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Management of liver diseases in pregnancy. Moderator-Prof. Anoop Saraya Candidate-Dr. Moka Praneeth. Contents. Pregnancy – physiologic changes Hepatitis-E Hepatitis-B Acute liver failure Cirrhosis & Portal hypertension ICP HG HELLP syndrome AFLP. - PowerPoint PPT Presentation
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Management of liver diseases in pregnancy
Moderator-Prof. Anoop SarayaCandidate-Dr. Moka Praneeth
Contents
Pregnancy – physiologic changes
Hepatitis-E
Hepatitis-B
Acute liver failure
Cirrhosis & Portal hypertension
ICP
HG
HELLP syndrome
AFLP
Physiological changes in liver tests during normal pregnancy
Test Normal Range
Bilirubin Unchanged or slightly decrease
Aminotransferases Unchanged
Prothrombin time Unchanged
Alkaline phosphatase Increases 2 to 4-fold
Fibrinogen Increases 50%
Globulin Increases in α and ß globulins
α -fetoprotein Moderate rise, esp. with twins
WBC Increases
Ceruloplasmin Increases
Cholesterol Increases 2-fold
Triglycerides Increases
Globulin Decreases in gamma-globulin
Hemoglobin Decrease in later pregnancy
Liver diseases in pregnancy
Only in thesetting of pregnancy
coincidental with pregnancy
Preeclampsia-associated
Chronic liver diseases e.g.: cholestatic liver disease,
autoimmune hepatitis,Wilson disease,
viral hepatitis, etc…
not associated withpreeclampsia
The preeclampsiaitself
HELLP-syndrome
AFLP
Hyperemesisgravidarum
Intrahepatic cholestasisof pregnancy
Study Patients (n)
Prevalence of HEV infection (%)
Prevalence of fulminant liver failure (%)
Mortality rate (%)
Jaiswal et al, 2001 (North India)
127 58 58 45
Singh et al, 2003 (North India)
60 37 64 64
Khuroo et al, 2003 (North India)
76 86 69 55
Beniwal et al, 2003 (North India)
97 47.4 75 39.1
Tsega et al, 1993 (Ethiopia)
32 59 - 42
Kumar et al, North India 2004
65 45 32 73
Patra et al 2007 North India
220 60 55 41
Stoszek et al 2006 (Egypt)
2428 84.3 0 0
Rasheeda et al (2008) 115 75 3.4 3.4
Hepatitis E virus infection and fulminant hepatic failure during pregnancy
50 pregnant and 50 non-pregnant women with FHF and 150
pregnant healthy females without liver disease as controls were
recruited for the study.
Serologically (38/50; 76%) as well as by RT-PCR (28/50; 56%), a
significantly higher HEV positivity rate was found in pregnant FHF
patients compared to non-pregnant women (serologically 15/50;
30%; RT-PCR 7/50; 14%).
Jilani N et al. J Gastroenterol Hepatol. 2007
Hepatitis E virus infection and fulminant hepatic failure during pregnancy
CD4 counts were lower (P < 0.05), while CD8 counts were higher (P <
0.05), and their ratio (CD4/CD8) in HEV positive pregnant FHF patients
was significantly lower (P < 0.01) when compared to that of HEV
negative pregnant FHF women or controls.
Levels of estrogen, progesterone and beta-HCG were also found to be
higher (P < 0.001) in HEV positive pregnant FHF patients when
compared to HEV negative patients or controls.
HEV infected pregnant FHF patients had a significantly higher mortality
rate of 65.8% (25/38) compared to 23.5% (4/15) in HEV positive non-
pregnant women (P < 0.001
Immunological alterations in pregnant women with acute hepatitis E.
Pregnant women with HEV had generalized immune suppression
characterized by decrease in lymphocyte response to
phytohemagglutinin (PHA) with a predominant Th2 bias as
compared to non pregnant women with hepatitis E and normal
healthy controls.
Neither normal healthy pregnant women nor nonpregnant HEV
infected women demonstrated decreased response to PHA.
Pal R et al. J Gastroenterol Hepatol. 2005
Pathogenesis of Hepatitis-E in pregnancy
Probable hypotheses for the variable pathogenesis of HEV
Termination of pregnancy in HEV-ALF?
