Jaundice in pregnancy can be due to either 1)Diseases related to pregnancy Hyperemesis gravidarum Intrahepatic cholestasis in pregnancy Acute fatty liver in pregnancy HELLP syndrome 2)Diseases coincident with pregnancy Hepatitis Fulminant hepatic failure Liver cirrhosis
Normal liver changes during pregnancy
1)Diseases related to pregnancy: Hyperemesis gravidarum Is defined by persistent vomiting, associated with loss of 5% or more of pre-pregnancy body weight, dehydration, and ketosis. Hyperemesis gravidarum is uncommon (0.3–2% of pregnancies), occurs early in the first trimester, and typically resolves by 20 weeks gestation. Although women with hyperemesis gravidarum have; Increased rates of low birth weight babies, and preterm birth Risk factors ; include molar pregnancy, multiple pregnancies, previous history of same condition, and fetal abnormalities (triploid, trisomy 21, and hydropsfetalis). Liver test abnormalities are common , and resolve when the vomiting stops. In all, 50-60% of hospitalized women with hyperemesis gravid rum will have a mild elevation in aminotransferase levels, Jaundice and hepatic synthetic dysfunction are uncommon .
All patients with severe or intractable vomiting and/or with ketonuria need to be admitted. The principles of management of severe vomiting in pregnancy are given as follows: • Immediate correction of dehydration ( hypovolaemia ), and electrolyte and metabolic derangements Medications to stop further vomiting •• Metoclopramide 10 mg (IV/IM/oral) 8-hourly—patient needs to be counselled regarding extra-pyramidal side effects. • Pyridoxine (vitamin B 6 ) 10 mg—may help to reduce severe nausea. Antacids (ranitidine 50 mg). Thiamine 50 mg In intractable vomiting, the following drugs may be administered: • Ondansetron 4 mg (IV/oral)—not licensed in pregnancy • Methyl prednisolone . Specific management of the aetiology —may require a ‘multidisciplinary’ approach • Counselling and improving the psychological well-being.
Intrahepatic cholestasis of pregnancy Occurs in incidence about 0.3-5.6% and it is the most common liver disease in Pregnancy. Risk factors : Advanced maternal age History of cholestasis secondary to oral contraceptives. personal or family history of same condition. Some studies suggest a higher prevalence in patients with hepatitis C, cholelithiasis, and non alcoholic fatty liver disease. Evaluation for alternative etiologies should be done if cholestasis fails to resolve after delivery.
Clinical features: persistent pruritus, typically involving the palms and soles as well as the rest of the body and resolves with delivery. Jaundice occurs in <25% , always after the onset of pruritus. Fat malabsorption can result in fat-soluble vitamin deficiencies requiring Supplementation. Maternal outcomes are excellent, however, there is a risk of fetal distress, preterm labor, prematurity , and intrauterine death. Early delivery at 37 weeks is encouraged, because intrauterine death is more common in the last month of pregnancy and few deaths occur before 37 weeks.
Investigation: 1)Increased bile salts Bile acid concentrations are typically >10 μ mol /l with increased cholic and chenodeoxycholic acid levels. Bile acid levels also correlate with fetal distress. Most complications occur when bile acid levels exceed 40 μ mol /l 2)Increased bilirubin level 3)Liver enzymes Aminotransferase levels may also be elevated, reaching values >1,000 U/l . 4)Ultrasonography should be performed to exclude cholelithiasis .
Treatment Ursodeoxycolic acid 10-15 mg /kg woman weight. Antihistamines Emollient Vitamin k supplementation to woman after 36 week and to the neonate after delivery in a dose of 0.1 mg I.M. Serial liver function monitoring Delivery at 37 weeks of gestational age.
Preeclampsia and eclampsia Preeclampsia is characterized by new onset hypertension (systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mm Hg) and proteinuria (≥300 mg/24 h) after 20 weeks of gestation. Eclampsia is present when grand mal seizures occur. Hepatic involvement can present with epigastric or right upper quadrant pain, likely From hepatomegaly stretching Glisson’s capsule. Liver injury results as a consequence of vasoconstriction & fibrin precipitation in the liver. Complications can include hematoma below Glisson’s capsule and hepatic rupture .
Asparate aminotransferase(AST) and alanine transaminase (ALT) elevations can be prominent. The magnitude of the liver chemistry abnormalities parallels the risk of adverse maternal but not fetal outcomes. Liver tests cannot exclusively be used to gauge clinical decisions, as the presence of normal liver enzymes does not exclude disease. Delivery is the only curative treatment and after 36–37 weeks, there is no advantage in continuing the pregnancy.
