Cirrhosis of the liver
The main cause is portal hypertension, in addition to other factors such as decreased colloidal pressure, decreased vascular strength, salt and water retention factors.
Cirrhosis - the Greek name "kirrhose," meaning cirrhosis of the liver, was coined by Laennec in 1819 when describing liver damage caused by chronic alcoholism. Since then, the disease has been named after him as Laennec cirrhosis.
Cirrhosis is defined as the anatomical lesions of the liver, Therefore, depending on the cause, cirrhosis, in addition to its general symptoms, may be accompanied by other clinical manifestations specific to the cause of the disease.
Lesions specific to cirrhosis are a process of chronic, irreversible damage to cirrhosis with diffuse fibrosis associated with the formation of regenerative liver parenchymal nodules. This damage leads to hepatocellular necrosis, deflating the liver's support network, thereby leading to the deposition of connective organizations, the blood vessel floors in the liver become meandering, twisting, and parenchyma. the remaining liver arises in nodules. This damage is the result of chronic liver damage from a variety of causes.
In France, the frequency of symptomatic cirrhosis is 3000/1 million people, of which wine is the majority (men: 90% -95%; women: 70% -80%); by beer: 10%, due to chronic viral hepatitis 10%. The number of people who drink a lot of alcohol: 30,000 / 1 million people have a risk of cirrhosis of 10%. If the average drink about 80 grams of alcohol/day for men and 60 grams/day for women for 10 years, the risk of cirrhosis is 50%. The death rate from cirrhosis: 300 people / 1 million people/year.
In Southeast Asia, sub-Saharan Africa, about 15% of the population is infected with hepatitis B and C viruses even at a young age, of which 25% lead to cirrhosis.
In the United States, the rate of B virus infection is less, more people at high risk such as homosexuality in men, drug addiction, hepatitis C after blood transfusion, about 50% lead to cirrhosis 20% life after 20 years. In Vietnam, there are no specific statistics.
There are many causes of cirrhosis; some are still unknown.
As a common cause in Europe, seen in people who drink a lot, glands with large ears, varicose nodules. SGOT / SGPT> 2, GGT increase, determined by liver biopsy, with vasodilator nodules.
Cirrhosis of the liver due to infection
The top-ranking is hepatitis B, C, and or a combination of D that causes large nodular cirrhosis (post necrotic cirrhosis). This is a consequence of active chronic hepatitis with no viral replication found. Serum tests showed chronic carriers of B, C: HBsAg +, AntiHBc +, HCV (+). Other less common infections are Brucellosis, Echinococcus, Schistosomiasis, Toxoplasmosis.
Cirrhosis of the liver due to metabolism
Serum iron is increased, ferritin saturation and blood transferrin are increased.
Copper cirrhosis: serum copper increased.
Uncommon diseases: Deficiency (antitrypsin, urinary porphyrin, hyper galactose disease, Gaucher disease, urinary fructose.
Cirrhosis of the liver due to an immune disorder
Primary biliary cirrhosis:
This is a small chronic inflammatory disease in the liver with incapacitated bile, seen in women, 30t-50t, manifesting chronic cholestasis, increased Gama-globulin IgM, and antibodies to mitochondria.
Chronic hepatocellular destruction often exacerbated blood tests with anti-smooth muscle antibodies, antinuclear antibodies, antibodies against mitochondria.
Mechanical cirrhosis of the liver
Secondary biliary cirrhosis:
Due to chronic obstruction of the main biliary tract, due to oddi muscle stenosis, due to stones.
Off hepatic veins in Budd-Chiari syndrome, long-term right heart failure, spasmodic pericarditis.
Drug-induced cirrhosis of the liver
Methotrexate, maleate de perhexiline, methyldopa, birth control pills, oxyphenisatin, isoniazid,
Other reasons have not been proven
Chronic inflammatory bowel disease, diabetes, sarcoidosis.
Mechanism of pathogenesis
The progression of cirrhosis is slow over many years, sometimes the cause is gone, but the disease continues to progress due to a vicious cycle.
Maintain damage to liver cells, it is possible to encounter antigens (KN) anti-hepatocytes, anti-red blood cells, anti-gamma- globulin established in the cirrhosis process, thereby causing damage to liver cells destruction of red blood cells, causing anemia and increased risk of infection.
Door pressure booster
Further, reduce blood circulation in the portal system, make relative anemia in liver cells, liver cells will receive a lack of oxygen and nutrients are susceptible to further necrosis, leading to fibrosis, scarring, structure reversal liver increases portal pressure.
For any reason, it will increase hepatocellular anemia, cause necrosis and liver failure.
The veins in the liver, lungs
Also reduces blood flow to the liver causing anemia, necrosis, and liver failure.