Banait VS et al. Indian J Gastroenterol 2007
Treatment algorithm for an HBV-infected woman who is already on
antiviral therapy and presents with an unexpected pregnancy
Impact of pregnancy on chronic HBV
No worsening of liver disease in majority
Overall increase in HBV DNA levels during pregnancy
Median ALT levels decreased during pregnancy
Increase in ALT (3 x lowest ALT) within 6 months after delivery
Case reports of postpartum hepatic exacerbations
1. Terrault et al. Semin Liver Dis. 20072. Soderstrom et al. Scand J Infect Dis 20033. Borg et al. J viral Hep 20084. Rasheed et al. Int J Gynaecol Obstet
2013
HBV Infection in Women Considering Starting a Family:
Which Drug? FDA classification: based on in vitro and animal studies
Pregnancy class B: telbivudine and tenofovir DF Pregnancy class C: interferon, adefovir, entecavir, and
lamivudine Human data:
Antiretroviral pregnancy registry: safety established for lamivudine and tenofovir, including exposure in first trimester[1]
Clinical studies of antiviral therapy to prevent perinatal transmission: safety established for lamivudine and telbivudine, mainly exposure in third trimester[2-5]
1. Antiretroviral Pregnancy Registry. December 2012. 2. Xu WM, et al. J Viral Hepat. 2009;16:94-103. 3. Shi Z, et al. Obstet Gynecol. 2010;116:147-159. 4. Han GR, et al. J Hepatology. 2011;55:1215-1221. 5. Pan CQ, et al. Clin Gastroenterol Hepatol. 2012;10:520-526.
Incidence of Birth Defects With in Utero Exposure to HBV Nucleos(t)ide
Analogues Data derived from Antiretroviral Pregnancy Registry, 1/1989
- 7/2012[6] International, voluntary, prospective, exposure-registration
cohort Data on exposure in HBV-monoinfected mothers began in
1/2003
Metropolitan Atlanta Congenital Defects Program, a population-based birth defects surveillance program administered by CDC[6,7]
Overall birth defects: 2.72% (95% CI: 2.68-2.76)6. Antiretroviral Pregnancy Registry. December 2012. 7. Correa A, et al. Birth Defects Res A Clin Mol Teratol. 2007;79:65-186.
Prevention of Perinatal HBV Transmission
Cornerstone: HBIG + HBV vaccine HBIG + first dose vaccine within 12 hrs
of birth, different sites Efficacy: ~ 95% Reasons for failure
Delay in administration of HBIG and first dose of vaccine
Failure to complete vaccine series/Poor quality vaccine
Mother HBeAg positive and/or high HBV DNA In utero infection HBsAg mutation/Escape mutants Immunocompromised host
1. Lok AS, et al. Hepatology. 2009;50:661-662. 2. Mast EE, et al. MMWR Recomm Rep. 2005;54(RR-16):1-31.
Meta-analysis of Lamivudine to Interrupt Perinatal Transmission of HBV
*Risk ratio calculated using the Mantel-Haenszel random-effects model.
Infant HBsAg Seropositive
Lamivudine,Events/N
Control ,Events/N
Risk Ratio(95% CI)*
Han 2005 0/43 5/35 0.07 (0.00-1.30)Li 2006 1/36 7/44 0.17 (0.02-1.35)Feng 2007 7/48 16/42 0.38 (0.17-0.84)Guo 2008 4/70 12/40 0.19 (0.07-0.55)Xu 2009 10/56 23/59 0.46 (0.24-0.87)Zhang 2010 1/50 8/50 0.13 (0.02-0.96)Total 23/303 71/270 0.33 (0.21-0.50)
17. Han L, et al. World J Gastroenterol. 2011;17:4321-4333.
Risk Ratio (95% CI)*
0.01 0.1 1 10 100Favors Lamivudine Favors Control
Infant HBV DNA Seropositive
Lamivudine,Events/N
Control ,Events/N
Risk Ratio (95% CI)*
Feng 2007 7/48 16/42 0.38 (0.17-0.84)Guo 2008 6/70 18/40 0.19 (0.08-0.44)Xu 2009 11/56 27/59 0.43 (0.24-0.78)Zhang 2010 1/50 8/50 0.13 (0.02-0.96)Total 25/224 69/191 0.32 (0.20-0.50)
Risk Ratio (95% CI)*
0.01 0.1 1 10 100Favors Lamivudine Favors Control
Algorithm for HBV Management in Women During Pregnancy
Pregnant women with HBV infection
1st trimester: assess HBV replication and liver disease
Active disease/suspected cirrhosis: consider initiating
treatment with tenofovir
End of 2nd trimester: quantitative HBV DNA and ALT levels
HBV DNA < 106 IU/mL* HBV DNA > 106 IU/mL*
Monitor;infant receives HBIG
+ vaccine at birth
Consider initiating treatment with tenofovir, lamivudine, or telbivudine at 28-32 wks†
Infant receives HBIG + vaccine at birth
*The cut-off level of maternal HBV DNA level for initiation of therapy is unclear, and HBV DNA from 6-8 log10 IU/mL can be considered for therapy based on physician and patient preference.†Tenofovir is preferred if treatment is expected to be > 12 weeks or if treatment is expected to continue while breastfeeding.
