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Gastrointestinal and hepatic disorders in pregnancy.pptx

Gastrointestinal and hepatic diseases during pregnancy can occur due to physiological or pathological changes, or due to pre-existing or pregnancy-specific conditions. This document provides an overview of common gastrointestinal and hepatic disorders encountered in pregnancy.

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Dr. Ajay Kumar Yadav DM Resident, NAMS 2081/06/16 Gastrointestinal and Hepatic Disorders in Pregnancy
Layout Physiological changes in Preganncy Endoscopyin Pregnancy Imaging in pregnancy GI disorders in Pregnancy Hepatic disorders unique to pregnancy
Physiological changes in pregnancy Intra-abdominal organs must move to accommodate uterine growth Hormonal factors alter motility – GERD, N/V, constipation Immunological adaptation to pregnancy affects response to disease
Esophagus and Gastrointestinal Function
Immune Function and the Intestinal Microbiota Maternal immune system adapt to presence of fetus  influence response to infection and modulate course of autoimmune diseases Shift from cellular to humoral immunity, downregulation of Th1 and upregulation of Th2 cytokines Alternation of maternal intestinal flora  alters host-microbial interaction in a beneficial fashion Bacteria from the mother colonize the neonate’s gut  potential long-lasting health consequences
GB and Hepatic Function
Biochemical changes during Pregnancy
Drug Safety in Pregnant Patients No medication or other therapeutic intervention can be considered definitely safe during pregnancy Letter categories (A, B, C, D, X) are not longer used FDA 2014: Physician labelling rule  risk-benefit ratio
Endoscopy during pregnancy • It is performed routinely if there is a clear indication • Safety of endoscopy not completely established • Pregnant women have safely undergone EGD, colonoscopy, sigmoidoscopy, ERCP, and percutaneous gastroscopy. • In addition to general contraindications to endoscopic procedures, specific contraindications during pregnancy include • imminent or threatened delivery, PROM, placental abruption, and PIH
• Given the extreme sensitivity of the fetus to maternal hypoxia, pregnant women should receive supplemental O2 with continuous SPO2 monitoring. • In the 2nd and 3rd trimesters, the supine position and external abdominal pressure s/b avoided compression of the IVC and AA hypotension and placental hypoperfusion. • ERCP s/b performed only with therapeutic intent and by EE, and every effort should be made to avoid fetal radiation • Avoid • Opioid analgesics  fetal hypoxia • BZDs, esp 1st trimester  fetal malformations • Lactating patients are advised to avoid breastfeeding and to discard breast milk for 4 hours after a procedure requiring sedation
Imaging and radiation exposure during pregnancy The National Commission on Radiation Protection recommends limiting exposure to ionizing radiation during pregnancy to less than 5cGy The potential for radiation damage to the fetus is determined by dose and gestational age at the time of exposure (Table 40.1). CT should be performed only when its potential benefits clearly outweigh its risks and should be done, if possible, after completion of organogenesis MRI is often a superior alternative to CT • There is a theoretical risk of thermal injury to the fetus from MRI in early pregnancy and thus MRI is not recommended during the first 12 weeks of gestation • Breastfeeding should not be interrupted after imaging with gadolinium (<0.04% excreted in breast milk)
GI Disorders and Pregnancy Nausea, Vomiting, and Hyperemesis Gravidarum • 1st trimester: Nausea (60% to 70%), Vomiting (40%) • Onset: 4th to 6th ; peak: 8th to 12th week; resolution by 20 wop • Hyperemesis gravidarum (< 2% of pregnancies) • Severe persistent vomiting demanding medical intervention • defined by the presence of ketonuria and a 5% decrease from pre-pregnancy weight • a/w fluid, electrolyte, and acid-base imbalances, nutritional deficiency, and LOW • usually begin at weeks 4 to 5 and improve by weeks 14 to 16 of gestation; 20% persists until delivery • frequently recurs in subsequent pregnancies
• Risk factors for hyperemesis • personal or family history • female fetus • ↑ed HCG • multiple gestation, GTN, fetal trisomy 21, hydrops fetalis • Pathophysiology • Pregnancy-related hormones, specifically HCG and estrogen, have been implicated • Estrogen and progesterone  by altering gastric motility and slowing GI transit time  N/V • Abnormal TFT: 2/3rd of patient • Indication for hospital admission • IV fluid and electrolyte replacement, nutritional support • affected individuals develop hypotension, tachycardia, ketosis, weight loss, or muscle wasting.
• Maternal complications: • Mallory-Weiss tears with UGIB, • Boerhaave syndrome, • Wernicke encephalopathy with or without Korsakoff psychosis, • central pontine myelinolysis, • retinal hemorrhage, and • spontaneous pneumomediastinum • The goals of therapy: maintenance of adequate maternal fluid intake and nutrition + symptom control • Management • Dietary modification: frequent small meals, avoid an empty stomach • Pharmacotherapy • 1st line: Antiemetic and antireflux medications: phenothiazines (chlorpromazine, prochlorperazine), metoclopramide, ondansetron, and pyridoxine (vitamin B6) • 2nd line: Glucocorticoids benefit individuals with severe symptoms
GERD • By the end of the 3rd trimester, 50% to 80% of pregnant patients have had new, or an exacerbation of preexisting, heartburn • Pregnant women with heartburn may also have regurgitation and N/V, as well as atypical reflux symptoms, such as persistent cough and wheezing. • Pathogenesis of GERD in pregnancy • Progesterone  ↓esophageal motility, LES tone, and gastric emptying • Enlarging uterus  compression of the stomach  increased intra-abdominal pressure • Management: • diet and lifestyle modifications • Pharmacotherapy: Liquid antacids and sucralfate  H2RA  PPI
PUD • Gastric acid secretion and the natural h/o Hp infection are not altered by gestation • Dyspeptic symptoms that accompany pregnancy, esp. N/V, heartburn may make diagnosis difficult • 1st line therapies: Ranitidine and sucralfate  2nd line: PPIs • Patients with Hp infection may be given antibiotics during pregnancy or after delivery.
