Presented by: Ahmad mukhtar MD.,M.B.B.Ch., M.Sc Obstetrics and GynecologyConsultant and Lecturer of Obstetrics and Gynecology, Faculty of MEDICINE, Zagazig University.

1. Jaundice in
Pregnancy
Presented by:
Ahmad mukhtar
MD.,M.B.B.Ch., M.Sc Obstetrics and
Gynecology., Consultant and Lecturer of
Obstetrics and Gynecology, Faculty of
MEDICINE, Zagazig University.

2.  Incidence: This occurs in about 1 in 1,000
pregnancies and is most common due to viral
hepatitis.
 Etiology: Classification is traditionally into the
following categories: Hemolytic, Hepatocellular,
and Obstruction.
 Causes may be consequential to, or independent
of, the pregnancy

3. Jaundice in pregnancy:
 Hemolytic:
- Incompatible blood transfusion
- Cl. Perfringens, E. coli/septicemia
 Hepatocellular:
- Viral hepatitis
- Severe preeclampsia
- Acute fatty liver of pregnancy
- Alcohol and drugs (e.g. halothane)
- Autoimmune chronic active hepatitis

4. Cont. of jaundice in pregnancy
 Obstructive:
- Cholestasis of pregnancy
- Cholelithiasis
- Drugs (e.g. Chlorpromazine)
- Primary biliary cirrhosis
- Pancreatic carcinoma

5. Diagnosis:
 Careful history and examination
 Biochemical test
 Ultrasound
Biochemical test will help to differentiate between
hepatocellular damage and obstruction:
- Hepatocellular: predominantly unconjugated
bilirubin and hepatocellular enzymes (aspartate
transaminase or alanine transaminase)
- Cholestasis (intrahepatic or extrahepatic):
predominantly conjugated bilirubin and alkaline
phosphatase

6. Cholestasis eof prgnancy:-
 Pathogenesis: is due to an estrogen sensitivity
effect and exhibits a familial tendency. It is
frequently recurrent in successive pregnancies or
if the women is prescribed oral contraceptives.
 Clinical features: mild jaundice, malaise, and
itching of the skin.
Liver function tests (alkaline phosphatase, urine
urobilinogen) suggest biliary obstruction, cholic
acid levels are typically elevated .
Serum bilirubin is rarely more than 85 mmol/L

7.  Effect of Cholestasis on pregnancy:
 Postpartum hemorrhage (reduced vitamin K
absorption)
 Premature labour (30%)
 Stillbirth.
 Management: Other causes of jaundice should be
excluded, USG and CTG (fetal well-being),
cholestyramine resin is effective for pruritus,
Induction of labour is indicated at 37-38 weeks or
earlier if there is fetal compromise.
The condition resolves rapidly after pregnancy.

8. Acute fatty liver of pregnancy:-
 Is unique to pregnancy
 More common in primigravidas
 frequently complicates the third trimester and is
commonly associated (or complicated ) with
preeclampsia (50 to 100 percent). Incidence : 1/7000
-11,000
 Age, (mean, range) 26 (16-39)
 Primiparous (%): 67 Male baby (%) :60
 Onset week of pregnancy :33% (28-38)
 Mortality (%): ( Maternal )18% - ( Fetal) 47%

9. Acute fatty liver of pregnancy:-
 The etiology is not known precisely. It may
follow intravenous tetracycline administration
or prolonged vomitingA genetic component has
been suggested
 Recent research suggests that AFLP is
associated with a Glu474Gln mutation in the
long-chain 3-hydroxy acyl-coenzyme A
dehydrogenase (LCHAD), a fatty acid β
oxidation enzyme.

