PREGNANCY
&
LIVER DISEASES
Dr Abdullah Ansari
MBBS, MD Medicine
Aligarh Muslim University
PHYSIOLOGICAL CHANGES IN THE LIVER
DURING PREGNANCY
Increased
 ALP rise 3-4 fold due to placental production
 Fibrinogen rise by 50 %, with other clotting factors
Decreased
 Gallbladder contractility
 Albumin and total protein
No change
 Liver size
 Liver blood flow despite increased blood volume
and cardiac output
 Liver aminotransferase levels, may decrease
 Bilirubin level
 Prothrombin time
THE POSSIBILITIES OF LIVER DISEASES
1. A worsening of pre-existing chronic liver or biliary
disease (may not have previously been
diagnosed)
2. A genuine first presentation of liver disease that is
not intrinsically related to pregnancy
3. A genuine pregnancy-associated liver injury
process
THE GENERAL RULE
 The earlier in pregnancy the liver abnormality
presents, the more likely it is to represent either
preexisting liver disease or non-pregnancy-related
acute liver disease
LFT IN PREGNANCY
 ALT levels and albumin normally fall in pregnancy
 ALP levels can rise due to contribution of placental
ALP
INTERCURRENT AND PRE-EXISTING
LIVER DISEASE
Viral hepatitis
 Acute hepatitis A: no effect on fetus
 Chronic hepatitis B: requires identification to
reduce perinatal transmission
 Chronic hepatitis C: perinatal transmission 1%
 Acute hepatitis E: progresses to fulminant hepatic
failure, with 20% maternal mortality
Autoimmune hepatitis
 Improves during pregnancy and flare-up
postpartum
 Azathioprine to be continued during pregnancy
Gallstones
 More common during pregnancy,
 May present with cholecystitis or biliary obstruction
 ERCP safely performed with lead protection
Cirrhosis
 Pregnancy uncommon as cirrhosis causes relative
infertility
 Ascites or polyhydramnios treated with amiloride
rather than spironolactone
Wilson’s disease
 Penicillamine to be continued during pregnancy
PREGNANCY-ASSOCIATED LIVER DISEASE
 Predominant in the third trimester and resolve post-
partum
 Maternal and fetal mortality and morbidity
prevented by early delivery
 Hyperemesis Gravidarum is a disease of 1st
trimester
HYPEREMESIS GRAVIDARUM
 0.3-2% of all pregnancies
 Presents with persistent vomiting, leading to
dehydration with associated ketosis and weight
loss of >5%
 Risk factors include previous pregnancies with
hyperemesis gravidarum, multiple gestations,
trophoblastic disease, nulliparity
 Hormonal peaking of HCG and estradiol probably
plays role
 Mild elevation of transaminase in 50% cases,
Bilirubin may rise to 4 mg/dl
 Amylase elevated in 10%
 A transient hyperthyroidism associated in 50-60%
cases
 Complications include electrolyte imbalance,
esophageal rupture, retinal hemorrhage, renal
failure
 Initial management is conservative
 The only FDA-approved drug for treating nausea
and vomiting in pregnancy is doxylamine/pyridoxine
 However, antihistamines, antiemetics of the
phenothiazine class, and promotility agents (eg,
metoclopramide) are used
 In refractory cases, ondansetron and steroids may
be considered
ACUTE CHOLESTASIS OF PREGNANCY
 20% of jaundice in pregnancy
 Presents with itching
 Associated with IUGR, premature birth and IU fetal
death (if pregnancy >36 weeks)
 Cholestatic LFT and elevated serum bile salts
 Delivery leads to resolution and pregnancy should
not be continued beyond term
 UDCA (15 mg/kg daily) effective in itching and
probably prevents premature birth
 UDCA requires long time for effective levels in bile
pool, hence of little use in late pregnancy
 Recurs in 60% subsequent pregnancies
ACUTE FATTY LIVER OF PREGNANCY
 More common in twins, first pregnancies and male
fetus
 Presents with vomiting and abdominal pain followed
by jaundice
 Fulminant hepatic failure in severe cases
 Defect in beta-oxidation of fatty acids in
mitochondria, leads to fat droplets formation in
hepatocyte (microvesicular fatty liver)
 Differentiates from toxaemia of pregnancy by high
levels of serum uric acid and absence of hemolysis
 Maternal and perinatal mortality 1% and 7%
respectively
 Delivery regardless of gestational age is the only
treatment
HELLP SYNDROME
 Hemolysis, elevated liver enzymes and low
platelets, a variant of pre-eclampsia
 Presents with hypertension, proteinuria and fluid
retention
 Jaundice only in 5% cases
 Blood tests shows low haemoglobin, with
fragmented red cells, markedly elevated serum
transaminases and raised D-dimers
 Complications include hepatic infarction and
rupture, DIC and placental abruption
 Maternal and perinatal mortality 1% and 30%
respectively
 Delivery leads to prompt resolution
 Recurs < 5% subsequent pregnancies
Thank You

Pregnancy and Liver Diseases

  • 1.