New nodules create fewer blood vessels
Causes pressure on blood vessels causing anemia
The clinical picture of cirrhosis is very variable, varies depending on the stage.
There is very little physical and physical evidence, detected by physical examination, of people at high risk.
Poor appetite, indigestion, epigastric pressure, decreased sex drive, menstrual disorders.
Large liver with firm, painless face, large spleen, no ascites, vasodilation in the cheeks, star-shaped vasodilatory nodules, erythema palms. Diagnosis is confirmed by liver biopsy.
This is the stage with many complications. The disease manifests itself in 2 syndromes:
Liver failure syndrome:
With anorexia, delayed indigestion, bloating, menstrual disturbances, impotence, large breasts, root bleeding, nosebleeds, bleeding under the skin, hair loss, meniscus nails, fingers drumstick is found in cirrhosis, thin chest and upper extremities, 2 soft ooedema, mild yellow skin, anaemia, star vasodilator nodules on chest and back, erythema palms, red lips, shiny red tongue , large breasts, testicular atrophy, peripheral neuritis, small liver.
The portal vein hypertension syndrome:
Beginning with bloating or stools or have bloody stools, vomiting blood. Exam has:
Aortic collateral circulation in the epigastric region and flanks, the hypotonic region and both sides of the pelvic fossa, or around the navel (jellyfish head) or sometimes as short connections between the portal system and the inner host. In the case of the inferior vena cyst, there will be more collateral circulation.
Large spleen: initially soft, later fibrosis becomes firm or stiff, detected by stone touch.
Ascites: free form. The main cause is portal hypertension, in addition to other factors such as decreased colloidal pressure, decreased vascular strength, salt and water retention factors.
Hemorrhoids: usually internal hemorrhoids due to increased pressure of the lower mesenteric vein, manifested by the passage of fresh blood.
Gate venous hypertension syndrome
Measurement of portal venous pressure:
Normal: 10-15cm water, increase when> 25cm water; splenic venous pressure increased, portal spleen time was prolonged.
The diameter of the portal vein, spleen vein:
Normally 8-11mm, when there is portal hypertension, the diameter is greater than 13mm, the diameter of the spleen venous is> 11mm (measured by ultrasound)
Dilated peritoneal veins, mesenteric veins, umbilical veins, or gastroesophagoscopy shows an enlarged esophagus, stomach.
Liver failure syndrome
Blood Protide: Reduced, especially albumin, increased gamma-globulin, A / G reversed.
Prothrombin ratio: Decreased, this is a heavy prognostic factor.
Blood cholesterol: Reduced, especially the esterified type.
Specific liver function tests: Urinary Galactose + test, caffeine clearance (+).
Electrolyte disorders: Blood sodium increased or decreased, blood khaki decreased, sodium urinary decreased (sodiumuria <25 mEq / 24 hours.
NH3 blood increases.
Fibrinogen blood: Increases> 4g / l.
LDH> 250vnd, CRP> 20mg / l, VS: Increased. (when there is progressive fiber).
Liver cell destruction syndrome
Expression when there is inflammation in advanced cirrhosis with increased ALAT, ASAT.
Isochromatosis, or 3 decreases in blood cell lines in the presence of splenomegaly.
Liver ultrasound: Small liver, irregular margin, serrated, nodular form, portal vein dilated, re-establishing umbilical vein, portal embolism.
Density tomography: for similar images
As a decisive test in the diagnosis of cirrhosis contributes to the diagnosis of the cause and classification of cirrhosis.
Implementing the quadrants
Based on the following factors:
History of chronic liver disease.
Clinical Based on 2 portal hypertensive syndromes and liver failure syndrome.
Subclinical: Blood tests, ultrasound, liver biopsy.
There is a history of protein loss such as bowel resection, prolonged exhaustion, and severe lack of food. Tests showed a decrease in blood protein but normal liver function, ultrasound, liver biopsy was normal.
Progressive edema, with proteinuria> 70 mg/kg or> 3.5g / 24 hours, blood protein electrophoresis with ß globulin predominantly, ultrasound and liver biopsy are normal
Tuberculosis of the peritoneum
Based on the history, history with signs of TB infection, free or localized groin, pain, drainage mainly lymphoid, find BK in the semen.
Drainage of secretions, with foreign cells, diagnosed by density tomography, tumor biopsy, or fine-needle aspiration.
Maybe more than 1 healthy liver or 1 cirrhosis liver. The liver grows fast, hard, groin can be blood fluid, Alpha - FP (+), DCP (+), ultrasound, CT, biopsy.
Progression and complications
Dull, lasting over many years, from the stage of compensation with very few symptoms, diagnosed by liver biopsy, to the decompensated stage with clear clinical symptoms, typical subclinical. This stage has many complications.
Much and complicated at the end.
Infection: Bowel, groin, portal vein, lung, kidney.
