Pregnancy Pearls



Pregnancy Pearls





(Am J Gastroenterol. 2004;99:2479-88 & 1999;94:1728-32)


GENERAL



  • Liver histology and function do not change during pregnancy


  • Maternal blood volume and cardiac output increase, without corresponding increase in hepatic blood flow = net decrease in blood flow to liver


  • Labs remain normal: AST, ALT, GGT, Bili, PT/INR



    • Aφ can ↑ 2-4x (due to placenta source), return to normal within 20 days; Also ↑ α1-AT, Ceruloplasmin, Fibrinogen, Cholesterol


    • Albumin can decrease slightly, due to dilution, contributing to ˜ 20% decline in total serum protein concentration; Also ↓ ferritin


  • Can see small esophageal varices in 50% of pregnant women



    • Maternal blood volume and cardiac output ↑ significantly, without a corresponding ↑ in hepatic blood flow = net decrease in fractional blood flow to liver


    • Enlargement of the uterus makes venous return via the IVC progressively more difficult


    • Hence, blood is shunted via the azygous system and the development of esophageal varices


  • Avoid estrogen-based contraceptives if history of acute liver disease: After 5 years of OCP use, risk of hepatic adenoma ↑ 116-fold



    • Hepatic adenomas often regress with stopping estrogen, but can recur during pregnancy; surgical resection recommended


    • Peliosis hepatic: small venular cavities or lakes within the liver arising from injury to sinusoids: OCP & Anabolic steroid use


ACUTE FATTY LIVER OF PREGNANCY (AFLP)



  • Sudden catastrophic illness occurring late in pregnancy with microvesicular fatty infiltration resulting in liver failure with PSE


  • Rare disorder-rapid progression of liver failure in 3rd trimester (can develop post-partum); Most are nulliparous (unlike HELLP)



    • Recessive disorder, recurrence rate of 15-25%; Women with AFLP should undergo genetic counseling


  • Etiology: Fetal-maternal interaction; Fetus has deficiency in long-chain hydroxyacyl co-A dehydrogenase (LCHAD),



    • Leads to abnormal mitochondrial B-oxidation of FFA that accumulate in the mother and are highly toxic to maternal liver


  • Histology: Microvesicular steatohepatitis with mild-modest necrosis See also Liver- Histopathology of Liver (Chapter 4.19)


  • Clinical:



    • Largely non-specific; jaundice in most patients, N/V, malaise, thirst, altered mentation, RUQ pain


    • Severe: FHF, DIC, ARF, Coma, Death


    • Can occur with coexistent preeclampsia (50-100%): hypertension, proteinuria and edema


  • Labs: ↑ PT, AST/ALT (<1000), Bili (<5), Ammonia, Uric acid, WBC; ↓ Platelets, Glucose; Viral serologies negative; ± DIC



    • More severe synthetic dysfunction of AFLP helps distinguish from HELLP (the two are often difficult to distinguish)


  • Treatment: Immediate delivery of baby, Supportive ICU care, Recovery is usually complete and transplant rarely necessary


  • Maternal mortality can range from 10-33%; AFLP may reoccur with subsequent pregnancies but its reoccurrence is very rare


  • Child outcome: Previous mortality high as 90%



    • Child presents about 8 months with acute hepatic dysfunction: HSM, PSE, Fatty liver



      • Avoid this child’s morbidity by testing for long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency


    • Prompt dietary intervention by treating with medium-chain fatty acids equates to a much longer survival


AUTOIMMUNE HEPATITIS



  • Usually not a problem, but may worsen


  • Continue immunosuppressive drugs; Azathioprine/Imuran usually safe, but try to lower prednisone dose



BUDD-CHIARI SYNDROME: See also Liver- Clots (Chapter 4.09)

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Aug 24, 2016 | Posted by in GASTROENTEROLOGY | Comments Off on Pregnancy Pearls

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