Acute fatty liver of pregnancy

Introduction to acute fatty liver during pregnancy Acute fatty liver in pregnancy, also known as obstetric acute pseudo-yellow liver atrophy, is a rare and rare disease in the late pregnancy. The onset of the disease is rapid, the condition changes rapidly, and the clinical manifestations are similar to those of fulminant hepatitis. Previous reports reported that the maternal and child mortality rates were 75% and 85%, respectively. However, if early diagnosis, early treatment, and timely termination of pregnancy can be achieved, the disease can be reduced. With maternal mortality, infant mortality can be reduced to 58.3%. basic knowledge The proportion of illness: 0.005% Susceptible population: pregnant women Mode of infection: non-infectious Complications: premature delivery postpartum hemorrhage pancreatitis

Acute fatty liver disease during pregnancy

(1) Causes of the disease

The cause of AFLP is unknown. Because AFLP occurs in the third trimester of pregnancy and only hopes to heal after termination of pregnancy, it is speculated that the hormone changes caused by pregnancy may cause obstacles in fatty acid metabolism, resulting in accumulation of free fatty acids in liver cells and kidneys, pancreas, brain, etc. Other organs have caused multiple organ damage. In recent years, there have been many cases of recurrent cases and their offspring have reported genetic defects. Therefore, it may be congenital genetic disease, in addition to viral infection, poisoning, drugs (such as tetracycline), malnutrition Multiple factors such as hypertensive disorder complicating pregnancy may also be related to the damage of mitochondrial fatty acid oxidation.

(two) pathogenesis

The main pathological change of AFLP is the infiltration of a large number of fat droplets in the liver cells. The overall structure of the liver does not change, the liver cells are swollen, the cytoplasm is filled with fat droplets, the fat droplets are tiny, and they surround the nucleus in the cytoplasm. HE stained tissue sections saw many unique vacuoles, and further development showed a small amount of large-sized fat vacuoles (Fig. 1), which may be related to steatosis, but inflammation and necrosis were not obvious, stained with special fatty oil red O, cells The fat droplets in the medium can be seen with special staining, and the positive rate is higher. The disease begins in the center and middle zone of the hepatic lobules, and later develops into the hepatocytes in the portal area. The condition worsens, and the kidneys, pancreas, brain tissue and other organs have Microcystic-like steatosis.

Due to obstruction of the bile duct or accumulation of intrahepatic bile, about 40% of gestational fatty liver has histological features of cholestasis. Although inflammation is not a unique manifestation of AFLP, it is also very common (50%). Serious AFLP can be expressed as Sparse small pieces of necrosis, but not large, necrosis of whole lobes, should be differentiated from hepatitis when histological changes are not typical.

Electron microscopy is located in the center of the cell, surrounded by fat droplets, mitochondria swelling, increased matrix density, fat droplets composed of free fatty acids, not triacylglycerol, rapid pathological changes in the liver after delivery, no sequelae, will not develop into Cirrhosis of the liver.

Acute fatty liver prevention during pregnancy

Pay attention to rest, work and rest, life in an orderly manner, and maintaining an optimistic, positive and upward attitude towards life can be of great help in preventing diseases.

Acute fatty liver complications during pregnancy Complications premature delivery postpartum hemorrhagic pancreatitis

At the time of AFLP, stillbirth, stillbirth, premature delivery and postpartum hemorrhage are common, and a small number of patients may also have pancreatitis and hypoproteinemia.

Acute fatty liver symptoms during pregnancy Common symptoms High blood pressure right upper quadrant pain Renal failure nausea abdominal pain Acute fatty liver in pregnancy Diabetes edema Hemorrhoids Vomiting

In the early stage of onset, there is only persistent nausea, vomiting, fatigue, upper abdominal pain or headache. There are jaundices from day to week and progressive deepening. There is often no itching. Abdominal pain can be limited to the right upper abdomen. It can also be diffuse and often high. Blood pressure, proteinuria, edema, a small number of people have had polyuria and polydipsia, such as no progress in childbirth, coagulation dysfunction (skin defects, ecchymosis, gastrointestinal bleeding, gum bleeding, etc.), hypoglycemia, consciousness Obstacles, psychiatric symptoms and hepatic encephalopathy, oliguria, no urine and renal failure, often die in a short period of time.

Examination of acute fatty liver during pregnancy

1. Blood routine: Peripheral blood white blood cell count increased, up to (15.0 ~ 30.0) × 109 / L, poisoning particles appeared, and see red blood cells and basophilic red blood cells; platelet count decreased, peripheral blood smear showed hypertrophy Platelets.

2. The serum total bilirubin is moderately or severely elevated, mainly direct bilirubin, generally not exceeding 200 mol/L; blood transaminase is mildly or moderately elevated, ALT does not exceed 300 U/L, and enzyme-biliary Separation phenomenon; blood alkaline phosphatase increased significantly; serum albumin was low, and beta lipoprotein was elevated.