Onset may be observed after enteritis, with the more rapid increase in the groin, spontaneous abdominal pain, fever. Abdominal pain with pressure, puncture, peritoneum fluid with cell proliferation> 500 / mm3 and more than 50% neutrophils, Rivalta reaction can (+), culture may contain pathogenic bacteria.
Door vein thrombosis caused by infection:
Clinically, there is a rapid increase in the groin, natural abdominal pain, fever, bloody stools. Ultrasonic diagnosis of thrombosis in the portal vein.
Pathology of the stomach and duodenum:
Peptic ulcers, gastric portal hypertension.
Peptic ulcers: More common ulcers in the duodenum than peptic ulcers. The ulcer usually has very few symptoms, is difficult to heal, and easily recurs, so there are many complications such as perforation, bleeding.
The stomach lining is red, but it's actually not inflamed. Gradually, the mucosa becomes mosaic-shaped and may be accompanied by gastric vein enlargement. This damage more often occurs in patients treated with varicose oesophageal varicose veins.
Skin, mucosa, internal organs, bleeding from the oesophageal artery province, from hemorrhoids in portal hypertension.
Bleeding from oesophageal enlargement: The portal pressure is too high. The disease has a sudden onset of blood vomiting but has no warning symptoms. Bleeding can sometimes be very severe with manifestations of dizziness due to blood loss, life-threatening. Grade 3 varicose esophagoscopy with bleeding. In addition, there may be bleeding in other venous distention sites such as hemorrhoids, gastric aneurysms, small intestinal varicose (rare).
Bleeding due to decreased clotting factor: Bleeding of the brain, bleeding under the skin.
The process of terminal cirrhosis. Often there are easy factors such as infection, hemorrhage, electrolyte water disorder, after bypass surgery of the aorta is also called encephalopathy.
Liver and kidney syndrome:
Is it a serious complication, high mortality? This is very severe acute renal failure, triggering on 1 impaired liver, too heavy groin, indiscriminate diuretics or nephrotoxic drugs. Clinical manifestations of oliguria or anuria, signs of renal failure, proteinuria, red blood cells, decreased blood sodium <130 mEq / L, urine osmolality is higher than plasma.
Common after cirrhosis except for cardiac cirrhosis and cholestatic cirrhosis.
Blood sugar disorders:
There is impaired glucose tolerance but rarely causes true diabetes or low blood sugar in severe liver failure.
Coagulation factor disorder.
Treat the cause
Once cirrhosis has occurred, the problem of treating the cause is too difficult. Eliminating harmful causes such as alcohol and toxins, with proper diet, rest, adequate nutrition, can recover if the fiber process is in an early stage.
Salt restriction is very important. Light eating 0, 5g salt /day, less fat <50g /day, protide about <2g / kg / day. Energy is about 1500-2000 calories/day, drinking water <1l /day based on water bilan. (Can be 100g meat/n g orreplace with 2 eggs, no more than 0.25l of milk/ng, unsalted bread with butter and mayonnaise, fruit, salad, ketchup, no chocolate milk, mint) should use vegetable protein, limit physical activity.
Treatment of ascites:
It is more difficult than ascites due to other causes. En nutrition and rest if there is no decrease in chorum and urinary Na + <25mmol / day, then a diuretic should be used.
Diuretics: Usually starts with anti-Aldosterone such as spironolactone 100-200mg / ng or Amiloride 10mg-15mg / ng or Triamterene. After 4 days if the response is poor, add Furosemide 80mg / ng or thiazide 50mg- 100mg / ng.
According to weight, daily urine output, electrolyte blood test 2 times / 1 week while still in the hospital to help monitor the treatment process. When there is peripheral edema and when the edema is gone, reduce the diuretic dose to maintain treatment depending on disease response, with salt restriction secretion.
Stretcher puncture: Only when the neck is stretched; oedema; Child B; Protrombin> 40%; Bilirubin blood <10mg / dl; Platelets> 40,000 / mm3; serum creatinine <3mg / dl; Sodium urinary> 10mmol / 24h. Intoxication 1 time a week, each time taking 1 to 5 liters and must return every 6g albumin / 1 pack (can use Dextran or polygeline).
Closed drainage: Drain the peritoneum into the cervical vein through a Teflon tube.
If none of the above methods are blistering, peritoneovenous shunts (peritoneovenous shunts) or TIPS, and finally liver transplantation
Treatment of portal hypertension:
Doorway connection: Lowers groin fast but has a risk of hepatic encephalopathy, and the effect does not improve much.
Sympathomimetics blockers: (Propranolol, nadolol) work to reduce portal pressure through the vasodilator effect on the visceral vein, reducing the size of the ascites and portal vein system, in combination with reducing cardiac output. The drug is used in a dose so that the pulse remains relative to the original pulse at rest with no contraindications. It can be combined with Isosorbide mononitrate (Imdur).
