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