Patient Registries, risks of gestational diabetes, preeclampsia, pre teI'm birth, and low-birthweight newborns were two-to threefold greater than in unafected women (Hagstrom, 2016). Yarrington and associates (2016) reported a high rate of gestational diabetes among nonobese women without liver disease, alcohol use, or diabetes, and who had elevated alanine transaminase levels in the irst trimester. s the obesity endemic worsens, adverse efects of this liver disorder on pregnancy will be clarified.
Irreversible chronic liver injury with extensive fibrosis and regenerative nodules is the inal common pathway for several disorders. Laennec cirrhosis from chronic alcohol exposure is the most frequent cause in the general population. But in young women-including pregnant women-most cases are caused by postnecrotic cirrhosis from chronic hepatitis Brand C. Many cases of cryptogenic cirrhosis are now known to be caused by NAFLD (Goh, 2016). Clinical manifestations of cirrhosis include jaundice, edema, coagulopathy, metabolic abnormalities, and portal hypertension with gastroesophageal varices and with splenomegaly that may cause thrombocytopenia. The incidence of deep-vein thromboembolism is increased (S0gaard, 2009). The prognosis is poor, and 75 percent have progressive disease that leads to death in 1 to 5 years.
Women with symptomatic cirrhosis frequently are infertile.
hose who become pregnant generally have poor outcomes. Common complications include transient hepatic failure, variceal hemorrhage, preterm delivery, fetal growth restriction, and maternal death (Tan, 2008). Outcomes are generally worse if esophageal varices coexist.
Another potentially fatal complication of cirrhosis arises from associated splenic artery aneurysms. Up to 20 percent of ruptures occur during pregnancy, and 70 percent of these rupture in the third trimester (Palatnik, 2017; Tan, 2008). In a review of 32 gravidas with aneurysm rupture, the mean aneurysm diameter was 2.25 cm, and in half of cases, the diameter was <2 cm (Ha, 2009). The 22-percent maternal mortality rate was likely related to the emergent presentation of these events. Parrish and colleagues (2015) described embolization of a 13 X 9 mm aneurysm in the third trimester leading to a splenic abscess and sepsis 3 weeks later.
In pregnant women, approximately half of cases of esophageal varices originate from cirrhosis or extrahepatic portal vein obstruction, which leads to portal system hypertension. Some cases of extrahepatic hypertension develop following portal vein thrombosis associated with one of the thrombophilia syndromes (Chap. 52, p. 1005). Others follow thrombosis from umbilical vein catheterization when the woman was a neonate, especially if she was born preterm.
With either intrahepatic or extrahepatic resistance to low, portal vein pressure rises from its normal range of 5 to 10 mm Hg, and values may exceed 30 mm Hg. Collateral circulation develops that carries portal blood to the systemic circulation. Blood drains into the gastric, intercostal, and other veins to the esophageal system, where varices develop. Bleeding is usually from varices near the gastroesophageal junction, and hemorrhage can be torrential. Bleeding during pregnancy from varices occurs in a third to half of afected women and is the major cause of maternal mortality within thisrgroup (Tan, 2008).