Constipation in Pregnancy • 2nd m/c symptom (40%) after nausea • Pathophysiology: ↓ colonic motility + ↑ colonic transit + ↓physical activity + medications (iron/calcium) + pressure effect of gravid uterus on rectosimoid
Diarrhea in Pregnancy • Prevalence unknown; 34% frequent bowel movement • Pathophysiology: same as for non-pregnant
Pharmacological treatment of abdominal pain/IBS in Pregnancy
IBD • The majority of cases of IBD present before age 30, the years of peak fertility • Pregnancy rates spuriously low • Self-image problems  sexual avoidance and voluntary childlessness • Fear of IBD in offspring • Fear of fetal malformation from maternal drug therapy • Female fertility does not appear to be impaired by uncomplicated IBD • A notable exception: patients treated with total colectomy and IPAA • meta-analysis: 3-fold increase risk • pelvic adhesions + fallopian tube scarring  infertility • Fertility in men with IBD is impaired by sulfasalazine treatment  reversible ↓ in sperm counts (usually return to normal within 6 months of discontinuing drug)
Cont.. • Initial presentation of IBD is is often during 1st trimester of pregnancy • no more severe than those in non-pregnant individuals • pregnancy does not appear to increase the severity of or morbidity due to preexisting IBD • Evidence suggests that active disease around the time of conception increases the risk of disease relapse during pregnancy • Relapse: UC > CD • The goals of therapy: to minimize IBD symptoms and morbidity prior to conception. • affected patients should continue optimized pre-pregnancy therapy to avoid possible flares resulting from medication withdrawal. • Exacerbations of IBD during pregnancy should be managed aggressively to avoid complications, including hemorrhage, perforation, sepsis, fetal demise, and premature labor.
Cont.. • Treatment of fulminant colitis • same as in non-pregnant individuals, namely high-dose glucocorticoids, IV antibiotics, cyclosporine, and salvage biological therapies. • indications for bowel surgery  same as in non-pregnant IBD patients, although bowel surgery is a/w premature labor as well as maternal and fetal mortality • Synchronous CS and subtotal colectomy for patients with fulminant colitis after 28 wog. • Major complications include premature birth, LBW and SGA • increased risk for thromboembolic event • Potentially teratogenic drugs s/b discontinued before conception, if at all possible. • Methotrexate and thalidomide • optimum period of abstinence: minimum of 6 months
Cont.. • The 5-ASAs are used to treat mild IBD. • A prospective study + large case series  no increased risk of teratogenicity • AZA/6-MP: discontinuation before or during pregnancy is not advisable. • Glucocorticoid t/t for moderate to severe IBD during pregnancy is a/w other complications, including maternal glucose intolerance and HTN (risks factor for preeclampsia), macrosomia, and fetal adrenal suppression. • Prednisolone: more efficiently metabolized by the placenta  less risk of adrenal suppression • Newer data support budesonide • There is still limited data on the effects of treatment with anti-integrin and anti-IL-12/23 antibodies (vedolizumab or natalizumab and ustekinumab, respectively) during pregnancy.
Cont.. • TNF-α antagonists • Serum infliximab levels increase, whereas serum adalimumab levels are stable, during pregnancy • Post-marketing registries of safety data and case series  no increased incidence of fetal malformations or miscarriage • Recently published guidelines recommend that TNF-α antagonists be continued throughout pregnancy, unless otherwise indicated • Babies exposed in utero to these drugs should not receive live vaccines during the first 6 months of life; however, other vaccines are recommended • Vaginal delivery is not contraindicated in IBD patients, but CS is recommended for patients with active perineal disease. • Patients with ileoanal pouches are often advised to avoid vaginal delivery in order to avoid anal sphincter injury.
Appendicitis • Acute appendicitis is the most common non- obstetric indication for exploratory laparotomy in pregnant women • complicates approx. 1 in 1500 pregnancies and may develop at any time during the course of gestation • Diagnosis may be difficult • enlarging uterus  displaces the cecum and appendix cephalad alters the location of pain  delayed detection as pregnancy progresses. • Late diagnosis  ↑ed maternal and fetal morbidity and mortality Fig. Location of appendix with gestation
Gallstone dIsease Prevalence of gallstones in asymptomatic pregnant women: 2.5-12% Increased predisposition to formation of CH stones Alternation in bile composition: CH supesaturation + ↓chenodeoxycholic acid + ↑cholic acid ↑bile acid pool Estrogen/progesterone  ↓GB contractility Surgical intervention, if needed, does not increase risk of preterm labour, fetal or maternal mortality
Acute Pancreatitis Uncommon: once in every 1066 to 3300 pregnancies Most cases caused by GB stones, and present during 3rd trimester or puerperium Cl/f  similar Complications  rare
Liver Diseases in Pregnancy
Hepatic Disorders unique to pregnancy Cholestasis of Pregnancy • form of intrahepatic cholestasis a/w pruritus, elevated serum bile acids, and bland cholestasis on liver biopsy. • usually presents in the 3rd trimester, but may be seen earlier as 1st trimester • Cllinical presentation: • Pruritus: most severe in the skin of the palms and soles and at night. • Jaundice: 10% to 25% • Intense cholestasis  steatorrhea, usually subclinical • Lab Findings: • Elevated SBA > 10 μmol/L • SALP: modestly↑, GGTP: normal or only marginally ↑ • AST/ALT ↑ (as high as ~1000 U/L ∞ viral hepatitis) • ↑ Sr. autotaxin level: sensitive and specific diagnostic test
Cont.. • Clinical improvement and laboratory resolution begins with delivery of the infant  usually prompt and complete. • Planned early elective delivery immediately after fetal maturity is recommended • no residual hepatic defect • increased risk for gallstones, cholecystitis, and pancreatitis. • 60% to 70% develop cholestasis during subsequent pregnancies (although recurrent episodes may be less severe than the initial one) or with use of OCPs contraceptives. • The risk of recurrence with subsequent pregnancies is increased by interval cholecystectomy. • Complications (with SBA > 40 μmol/L) • Fetal distress, stillbirth, and premature delivery
Cont.. • Pathogenesis: • mutations of the MDR3 (ABCB4) gene: approx. 15% of cases • no relationship to HLA type • increased sensitivity to the cholestatic effects of exogenous estrogen • D/D: PBC, PSC, BRIC, cholestatic viral hepatitis, DILI, and bile duct obstruction • Management of cholestasis of pregnancy is primarily palliative. • UDCA: symptomatic relief + ↓fetal complications • Dose: 15 mg/kg/day, one report  higher dose (20 to 25mg/kg/day): more effective. • Bile-acid binders s/a cholestyramine and guar gum • May worsen steatorrhea and resultant fat-soluble vitamin deficiencies. • Glucocorticoid (e.g., oral dexamethasone 12mg/day for 7 days): reduce itching and SBA • Phenobarbital: may relieve itching but may adversely affect the fetus.