HELLP syndrome HELLP syndrome is characterized by hemolytic anemia, increased liver enzymes, and low platelets. HELLP affects a minority of pregnancies but complicates up to 20% of cases of sever PET, although HELLP typically presents between 28 and 36 weeks of gestation,30% manifest symptoms in the first week postpartum. Risk factors include advanced maternal age, nulliparous. The diagnosis of HELLP is most often made through recognition of typical laboratory results.
Sign of hemolytic anemia and thrombocytopenia with platelets <100,000 cells/μ l, elevations in AST, ALT, serum bilirubin, and lactate dehydrogenase are expected. There are no pathognomonic clinical signs and some women with HELLP may be asymptomatic. Right upper quadrant &epigastric pain, nausea, vomiting, malaise, headache , edema, and weight gain are common complaints. Hypertension and proteinuria should be expected, occurring in up to 80% of cases. Jaundice is rare, occurring in only 5% of patients.
Maternal consequences can be sever with mortality rates of 1–3% . Progression can also be rapid but laboratory values typically begin to normalize 48 hour post partum. Fetal prognosis is most strongly linked to gestational age at delivery and birth weight. Hepatic consequences include hepatic infarction, sub capsular hematomas, and intra parenchymal hemorrhage. Hepatic infarction should be suspected with right upper quadrant pain with fever, whereas abdominal swelling or shock presentation can occur with hepatic rupture.
Management • Blood pressure control • Termination of pregnancy • Glucose supplementation • Platelet transfusion . • Glucocorticoid is of no evidence for benefit. • Surgery indicated only in unstable patient with hepatic hematoma or rupture capsule.
Acute fatty liver disease of pregnancy Is a rare, life-threatening condition characterized by micro vesicular fatty infiltration of the liver ( due to deficiency of long chain 3 hydroxyacyl CoA dehydrogenase LCHAD enzyme) , leading to hepatic failure. The median gestation age at the time of identification is 36 weeks. Risk factors; include twin pregnancies and low body mass index , male sex pregnancy ,and previous history of same condition. Maternal mortality rate reach 12.5-18%, and neonatal mortality reach 50%. Clinical features: Presenting symptoms are non-specific: nausea, vomiting, and abdominal pain. Concomitant preeclampsia is present in roughly one half of the affected women. Hepatic failure can manifest with signs of hepatic dysfunction such as encephalopathy, coagulopathy, and hypoglycemia. Renal dysfunction and pancreatitis are common.
Treatment Early recognition, prompt delivery, and supportive care are essential to optimize maternal and fetal prognosis including correction of hypoglycemia ,coagulopathy and electrolyte disturbance, as the postpartum clinical course is dependent on the interval between symptoms and termination of the pregnancy. If hepatic function does not rapidly improve, evaluation for liver transplantation offers the patient the best chance for survival.
2) Disorders coincident to pregnancy : viral hepatitis Clinical features of viral hepatitis in pregnancy Signs and symptoms , complications identical in pregnant and non-pregnant female . H A : abrupt onset . H B , C , D: prolonged onset . Nausea , vomiting , abdominal pain appear before jaundice , anorexia , malaise , fever , dark urine, hepatomegaly.
Investigations : Increase serum transaminase with or without total serum bilirubin. Increase in serum alanine transaminase indicates acute hepatic injury. Anti-hepatitis A and E IgM. Moderate increase alkaline phosphatase . Leukocyte count normal . Prolonged PT , Thrombocytopenia . Renal function test normal
Hepatitis B : 1. Its course is not altered by pregnancy . 2. Hepatitis B may lead to acute fulminant hepatic failure occasionally . 3. Preterm labour . 4. Feto -maternal transmission occur with Hepatitis B Routes of transmission : 1) Trans placental ( rare ) 2) Vertical transmission during delivery by contaminated amniotic fluid and birth canal secretion. 3) Through breast feeding . 4) Salivary contamination .
Prevention of neonatal infection of hepatitis B 1. Serological screening for all pregnancy ( routinely ) offered at their antenatal Booking visit for anti core-antibody if positive for first time the infections status of the patient should be achieved by serology and testing of the partner and testing for other sexually transmitted disease. 2. Intra partum fetal scalp electrodes and fetal blood sampling should be avoided and use of forceps rather than ventouse ( if needed ) . 3. Keep the membranes intact for as long as possible . 4. Administer hepatitis B Immunoglobulin to those neonates born to high-infectivity mother .
Hepatitis C : The same as B , But with : Screening for Hepatitis C is not offered routinely in the antenatal care . Breast feeding does not appear to risk of the mother to child transmission . Biliary disease in pregnancy Cholelithiasis ; the presences of stones in the gallbladder, is common in pregnancy owing to the increased estrogen levels, Causing cholesterol super saturation and increased gallstone formation. The incidence of cholelithiasis in pregnant women is 3.5% . Management *conservative *surgical in sever cases.