation of portal hypertension. The specific performance is as follows:

(1) Spleen: The spleen can be moderately enlarged, sometimes it can be a giant spleen. When the upper gastrointestinal tract is bleeding, the spleen is obviously reduced and can not be touched.

(2) collateral circulation establishment and opening: when the portal pressure increases more than 200mmH2O, the returning blood of normal digestive organs and spleen is blocked by the liver, resulting in the establishment of portal-body collateral circulation between multiple parts of the portal system and the vena cava. Clinically, There are 3 important side branches open.

1 esophagus and gastric varices.

2 abdominal wall varices.

3 venous dilatation, in addition, liver and sputum, spleen and renal ligament, abdominal organs and retroperitoneal tissue see veins, can also be connected to each other.

(3) Ascites: suggesting that cirrhosis enters the stage of late decompensation, abdominal distension, increased intra-abdominal pressure, severe umbilical hernia, high ascites, dyspnea, upper gastrointestinal bleeding, infection, Portal vein thrombosis, surgery, etc. can rapidly form ascites, the formation of ascites is sodium, excessive water retention, and the following abdominal local and systemic factors:

1 portal pressure increased: when the pressure is greater than 300mmH2O, the absorption of peritoneal tissue fluid is reduced and leaks into the abdominal cavity.

2 hypoproteinemia: when albumin is less than 30g / L, the plasma colloid osmotic pressure is reduced, resulting in extravasation of blood components.

3 Lymph fluid production is excessive, exceeding the drainage capacity of the thoracic duct, and the lymph fluid leaks from the liver capsule and the hilar lymphatic duct to cause the peritoneum.

4 secondary aldosterone increased renal sodium reabsorption increased.

5 increased secretion of vasopressin increased water reabsorption.

6 effective circulation of insufficient blood volume: increased renal sympathetic activity, prostaglandin, atrial peptide and kallikrein-kinin activity decreased, resulting in renal blood flow, sodium and urine output decreased.

(4) pleural effusion: 5% to 10% of patients with ascites with pleural effusion, usually the right side, bilateral and left side are rare, may be related to the following factors: hypoproteinemia, azygous vein, semi-singular venous system The pressure is increased, the lymphatic flow of the liver is increased, the pleural lymphatic vessels are dilated, siltation and rupture, the lymphatic fluid overflows to form pleural effusion, the abdominal pressure is increased, the tendon of the diaphragm is thinned, and the pores are formed, and the ascites leaks into the abdominal cavity.

3. Liver palpation

Liver properties and intrahepatic fat infiltration, liver cell regeneration and connective tissue hyperplasia, early liver slightly larger, ribs 1 ~ 3cm, medium hard, smooth surface, late reduction, hard, surface nodules, sharp edges, under the ribs Can not be touched, the left lobe compensatory hyperplasia can be reached under the xiphoid.

Examination of cirrhosis in the elderly

Blood routine

In hypersplenism, whole blood cells are reduced, and white blood cells and thrombocytopenia are common, but some patients have positive red blood cell anemia, and a few patients may have large cell anemia.

2. Urine routine

There is no change in the compensation period. When there is jaundice, bilirubin can occur, and there is an increase in urinary biliary, and sometimes protein, tuberculosis and hematuria can be seen.

3. Liver function test

Liver function is very complicated, many clinical tests, but it is difficult to reflect all functional status, combined with disease analysis, commonly used biochemical indicators:

(1) elevated ALT and AST, degree of reactive cell damage, compensated cirrhosis or cirrhosis without active inflammation may not increase.

(2) Serum bilirubin responds to liver uptake, binding and excretion. More than half of patients with decompensation have jaundice. When there is active hepatitis or bile duct obstruction, direct bilirubin and total bilirubin can be increased.

(3) The reduction of serum albumin is seen in moderate to above lesions, and its continued low prognosis has prognostic value.

(4) Protein electrophoresis: albumin decreased during liver cirrhosis, globulin increased, globulin changed little, gamma globulin often increased, protein components in protein electrophoresis except for immunoglobulin, were synthesized by hepatocytes. Albumin is significantly lower, gamma globulin is significantly increased, and often reflects chronic progressive liver disease.