3. Blood sugar can be reduced to l/3~1/2 of normal value, which is a prominent feature of AFLP; blood ammonia is elevated, and it can be up to 10 times of normal value when hepatic encephalopathy occurs.

4. Prothrombin time and partial thromboplastin time prolonged, fibrinogen decreased.

5. Blood uric acid, creatinine and urea nitrogen are elevated, especially the increase of uric acid is not proportional to renal function. Sometimes hyperuricemia can exist before the onset of AFLP.

6. Urine protein positive, urinary bilirubin negative, urinary bilirubin negative is one of the more important diagnoses, but urinary bilirubin positive can not rule out AFLP.

7. Imaging examination

B superficially see the diffuse high-density area of the liver area, the echo is uneven, snow-like, typical fatty liver waveform, CT and MRI examination can show excess fat in the liver, the liver parenchyma is uniform and the density is reduced.

8. Pathological examination

It is the only way to diagnose AFLP, and it can be used for B-ultrasound liver biopsy.

(1) Light microscopic observation: typical changes in liver histology are normal hepatic lobular structure, diffuse hepatocytes, microscopic fatty degeneration, hepatocyte enlargement, and more common hepatocytes near the central vein of the lobule; Fat vacuoles, the nucleus is still in the center of the cell, the structure is unchanged; visible cholestasis, no inflammatory cell infiltration, HE staining, hepatocytes are balloon-like changes, is the earliest morphological changes of the disease, visible in the liver sinus Acidic bodies, such as severe damage to liver cells, have significant necrotic and inflammatory responses.

(2) Electron microscopy: Under electron microscope, mitochondria were obviously enlarged, ruptured, loose and sputum decreased, and crystal-like inclusion bodies, smooth surface and rough endoplasmic reticulum were seen. Golgi was filled with lipid and expanded.

Diagnosis and diagnosis of acute fatty liver in pregnancy

diagnosis

AFLP is prone to occur in the third trimester of pregnancy, primipara, pregnancy-induced hypertension, multiple births are a high risk factor for AFLP, more than half of AFLP is associated with pregnancy-induced hypertension, diagnosis in addition to medical history, clinical features, refer to auxiliary examination, diagnosis depends on the organization Learn to check.

Differential diagnosis

Acute severe viral hepatitis

Liver failure is the main manifestation of acute severe viral hepatitis. It is clinically similar to AFLP. Special attention should be paid to the identification. The serum immunological examination of acute severe viral hepatitis is often positive (including hepatitis virus antigen and antibody detection); transaminase is extremely elevated. High, often >1000U/L; urinary tricholic positive, blood uric acid is not obvious, white blood cell count is normal, renal function abnormality occurs later, peripheral blood smear without young red blood cells and dot color cells, liver histological examination see liver cells Extensive, large flake necrosis, destruction of hepatic lobular structure.

2. Intrahepatic cholestasis of pregnancy

Intrahepatic cholestasis of pregnancy manifests as itching, elevated transaminase, jaundice, and elevated bile acids; whereas AFLP has no pruritus and elevated bile acids, and histological changes in cholestasis during pregnancy are mainly in the central capillary of the hepatic lobules. Cholestatic, placental tissue also has bile deposition; while AFLP liver cells are mainly fat droplet infiltration, no significant changes in placenta.

3. Pregnancy-induced hypertension liver damage and HELLP syndrome

AFLP's renal tubular epithelial cells have free fatty acid deposition, reabsorption of renal tubules, leading to retention of sodium and water, nausea and vomiting, hypertension, proteinuria, edema, etc., similar to the performance of pregnancy-induced hypertension; High blood pressure can also occur in liver function, renal function and coagulation function; when the pregnancy-induced hypertension develops further, the clinical manifestations and laboratory tests are similar to AFLP when HELLP syndrome occurs. The identification between the two must be caused. Clinical attention, pregnancy-induced hypertension, pre-eclampsia and HELLP syndrome rarely appear hypoglycemia and high blood ammonia, which is not only an important identification point, but also a sign of the severity of AFLP disease, indicating liver failure and poor prognosis, liver area ultrasound And CT examination is helpful for differential diagnosis, but the diagnosis can only rely on liver biopsy. Pregnancy-induced hypertension has few liver failure and hepatic encephalopathy. Liver histology shows hemorrhage around the portal vein. Fibrin deposition, hepatocyte necrosis; inflammatory cell infiltration in liver tissue, immunohistochemistry in liver tissue, tumor necrosis factor (TNF) and neutrophil Staining of the enzyme is very obvious.

Sometimes the clinical manifestations of the two are very similar, and the two may exist at the same time. The clinical identification is very difficult. Because the obstetric treatment of the two is consistent, both of them are strengthened monitoring and early termination of pregnancy, so clinical identification is not the main contradiction.

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