Jaundice in Pregnancy

M2 – FMBS
Dr DOHBIT SAMA
Prof MBOUDOU E. T.
Background knowledge
Bilirubin metabolism
Physiologic changes of pregnancy
Objectives
At the end of this lecture, the student should be
able to:
1. State six (06) main disease entities causing
jaundice in pregnancy
2. Make an etiological diagnosis of the common
causes
3. Manage viral hepatitis in pregnancy
4. Treat and follow up cases of jaundice in
pregnancy
Plan
1. Main causes
2. For each etiology:
1. Diagnosis
2. Treatment
3. Prognosis

Conclusion
Main causes
They include: (Pre Intra and post Hepatic)
1. Haemolytic anaemia
2. Acute fatty liver
3. HELLP syndrome
4. Viral hepatitis
5. Cholestatic jaundice
6. Cholecystitis
7. Acute pancreatitis
1. Haemolytic anaemia
Occurs at any stage of pregnancy
The causes are varied;
Drugs induced, like anaesthetic drugs,
Incompatible blood    transfusion,
Hemoglobinopathies: sickle cell, Thalassemia
Parasitic infections like plasmodium spp.
Cases present with anaemia and jaundice.
The prognosis is good if proper diagnosis and
treatment of the underlying cause is done.
2. Acute fatty liver
Very rare and deadly condition of the 3rd
trimester, 1 in 13,000 and no increased risk of
recurrence
Occurs in the last quarter of pregnancy
Related to protein malnutrition, Eclampsia &
pre- eclampsia.
Early recognition and TOP (delivery) and
extensive supportive therapy will reduce
mortality from 80 to 20%.
Acute fatty liver 2
Possible association between fetal recessive
inheritance of long-chain 3-
hydroxyacetylCoA dehydrogenase deficiency
That is a recessively inherited mitochondrial
abnormalities of fatty acid oxidation
Patients often present with severe nausea and
vomiting late in pregnancy, associated with
abdominal (epigastric) pain, jaundice and
haematemesis.
Acute fatty liver 3
Laboratory investigation shows:
Elevated LDH, ASAT, ALAT, bilirubin, and
prolonged prothrombin time.
Glucose, platelets, cholesterol, triglycerides,
and fibrinogen are notably decreased.
Liver biopsy reveals microvesicular hepatic
steatosis and mitochondrial disruption on
electron microscopy.
Acute fatty liver 4
Complications such as:
Acute renal failure,
DIC,
Encephalopathy, and
Sepsis can be severe
Very poor prognosis, with maternal mortality
up to 80%.
Consider TOP whenever the diagnosis is
made considering its very poor prognosis
3. HELLP Syndrome
Stands for: Hemolysis, Elevated Liver
Enzymes (dysfunction), and low Platelets
Typically occurs with severe preeclampsia
and eclampsia
Occurs in the last trimester of pregnancy
Characterized by vomiting, upper quadrant
pain and progressive nausea.
Liver function deteriorates rapidly, and
delivery is essential in treatment
HELLP Syndrome 2
Stillbirth is frequent (10 – 15%), with a high
neonatal loss (20 – 25%), usually due to
prematurity
Corticosteroids and dexamethasone 10mg twice
daily have been used to help resolve the HELLP
syndrome
Terminate the pregnancy as soon as it is
diagnosed !
The prognosis highly depends on the early
diagnosis
4. Viral hepatitis
Occurs at any age of pregnancy
Complicates 0.2% of all pregnancies
Hepatitis may be caused by numerous viruses,
drugs, or toxic chemicals.
The clinical manifestation of all forms are
similar
Viral agents causing hepatitis in pregnancy are
hepatitis A virus, B, C (non-A, non-B virus), E,
G,EBV, and Delta agent.
Viral hepatitis 2
Patients will present with:
- malaise, anorexia,
- nausea and vomiting,
- pyrexia,
- upper abdominal pain,
- myalgia, fatigue,
- low grade fever and
- hepatomegaly and splenomegaly.
Viral hepatitis 3
WBC count depressed, mild proteinuria
ASAT, ALAT, bilirubin and alkaline
phosphatase are usually elevated
Clotting profile: TP and partial thromboplastin
time are prolonged with severe liver
involvement
The cases are handled accordingly.
The immediate prognosis is good, but poor in
situations of malnutrition.
Viral hepatitis 4
Diagnosis made using serologic markers:
- anti-HA IgM, HBsAg, HC PCR, antiHBc
IgM, HD PCR, anti-HE IgM, and anti-HG
IgM.
Liver biopsy shows extensive hepatocellular
injury and inflammatory infiltrate
Differential diagnosis: A, B, C, and delta;
EBV; CMV; cholestasis; PET; acute fatty
liver; TORCH; 2 syphilis; autoimmune;
toxic or drug induced hepatitis; bile duct
Viral hepatitis 5
Treatment: bed rest ++, IV hydration and
supportive measures
- avoid hepatotoxic drugs
- Gamma globulin prophylaxis for exposure to
hepatitis A or non-A, non-B
- Inactivated virus A vaccine available
- Hepatitis B immunoglobulin to those exposed
- Hepatitis B vaccine for those HBsAg negative
Viral hepatitis 6
Passive and active immunization of the
neonate is 85 – 95% effective Sero-
Vaccination
Breastfeeding not contraindicated when the
baby is immunized
Maternal course unaltered by viral hepatitis
but risk of premature delivery is increased
Severe liver disease will lead to infertility
Interferon improves prognosis for chronic
active hepatitis
Viral hepatitis A