10. CLINICAL PRESENTATION
Vomiting 80
Abdominal pain 52
Jaundice 93
Encephalopathy 87
Polydipsia 80
Pruritus 60
Ascitis 47
Symptoms/
Signs %

11. LABORATORY FEATURES
 Liver test abnormalities
 conjugated hyperbilirubinemia (usually
between 5 and 15 mg/dL)
 increased alkaline phosphatase (normal <170)
 and modest increases in serum
aminotransferases normal <50 (usually<1000
IU/L)
 Leukocytosis occurs commonly
 thrombocytopenia
 decreased clotting factors
 Hypoglycemia and renal dysfunction

12. Management of AFL:
 Intensive Unit Care
 Adequate intravenous fluids
 Albumin, glucose and vitamin K
 Correction of coagulation defects
 The pregnancy should be terminated, usually
by CS.

13. Fate & complicationsFate & complications

14. Fate & complications
Usually
By 2 - 3 days
postpartum
liver enzymes
& encephalopathy
improve
Sometimes
laboratory abnormalities
persist after delivery
& may initially worsen during
first postpartum week
Rarely
patients progress to fulminant hepatic failure
with need for liver transplantation.
Most patients improve in 1 to 4 weeks postpart

15. HELLP syndrome

16. HELLP syndrome
 Severe preeclampsia is complicated in 2-12% ofSevere preeclampsia is complicated in 2-12% of
cases (0.2-0.6% of all pregnancies) by hemolysiscases (0.2-0.6% of all pregnancies) by hemolysis
(H), elevated liver tests (EL), and low platelet count(H), elevated liver tests (EL), and low platelet count
(LP), fibrin deposition the HELLP syndrome.(LP), fibrin deposition the HELLP syndrome.
 EtiologyEtiology:: microangiopathic hemolytic anemiamicroangiopathic hemolytic anemia ++
vascular endothelial injury in blood vesselsvascular endothelial injury in blood vessels ++
platelet activation & consumption, small to diffuseplatelet activation & consumption, small to diffuse
areas of hemorrhage and necrosis large hematomasareas of hemorrhage and necrosis large hematomas
++ capsular tearscapsular tears ++ intraperitoneal bleedingintraperitoneal bleeding..

17. Clinical Picture:Clinical Picture:
Most patientsMost patients
Less commonlyLess commonly
upper abd. painupper abd. pain
& tenderness& tenderness
NauseaNausea
vomitingvomiting
MalaiseMalaise
headacheheadache
EdemaEdema
weight gainweight gain
jaundicejaundice
uncommon (5%)uncommon (5%)
HypertensionHypertension
proteinuriaproteinuria
renal failurerenal failure
+ uric acid+ uric acid
DIDI
AntiphospholipidAntiphospholipid
syndromesyndrome
some patients havesome patients have no obviousno obvious preeclampsiapreeclampsia

18. •DiagnosisDiagnosis requires the presencerequires the presence of all 3 laboratoryof all 3 laboratory
criteria:criteria:
Based on platelet count, may be:
•severe/ Class 1 (platelets 50,000),
•moderate/Class 2 (50 –99,000),
•mild/Class 3 (100 –150,000).
Lately, DIC, pulmonary edema, placental
abruption, and retinal detachment may be present.
H ……………………H ……………………
HemolysisHemolysis
EL…………………EL…………………
Elevated Liver TestsElevated Liver Tests
LP……………LP……………
Low PlateletsLow Platelets
LDH>600 U/LLDH>600 U/L
↑↑ indirect bilirubinindirect bilirubin
AST> 70U/LAST> 70U/L <150,000<150,000

19. Severe Preeclampsia (including
HELLP syndrome)
 May be part of the spectrum of Acute fatty liver
 Has a predisposition for late pregnancy and
primigravidas
 Widespread endothelial cell damage resulting in
hemolysis and thrombocytopenia
 The women needs to be stabilized and delivered
regardless of gestational age
 There are some reports of a beneficial effect of
coticosteroids.

20. CT abdomen of a woman with severe HELLP syndrome (39 weeks). A
large subcapsular hematoma extends over the Lt lobe; Rt lobe has
heterogeneous, hypodense appearance due to widespread necrosis, with
“sparing” of the areas of lt lobe (compare perfusion with the normal
spleen).