Pregnant Women With High HBV DNA and Not Initially on Antiviral
Therapy When to stop antiviral after delivery?
To prevent perinatal transmission: immediately, especially if mother plans to breast-feed, or up to 3 mos postdelivery
To treat liver disease: continue until therapeutic endpoint
What is the risk of posttreatment flare? Seemingly rare, but mild ALT elevation common;
also seen in postpartum period for women not receiving antiviral
Decompensation not reported in clinical trials; likelihood low because most pregnant women have early-stage liver disease
Important to closely monitor ALT after antiviral therapy is discontinued (eg, 1, 3, and 6 mos posttreatment)
19. Ter Borg MJ, et al. J Viral Hepat. 2008;15:37-41.
Cesarean vs Vaginal delivery in CHB- a meta-
analysis Infant serum Anti-HBs postivity at birth (RR= 1.24, 95% CI 0.89-1.74,
p = 0.2) or at 6-7 months (RR= 0.98, 95% CI0.86-1.11, p = 0.73) was
not significantly different
The incidence of infant CHB infection may have been higher in the
vaginal delivery group (R=2.2, 95% CI 1.02-4.74, P = 0.04)
Xu et al. Dig Dis Sci. 2014
Acute HBV in pregnancy
Transmission rates:
10% in early pregnancy
60% at or near time of delivery
Prophylaxis of vertical transmission
Hepatitis Maternal status
Transmission Prophylaxis
A Infection within 2 weeks before or after delivery
Rare Immune globulin + HAV vaccine after delivery
C HCV RNA positiveHCV RNA + HIV positive
5-8%Upto 30%
NoneNone
E Active infection at time of birth
50-100% None
ALF in pregnancy
1015 consecutive patients of ALF in reproductive age group,
admitted in AIIMS from January 1986 to December 2006
249 (38.5%) were pregnant females
The mortality rate of pregnant women and girls (53.8%) was similar
to nonpregnant women and girls (57.2%), and men and boys
(57.9%); P = 0.572.
Bhatia V, Acharya SK et al. Hepatology 2008
ALF in pregnancy
A significantly higher proportion of ALF was attributable to HEV
among pregnant women (59.4%), as compared with nonpregnant
women (30.4%), and men (23.1%) (p < 0.001)
The outcome of HEV-related ALF was independent of the sex and
pregnancy status of the patients (P = 0.103).
ALF in pregnancy
Mortality in HEV-ALF and non-HEV-ALF patients in pregnant women
and girls was 51% (74/145) and 54.7% (52/95)(P > 0.1), respectively.
The outcome of pregnant ALF patients was also unrelated to the
trimester of pregnancy.
The mortality of non-HEV-related ALF among the pregnant women
and girls (54.7%), age-matched nonpregnant women and girls
(61.7%), and men and boys (62.8%) were also similar (P > 0.1).
Bhatia V, Acharya SK et al. Hepatology 2008
Induction of delivery in ALF with IUD
Increased risk of peripartum hemorrhage due to
associated coagulopathy 1
rFVIIa is a useful adjunct to standard management in
postpartum hemorrhage secondary to acute liver
failure of pregnancy-related liver disorders.1
When a dead fetus has been in utero for 3-4 weeks,
fibrinogen levels may drop, leading to a coagulopathy.2
Does a dead (< 2 weeks) fetus lead to sepsis?
Should we routinely remove the dead fetus in
pregnant women with ALF with IUD?1. Goel a et al. Indian J Gastroenterol. 2013 Jul2. Tempfer CB et al. J Womens Health (Larchmt). Apr
2009
CLD- pregnancy Most patients with CLD infertile due to hypothalamic- pituitary dysfunction. Russell MA et al. Semin Perinatol 1998;22:156-165.
