Toxic-induced liver damage

Introduction Explosive liver failure may occur in the history of hepatitis exposure or in the history of liver damage caused by drugs or poisons. 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.

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

MRI examination of liver, gallbladder, pancreas and spleen, hepatobiliary dynamic imaging, ultrasound diagnosis of liver disease

In the course of the disease, the clinical symptoms are complicated and diverse due to the involvement of multiple organs. The onset is urgent and the disease progresses rapidly.

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, persisting, and regressing. 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. Continuous low heat

There may be low fever at the beginning of the disease, 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 very 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, nasal discharge, bleeding gums, a small number of upper gastrointestinal bleeding, etc., suggesting coagulopathy, liver failure.

6. Ascites appears quickly

Due to the long half-life of albumin (about 2 weeks), hypoalbuminemia usually occurs 2 to 3 weeks after the disease, and ascites is more common in patients with a course of more than 2 to 8 weeks.

7. Personality change

If 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

In the extreme stage of the course of the disease, hepatic encephalopathy is mainly manifested, followed by the following symptoms, during which the transition phase is not easily separated.

Brain edema

When there is a hernia, the pyramidal tract is positive, there is brain edema, or there is conjunctival edema, pupil dilated, slow breathing, irregular rhythm, and papilledema show cerebral edema.

2. Coagulopathy and bleeding

The bleeding site is common to the skin, gums, nasal mucosa, bulbar conjunctiva and gastric mucosa.

(1) abnormal platelet mass and quantity: platelets are smaller than normal at FHF, and vacuoles, pseudopods, and serosa are blurred by electron microscopy. 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 coagulation factors in plasma are reduced, especially in the extrahepatic synthesis of factor VII, but increased. Prothrombin time was significantly prolonged.

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

3. Infection

Respiratory tract infections are the most common, and other urinary infections, mostly G-bacteria, G+ cocci, may also have anaerobic and mold infections.

4. Renal failure

Renal dysfunction was 70% at FHF and acute tubular necrosis was 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

Low blood sodium, low blood calcium, low blood magnesium, hypokalemia, respiratory alkalosis, hypokaline alkalosis and metabolic acidosis.

6. Other

Hypoglycemia, hypoxemia, pulmonary edema, arrhythmia, portal hypertension and acute pancreatitis.

Differential diagnosis

1. Hepatic rupture of the hepatic membrane: rupture under the capsule, rupture of the liver parenchyma under the capsule, forming a subdural hematoma is a kind of liver rupture, and liver rupture refers to liver rupture caused by blunt action. Since the external force acts directly on the liver area, the liver is squeezed between the anterior and posterior abdominal wall and the spine, or the body can be damaged by acceleration, deceleration, and torsion during exercise. The liver was enlarged, the abdomen had a mobile dullness, and the liver dull area was enlarged.

2. Cirrhosis caused by schistosomiasis: Schistosomiasis japonica is a disease caused by Schistosoma japonicum parasitic in the portal system. Infected by skin contact with cercaria-containing plague water, the main lesion is granuloma caused by eggs in the liver and colon. In the acute phase, there is fever, hepatomegaly and tenderness, diarrhea or pus and blood, and the number of eosinophils in the blood increases significantly. The chronic phase is mainly caused by hepatosplenomegaly. In the late stage, it is mainly caused by fibrosis around the portal vein, which can develop into portal hypertension, spleen and ascites.

Impaired liver function: The liver is most susceptible to toxic substances, causing chemical liver damage. Impaired liver function refers to certain pathogenic factors, including infectious and non-infectious, which cause changes in liver function, causing the liver to fail to perform its normal function, causing its function to undergo impaired changes. .

3, "Diffuse Liver Lesions": It is a manifestation of liver tissue lesions in imaging examination, which can also be called liver fibrosis. Hepatic fibrosis is an excessive deposition of diffuse extracellular matrix in the liver. It is the result of a large amount of collagen deposited in the hepatic cell space stimulated by activated hepatic stellate cells under the stimulation of various pathogenic factors. If the fibrous tissue continues to proliferate, invade the liver cells, destroy the structure of normal liver tissue, form many nodules surrounded by fibrous tissue, and the liver texture becomes hard, which is cirrhosis.

In the course of the disease, the clinical symptoms are complicated and diverse due to the involvement of multiple organs. The onset is urgent and the disease progresses rapidly.

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