Preeclampsia • multi-system disorder characterized by de novo hypertension associated with endothelial damage and maternal organ dysfunction, possibly including the liver, that may produce severe, even life-threatening, complications and affect pregnancy outcome • Pathology: placental ischemia • complicates 3% to 10% of pregnancies • Occurs >20th WOP and puerperium < 12 weeks • Criteria • sustained BP ≥ 140/90 mm Hg after the 20th WOP in a previously normotensive woman, • Proteinuria (≥300 mg/24 hr) ~Urine protein of 30 mg/dL (“1+ dipstick”) • Pedal edema
HELLP Syndrome 12% of pre-eclampsia, 0.2-0.8% of all pregnancies
Liver biopsy: periportal hemorrhage, intrasinusoidal fibrin deposition, irregular areas of hepatic necrosis with mild reactive hepatitis
Indication for abdominal imaging • Severe abdominal pain, neck or shoulder pain, or a sudden drop in BP • USG/CT/MRI: intrahepatic h’ge and infarction, subcapsular hematoma ITP TTP APS D/D • Family History: may be present • AR, AD with variable penetrance • women with hypercoaguable state  early and severe PE • Increasing evidence: ↑ sFlt1  antagonist of VEGF, PGF, sEng • Clinical and laboratory resolution after delivery of fetus  can recur in subsequent pregnancies but usually does not • Severe PE and HELLP  platelet transfusion, HD, PE (occ) • Glucocorticoid: improve platelet count and ALT, ↓hospitalization and ICU stay, but NO IMPROVEMENT IN MATERNAL MORBIDITY AND MORTALITY
Acute Fatty Liver of Pregnancy • Characterised by • microvesicular fatty liver • presents late in pregnancy as ALF, s/t as fulminant ALF with sudden onset of coagulopathy and HE • without prior h/o liver disease • Pathophysiology: • Unknown • Well established a/w inherited fatty-acid- oxidation defect ~ Jamaican vomiting sickness • Management • Early diagnosis and prompt delivery of fetus 100% survival • Supportive therapy: antibiotic, MV, HD Hypoglycemia and HE s/b suspected when patients exhibit altered sensorium
• Usually presents late in pregnancy (1 in 6700 3rd trimester preganancies) , usually between 34-37 WOP, as early as 19-20 weeks, rarely after delivery • m/c in primiparous women and multiple gestation • Pre-eclampsia accompanies in 21-64% of cases • Complications: ascites, pleural effusion, AP, respiratory failure, renal failure, infection • Hepatic imaging: staetosis, hematoma, rupture, and infarction • Histological hallmark: • Small-droplet fatty infiltration • Spares hepatocytes surrounding portal areas • Most prominent in zone 3 • No periportal h’ge and sinusoidal fibrin deposition • D/D: Viral hepatitis, DILI
• Perinatal mortality rates < 7%. • Surviving infants may have LCHAD deficiency • nonketotic hypoglycemia and obtundation • Recurrence of AFLP, particularly in women with LCHAD deficiency. • In all cases of AFLP the mother, father, and child should be tested for the G1528C LCHAD mutation
Other Hepatic Disorders in Pregnancy Viral Hepatitis • Hepatitis A • unless unusually severe, does not appear to alter the normal course of pregnancy, nor does pregnancy appear to influence the natural history of disease. • Hepatitis E • enterically transmitted RNA virus with 4 genotypes and 1 serotype. • Genotypes 1 and 2 only infect humans and usually cause epidemic disease during the monsoon season in central and south Asia and India. • 3rd trimester: fulminant ALF; mortality rate of up to 20%. • a/w IUFD and abortion • Risk greater in any trimester than uninfected counterparts Hepatitis A Hepatitis E
HBV and HDV • HBV infection in pregnant women is the most important factor perpetuating the worldwide epidemic of CHB • HBV transmission can occur at any time during gestation, at the time of delivery or after birth • most MTCT occurs during delivery (neonate’s immune system is incapable of clearing the virus). • Vertical transmission of HBV is responsible for most cases of CHB in endemic areas, esp.SEA and Africa • W/out t/t, 90% of infants born to HBeAg positive mothers and 10% of infants born to HBeAg negative mothers develop CHB infection • Antiviral therapy beginning in the 3rd trimester is recommended for pregnant women • inactive hepatitis B and serum HBV DNA levels > 200,000 IU/mL. • active hepatitis B  same as for non-pregnant women. • When there is an indication for t/t, it should be stopped at, or within 4 weeks of delivery • Continued treatment for up to 12 weeks postpartum does not protect the mother from disease flares.
Cont.. • Invasive procedures during pregnancy, such as amniocentesis, may pose a risk of MTCT, especially when the maternal HBV-DNA level is ≥ 7 log copies/mL. • The infants of mothers with a reactive serum test for HBsAg should receive HBIG and hepatitis B vaccine within 12 hours of delivery. • 1% to 2% of treated infants will become chronically infected with HBV • In a recent study, approximately 25% of women with CHB had disease flares in the first few months after delivery • pregnant and postpartum patients with CHB s/b monitored closely for up to 6 months after delivery • TDF is preferred: reliable efficacy + high barrier to resistance. • Vaccination of non-immune pregnant women against HBV infection is safe and effective.