(5) Prothrombin time measurement: plasma prothrombin in early cirrhosis is normal, while plasma prothrombin in normal active cirrhosis and cirrhosis is normal, while late active cirrhosis and severe damage to liver cells are obvious. Prolonged, if vitamin K and treatment can not be corrected, suggesting a poor prognosis.

(6) Urea nitrogen only reflects the ability of liver to synthesize urea, <50mg/L is found in ethanolic cirrhosis.

(7) Blood ammonia: Blood ammonia can be elevated in hepatic encephalopathy, and normal blood ammonia is 34 to 100 mol/L.

(8) The ratio of serum combined with bile acid and cholic acid/chenodeoxycholic acid has diagnostic value. The change of bile acid after meal indicates that there is liver circulation disorder, which is especially valuable in primary and secondary biliary cirrhosis.

(9) Serum cholinesterase (ChE): ChE activity is often decreased when cirrhosis is decompensated, and its decrease is parallel with serum albumin. This enzyme reflects liver reserve capacity.

(10) Determination of serum adenosine deaminase (ADA); ADA is considered to be a good indicator of liver damage, generally consistent with ALT, and residual disease in response to liver disease is superior to ALT.

4. Detection of liver reserve function

CT measurement of liver size and volume, galactose clearance rate, urea synthesis rate, ICG, retention rate: BSP maximum operation and storage capacity, and drug conversion ability, etc., can estimate the functional amount of residual hepatocyte population, estimate cirrhosis Severity is also valuable for estimating the risk of liver disease surgery.

5. Liver fibrosis test

The best indicator of liver fibrosis is serum type III procollagen (P-III-P), followed by monoamine oxidase (MAO), prolyl hydroxylase, lysine oxidase, serum NB-amino-glucosidase ( NAG), proline, hydroxyproline, etc., have been measured in recent years, the Fab fragment and lamellar protein concentration of type III procollagen antibody are significantly increased in cirrhosis and slow-lived liver, especially ethanolic cirrhosis.

6. Immunological examination

(1) Cellular immunity: In patients with cirrhosis, the rate of E rose formation, lymphocyte conversion rate decreased, CD3, CD4, and CD8 cells were all decreased, and T cells were also decreased in patients with cirrhosis.

(2) Humoral immunity: Immunoglobulins are often elevated by gamma globulin, especially IgG, hyperglobulin and liver damage, reduced phagocytic clearance, defective T cell function, B cell hyperfunction, autoimmunity Slow-acting livers also have autoimmune antibodies.

7. Ascites examination

Generally for leakage, such as spontaneous peritonitis, the transparency of ascites is reduced, the specific gravity is between the leakage and exudate, the number of white blood cells is increased, often above 500×106/L, and the polymorphonuclear leukocyte count is greater than 250× 106/L, complicated by tuberculous peritonitis, lymphocyte-based, ascites hematopoietic should be highly suspected of cancer, should be done cytological examination, when suspected spontaneous peritonitis, bedside blood culture flask for ascites bacterial culture It can increase the positive rate and use the drug sensitivity test as a reference for the selection of antibiotics.

8. Ultrasound examination

In cirrhosis, it shows uniform, diffuse dense point echo, late echo enhancement, liver shrinkage, portal vein widening, and spleen thickening.

9. Esophageal X-ray barium meal examination

Observing the presence or absence of esophagus, gastric varices, and varicose veins, the sputum was unevenly distributed on the mucosa, and there was a worm-like filling defect. When the varicose veins were found, the tincture was filled with chrysanthemum-like filling defects.

10.CT scan

For advanced cirrhosis, CT diagnosis can replace laparoscopic and liver biopsy, showing liver deformation, imbalance of liver and leaf size, enlargement of left lobe, especially caudal lobe, hepatic portal widening and gallbladder translocation, intrahepatic fat When infiltrating, the liver density is reduced and the spleen density is equal, even lower than the kidney, which can affect the whole liver, or a leaf or focal, with low density shadow in one circle of ascites, splenomegaly in portal hypertension, more than 6 rib units In the hilar and stomach, spleen, sacral ligament, paraumbilical and anterior abdominal wall, spherical or worm-like soft tissue is seen as collateral vein.