    PREGNANCY & LIVER DISEASES Dr AbdullahAnsari MBBS, MD Medicine Aligarh Muslim University
  • 2.
    PHYSIOLOGICAL CHANGES INTHE LIVER DURING PREGNANCY Increased  ALP rise 3-4 fold due to placental production  Fibrinogen rise by 50 %, with other clotting factors Decreased  Gallbladder contractility  Albumin and total protein
  • 3.
    No change  Liversize  Liver blood flow despite increased blood volume and cardiac output  Liver aminotransferase levels, may decrease  Bilirubin level  Prothrombin time
  • 4.
    THE POSSIBILITIES OFLIVER DISEASES 1. A worsening of pre-existing chronic liver or biliary disease (may not have previously been diagnosed) 2. A genuine first presentation of liver disease that is not intrinsically related to pregnancy 3. A genuine pregnancy-associated liver injury process
  • 5.
    THE GENERAL RULE The earlier in pregnancy the liver abnormality presents, the more likely it is to represent either preexisting liver disease or non-pregnancy-related acute liver disease
  • 6.
    LFT IN PREGNANCY ALT levels and albumin normally fall in pregnancy  ALP levels can rise due to contribution of placental ALP
  • 7.
    INTERCURRENT AND PRE-EXISTING LIVERDISEASE Viral hepatitis  Acute hepatitis A: no effect on fetus  Chronic hepatitis B: requires identification to reduce perinatal transmission  Chronic hepatitis C: perinatal transmission 1%  Acute hepatitis E: progresses to fulminant hepatic failure, with 20% maternal mortality
  • 8.
    Autoimmune hepatitis  Improvesduring pregnancy and flare-up postpartum  Azathioprine to be continued during pregnancy Gallstones  More common during pregnancy,  May present with cholecystitis or biliary obstruction  ERCP safely performed with lead protection
  • 9.
    Cirrhosis  Pregnancy uncommonas cirrhosis causes relative infertility  Ascites or polyhydramnios treated with amiloride rather than spironolactone Wilson’s disease  Penicillamine to be continued during pregnancy
  • 10.
    PREGNANCY-ASSOCIATED LIVER DISEASE Predominant in the third trimester and resolve post- partum  Maternal and fetal mortality and morbidity prevented by early delivery  Hyperemesis Gravidarum is a disease of 1st trimester
  • 11.
    HYPEREMESIS GRAVIDARUM  0.3-2%of all pregnancies  Presents with persistent vomiting, leading to dehydration with associated ketosis and weight loss of >5%  Risk factors include previous pregnancies with hyperemesis gravidarum, multiple gestations, trophoblastic disease, nulliparity  Hormonal peaking of HCG and estradiol probably plays role
  • 12.
     Mild elevationof transaminase in 50% cases, Bilirubin may rise to 4 mg/dl  Amylase elevated in 10%  A transient hyperthyroidism associated in 50-60% cases  Complications include electrolyte imbalance, esophageal rupture, retinal hemorrhage, renal failure
  • 13.
     Initial managementis conservative  The only FDA-approved drug for treating nausea and vomiting in pregnancy is doxylamine/pyridoxine  However, antihistamines, antiemetics of the phenothiazine class, and promotility agents (eg, metoclopramide) are used  In refractory cases, ondansetron and steroids may be considered
  • 14.
    ACUTE CHOLESTASIS OFPREGNANCY  20% of jaundice in pregnancy  Presents with itching  Associated with IUGR, premature birth and IU fetal death (if pregnancy >36 weeks)  Cholestatic LFT and elevated serum bile salts
  • 15.
     Delivery leadsto resolution and pregnancy should not be continued beyond term  UDCA (15 mg/kg daily) effective in itching and probably prevents premature birth  UDCA requires long time for effective levels in bile pool, hence of little use in late pregnancy  Recurs in 60% subsequent pregnancies
  • 16.
    ACUTE FATTY LIVEROF PREGNANCY  More common in twins, first pregnancies and male fetus  Presents with vomiting and abdominal pain followed by jaundice  Fulminant hepatic failure in severe cases  Defect in beta-oxidation of fatty acids in mitochondria, leads to fat droplets formation in hepatocyte (microvesicular fatty liver)
  • 17.
     Differentiates fromtoxaemia of pregnancy by high levels of serum uric acid and absence of hemolysis  Maternal and perinatal mortality 1% and 7% respectively  Delivery regardless of gestational age is the only treatment
  • 18.
    HELLP SYNDROME  Hemolysis,elevated liver enzymes and low platelets, a variant of pre-eclampsia  Presents with hypertension, proteinuria and fluid retention  Jaundice only in 5% cases  Blood tests shows low haemoglobin, with fragmented red cells, markedly elevated serum transaminases and raised D-dimers
  • 19.
     Complications includehepatic infarction and rupture, DIC and placental abruption  Maternal and perinatal mortality 1% and 30% respectively  Delivery leads to prompt resolution  Recurs < 5% subsequent pregnancies
  • 20.