A slideshow regarding jaundice in pregnancy.

1. Jaundice in Pregnancy
BY,
AHMAD ALI KHAN
ROLL NO.183

2. Learning Objectives
 Define Jaundice
 Learn all causes of jaundice in a pregnant woman
 How to treat jaundice women with pregnancy

3. Case Scenario
 Question:
You are called to the Emergency Department to review a nulliparous 28 year old
woman. She is currently 35 weeks pregnant, and has presented with 72 hours of
nausea and vomiting accompanied by epigastric and right upper quadrant
pain. On examination she was jaundiced, confused and had a blood pressure of
120/70. List three likely diagnosis.

4. Definition of Jaundice
 Jaundice is the clinical manifestation of raised bilirubin levels in blood, that is,
yellow staining of the skin and sclera (the whites of the eyes). The yellowing
extends to other tissues and body fluids
 It is detected clinically at bilirubin levels of 2 mg/dl.
(Normal being 0.2 – 0.8 mg/dl )

5. Bilirubin Cycle

7. Intrahepatic Cholestasis of
Pregnancy

8. Intrahepatic Cholestasis of Pregnancy
 It is also known as Recurrent Jaundice of Pregnancy,
Cholestatic Jaundice of Pregnancy, Jaundice of late
Pregnancy, and Hepatosis of Pregnancy.
 It is a form of intrahepatic cholestasis associated with
pruritus, elevated serum bile acid levels and the findings of
bland cholestasis on liver biopsy.
 Epidemiology: It occurs in 1.5 - 2% of pregnancies.

9. Pathogenesis
 Its etiology is unknown.
 Genetically predisposed women
 Low plasma selenium levels
 Enhanced sensitivity to Estrogen
 A variation in metabolism of Progesterone (diminished secretions of sulfated
progesterone metabolites)
 Molecular mechanism show many gene mutations that control hepatocellular
transport systems.

10. Clinical Findings
 Pruritus
1)Dominant and the main symptom
2)More in the 3rd Trimester
3)usually includes the trunks and the extremities especially the palms and soles
of the feet.
4)Disappears 24 – 48 hours post-partum
 Mild Jaundice
1) Only 10 – 25% of patients develop it
 Malaise and insomnia
 Dark Urine, Anorexia, Steatorrhea

11. Laboratory Findings
 Raised Bile Acids
 Moderate Elevation in ALT
 Raised alkaline phosphatase
 Raised Bilirubin
 Raised GGt

12. Effects on the Mother
 Improvements of symptoms and laboratory test results begins with the delivery
of the fetus and is usually prompt and complete.
 There is no residual hepatic defect after resolution of the disorder
MATERNAL RISKS
 Increased risk for post-partum hemorrhage
 Vitamin K deficiency
 Increased risk for development of gallstones, cholecystitis and pancreatitis

13. Fetal Risks
 Increased risk for intrauterine fetal death
 Spontaneous Preterm delivery
 Intrapartum Fetal Distress
 Neonatal Respiratory Distress
 Meconium Aspiration

14. Management
 The treatment is mainly palliative
 Antihistamines and Topical emollients
 Ursodeoxycholic Acid 10 – 15 mg/kg/day
 Cholestyramine
1) These are bile acid binders
2) But they worsen steatorrhea resulting in fat soluble and vitamin K deficiency.
3) Side effects include Fetal Coagulopathy, intracranial hemorrhage, and still birth.
 S-Adenosyl-1-methionine
1) Significantly improves pruritus and serum transaminase and bile levels, perhaps, by
reducing the negative effects of estrogen on bile secretion.
 Women are counselled to avoid combines Oral Contraceptive pills.

15. Pre-Eclampsia

16. Pre - Eclampsia
 It is a form of pregnancy related hypertension that is
associated with damage and dysfunction of one or more
maternal organs, possibly including liver that may produce
severe, life threatening complications and may affect
pregnancy outcome.

17. HELLP Syndrome

18. HELLP Syndrome
 H – Hemolysis
EL – Elevated Liver Enzymes
LP – Low platelet counts
 It is a multisystem disease characterized by
1) Microangiopathic Hemolytic Anemias
2) Hepatic Dysfunction
3) Thrombocytopenia ( platelet count less than <100,000/ mm3 )
4) syndrome’s severe form is DIC.
 Incidence : 10 – 20 % of Pre-eclampsia patients

19. Clinical Findings
 90% of the patients present with malaise
 Epigastric pain
 Nausea
 Vomiting
 Headache

20. Management
 First of all, assessment and stabilization of the woman’s condition especially
coagulation dysfunction
 Fluid management
 Control of Hypertension
 Prevention of Seizures
 Platelet Transfusion
 Evaluation of fetal well – being
 Decision about delivery

21. Complications
 Placental Abruption
 Disseminated Intravascular Coagulation (DIC)
 Retinal Detachment
 Acute Renal Failure
 Pulmonary Oedema
If not treated in timely manner, the mother can become critically ill or die due to
liver rupture and hemorrhage.