Cont.. • HDV infection requires simultaneous acute or chronic hepatitis B virus infection. • Pregnant patients with hepatitis B who are most likely to have HDV co-infection HIV and immigrants from areas of high HDV endemicity. • anti-HDV antibody  HDV infection • There is no evidence that pregnancy changes the natural course of hepatitis D. • Prevention of vertical transmission of HDV is best accomplished by • vaccination of the mother against infection with hepatitis B virus, or • existing maternal CHB: infant vaccination + HBIG within 12 hours of delivery
• No recommendation for universal HCV screening of pregnant women • HCV antibody testing: risk factor for viral exposure, s/a IVDU, HIV co-infection • Reactive antibody test  confirmatory HCV RNA • MTCT is the principal cause of hepatitis C in children • Incidence of HCV vertical transmission • HCV RNA-positive, HIV-negative women: 5.8% • HCV RNA-positive, HIV-positive women: 10.8% • HCV-RNA ≥ 106 /mL  36% of cases • The incidence of perinatal HCV infection does vary whether the baby is delivered vaginally or by CS HCV
HCV Cont.. • Although HCV RNA can be detected in breast milk, breastfeeding is not considered to be a risk factor for neonatal HCV infection • Chronic hepatitis C may be independently a/w development of GDM, preterm delivery, LBW, IUGR, and cholestasis of pregnancy • When possible, women of reproductive age with hepatitis C should receive antiviral therapy before becoming pregnant • DAA are not approved for use during pregnancy • No treated with INF/ribavirin (teratogen) • Previously infected individuals may have spontaneous HCV-RNA clearance after delivery
HSV • Immunocompetent: sub-clinical hepatitis • Immunosuppressed/pregnant: severe liver disease (fulminant liver failure) • May have subtle oropharyngeal or genital herpetic lesions. • Encephalopathy may result from herpes encephalitis. • T/t with oral acyclovir or valacyclovir: highly effective + prevent MTCT
Chronic Liver Disease and Portal Hypertension • Women with significant CLD/COL often have anovulatory menstrual cycles or are amenorrheic  unlikely to become pregnant • PHTN, ascites, and compensatory dilation of submucosal esophageal veins connecting the portal circulation to the azygos vein can occur in pregnant women with NCPH aggravated by physiologic increases in circulating blood volume • ↑ed maternal blood volume  ↑risk of variceal bleeding in pts with underlying PHTN • with cirrhosis: 18% to 32% • with known PHTN: 50% • with preexisting varices: 78% • EBL: preferred initial therapy • Also a/w increased risk of death, hepatic decompensation, splenic artery rupture, and uterine hemorrhage
• Vasopressin and octreotide infusions may theoretically cause uterine ischemia and induce premature labor • The AASLD has recommended that every individual with cirrhosis who have a liver stiffness > 20 kPa (FibroScan) and a platelet count < 150,000/mm3 should have endoscopic screening for EV. • No formal guidelines for prophylactic management of EV in pregnant women. • β-Adrenergic receptor antagonists are tocolytic, but these drugs do not repress normal labor in chronically treated pregnant patients. • Ascites and HE in pregnant women with CLD are managed in the customary manner. • The only therapy available for severe hepatic decompensation during pregnancy is LT. • The MELD score can help predict clinical decompensation in a cirrhotic woman during pregnancy.
Safety of drugs used for CLD in Pregnancy
Wilson Disease • WD in women of childbearing age is a/w amenorrhea and infertility. • T/t  removal of excess copper  resumption of ovulatory cycles subsequent pregnancy. • Discontinuation of therapy during pregnancy  sudden copper release  hemolysis, ALF, and death. • d-Penicillamine is potentially teratogenic • Zinc salts s/a zinc acetate do not appear to be teratogenic  preferred therapy for WD in pregnancy
Autoimmune Liver Diseases • Classic (type-1) AIH • typically presents around the expected time of menarche, but is a/w amenorrhea. • Pregnancy is a/w ↑ed incidence of spontaneous abortion and preterm delivery. • Pregnant women with prior AIH may have disease flare during pregnancy and postpartum. • Azathioprine: non-teratogenic • PBC • much more common in postmenopausal women • may experience an exacerbation of pruritus during pregnancy. • safety of UDCA during pregnancy has not been formally proved
Hepatic Tumors and Mass Lesions • Benign liver lesions found commonly in women of childbearing age include adenomas, FNH, and hemangiomas. • Hepatic adenomas are a/w OCP use and may enlarge during pregnancy • Enlarging lesions can bleed and rupture into the abdominal cavity. • FNH and hemangiomas in pregnant pts have also been reported to hemorrhage. • HCC occurs almost exclusively in persons with CLD and may present in the absence of cirrhosis in young people with chronic HBV infection • MSAFP has limited predictive value for HCC • Can also increase in Down syndrome, NTD, and molar pregnancy.
• Fibrolamellar carcinoma • slow-growing liver cancer usually found in young adults and also in pregnancy. • Aggressive neoplasm: 5Y survival < 50%. • Hepatic metastases from other cancers are rare in women of childbearing age.
Budd-Chiari Syndrome • Pregnancy: predisposing factor for the development of venous thrombosis. • Hepatic vein thrombosis may occur in a/w HELLP syndrome and with preeclampsia in women who have an APLA. • Pregnant women who develop hepatic vein thrombosis s/b evaluated for the presence of APLA and other circulating procoagulants (e.g., factor V Leiden), and also for JAK-2 mutation.
Pregnancy After Liver Transplantation • Women of childbearing age may become pregnant after successful orthotopic LT and deliver normal Infants. • Transplant patients must continue immunosuppressive therapy during gestation but may need to have their treatment modified.
Summary of Pharmacological treatment of Liver Disease during Pregnancy
Reference • Sleisinger and Fordtran’s Gastrointestinal and Liver Diseases 11th E • Yamada’s Textbook of Gastroenterology 7th E

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Gastrointestinal and hepatic disorders in pregnancy.pptx

  • 1.
    Dr. Ajay KumarYadav DM Resident, NAMS 2081/06/16 Gastrointestinal and Hepatic Disorders in Pregnancy
  • 2.