May occur sporadically or in epidemics
Fecal-oral route of transmission
Excretion of virus in stool begins 2 weeks
to onset of symptoms and is complete 3
weeks following onset of clinical symptoms
No known carrier state.
Viral hepatitis A (2)
Both blood and stool are infectious during
the 2 to 6 week incubation period
Perinatal transmission does not occur
Belongs to the picornavirus group like the
poliomyelitis virus and coxsackievirus
Viral hepatitis B
DNA hepadnavirus, pleomorphic
Transmitted by inoculation of infected
blood or blood products, or sexual
intercourse.
5 to 10% infected persons become chronic
carriers
Incubation period 6 weeks to 6 months
Clinical features similar for A and B.
Fulminant hepatitis affects 1% of B
infections, rare with hepatitis A
Viral hepatitis B (2)
HBsAg is the marker measured in blood
Its persistence after the acute phase of
hepatitis is usually associated with clinical
and laboratory evidence of chronic hepatitis
The core antibody HBcAb is against the
27nm Dane particle. Particle only present in
overwhelming infections.
HBcAb occurs at onset of clinical illne ss
Viral hepatitis B (3)
HBeAg is a soluble non particulate Ag
Serves as an accurate indicator of viral replication
and infectivity.
Pregnant women in 3rd trimester positive for HBeAg
frequently transmit this infection to their foetuses (80
– 90%) in the absence of immunoprophylaxis.
Those who are negative rarely infect their foetuses.
DNA polymerase activity usually transient, occurring
with peak HBsAg positivity.
Its persistence usually suggests continued infectiv ity
Viral hepatitis C (Non-A, Non-B)
Up to 80% infected individuals become
chronic carriers.
Cause of 90% post transfusion hepatitis.
Incubation period 7 – 8 weeks
Course of infection similar to hepatitis B
Antibody present in 90% of patients, may
require PCR for its RNA in early infection
Vertical transmission 7 – 8% infected
pregnancies
Epstein-Barr Virus
Causes clinical picture of infectious
mononucleosis with hepatitis
Antibody titers like anti-EGNA, early
replication cycle (anti-EA), or late
replication cycle (anti-VCA) viral proteins
Other Viral Hepatitis
Delta agent: HDAg, HDAb are serologic
markers (with B)
E is transmitted through the fecal-oral route.
15% risk of fulminant hepatitis with a
mortality of 5%
G more like in patients with hepatitis B or
C. There is vertical transmission, no chronic
carrier state
5. Cholestatic jaundice of pregnancy
Usually occurs in the last quarter of pregnancy
Cause related to elevated levels of oestrogen and
progesterone.
Familial tendency.
Accumulation of bile acids in the liver with
subsequent accumulation in the plasma.
Causes pruritus and jaundice.
Similar to the cholestasis during COC therapy
Cholestatic jaundice of pregnancy 2
Ultrasound examination of gall bladder helps
rule out cholelithiasis
In the absences of hepatitis, the most likely
diagnosis is cholestasis associated with
pregnancy
Labo: ↑alkaline phosphatase, bilirubin, and
serum bile acids (chenodeoxycholic acid,
deoxycholic acid, and cholic acid), ASAT and
ALAT may be mildly elevated as well
Cholestatic jaundice of pregnancy 3
Symptomatic treatment of pruritus with
diphenhydramine.
Ursodeoxycholic acid 300mg twice daily
will inhibit absorption of toxic bile acids
and increase their biliary secretion.
This improves liver function and alleviates
pruritus.
Oral steroids have been used to relieve
symptoms.
Symptoms resolve postpartum
Cholestatic jaundice of pregnancy 4
Spontaneous resolution often takes place
but this condition recurs with pregnancy and
hormonal therapy.
There is slight increase in preterm births
and stillbirth from foetal toxicity by bile
acids.
Foetal monitoring with biophysical studies
6. Cholecystitis
Rare in pregnancy, 0.3% because the gall
bladder and biliary duct smooth muscles are
relaxed by progesterone
Occurs at all stages of pregnancy
Often caused by biliary obstruction.
Patients present with pain (hypochondrial),
vomiting, malaise and jaundice.
Surgical treatment is rarely required.
Cholecystitis 2
Acute inflammation is treated with IV fluids
and nasogastric suction.
If inflammation does not resolve or
pancreatitis develops, cholecystectomy
should be considered.
Surgery in 1st trimester increases foetal loss,
in 3rd trimester it will cause preterm labour
The prognosis is often good.
7. Acute pancreatitis
This condition is common in late pregnancy
Patients present with severe abdominal
pain, vomiting, hypotension, rapid pulse.
The diagnosis is very essential for
management, including TOP.
Ransom criteria for healing
The prognosis is not good, with a high
mortality of 20%.
Conclusion
Jaundice in pregnancy can have very varied
causes
Most of the disease conditions have very
favourable outcome
Acute fatty liver and acute pancreatitis
constitute the most deadly conditions
Early diagnosis with adequate management
are essential for survival
Thank you

Merci