21.  TreatmentTreatment
 Hospitalization & ICU careHospitalization & ICU care for:for:
o antepartum stabilization of BP and DIC,antepartum stabilization of BP and DIC,
o seizure prophylaxis,seizure prophylaxis,
o fetal monitoringfetal monitoring..
pregnancy is > 34 wk
gestational age
24-34 wk
immediate induction
corticosteroids for 48 h
(fetal lung maturity)
delivery
The only definitive treatment is deliveryThe only definitive treatment is delivery

22. After deliveryAfter delivery continue close monitoring of the mothercontinue close monitoring of the mother
Up to 48 h
postpartum
worsening thrombocytopeniaworsening thrombocytopenia
& increasing LDH levels& increasing LDH levels
Most lab. values normalizeMost lab. values normalize
After 48 h
persistent or worseningpersistent or worsening
lab. Abnormalitieslab. Abnormalities
by 4by 4thth
postpartum daypostpartum day
PostpartumPostpartum
complicationscomplications
May
be
normalization of plateletsnormalization of platelets
55
daysdays
RARELY

23.  ReportedReported maternal mortalitymaternal mortality isis 1%1%
 Perinatal mortalityPerinatal mortality rate ranges fromrate ranges from 7%-22%7%-22% and may beand may be
due to:due to:
 premature detachment of placenta,premature detachment of placenta,
 intrauterine asphyxia,intrauterine asphyxia,
 prematurity.prematurity.
 Other complicationsOther complications::
• abruptio placentaeabruptio placentae
• DICDIC
• ARFARF
• ARDSARDS
•pulmonary edemapulmonary edema
•strokestroke
•liver failureliver failure
•hepatic infarctionhepatic infarction

24. HOW TOHOW TO
DIFFERENTIATEDIFFERENTIATE

25. HELLPHELLP AFLPAFLP
%%PregnanciesPregnancies 0.2%0.2%––0.6%0.6% 0.005%0.005%––0.01%0.01%
Onset/trimesterOnset/trimester 33or postpartumor postpartum 33or postpartumor postpartum
Family historyFamily history NoNo OccasionallyOccasionally
Presence ofPresence of
preeclampsiapreeclampsia
YesYes 50%50%
Typical clinicalTypical clinical
featuresfeatures
Hemolysis (anemiaHemolysis (anemia((
ThrombocytopeniaThrombocytopenia
(50,000 often(50,000 often((
Liver failure withLiver failure with
coagulopathy,coagulopathy,
encephalopathyencephalopathy
hypoglycemia,hypoglycemia,
DICDIC
Aminotransfer-Aminotransfer-
asesases
MildMild, but may be up, but may be up
to 10-20-fold riseto 10-20-fold rise
300-500300-500typicaltypical
but variablebut variable

26. HELLPHELLP AFLPAFLP
BilirubinBilirubin >>55mg/dL unlessmg/dL unless
massive necrosismassive necrosis
oftenoften >5>5 mg/dL, higher ifmg/dL, higher if
severesevere
HepaticHepatic
imagingimaging
Hepatic infarctsHepatic infarcts
Hematomas,Hematomas,
rupturerupture
Fatty infiltrationFatty infiltration
HistologyHistology Patchy/extensivePatchy/extensive
necrosis, periportalnecrosis, periportal
hge, fibrin depositshge, fibrin deposits
Microvesicular fat in zone 3Microvesicular fat in zone 3
MaternalMaternal
mortalitymortality
1%1%––25%25% 7%7%––18%18%
Fetal/perinatalFetal/perinatal
mortalitymortality
11%11% 9%9%––23%23%
Recurrence inRecurrence in
subsequentsubsequent
PregnanciesPregnancies
4%4%––19%19% sfatty acid oxidation defectsfatty acid oxidation defect
25%25%
No fatty acid oxidation defectNo fatty acid oxidation defect
rarerare