Hepatic Disease in Pregnancy
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- Noreen Hunt
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1 Hepatic Disease in Pregnancy Objectives 1. Describe normal physiologic changes to the liver during pregnancy 2. Identify common liver disorders associated with pregnancy 3. Discuss current management guidelines and options for the treatment of liver disorders in pregnancy 1
2 Physical findings associated with Pregnancy Palmar erythema** Spider Angiomas** **Interestingly, these are also associated with Liver disease Jaundice/Icterus associated with Liver damage or hemolysis regardless of pregnancy status. Liver palpation beyond the late 2 nd trimester is not a clinically normal finding, as it is often displaced by the gravid uterus. Palpation of the Liver in the late 2 nd /3 rd trimester should be considered pathologic. Normal Physiologic Changes of the Liver in Pregnancy Albumin & Total Protein: decreased from the 1 st trimester Alkaline Phosphatase: increased in the 2 nd and 3 rd trimester Bilirubin: slight decrease from the 1 st trimester GGT (gamma glutamyltransferase): slight decrease in 3 rd trimester Serum Aminotransferase (ALT &AST): no change Prothrombin Time (PT): no change Total Bile Acids (fasting): no change LDH (lactate dehydrogenase): no change (Normal Laboratory Changes associated with Pregnancy) Unchanged Increases Decreases Albumin Total Protein Alkaline Phosphatase +++ Bilirubin Gamma glutamyl transferase (GGT) Serum Aminotransferase (ALT/AST) *** Prothrombin Time (PT) *** Lactate Dehydrogenase (LDH) *** Bile Acids *** 2
3 Clinical characteristics of liver diseases in pregnancy (UpToDate 2013) Liver diseases specific to pregnancy Acute Fatty Liver Disease of Pregnancy (AFLP) Multisystem diseases with hepatic manifestations Preeclampsia/HELLP Hyperemesis Gravidarum Hepatic diseases impacted by Pregnancy Cholelithiasis Thrombotic Disease (Budd Chiari Syndrome) Hepatic diseases unrelated and Not influenced by Pregnancy Viral Hepatitis NDD 28 yo G1P0 Sudanese woman with an uncomplicated pregnancy thru 22 weeks. At her prenatal visit around that GA, she described itching over her entire body, including the palms of her hands and the soles of her feet. She also had ongoing nausea and vomiting, Hyperemesis Gravidarum, for which she using anti emetic medication (Ondansterone), as well as treatment for GERD. Laboratory analysis was performed which revealed a mild elevation in her serum aminotransferases (ALT =167 & AST =167), and a significant elevation of her serum bile acids: 110 umol/l (0 19). Pt was started on ursodiol, and diphenhydramine prn. Pt went on to have debilitating GERD, profound anemia, uncontrollable pruritus, and ultimately gestational diabetes. She was transferred to the high risk OB group after the diagnosis of gestational diabetes at 27 weeks GA. 3
4 Histologically characterized by cholestasis without inflammation. HOWEVER, Liver biopsy is RARELY indicated Incidence cited as % of pregnancies worldwide (in the U.S. Bridgeport, CT, up to 6% in a primarily Latino population in Los Angeles, CA). Highest incidence noted in Bolivia and the Araucanos Indians of Chile. Estrogen is known to contribute to cholestasis, thus in those scenarios with elevated estrogen concentration, risk of ICP is increased ( twins). Also, may be impacted by altered progesterone metabolism. The formation of large amounts of sulfated progesterone metabolites,., may result in saturation of the hepatic transport system(s) utilized for biliary excretion. THUS, caution is advised in patients with history of ICP and use of progestins in pregnancy. LAB value abnormalities Serum total bile acids: Elevated Serum aminotransferases: Elevated PT (prothrombin time): Normal, BUT may be prolonged due to vitamin K deficiency of cholestasis, only to be further exacerbated by the use of bile acid sequestrants (i.e. cholestyramine) Clinical Manifestations: PRURITUS! May be generalized, but commonly involves the palms and soles. No Rash, but may see skin excoriations due to excessive scratching Abdominal pain is uncommon Other stigmata of liver disease, should encourage investigation into other sources of liver abnormalities. Imaging: Liver Appears Normal 4
5 Pathogenesis: Likely genetic component, specifically the ABCB4 (adenosine triphosphate binding cassette, subfamily B, member 4) encoding the MDR3 protein (multidrug resistance 3 gene). Whatever the cause(s): BILE ACIDS are incompletely cleared and accumulate in the plasma. 5
6 Treatment: should be focused on reducing maternal symptoms, and preventing maternal and fetal complications. Maternal Symptoms: ITCHING 10% may develop Jaundice Maternal Complications: Fat Soluble Vitamin Deficiency ( DAKE ) Rarely formation of gallstones exceedingly RARE encephalopathy. Maternal Comorbidities: Chronic Hepatitis C results in a 20X increased incidence of Cholestasis (Paternoster et al, 2002) Fetal Morbidity and Mortality: PREMATURITY Meconium stained amniotic fluid Neonatal Respiratory Distress Syndrome (due to bile acids in lungs) Intrauterine Fetal Demise (IUFD) Rarely occurs before final 4 weeks of gestation Median age of demise in 1 study was 38 weeks (20 IUFD s eval d) Pathophysiology of IUFD poorly understood, BUT emerging data suggests..an acute event due to fetal cardiac arrhythmia or vasospasm of the placental chorionic surface vessels, induced by high levels of bile acids. (Williamson et al, 2011 & Sepulveda et al 1991) Treatment: Maternal Ursodeoxycholic acid (UDCA, ursodiol) Improves pruritus, reduces bile acid concentration, increases prolongation of pregnancy No Adverse effects on mother or fetus 300mg TID or 500mg BID Cholestyramine Less effective than Ursodiol Increase risk of fat soluble vitamin deficiency, especially vitamin K 6