    Layout Physiological changes in Preganncy Endoscopyin Pregnancy Imaging in pregnancy GIdisorders in Pregnancy Hepatic disorders unique to pregnancy
  • 3.
    Physiological changes inpregnancy Intra-abdominal organs must move to accommodate uterine growth Hormonal factors alter motility – GERD, N/V, constipation Immunological adaptation to pregnancy affects response to disease
  • 4.
  • 5.
    Immune Function andthe Intestinal Microbiota Maternal immune system adapt to presence of fetus  influence response to infection and modulate course of autoimmune diseases Shift from cellular to humoral immunity, downregulation of Th1 and upregulation of Th2 cytokines Alternation of maternal intestinal flora  alters host-microbial interaction in a beneficial fashion Bacteria from the mother colonize the neonate’s gut  potential long-lasting health consequences
  • 6.
  • 7.
  • 8.
    Drug Safety inPregnant Patients No medication or other therapeutic intervention can be considered definitely safe during pregnancy Letter categories (A, B, C, D, X) are not longer used FDA 2014: Physician labelling rule  risk-benefit ratio
  • 9.
    Endoscopy during pregnancy •It is performed routinely if there is a clear indication • Safety of endoscopy not completely established • Pregnant women have safely undergone EGD, colonoscopy, sigmoidoscopy, ERCP, and percutaneous gastroscopy. • In addition to general contraindications to endoscopic procedures, specific contraindications during pregnancy include • imminent or threatened delivery, PROM, placental abruption, and PIH
  • 10.
    • Given theextreme sensitivity of the fetus to maternal hypoxia, pregnant women should receive supplemental O2 with continuous SPO2 monitoring. • In the 2nd and 3rd trimesters, the supine position and external abdominal pressure s/b avoided compression of the IVC and AA hypotension and placental hypoperfusion. • ERCP s/b performed only with therapeutic intent and by EE, and every effort should be made to avoid fetal radiation • Avoid • Opioid analgesics  fetal hypoxia • BZDs, esp 1st trimester  fetal malformations • Lactating patients are advised to avoid breastfeeding and to discard breast milk for 4 hours after a procedure requiring sedation
  • 13.
    Imaging and radiationexposure during pregnancy The National Commission on Radiation Protection recommends limiting exposure to ionizing radiation during pregnancy to less than 5cGy The potential for radiation damage to the fetus is determined by dose and gestational age at the time of exposure (Table 40.1). CT should be performed only when its potential benefits clearly outweigh its risks and should be done, if possible, after completion of organogenesis MRI is often a superior alternative to CT • There is a theoretical risk of thermal injury to the fetus from MRI in early pregnancy and thus MRI is not recommended during the first 12 weeks of gestation • Breastfeeding should not be interrupted after imaging with gadolinium (<0.04% excreted in breast milk)
  • 14.
    GI Disorders andPregnancy Nausea, Vomiting, and Hyperemesis Gravidarum • 1st trimester: Nausea (60% to 70%), Vomiting (40%) • Onset: 4th to 6th ; peak: 8th to 12th week; resolution by 20 wop • Hyperemesis gravidarum (< 2% of pregnancies) • Severe persistent vomiting demanding medical intervention • defined by the presence of ketonuria and a 5% decrease from pre-pregnancy weight • a/w fluid, electrolyte, and acid-base imbalances, nutritional deficiency, and LOW • usually begin at weeks 4 to 5 and improve by weeks 14 to 16 of gestation; 20% persists until delivery • frequently recurs in subsequent pregnancies
  • 15.
    • Risk factorsfor hyperemesis • personal or family history • female fetus • ↑ed HCG • multiple gestation, GTN, fetal trisomy 21, hydrops fetalis • Pathophysiology • Pregnancy-related hormones, specifically HCG and estrogen, have been implicated • Estrogen and progesterone  by altering gastric motility and slowing GI transit time  N/V • Abnormal TFT: 2/3rd of patient • Indication for hospital admission • IV fluid and electrolyte replacement, nutritional support • affected individuals develop hypotension, tachycardia, ketosis, weight loss, or muscle wasting.
  • 16.
    • Maternal complications: •Mallory-Weiss tears with UGIB, • Boerhaave syndrome, • Wernicke encephalopathy with or without Korsakoff psychosis, • central pontine myelinolysis, • retinal hemorrhage, and • spontaneous pneumomediastinum • The goals of therapy: maintenance of adequate maternal fluid intake and nutrition + symptom control • Management • Dietary modification: frequent small meals, avoid an empty stomach • Pharmacotherapy • 1st line: Antiemetic and antireflux medications: phenothiazines (chlorpromazine, prochlorperazine), metoclopramide, ondansetron, and pyridoxine (vitamin B6) • 2nd line: Glucocorticoids benefit individuals with severe symptoms
  • 18.
    GERD • By theend of the 3rd trimester, 50% to 80% of pregnant patients have had new, or an exacerbation of preexisting, heartburn • Pregnant women with heartburn may also have regurgitation and N/V, as well as atypical reflux symptoms, such as persistent cough and wheezing. • Pathogenesis of GERD in pregnancy • Progesterone  ↓esophageal motility, LES tone, and gastric emptying • Enlarging uterus  compression of the stomach  increased intra-abdominal pressure • Management: • diet and lifestyle modifications • Pharmacotherapy: Liquid antacids and sucralfate  H2RA  PPI
  • 19.
    PUD • Gastric acidsecretion and the natural h/o Hp infection are not altered by gestation • Dyspeptic symptoms that accompany pregnancy, esp. N/V, heartburn may make diagnosis difficult • 1st line therapies: Ranitidine and sucralfate  2nd line: PPIs • Patients with Hp infection may be given antibiotics during pregnancy or after delivery.
  • 20.
    Constipation in Pregnancy •2nd m/c symptom (40%) after nausea • Pathophysiology: ↓ colonic motility + ↑ colonic transit + ↓physical activity + medications (iron/calcium) + pressure effect of gravid uterus on rectosimoid
  • 21.
    Diarrhea in Pregnancy •Prevalence unknown; 34% frequent bowel movement • Pathophysiology: same as for non-pregnant
  • 22.