11. Magnetic resonance imaging (MRI)

Magnetic resonance imaging is similar to CT in that it can see liver shape, fat infiltration, ascites and blood vessels are unobstructed, and each has its own advantages and disadvantages.

12. Selective hepatic angiography

Hepatic venography is rarely used in cirrhosis, it can reflect the degree, extent and type of cirrhosis, and has a certain significance in the identification of primary liver cancer. Hepatic venous catheter is mainly used for the measurement of free pressure in cirrhosis with portal hypertension. Embedded pressure research.

13. Radionuclide scanning

Liver Kupffer cell uptake and phagocytosis of nuclear function have changed, can show liver shape changes, common right leaf atrophy, left lobe enlargement, spleen and bone marrow development, compensated liver shadow enlargement, advanced liver shadow reduction, spleen shadow Increase.

14. Gastroscopy

The diagnosis rate is higher than that of esophageal X-ray barium meal. It can directly observe the degree of esophageal varices, varicose veins, red signs and fibrinous exudation, and erosion, which helps to predict the bleeding.

15. Liver biopsy

The diagnosis can be determined to understand the tissue blood type of cirrhosis and the extent of hepatocyte damage and connective tissue formation.

16. Laparoscopy

The liver shape, surface, color, edge and spleen can be directly observed, and the hardness can be touched with a stick. The biopsy is performed on the lesion under direct vision, which is helpful for determining the cause of cirrhosis.

Diagnostic diagnosis of cirrhosis in the elderly

Diagnostic criteria

There is no symptom or only some non-specific gastrointestinal symptoms in the early stage of cirrhosis, and the signs are not obvious. Therefore, it is difficult to diagnose, and the decompensated cirrhosis is easy to diagnose. The main basis for diagnosis is:

1. There are viral hepatitis, long-term alcohol abuse, malnutrition, and medications such as liver damage.

2. The liver is large, the texture is hard, the surface is not smooth, and there are often splenomegaly.

3. There are clinical manifestations of liver dysfunction and portal hypertension.

4. Some liver function tests showed positive changes, among which serum albumin decreased, globulin increased, white/ball ratio decreased or inverted, protein-electrophoresis showed - bridge; serum liver fibrosis index increased; coagulation Prolonged zymogen time.

5. Ultrasound, CT or magnetic resonance examination revealed that the liver was large or small, the surface was not smooth or even uneven, the inner diameter of the portal vein and splenic vein was widened, the spleen was large, and the ascites was observed.

6. Laparoscopy, liver biopsy pathological examination found false leaflet formation.

Differential diagnosis

The differential diagnosis is mainly differentiated from diseases that cause hepatosplenomegaly and diseases of ascites.

1. Hepatosplenomegaly disease

(1) Chronic hepatitis: Chronic hepatitis and early cirrhosis are often the process of migration, without obvious boundaries, so they can coexist in the same patient. If the serum reflects liver fibrosis, the index is obviously increased. Ultrasound has portal hypertension, rectum. Portal vein radionuclide scintigraphy was used to determine the ratio of heart/liver imaging and liver biopsy to find false leaflets, which is helpful in diagnosing cirrhosis.

(2) Primary liver cancer: patients with liver cirrhosis often have liver cancer, and some hepatocyte regeneration nodules are difficult to distinguish from liver cancer in imaging. If AFP is >200g/L for 8 weeks, >500g/L for 4 weeks. Above; B-ultrasound or CT or MRI found that there is a space-occupying lesion, and fine needle aspiration for pathological examination under the guidance of B-ultrasound is helpful in diagnosing liver cancer.

2. Differential diagnosis of ascites disease

Cirrhosis is leakage of ascites, but it can be complicated by infection (spontaneous peritonitis or tuberculous peritonitis). At this time, ascites has leakage and exudative components. The ratio of the patients to different patients or different stages is different. The composition is obviously more than the exudation component, the ascites examination is biased to the leakage change, so the diagnosis is difficult. Table 1 lists the identification points of exudate and leakage, and cirrhosis can also be complicated by cancerous peritonitis. Table 2, the values in the table can be different for different detection methods, so it is only the reference value.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.