22. Acute Fatty Liver of
Pregnancy

23. Acute Fatty Liver Disease
 It is a rare occurrence in pregnancy. It is a form of micro vesicular fatty liver
disease unique to human gestation that presents late in pregnancy often as
fulminant hepatic failure with sudden onset of coagulopathy and encephalopathy
in a woman without a prior history of liver disease.
 Incidence: 1 in 10,000 pregnancies.
 It is associated with
1) Maternal Obesity
2) Male Fetus (3 times more common)
3) Multiple Pregnancy
 It is has a considerable overlap with Pre – Eclampsia

24. Clinical Features
 Nausea, Vomiting
 Malaise and Fatigue
 Abdominal Pain. Features of jaundice within 2 weeks of onset of symptoms
 Increased thirst, headaches, pruritus and altered mental status
 DIC and Renal Failure
 Hypertension and Proteinuria
 Extreme polydipsia and pseudo – diabetes.

25. Laboratory Findings
 Raised Transaminases and Alkaline Phosphatase
 Hypoglycemia
 Hyperuricemia
 USG, MRI, CT. They may show evidence of fat infiltration
 Gold Standard is Liver Biopsy. The histological hallmark is micro vesicular fatty
infiltration of the liver that is most prominent in hepatocytes surrounding the
central veins and spares those surrounding portal areas.

26. Complications
 Maternal Risks:
1) Fulminant hepatic failure
2) Hepatic Encephalopathy
3) Coagulopathy
4) Death
 Fetal Risks:
1) Intrauterine fetal death
2) Neonatal risks include transient derangement of LFT’s and hypoglycemia

27. Management
 Early Diagnosis, Prompt Delivery and supportive care are the cornerstones in the
management
 Maternal resuscitation and stabilization
 Fetal Monitoring
 Urgent Delivery ( Vaginal delivery probably better)
 Admit to Intensive Care Unit
 Parenteral Glucose
 Neomycin and Lactulose
 Multivitamin Supplementation
 In fulminant hepatic failure, liver transplant is the only option

28. Hyperemesis Gravidarum

29. Hyperemesis Gravidarum
 It occurs mainly in the first trimester. It is the onset of severe or protracted
vomiting causing fluid and electrolyte imbalance.
 The patient usually loses 3 kg of weight
 Incidence: 0.5 – 1% of all pregnancies

30. Investigations
 Raised Hematocrit and White cell count.
 Hyponatremia, hypokalemia, hypochloraemic metabolic alkalosis.
 Serum Urea is low
 Elevated Urea : Creatinine ratio. It is an indicator of dehydration
 Liver Function Test serves as a mark of severity
 Biochemical Thyrotoxicosis
 Urine Analysis show Ketonuria
 Pelvic Scan to confirm a viable single pregnancy

31. Complications
 Maternal Risks:
1) Anemia and peripheral neuropathy
2)Wernicke’s Encephalopathy
3) Malloy – Weiss Tear
4) Catabolic State
5) Hyponatremia
 Fetal Risks:
1) No increase in congenital abnormalities
2) Lowe Birth Weights
3) Risk of fetal death ( 40% )

32. Management
 First and foremost rehydrate the patient with normal saline or Hartmann’s Solution
 Regular Urine Analysis to monitor ketonuria
 Anti – emetics
1) Ondansetron
2) Intravenous hydrocortisone in severe cases
 Vitamin Supplements
 Anti – gastroesophageal reflux measures:
1) Elevation of head of bed
2) Small frequent bland meals
3) H2 receptor antagonists
 Psychological Support and Reassurance
 Termination of pregnancy in intractable cases

33. Viral Hepatitis

34. Hepatitis A
 The management and the prognosis is same as that of a
non-pregnant woman.
 Post exposure immunoprophylaxis may not prevent viral
shedding
 The potentially infected individuals should be isolated

35. Hepatitis B
 This is much importance owing to the fact that this virus spreads predominantly
through vertical transmission.
 Prognosis:
1) Complete resolution of 90% of cases within 6 months
2) Remaining 10% becomes chronic carriers.
 Diagnosis:
1) Through detection of viral specific antigens and antibodies
2) HbsAg indicates infectivity
 Majority of the infants are infected at the time of the birth and thus, antenatal
detection of HbsAg mandates preventive program of active and passive
immunization at birth.

36. Hepatitis C
 It is an even more higher risk of vertical transmission if the mother is positive for
both HCV RNA and anti- HCV antibodies.
 Currently, there are no vaccines for HCV infections

37. Hepatitis E
 Obstetric Significance: Predilection to pregnancy for unknown reasons.
 In 61% of the cases, it results in fulminant hepatic failure.
 Infection in the 3rd trimester of pregnancy is associated with increased maternal
mortality
 No immunoprophylaxis available

38. Anti viral Therapy
 It is based on the severity of the disease, hepatic activity and fibrosis
 Interferon therapy is contraindicated in pregnancy.
 Oral Agents:
1) Telbivudine Tenofovir are pregnancy category B drugs and are preferred.
2) Lamivudine is category C drug but it is thought to be associated with a low
risks of complications
3) There is insufficient data for other drugs.

39. Autoimmune Hepatitis

40. Autoimmune Hepatitis
 Women with autoimmune hepatitis can get pregnant and can still carry a
successful pregnancy
 The coarse of the disease is unpredictable
 Although spontaneous remission may occur, maternal death and exacerbation
during pregnancy and after delivery have been reported.

41. Treatment
 Corticosteroids are the treatment of choice and appear to be safe in pregnancy.
 They seem to induce rapid remission of autoimmune hepatitis.
 Azathioprine:
1) FDA category D

42. Hope you learned a lot.
Have a nice day
Thank you