    Pharmacological treatment ofabdominal pain/IBS in Pregnancy
  • 23.
    IBD • The majorityof cases of IBD present before age 30, the years of peak fertility • Pregnancy rates spuriously low • Self-image problems  sexual avoidance and voluntary childlessness • Fear of IBD in offspring • Fear of fetal malformation from maternal drug therapy • Female fertility does not appear to be impaired by uncomplicated IBD • A notable exception: patients treated with total colectomy and IPAA • meta-analysis: 3-fold increase risk • pelvic adhesions + fallopian tube scarring  infertility • Fertility in men with IBD is impaired by sulfasalazine treatment  reversible ↓ in sperm counts (usually return to normal within 6 months of discontinuing drug)
  • 24.
    Cont.. • Initial presentationof IBD is is often during 1st trimester of pregnancy • no more severe than those in non-pregnant individuals • pregnancy does not appear to increase the severity of or morbidity due to preexisting IBD • Evidence suggests that active disease around the time of conception increases the risk of disease relapse during pregnancy • Relapse: UC > CD • The goals of therapy: to minimize IBD symptoms and morbidity prior to conception. • affected patients should continue optimized pre-pregnancy therapy to avoid possible flares resulting from medication withdrawal. • Exacerbations of IBD during pregnancy should be managed aggressively to avoid complications, including hemorrhage, perforation, sepsis, fetal demise, and premature labor.
  • 25.
    Cont.. • Treatment offulminant colitis • same as in non-pregnant individuals, namely high-dose glucocorticoids, IV antibiotics, cyclosporine, and salvage biological therapies. • indications for bowel surgery  same as in non-pregnant IBD patients, although bowel surgery is a/w premature labor as well as maternal and fetal mortality • Synchronous CS and subtotal colectomy for patients with fulminant colitis after 28 wog. • Major complications include premature birth, LBW and SGA • increased risk for thromboembolic event • Potentially teratogenic drugs s/b discontinued before conception, if at all possible. • Methotrexate and thalidomide • optimum period of abstinence: minimum of 6 months
  • 26.
    Cont.. • The 5-ASAsare used to treat mild IBD. • A prospective study + large case series  no increased risk of teratogenicity • AZA/6-MP: discontinuation before or during pregnancy is not advisable. • Glucocorticoid t/t for moderate to severe IBD during pregnancy is a/w other complications, including maternal glucose intolerance and HTN (risks factor for preeclampsia), macrosomia, and fetal adrenal suppression. • Prednisolone: more efficiently metabolized by the placenta  less risk of adrenal suppression • Newer data support budesonide • There is still limited data on the effects of treatment with anti-integrin and anti-IL-12/23 antibodies (vedolizumab or natalizumab and ustekinumab, respectively) during pregnancy.
  • 27.
    Cont.. • TNF-α antagonists •Serum infliximab levels increase, whereas serum adalimumab levels are stable, during pregnancy • Post-marketing registries of safety data and case series  no increased incidence of fetal malformations or miscarriage • Recently published guidelines recommend that TNF-α antagonists be continued throughout pregnancy, unless otherwise indicated • Babies exposed in utero to these drugs should not receive live vaccines during the first 6 months of life; however, other vaccines are recommended • Vaginal delivery is not contraindicated in IBD patients, but CS is recommended for patients with active perineal disease. • Patients with ileoanal pouches are often advised to avoid vaginal delivery in order to avoid anal sphincter injury.
  • 29.
    Appendicitis • Acute appendicitisis the most common non- obstetric indication for exploratory laparotomy in pregnant women • complicates approx. 1 in 1500 pregnancies and may develop at any time during the course of gestation • Diagnosis may be difficult • enlarging uterus  displaces the cecum and appendix cephalad alters the location of pain  delayed detection as pregnancy progresses. • Late diagnosis  ↑ed maternal and fetal morbidity and mortality Fig. Location of appendix with gestation
  • 30.
    Gallstone dIsease Prevalence ofgallstones in asymptomatic pregnant women: 2.5-12% Increased predisposition to formation of CH stones Alternation in bile composition: CH supesaturation + ↓chenodeoxycholic acid + ↑cholic acid ↑bile acid pool Estrogen/progesterone  ↓GB contractility Surgical intervention, if needed, does not increase risk of preterm labour, fetal or maternal mortality
  • 31.
    Acute Pancreatitis Uncommon: oncein every 1066 to 3300 pregnancies Most cases caused by GB stones, and present during 3rd trimester or puerperium Cl/f  similar Complications  rare
  • 32.
  • 33.
    Hepatic Disorders uniqueto pregnancy Cholestasis of Pregnancy • form of intrahepatic cholestasis a/w pruritus, elevated serum bile acids, and bland cholestasis on liver biopsy. • usually presents in the 3rd trimester, but may be seen earlier as 1st trimester • Cllinical presentation: • Pruritus: most severe in the skin of the palms and soles and at night. • Jaundice: 10% to 25% • Intense cholestasis  steatorrhea, usually subclinical • Lab Findings: • Elevated SBA > 10 μmol/L • SALP: modestly↑, GGTP: normal or only marginally ↑ • AST/ALT ↑ (as high as ~1000 U/L ∞ viral hepatitis) • ↑ Sr. autotaxin level: sensitive and specific diagnostic test
  • 34.
    Cont.. • Clinical improvementand laboratory resolution begins with delivery of the infant  usually prompt and complete. • Planned early elective delivery immediately after fetal maturity is recommended • no residual hepatic defect • increased risk for gallstones, cholecystitis, and pancreatitis. • 60% to 70% develop cholestasis during subsequent pregnancies (although recurrent episodes may be less severe than the initial one) or with use of OCPs contraceptives. • The risk of recurrence with subsequent pregnancies is increased by interval cholecystectomy. • Complications (with SBA > 40 μmol/L) • Fetal distress, stillbirth, and premature delivery
  • 35.