7 Treatment (con t): Dexamethasone No benefit when compared to either Ursodiol or Cholestyramine Hydroxizine Reduces symptomatic pruritus Diphenhydramine Reduces symptomatic pruritus No Adverse effects on mother or fetus 50mg q8h prn Antenatal Management: Ursodiol as previously discussed for maternal symptoms, has also been shown to decrease fetal morbidity Benefit of Antenatal surveillance remains controversial There is mounting evidence to induce at 37 weeks EGA, regardless of Fetal Lung Maturity. Some experts promote performing amniocentesis at 37 weeks and if mature deliver. If immature, delivery at 38 weeks without repeating amniocentesis Despite reactive NST s and reassuring BPP, there has been documented IUFD within the following hours. J.S. 25 y.o. G2P0 (ectopic x1) female at 38 weeks EGA with an uncomplicated antepartum course to date. At routine prenatal office visit (normal high BP/ normal UA/ normal FHR), patient stated she just feels different. Her partner brought up that the patient was drinking a ton of water and doesn t seem to go to the bathroom that often. At which point patient noted that her urine was darker. Given the subjective complaints, laboratory evaluation was ordered, and later that evening came back as a STAT result with the following values. Alk Phos 358 (20 125), ALT 304 (3 40), AST 463 (3 35), Bilirubin Total 6.8 ( ), Cr 1.4, BUN 7, Lytes:wnl, Glucose 127, plts 244k, Hct 32%, WBC 14k, Urine Protein: negative. Patient was contacted and instructed to come to L&D for further E&M. 7
8 histologically characterized by microvesicular fatty infiltration of hepatocytes That said, again, liver biopsy is RARELY indicated for diagnosing liver disease in pregnancy. Incidence: 1:10,000 1:20,000 deliveries, may be more common with multiple gestations Disease is ALWAYS present before delivery, but sometimes diagnosed post partum. LAB value abnormalities Serum Aminotransferases: modest elevation up to the 1000 s IU/ml. Serum Bilirubin: elevated usually Platelets (lower)/thrombocytopenia, which is associated with a MARKED reduction in Anti Thrombin III levels. Glucose (serum): Decreased, due to liver failure and lack of gluconeogenesis PT (prothrombin time): Prolonged Ammonia levels: elevated with liver failure Serum Creatinine: elevate with ARF Common symptoms include: Nausea & Vomiting Abdominal Pain (epigastric) Preeclampsia like symptoms may be present Transient Polyuria and/or Polydipsia may occur, due to renal impairment, which can by related to diabetes insipidus (DI). Transient Oliguria may ensue due to Acute Renal Failure (ARF) 8
9 Pathogenesis: thought to be associated with a defect in one of the inherited mitochondrial beta oxidation pathways. Specifically, long chain 3 hydroxyacyl CoA dehydrogenase deficiency (LCHAD) It is hypothesized that a mother who may or may not be a carrier of an LCHAD deficiency, is more likely to develop AFLP is the fetus she is carrying also harbors an LCHAD deficiency. Briefly, LCHAD catalyzes beta oxidation of fatty acids in the mitochondria. If this process is compromised due to a deficiency in the fetus, the accumulation of the precursor long chain fatty acid metabolites are toxic to the liver. Not all LCHAD mutations lead to AFLP, and some cases of AFLP have no identified mutation in LCHAD of the newborn. 9
10 Providers caring for the newborn should be informed of the diagnosis of AFLP and the association with LCHAD deficiency in the newborn. Testing or the newborn (and mother) should be done, and can be life saving for the infant, and informative for the mother for future pregnancies. When stressed, infants with LCHAD deficiency are at risk to develop nonketotic hypoglycemia, which mimics Reye s syndrome. Diagnosis and Treatment: Diagnosis is usually clinically acquired with laboratory support of the diagnosis. Major differential diagnosis confounder is HELLP syndrome Hypoglycemia and encephalopathy support AFLP Liver biopsy is diagnostic, BUT rarely indicated 10
11 Treatment is supportive with delivery and maintenance of euglycemia via glucose infusions, and avoidance of coagulopathy with transfusions of necessary blood products. May require ICU treatment/care Intubation for respiratory support Continued treatment of coagulopathy and bleeding, especially if MOD via C section Historically (1940 s): universally fatal for mother and infant. Today Maternal mortality rate of 1% and infant mortality rate of 10%. Recurrence risk is unknown. Mother and Infant should be tested for LCHAD mutation(s) HELLP Syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) 11
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