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Jaundice with pregnancy
- 1. Dr. Abdelhamid Ahmed Abdelmaksoud M.D of obstetrics and gynecology Consultant of OB&GYN, Damanhour Medical National Institute
- 2. Training Methods 1-lecture: It is effective with large groups. 2-Group discussion: It is very effective for small groups. 3-Role playing: It involves creating a realistic scenario. 4-Simulation: It likes the case study and providing practical experience to learners.
- 3. Jaundice in pregnancy Case study - A 36 years old female G1P0 at 34 weeks with twin gestation, presents to the delivery unit with a 4 days history of nausea, vomiting and epigastric pain. - Her skin and eyes changed slightly to the yellowish color. - Her prenatal course until now has been uneventful. - Blood pressure is normal. - Prenatal laboratory studies are in normal range. - Her past medical and surgical history are unremarkable. - By examination: 1-General Malaise - 2-scleral icterus - 3-slight right hypochonria tenderness
- 4. Why this case is jaundice with pregnancy? By definition: jaundice is the clinical manifestations of raised bilirubin in blood Detected clinically at bilirubin concentration of 2mg% or more Normal range: 0.2-0.8 mg%
- 5. What is the normal liver physiology in pregnancy? - The liver receives up to 25-35% of the cardiac output which doesnt change during pregnancy. - The size of the liver doesnt increase. - Palpably enlarged liver is abnormal in pregnancy. - The metabolic, synthetic and excretory function of the liver are affected by increased E.&P. in pregnancy.
- 6. What is the liver function tests changes in pregnancy? - Aspartate transaminase (AST) and Alanine transaminase (ALT): unchanged initially, but 25% decreased by 3rd trimester. - Gamma glutamate transaminase (GGT): unchanged or slightly decreased. - Alkaline phosphatase: 2-4 fold increase in 3rd trimester. - Cholesterol: two fold increase. - Triglycerides: 2-3 fold increase. - Globulin: increase in alpha and beta globulins
- 7. What is the effect of hyperbilirubinemia on the fetus? Elevated levels of maternal unconjugated bilirubin dont have deleterious effect on neurodevelopmental status of offspring.
- 8. What is the main cause of jaundice in pregnancy? I. Unique to pregnancy 1- Severe hyperemesis gravid arum. 2- Intrahepatic cholestasis of pregnancy. 3- HELLP syndrome. 4 Acute fatty liver of pregnancy II. Coincidental to pregnancy 1- Viral hepatitis. 2- Gallstone disease. 3- Congenital disorders of bilirubin metabolism. 4- Autoimmune hepatitis. 5- Drug induced: Isoniazid phenothiazine. 6- Hemolytic jaundice. 7- Cirrhosis. 8-Neoplasia.
- 9. What is the most common cause of jaundice in the pregnant patient? Hepatitis 40%
- 10. What laboratory values in this case? - s.ALT & AST: Moderately elevated. - P.T & PTT: Prolonged. - Fibrinogen: Decreased. - Glucose: Decreased. - Bilirubin: Elevated. - Platelets: Mildly decreased=100,000/mm3
- 11. What is the diagnosis in this case? Acute fatty liver of pregnancy (AFLP)
- 12. What are the clinical features observed in AFLP? AFLP incidence= 1/10,000 Occurs in 3rd trimester. Associated with: 1- maternal obesity 2- male fetus(3 times more common) 3- multiple pregnancy o Considerable overlap with HELLP syndrome. o AFLP may be a variant of PE symptoms and signs. o Nausea, anorexia and malaise. o Severe vomiting and abdominal pain. o Jaundice within 2 weeks of onset symptoms. o Ascites. o Signs and symptoms of liver failure. o Hepatic encephalopathy. o DIC and renal failure. o Hypertension and proteinuria in 50% of cases. o Extreme polydipsia or pseudodiabetes. o Rarely may present after delivery.
- 13. What are the pathogenesis of AFLP? - Long-chain 3-OH-acyl CoA fatty acid is secreted from the placenta or the fetus. - The metabolites of this fatty acid is toxic to the liver of the mother. - The enzyme long chain-3-hyroxy acyl coenzyme A(CoA) is important mitochondrial beta oxidation of fatty acids to non toxic metabolites and its deficiency is the cause of AFLP in the mother and can cause cardiomyopathy and progressive neuromyopathy and hypoglycemia in the neonates, so it is important to exclude LCHAD in both mother and infant.
- 14. What are the lab abnormalities seen in both HELLP syndrome and AFLP? AFLP - Hypoglycemia - Slight elevation of transaminases - Elevated bilirubin - Increase Ammonia - WBCs = 20,000- 30,000 HELLP - Increase in transaminase - Increase in bilirubin - Hemolysis in peripheral blood smear - Increase LDH level - Decrease platelets count
- 15. What are the complications of AFLP? I. Maternal: - Fulminant hepatic failure - Hepatic encephalopathy - Coagulopathy - Death 10-15% II. Fetal complications: - IUFD - Perinatal mortality rate 15%-65% - Neonatal risks include: 1) Derangement in LFTs 2) Hypoglycemia 3) Cardiomyopathy 4) Progressive neuromyopathy
- 16. What is the treatment of AFLP? 1) Maternal resuscitation and stabilization 2) Fetal monitoring 3) Urgent delivery 4) ICU 5) Vaginal delivery probably better 6) Parenteral glucose 7) Neomycin and lactulose 8) Reversal of coagulopathy by: a) Packed red cells b) Cryoprecipitate c)FFP (Fresh Frozen Plasma) d)Platelets 9) Careful monitoring of fluid status and renal functions. 10) Postnatal managements: - If abnormal LTTs persist beyond 6 weeks consider alternative pathologies - Recurrence is 20% in subsequent pregnancy
- 17. Thank You