    Cont.. • Pathogenesis: • mutationsof the MDR3 (ABCB4) gene: approx. 15% of cases • no relationship to HLA type • increased sensitivity to the cholestatic effects of exogenous estrogen • D/D: PBC, PSC, BRIC, cholestatic viral hepatitis, DILI, and bile duct obstruction • Management of cholestasis of pregnancy is primarily palliative. • UDCA: symptomatic relief + ↓fetal complications • Dose: 15 mg/kg/day, one report  higher dose (20 to 25mg/kg/day): more effective. • Bile-acid binders s/a cholestyramine and guar gum • May worsen steatorrhea and resultant fat-soluble vitamin deficiencies. • Glucocorticoid (e.g., oral dexamethasone 12mg/day for 7 days): reduce itching and SBA • Phenobarbital: may relieve itching but may adversely affect the fetus.
  • 36.
    Preeclampsia • multi-system disordercharacterized by de novo hypertension associated with endothelial damage and maternal organ dysfunction, possibly including the liver, that may produce severe, even life-threatening, complications and affect pregnancy outcome • Pathology: placental ischemia • complicates 3% to 10% of pregnancies • Occurs >20th WOP and puerperium < 12 weeks • Criteria • sustained BP ≥ 140/90 mm Hg after the 20th WOP in a previously normotensive woman, • Proteinuria (≥300 mg/24 hr) ~Urine protein of 30 mg/dL (“1+ dipstick”) • Pedal edema
  • 37.
    HELLP Syndrome 12% ofpre-eclampsia, 0.2-0.8% of all pregnancies
  • 38.
    Liver biopsy: periportalhemorrhage, intrasinusoidal fibrin deposition, irregular areas of hepatic necrosis with mild reactive hepatitis
  • 39.
    Indication for abdominalimaging • Severe abdominal pain, neck or shoulder pain, or a sudden drop in BP • USG/CT/MRI: intrahepatic h’ge and infarction, subcapsular hematoma ITP TTP APS D/D • Family History: may be present • AR, AD with variable penetrance • women with hypercoaguable state  early and severe PE • Increasing evidence: ↑ sFlt1  antagonist of VEGF, PGF, sEng • Clinical and laboratory resolution after delivery of fetus  can recur in subsequent pregnancies but usually does not • Severe PE and HELLP  platelet transfusion, HD, PE (occ) • Glucocorticoid: improve platelet count and ALT, ↓hospitalization and ICU stay, but NO IMPROVEMENT IN MATERNAL MORBIDITY AND MORTALITY
  • 40.
    Acute Fatty Liverof Pregnancy • Characterised by • microvesicular fatty liver • presents late in pregnancy as ALF, s/t as fulminant ALF with sudden onset of coagulopathy and HE • without prior h/o liver disease • Pathophysiology: • Unknown • Well established a/w inherited fatty-acid- oxidation defect ~ Jamaican vomiting sickness • Management • Early diagnosis and prompt delivery of fetus 100% survival • Supportive therapy: antibiotic, MV, HD Hypoglycemia and HE s/b suspected when patients exhibit altered sensorium
  • 41.
    • Usually presentslate in pregnancy (1 in 6700 3rd trimester preganancies) , usually between 34-37 WOP, as early as 19-20 weeks, rarely after delivery • m/c in primiparous women and multiple gestation • Pre-eclampsia accompanies in 21-64% of cases • Complications: ascites, pleural effusion, AP, respiratory failure, renal failure, infection • Hepatic imaging: staetosis, hematoma, rupture, and infarction • Histological hallmark: • Small-droplet fatty infiltration • Spares hepatocytes surrounding portal areas • Most prominent in zone 3 • No periportal h’ge and sinusoidal fibrin deposition • D/D: Viral hepatitis, DILI
  • 42.
    • Perinatal mortalityrates < 7%. • Surviving infants may have LCHAD deficiency • nonketotic hypoglycemia and obtundation • Recurrence of AFLP, particularly in women with LCHAD deficiency. • In all cases of AFLP the mother, father, and child should be tested for the G1528C LCHAD mutation
  • 44.
    Other Hepatic Disordersin Pregnancy Viral Hepatitis • Hepatitis A • unless unusually severe, does not appear to alter the normal course of pregnancy, nor does pregnancy appear to influence the natural history of disease. • Hepatitis E • enterically transmitted RNA virus with 4 genotypes and 1 serotype. • Genotypes 1 and 2 only infect humans and usually cause epidemic disease during the monsoon season in central and south Asia and India. • 3rd trimester: fulminant ALF; mortality rate of up to 20%. • a/w IUFD and abortion • Risk greater in any trimester than uninfected counterparts Hepatitis A Hepatitis E
  • 45.
    HBV and HDV •HBV infection in pregnant women is the most important factor perpetuating the worldwide epidemic of CHB • HBV transmission can occur at any time during gestation, at the time of delivery or after birth • most MTCT occurs during delivery (neonate’s immune system is incapable of clearing the virus). • Vertical transmission of HBV is responsible for most cases of CHB in endemic areas, esp.SEA and Africa • W/out t/t, 90% of infants born to HBeAg positive mothers and 10% of infants born to HBeAg negative mothers develop CHB infection • Antiviral therapy beginning in the 3rd trimester is recommended for pregnant women • inactive hepatitis B and serum HBV DNA levels > 200,000 IU/mL. • active hepatitis B  same as for non-pregnant women. • When there is an indication for t/t, it should be stopped at, or within 4 weeks of delivery • Continued treatment for up to 12 weeks postpartum does not protect the mother from disease flares.
  • 46.
    Cont.. • Invasive proceduresduring pregnancy, such as amniocentesis, may pose a risk of MTCT, especially when the maternal HBV-DNA level is ≥ 7 log copies/mL. • The infants of mothers with a reactive serum test for HBsAg should receive HBIG and hepatitis B vaccine within 12 hours of delivery. • 1% to 2% of treated infants will become chronically infected with HBV • In a recent study, approximately 25% of women with CHB had disease flares in the first few months after delivery • pregnant and postpartum patients with CHB s/b monitored closely for up to 6 months after delivery • TDF is preferred: reliable efficacy + high barrier to resistance. • Vaccination of non-immune pregnant women against HBV infection is safe and effective.
  • 47.