MATERNAL RISKS: Variceal Bleeding ( 18-32 %) Hepatic Decompensation(24%) Hepatic Encephalopathy PPH ( 7-10%) Rupture of splenicA aneurysms(2.6%)
FETAL RISKS : ↑ risk of abortions (30-40%) ↑ risk of prematurity / IUGR (25%) Perinatal death (18%) Hay et al. Hepatology 2008
Preexisting varices : 78% GI bleeding during pregnancy T2/T3 as maternal blood volume maximally expanded and fetus causes ↑ compression of IVC collateral vasculatureMortality rate of 18% to 50%.
Treatment of variceal bleeding
Endoscopic variceal band ligation Superior to sclerotherapy – no chemicals instilled into blood
stream. -Expert opinion Octreotide (B)
Safety in pg not determined Could cause arterolar vasospasm
Decreased placental perfusion and increased risk of placental abruption as well as
HTN, MI, peripheral ischemia Endoscopy
Safe when done with caution
Pregnancy and cirrhosis
Review of data from 1984 – 2009
Kings College Hospital
62 pregnancies in 29 women
Median MELD was 7 (range 6 – 17)
Median CPS was 5 ( range 5-8)
Live birth rate was 58%
Median gestational age 36 w
Westbrook RH et al ClinGastroHep 2011;9: 694-9
Pregnancy and cirrhosis Maternal complications occurred in 10%
Ascites Encephaolpathy Variceal hemorrhage
Associated with MELD > 10
MELD predicted which patients were to have liver related
complications AUC 0.8
83% sensitivity and 83% specificity
No one with MELD <6 had any liver related complications
Westbrook RH et al ClinGastroHep 2011;9: 694-9
Cesarean vs vaginal delivery in CLD
Experts use elective cesarean section or forceps delivery under
extradural analgesia to decrease the risk of variceal rupture (no
RCTs are available)1, 2
If a prophylactic cesarean section is performed, a vascular surgeon
should be available as bleeding from pelvic or abdominal wall
collaterals may occur3
1. Benjaminov FS, Heathcote J. Am J Gastroenterol 20042. Heriot JA et al. Br J Anes 19963. Misra S, Sanyal AJ. Clin Liver Dis 1999
Intrahepatic Cholestasis of Pregnancy (ICP)
Incidence 0.1% - 1% of pregnancies, 20% among twins, 7.5% of
pregnancies (AIIMS)
Recurrence rate of 50-70% in subsequent pregnancies
Pruritus (initially in soles & palms, only at night, and later
continuously progressing to trunk and face) develops in late 2nd and
3rd trimester
ICP
Jaundice (usually mild- bilirubin < 5 mg/dL) develops 2 weeks later,
plateaus and remains constant until delivery
Pruritus worsens with the onset of jaundice
Symptoms usually abate within 2 days of delivery.
ICP-lab investigations
The most specific and sensitive marker of ICP is total serum bile acid
(BA) levels > 10 µmol/L
Chenodeoxycholic acid and cholic acid ↑ sed 10 times N( >
11µmol/L), ↑ cholic acid % ( > 42 %), ↓ glycine/ taurine bile acid
ratio (<1)
ALT, AST- mild to 10-25 fold increase, SAP- increased upto 4 fold
GGT-mildly elevated in 30%, more likely in those with genetic
component
Glutathione s- transferase α - new marker being investigated
Deposition of bile acids in the skin → pruritus → dermatitis artefacta.
Hepatic impairment → prolonged prothrombin time → post partum hemorrhage
RCOG 2011
Arrese. Annals of Hepatology 2006; 5 (3): 216-218
Prematurity: ↑ iatrogenic prematurity ( 7- 25 % ) vs ( 4- 12 %) .
Passage Of Meconium : preterm than in term (25% vs 12%)
preterm controls (18% vs 3%). mc if BA > 40 umol/l vs 20 Risk ↑ linearly ( 19.7% ↑ for each
10 umol/l ↑ BA conc.) .
