2. 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
4. 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.
5. 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
B6 ) 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.
6. 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.
7. 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.
8. 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.
9. 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.
10. 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.
11. 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.
12. 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.
13. 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.
14. 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.
15. 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.
16. 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.
17.
18. 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.
19. 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.
20. 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
21. 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 .
22. 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 .
23. 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.