    Cont.. • HDV infectionrequires simultaneous acute or chronic hepatitis B virus infection. • Pregnant patients with hepatitis B who are most likely to have HDV co-infection HIV and immigrants from areas of high HDV endemicity. • anti-HDV antibody  HDV infection • There is no evidence that pregnancy changes the natural course of hepatitis D. • Prevention of vertical transmission of HDV is best accomplished by • vaccination of the mother against infection with hepatitis B virus, or • existing maternal CHB: infant vaccination + HBIG within 12 hours of delivery
  • 49.
    • No recommendationfor universal HCV screening of pregnant women • HCV antibody testing: risk factor for viral exposure, s/a IVDU, HIV co-infection • Reactive antibody test  confirmatory HCV RNA • MTCT is the principal cause of hepatitis C in children • Incidence of HCV vertical transmission • HCV RNA-positive, HIV-negative women: 5.8% • HCV RNA-positive, HIV-positive women: 10.8% • HCV-RNA ≥ 106 /mL  36% of cases • The incidence of perinatal HCV infection does vary whether the baby is delivered vaginally or by CS HCV
  • 50.
    HCV Cont.. • AlthoughHCV RNA can be detected in breast milk, breastfeeding is not considered to be a risk factor for neonatal HCV infection • Chronic hepatitis C may be independently a/w development of GDM, preterm delivery, LBW, IUGR, and cholestasis of pregnancy • When possible, women of reproductive age with hepatitis C should receive antiviral therapy before becoming pregnant • DAA are not approved for use during pregnancy • No treated with INF/ribavirin (teratogen) • Previously infected individuals may have spontaneous HCV-RNA clearance after delivery
  • 51.
    HSV • Immunocompetent: sub-clinicalhepatitis • Immunosuppressed/pregnant: severe liver disease (fulminant liver failure) • May have subtle oropharyngeal or genital herpetic lesions. • Encephalopathy may result from herpes encephalitis. • T/t with oral acyclovir or valacyclovir: highly effective + prevent MTCT
  • 52.
    Chronic Liver Diseaseand Portal Hypertension • Women with significant CLD/COL often have anovulatory menstrual cycles or are amenorrheic  unlikely to become pregnant • PHTN, ascites, and compensatory dilation of submucosal esophageal veins connecting the portal circulation to the azygos vein can occur in pregnant women with NCPH aggravated by physiologic increases in circulating blood volume • ↑ed maternal blood volume  ↑risk of variceal bleeding in pts with underlying PHTN • with cirrhosis: 18% to 32% • with known PHTN: 50% • with preexisting varices: 78% • EBL: preferred initial therapy • Also a/w increased risk of death, hepatic decompensation, splenic artery rupture, and uterine hemorrhage
  • 53.
    • Vasopressin andoctreotide infusions may theoretically cause uterine ischemia and induce premature labor • The AASLD has recommended that every individual with cirrhosis who have a liver stiffness > 20 kPa (FibroScan) and a platelet count < 150,000/mm3 should have endoscopic screening for EV. • No formal guidelines for prophylactic management of EV in pregnant women. • β-Adrenergic receptor antagonists are tocolytic, but these drugs do not repress normal labor in chronically treated pregnant patients. • Ascites and HE in pregnant women with CLD are managed in the customary manner. • The only therapy available for severe hepatic decompensation during pregnancy is LT. • The MELD score can help predict clinical decompensation in a cirrhotic woman during pregnancy.
  • 54.
    Safety of drugsused for CLD in Pregnancy
  • 55.
    Wilson Disease • WDin women of childbearing age is a/w amenorrhea and infertility. • T/t  removal of excess copper  resumption of ovulatory cycles subsequent pregnancy. • Discontinuation of therapy during pregnancy  sudden copper release  hemolysis, ALF, and death. • d-Penicillamine is potentially teratogenic • Zinc salts s/a zinc acetate do not appear to be teratogenic  preferred therapy for WD in pregnancy
  • 56.
    Autoimmune Liver Diseases •Classic (type-1) AIH • typically presents around the expected time of menarche, but is a/w amenorrhea. • Pregnancy is a/w ↑ed incidence of spontaneous abortion and preterm delivery. • Pregnant women with prior AIH may have disease flare during pregnancy and postpartum. • Azathioprine: non-teratogenic • PBC • much more common in postmenopausal women • may experience an exacerbation of pruritus during pregnancy. • safety of UDCA during pregnancy has not been formally proved
  • 57.
    Hepatic Tumors andMass Lesions • Benign liver lesions found commonly in women of childbearing age include adenomas, FNH, and hemangiomas. • Hepatic adenomas are a/w OCP use and may enlarge during pregnancy • Enlarging lesions can bleed and rupture into the abdominal cavity. • FNH and hemangiomas in pregnant pts have also been reported to hemorrhage. • HCC occurs almost exclusively in persons with CLD and may present in the absence of cirrhosis in young people with chronic HBV infection • MSAFP has limited predictive value for HCC • Can also increase in Down syndrome, NTD, and molar pregnancy.
  • 58.
    • Fibrolamellar carcinoma •slow-growing liver cancer usually found in young adults and also in pregnancy. • Aggressive neoplasm: 5Y survival < 50%. • Hepatic metastases from other cancers are rare in women of childbearing age.
  • 59.
    Budd-Chiari Syndrome • Pregnancy:predisposing factor for the development of venous thrombosis. • Hepatic vein thrombosis may occur in a/w HELLP syndrome and with preeclampsia in women who have an APLA. • Pregnant women who develop hepatic vein thrombosis s/b evaluated for the presence of APLA and other circulating procoagulants (e.g., factor V Leiden), and also for JAK-2 mutation.
  • 60.
    Pregnancy After LiverTransplantation • Women of childbearing age may become pregnant after successful orthotopic LT and deliver normal Infants. • Transplant patients must continue immunosuppressive therapy during gestation but may need to have their treatment modified.
  • 61.
    Summary of Pharmacologicaltreatment of Liver Disease during Pregnancy
  • 63.
    Reference • Sleisinger andFordtran’s Gastrointestinal and Liver Diseases 11th E • Yamada’s Textbook of Gastroenterology 7th E