Intrapartum Fetal Distress
Kenyon et al.. BJOG 2002; 109
Higher Caesarean Rates (10 – 36 %) → ↑ RDS & TTN
Stillbirth : (1.5 %) to that of general
population (0.5%). • RCOG 2011
FETAL RISKSMATERNAL RISKS
IUD seems to be due to – acute anoxia (placental chorionic vein spasm , umbilical vein spasm)
umbilical vein constriction
fetal cardiac arrest ( infiltration of fetal cardiomyocytes by bile salts) Kenyon et al. BJOG 2002 Gorelik et al. BJOG 2006
T. UDCA 15 mg/kg/d (or > 1 g/day) (– drug of choice) reduces
pruritus, ↓ total serum bile acids, ALT values and bilirubin levels,
improves cholic/CDCA ratio
Other agents with limited benefit: Phenobarbital 100 mg OD,
Hydroxyzine, SAME 1600 mg OD, Cholestyramine- takes 2 weeks to
work, Aluminium containing antacids, Dexamethasone 12 mg QID
for 7 days
at
Hyperemesis gravidarum
Investigations for HG
Urinalysis for ketones & specific gravity
Serum electrolytes: Na, K, Cl
LFTs- Elevated transaminases (50-65%) upto 200 IU/L,
SAP upto 2 times, serum bilirubin upto 4 mg/dL-
makes it a liver disease?
Serum amylase & lipase upto 5 times
TSH, FT4, Urine culture, Hct, screening for HAV, HBV,
HCV
Obstetric & abdominal USG
Management of HG
i.v. fluids (NS, RL) over 2-3 hours Thiamine/vitamin B1 Enteral/Parenteral nutrition Separating solids & liquids, Eating
small frequent meals of bland foods, Avoiding fatty foods (eg: Potato chips)
Avoid drinking cold/sweet beverages Eliminate pills with iron; give high
protein snacks
COMPLICATIONS
Maternal complications • Hypokalemia - lethargy, skeletal
muscle weakness and cardiac
arrhythmias
• Hyponatremia and CPM.
• Vitamin B6/B12 def
• Malnutrition.
• Mallory-Weiss oesophageal tears.
• Wernicke’s encephalopathy.
• Venous thromboembolism .
• Psychological morbidity.
Fetal complications
No increased risk of congenital
malformations .
Growth restriction.
Wernicke’s encephalopathy is
associated with a 40%
incidence of fetal death.
NICE 2010
HELLP Syndrome
1 in 1000 , 10-20 % of severe preeclampsia /
eclampsia
Most common in white, multiparous and older
women
90
65
30 31
0
10
20
30
40
50
60
70
80
90
symptoms
general malase
epigastric pain
vomiting
haedache
Clinical Presentation
SYMPTOMS
90
30 30
0
10
20
30
40
50
60
70
80
90
signs
Rt.hypochond.pain
edema
hypertention + proteinuria
signs
Clinical Presentation
Laboratory Diagnostic Criteria for HELLP syndrome
Haemolysis Abnormal peripheral smear : spherocytes,
schistocytes, triangular cells and burr cells Total Bilirubin level > 1.2 mg/dL Lactate dehydrogenase level > 600U/L
Elevated liver function test result Serum aspartate amino transferase level > 70U/L Lactate dehydrogenase level >600 U/L
Low platelet count (Most reliable indicator)Platelet count < 150 000/mm3 o Requires at least 2 of above mentioned abnormalities
Classificationon the basis of platelet
count
class I, less than 50,000 per mm3
class II, 50,000 to less than 100,000 per mm3
class III, 100,000 to 150,000 per mm3
The antenatal administration of dexamethasone (Decadron) in a high dosage of 10 mg intravenously every 12 hours has been shown to markedly improve the laboratory abnormalities associated with HELLP syndrome.
Steroids given antenatally do not prevent the typical worsening of laboratory abnormalities after delivery. However, laboratory abnormalities resolve more quickly in patients who continue to receive steroids postpartum.
Magann EF, Bass D, Chauhan SP, Sullivan DL, Martin RW, Martin JN Jr. Am J Obstet Gynecol 1994;171:1148-53.
Corticosteroid therapy should be instituted in patients with HELLP syndrome who have a platelet count of less than 100,000 per mm3 .And should be continued until liver function abnormalities are resolving and the platelet count is greater than 100,000 per mm3
Magann EF, Perry KG Jr, Meydrech EF, Harris RL, Chauhan SP, Martin JN Jr. Am J Obstet Gynecol 1994;171:1154-8.
Patients with HELLP syndrome should be treated
prophylactically with magnesium sulfate to prevent
seizures, whether hypertension is present or not
Antihypertensive therapy (most commonly
Hydralazine, Labetalol, Nifedipine) should be initiated
if blood pressure is consistently greater than 160/110
mm hg despite the use of magnesium sulfate.
The goal is to maintain diastolic blood pressure
between 90 and 100 mm hg.
