Neonatal hepatitis syndrome occurred in the neonatal period refers to the combination of increased bilirubin jaundice. Tuse feces were white pottery, liver, spleen, and liver damage to the main clinical syndrome. The main cause is (1) : all CMV virus, hepatitis viruses; (2) or intrahepatic cholestasis. extrahepatic biliary atresia; (3) : If galactose metabolic diseases hyperlipidemia, alpha1-antitrypsin protein in the United States lack disorders. The disease infected more than intrauterine pregnancy by the mothers of rubella virus, cytomegalovirus, herpes simplex virus, toxoplasmosis caused. Direct transmission to the fetus by the mother, the mother may incidence. Mothers with hepatitis B and intrauterine infection, and neonatal morbidity rates. Disease prevention is the key to avoiding maternal infection and contracted various diseases, the incidence of the disease will decline. The efficacy of treatment was not satisfactory, in part to patients with chronic hepatitis, cirrhosis of development is that there should be early diagnosis and treatment.

Clinical manifestations :

1. Physiologic jaundice is also regressive, or has been persistent.

2. Slow onset, Tunai, anorexia, weight gain, abdominal distension, fecal color of pale yellow. With a variable serious, dark yellow urine.

3. Hepatosplenomegaly, moderately enlarged liver mainly large.

4. Often with vitamin A, D deficiency.

Diagnosis :

1. Have a family history of liver disease, genetic diseases and maternal infection.

2. Slow onset, persistent physiological jaundice or who retire now, while continuing to deepen.

3. Have Tunai, anorexia, flatulence, weight gain, stool light yellow, gray and white was serious. urine dark yellow.

4. Hepatosplenomegaly, mainly to large liver. Mostly middle degree.

5. Liver function test serum transaminase Valley C U.S., alkaline phosphatase increased.

6. Directly or indirectly to increased serum bilirubin, direct bilirubin mainly higher, ¦Ã - glutamyl Hill aminotransferase U.S. may increase.

7. Urobilinogen, bilirubin positive urine.

8.HBsAg be positive.

Treatment principles :

1. Etiology treatment.

2. Vitamin nutrition : high supply, high-carbohydrate diets.

3. Infection prevention and control in a timely manner.

4. Hormones : short-term prednisone use, reducing withdrawal symptoms improved gradually.

5. Hugan : Hugan to avoid the use of harmful drugs and liver medicines and food.

6. Lidan.

7. Chinese medicine.

Medication principles :

1. Multi-vitamin supplement to the ordinary case, Hugan Lidan mainly short-term use of estrogen.

2. In addition to the above treatment can be severe cases intravenous drug use Hugan, Gan intravenous muscle, liver a bit too optimistic. A U.S. support to secondary treatment, intravenous infusion, plus medicine Lidan severe jaundice.

Supplementary examination :

1. Neonatal hepatitis syndrome bound by the limitations of the ad hoc inspections to the "A" main.

2. The ad hoc inspections of unknown etiology may include inspection bound by the limitations of the "A, B."

3. With biliary atresia, glycogen storage disease and other identification, Inspection bound by the limitations of the ad hoc inspections could include "A, B, C."

Evaluation :

1. Cured (1) general, and the spirit of good appetite, jaundice persisted weight. (2) of the liver, spleen enlargement, recovery to normal or near normal range. (3) resume normal liver function tests.

2. Improved (1) The general situation has improved and enhanced appetite, jaundice not completely dissipated. Hepatosplenic more narrow, but returned to the normal range.

This article was posted on 2007-02-27