However, portal hypertension in cirrhosis is irreversible, so the treatment of choice is a liver transplant.
Treatment of liver failure
There is no specific treatment.
Fat metabolism drugs: Choline, Methionine, Inositol do not restore liver function.
Vitamins B, C, A, D, K, folic acid, folate, zinc.
Testosterone: do not use it because it makes the breast bigger, the mortality rate increases.
Corticoids: Used only in autoimmune hepatitis.
Prolyl hydroxylase inhibitors such as HOE 077 were still in the test
Colchicine: L short process alcohol cirrhosis, use 1 mg/day, 5 days 1 week for several months has not strongly convinced
Treatment of complications
Treatment of venous bleeding of the esophagus:
This is an emergency treatment aimed at maintaining circulatory volume, however too much rehydration can increase portal pressure, resulting in more bleeding and therefore care should be taken.
Transfusion of fresh blood or fresh plasma and monitor with central venous pressure, urine output, mental status. About 50% of cases can be stopped on their own, but the risk of bleeding remains high.
Vasopressin’s: (use acute phase): Vasopressin or Somatostatin. Vasopressin infusion (Pitressin) 20 units / 100ml of dextrose 5% IV in 10 minutes of pressure will decrease after 45-60 minutes, or 0, 4v / ml for 2 hours causes vasoconstriction to reduce blood in the portal system, 80% effective and more than ½ do not bleed. Side effects: myocardial anemia, gastrointestinal anemia, acute renal failure, hyponatremia. To alleviate this complication, a combination of nitro-glycerine iv 40 mg/ph can be used. Glycerine (Terlipressin) has a longer effect than Vasopressin, infused 1mg / every 4 hours for 24 hours.
Somatostatin or Octreotide for direct vasoconstriction, good bleeding control, and fewer side effects than Vasopressin, first dose 250 (g followed by infusion 25-50 mg / h.
Hemostasis with sonde Blakemore or sonde Minnesota. The risk of choking in the lungs and rupture of the esophagus due to ulcers, perforation.
Fiber injection: Treatment for acute bleeding and repeated injections until atelectasis. The commonly used drug is polidocanol. Complications: mucosal ulcers can cause bleeding or narrowing of the esophagus, perforation.
Endoscopic dilated venous constriction provides better bleeding control and reduces complications and recurrent bleeding.
Emergency surgery: Put TIPS.
Remove the emergency esophagus with a gun clip through the front gastrointestinal tract. Short procedure time with few complications, low mortality.
Cimetidine or Ranitidine: for prevention of acute stress ulcers.
Antibiotics for high risk of gastrointestinal infections: use Norfloxacin.
Stool removal: removing blood from the intestine, using lactulose.
Treatment of prevention of primary bleeding: Combination of Nadolol and Isosorbide mononitrate with periodic fibrosis injection or with band ligation
Treatment of gastric disease caused by portal hypertension:
Determined by endoscopy. There is an indication for the use of a sympathomimetic ß blocker, while resistance to H2 is less effective.
Treatment of primary infectious peritonitis (SBP):
The antibiotic of choice is Cefotaxime 6g / 24h x 5-7 days. Just use intravenously after 48 hours has seen leukopenia in the semen. Thereafter, prophylactic therapy with Norfloxacin 400 mg/ng, or Ciprofloxacin 750 mg/week, or Bactrim for 5 days/week, for a minimum of 6 months, is effective in preventing recurrence.
Treatment of liver and kidney syndrome:
Limit fluid, salt, protein, potassium, do not use hepatotoxic drugs, treat bacterial infections if any, do not use Mannitol. Vasoconstrictors such as metaraminol, angiotensin II, ornipressin are less effective on the kidneys. Nitric oxide inhibitors were still in the test. TIPS implemented for Child C is less effective and should raise the issue of liver transplantation.
Avoid alcoholism, prevent hepatitis with compulsory vaccination for people at high risk and mobilize the entire population to get the hepatitis B vaccine 3 doses 1 month apart after 1 year of repeat, advocate for self-transfusion safe blood transfusion, be careful when using drugs that are toxic to the liver; prevention and treatment of malnutrition, chronic cholangitis.
The long-term prognosis is bad, 5% live after 5 years, depending on complications. The prognosis is poor with persistent jaundice, hemorrhage, hepatic coma, acute macular atrophy, bacterial infection, Child C of Child-Pugh classification.
Table: Scale to evaluate cirrhosis stage according to Child-Pugh index
< 35 μ mol/l
> 50 μmol/l
> 35 g/l
< 28 g/l
> 50 %
< 40 %
The scale to evaluate the stage of cirrhosis according to the Child-Pugh index is Child A: Score 5 or 6. Child B: score from 7-9. Child C scores 10-15.