Between 38 -93 % of patients with HELLP syndrome receive some form of blood product.
Patients with a platelet count greater than 40,000 per mm3 are unlikely to bleed.
Patients who undergo cesarean section should be transfused if their platelet count is less than 50,000 per mm3 ,
Prophylactic transfusion of platelets at delivery does not reduce the incidence of postpartum hemorrhage or hasten normalization of the platelet count. .
Patients with DIC should be given fresh frozen plasma and packed red blood cells.
Acute Fatty Liver of Pregnancy: Introduction
A rare, sudden catastrophic condition, 1/7000 – 1/16000 deliveries
40%-50% of patients are nulliparous
Almost exclusively occur in the 3rd trimester
The presentation can vary from asymptomatic to fulminant liver
failure
>50% have coexisting preeclampsia/HELLP syndrome
58
(B) Hematoxylin-eosin stain (high power) shows hepatocytes stuffed with microvesicular fat (free fatty acids) and centrally located nuclei.
Histological appearance of the liver in AFLP.
(A) Sudan stain (low power) shows diffuse fatty infiltration (red staining) involving predominantly zone 3, with relative sparing of periportal areas.
AFLP- CLINICAL FEATURES
COMMON SIGNS AND SYMPTOMS PREVALENCE(%)
Jaundice > 70
Abdominal pain ( usually R upper quadrant, mid-epigastric or radiating to back )
50- 60
CNS ( altered sensorium, confusion, disorientation, psychosis, restlessness, seizures, coma)
60- 80
Disseminated intravascular coagulation 55
Nausea and vomiting 50- 60
Gastrointestinal bleeding 20- 60
Acute renal failure 50
Oliguria 40- 60
Tachycardia 50
Late onset pyrexia 50
Steer et al. High Risk Pregnancy, 4th edition 2011
Proposed (Swansea) diagnostic criteria for AFLP
At least 6 of:
64
Imaging Hepatic ultrasound or CT
scan The clinical value of
imaging in the diagnosis of AFLP is not yet established Not to confirm the
diagnosis of fatty liver To rule out organic lesions
in liver, liver rupture infarct or biliary disease
65
MATERNAL RISKS• Maternal mortality 18 %.• Death due to sepsis, renal
failure(60%), circulatory collapse, pancreatitis, GI bleed(33%)
• Recurrence in future pregnancy 25 %.
• Full clinical recovery in several wks.• Liver recovery in several months.• Post- partum:
- diabetes insipidus
- acute pancreatitisFETAL RISKS mortality of around 23 %
Ko et al. Can J Gastroenterol 2006; 20 (1)
•Multidisciplinary approach.
• Senior obstetrician, anesthesiologist haematologist, hepatologist should be involved at an early stage.
•Correct coagulopathy and arrange adequate blood & blood products prior to induction
•Vitals monitoring and level of consciousness hourly
•BS monitoring 2 hrly- risk of hypoglycemia
•LFT’s, RFT,CBC 6 hrly•Most patients requires ICU care
Saketh et al. Crit Care Med 2005; 33(10)
AFLP- COMPLICATIONS AFLP- MANAGEMENT
Management
Immediate termination of pregnancy No report of recovery before delivery Broad spectrum antibiotics Monitor liver function
67
Maternal Outcome
AFLP is a reversible form of acute hepatic failure
48hrs after the delivery: often worsening of liver
function, renal function and coagulopathy
By 2 to 3 days after delivery: the aminotransferases
and encephalopathy will improve
Most patients improve in 1 to 4 weeks postpartum
Recovery can occur in days or be delayed for months
but is complete with no signs of chronic liver disease
68
69
Maternal Outcome
Maternal and fetal mortality Before the 1980s: ~85% Now: 18 – 12.5% (fetal: 7 – 58%)
70
Summary
• Further research is needed on Hepatitis-E in pregnancy in India
• Keep all possibilities in mind when a pregnant woman presents
with jaundice.
• Fetal surveillance important.
• Immunoprophylaxis important for fetus in viral hepatitis B
• Careful about coagulation disorders and risk of postpartum
hemmorhage
• Unique liver diseases of pregnancy terminate rapidly with
delivery
Prophylactic treatment of varices in cirrhosis
Screening EGD Before pregnancy Or at beginning of second trimester*
Blood volume increased Gravid uterus compressing IVC
Prophylaxis – options
non selective beta blockers Or variceal band ligation
* AASLD recommendations