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 doesn’t change during
pregnancy.
- The size of the liver doesn’t 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 don’t 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%
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 LFT’s
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 LTT’s persist beyond 6 weeks consider
alternative pathologies
- Recurrence is 20% in subsequent pregnancy
