Progressive liver shrinkage

Introduction Fulminant hepatic failure is a syndrome in which hepatic cell necrosis and severe liver function damage are caused by a variety of causes, and there is no history of liver disease and hepatic encephalopathy within 8 weeks after the disease. The onset is urgent, the progress is fast, and the mortality rate is high. Early diagnosis and early treatment can reduce the mortality rate. Early symptoms include jaundice, persistent hypothermia, low fever, gastrointestinal symptoms, bleeding tendency, progressive liver shrinkage, liver odor, flapping tremor, heart rate, hypotension, etc., late symptoms It is characterized by hepatic encephalopathy. Cerebral edema is characterized by convulsions, slow breathing, irregular rhythm, coagulopathy and hemorrhagic bleeding with skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa.

Cause

FHF caused by hepatitis virus, drug poisoning and poisonous poisoning, its liver pathological features are extensive hepatocyte necrosis, liver cells disappear, and liver volume shrinks. Generally, there is no hepatocyte regeneration, and there are many reticular stent collapses, residual hepatic cells, and inflammatory cell infiltration in the portal area. Liver pathology such as acute fatty liver and Reye syndrome during pregnancy is characterized by severe damage to mitochondria in hepatocytes and metabolic dysfunction. The cells in the hepatic lobule to the middle zone are enlarged, and the cytoplasm is filled with fat vacuoles, which are honeycomb-shaped and have no necrosis of large hepatocytes. Liver shrinkage is not as significant as acute severe hepatitis.

an examination

Related inspection

Liver function test liver ultrasound examination hepatobiliary imaging

I. Early symptoms

1. Huangqi has three characteristics:

(1) After the appearance of jaundice, it will rapidly deepen in the short term, such as total bilirubin >171mol/L, and other manifestations of severe liver damage, such as bleeding tendency, prolonged prothrombin time, and elevated ALT. If only deep jaundice, no other serious liver function abnormalities, shown as intrahepatic cholestatic;

(2) The duration of jaundice is long. Generally, the law of jaundice is three stages: deepening, persistence, and regression. If jaundice is still not retreated after 2 to 3 weeks, it indicates that the condition is serious;

(3) After the appearance of jaundice, the condition did not improve. The general rule was acute jaundice hepatitis. When jaundice appeared, the appetite gradually improved, and nausea and vomiting were alleviated. If the symptoms do not improve 1 week after the onset of jaundice, you need to be alert to severe hepatitis.

2. There may be low fever at the beginning of low fever, and the body temperature drops to normal after the appearance of jaundice. If accompanied by jaundice with persistent hypothermia, it suggests hepatocyte necrosis or endotoxemia.

3. The general situation is extremely poor, such as fatigue, burnout, loss of appetite, and even life can not take care of themselves.

4. Obvious gastrointestinal symptoms, frequent nausea, vomiting, hiccups, obvious abdominal distension, disappearance of bowel sounds, intestinal paralysis.

5. Bleeding tendency such as skin ecchymosis, purpura, epistaxis, gum bleeding, a few upper gastrointestinal bleeding, etc., suggesting coagulopathy, liver failure.

6. Ascites rapidly appears due to the long half-life of albumin (about 2 weeks), usually low albuminemia occurs 2 to 3 weeks after the disease, and patients with more than 2 to 8 weeks have ascites.

7. The personality changes as the original character is cheerful, the mutation is melancholy, or vice versa. Sleep rhythm is reversed, language is repeated, can not be conceived, disorientation, behavioral quirks, behavioral quirks, casual stools, etc., are signs of hepatic encephalopathy. Then there is a disturbance of consciousness and a hepatic coma.

8. Progressive liver reduction, liver odor, flapping tremor, increased muscle tone, positive pyramidal tract sign, sputum sputum, etc., suggesting severe liver damage.

9. Increased heart rate, low blood pressure, associated with endotoxemia or internal bleeding.

Second, the symptoms

It manifests as hepatic encephalopathy, which in turn causes the following symptoms, and the transition phase is not easily separated.

1. Cerebral edema has cerebral edema when there is a sputum sputum, positive pyramidal tract, or conjunctival edema, dilated pupils, slow breathing, irregular rhythm, and edema of the papillary edema.

2. Coagulation dysfunction and hemorrhagic bleeding sites are common to the skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa.

(1) Platelet quality and quantity abnormality FHF platelets were smaller than normal, and electron microscopy showed vacuoles, pseudopods, and serosa. Platelets are normal in the absence of hepatic encephalopathy. Thrombocytopenia can be caused by bone marrow suppression, hypersplenism, and consumption by intravascular coagulation.

(2) Coagulation factor synthesis disorder All plasma coagulation factors are decreased, especially in the extrahepatic synthesis of factor VII, but increased. Prothrombin time was significantly prolonged.

(3) DIC accompanied by local secondary fibrinolysis plasma plasma and its activating substances decreased, while fibrin/fibrinogen degradation products increased.

3. Infection is most common in respiratory infections, and other urinary infections, mostly G-bacteria, G+ cocci, may also have anaerobic and mold infections.

4. Renal failure FHF has 70% renal dysfunction and acute tubular necrosis accounts for half. There are high sodium, isotonic urine and tubular necrosis. It is related to hepatocyte necrosis, endotoxemia, improper use of diuretics, hypovolemia caused by gastrointestinal hemorrhage and hypotension. Renal failure has been reported to be the leading cause of FHF death, notable.

5. Electrolyte acid-base balance disorder hyponatremia, hypocalcemia, hypomagnesemia, hypokalemia, respiratory alkalosis, hypokaline alkalosis and metabolic acidosis.

6. Other hypoglycemia, hypoxemia, pulmonary edema, arrhythmia, portal hypertension and acute pancreatitis.

Differential diagnosis

Explosive liver failure, on the basis of liver disease, rapid jaundice, liver shortening in a short time, neuropsychiatric symptoms, elevated transaminases or bile enzyme separation (normal or slight increase in transaminase and significant increase in bilirubin) should be performed Consider the possibility of this disease. In general, when liver parenchymal cells are dysfunctional, the first is impaired secretion function (hyperbilirubinemia), followed by synthetic dysfunction (reduction of coagulation factor, hypoalbuminemia, etc.), and finally detoxification. Obstacles (inferior inactivation of hormones, elevated levels of aromatic amino acids, etc.). In addition to its powerful phagocytic function, Kupffer cells also regulate intrahepatic microcirculation, participate in certain biochemical reactions (such as synthetic urea and insulin degradation, etc.), and can secrete a variety of cytokines and inflammatory mediators, defense against the body, Immune function plays an extremely important role. Kupffer cell damage or dysfunction will lead to intestinal endotoxemia, which can aggravate liver damage and cause a variety of extrahepatic complications such as DIC, functional renal failure, refractory ascites, etc. .

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