Fetal hepatic calcifications can be divided into three main categories: peritoneal, parenchymal, and vascular. Peritoneal hepatic calcifications present as calcified masses on the surface of the fetal liver. Most commonly, this is due to meconium peritonitis resulting from in utero bowel rupture. Meconium peritonitis is the most common cause of fetal abdominal calcifications (Lince et al., 1985) (see Chapter 70). Parenchymal calcifications are due to the presence of intrauterine infection or tumor. Fetal tumors may be primary in the liver or metastatic, presenting as a complex mass with areas of increased echogenicity and possible shadowing. Fetal tumors encompass both benign and malignant varieties, including hemangioendotheliomas, hamartomas, and hepatoblastomas. Parenchymal calcifications appear as scattered nodules, with or without additional evidence of other affected organs. The most common in utero infections that can cause fetal liver calcifications include varicella and the TORCH agents (Figure 69-1). Hepatic calcifications due to vascular abnormalities result from calcified portal or hepatic venous clots, which are due to hypoperfusion or thromboembolism (Nguyen and Leonard, 1986; Bronshtein and Blazer, 1995).

With the increased utilization of prenatal sonographic screening, fetal hepatic calcifications are detected prenatally more frequently than they are observed in newborn infants. In one study, evidence of hepatic calcifications was noted in 14 of 24,600 fetuses, an incidence of approximately 1 in 1700 (0.05%) of screened fetuses, (Bronshtein and Blazer, 1995). In a population of 1500 spontaneously aborted fetuses, 33 were demonstrated to have hepatic calcification, an incidence of 2.2% in this abnormal patient population (Hawass et al., 1990). In the 33 affected fetuses, 17 hepatic calcifications were found in the first trimester and 16 in the second trimester.

Fetal liver calcifications can be detected reliably by the beginning of the second trimester of pregnancy (Figure 69-2). Bronshtein and Blazer, (1995) reported their 8-year experience in extensive targeted second trimester sonographic screening for fetal abnormalities, which included hepatic calcifications in 24,600 consecutive pregnancies. Hepatic calcification was identified in 14 fetuses; of these, 12 had one or two areas of focal calcifications. One fetus had evidence of four different foci of calcifications. In one fetus, there were diffuse hepatic, peritoneal, and intestinal calcifications. No correlation was seen between the number or location of calcifications and the occurrence of malformations or eventual outcome for the child. Of the 14 affected fetuses, 13 had persistent hepatic calcifications noted on serial sonographic scans. In one case initially diagnosed at 15 weeks of gestation, calcifications resolved by 24 weeks. Four fetuses had associated anomalies, which included two cases of trisomy 18, one case of dwarfism and hydronephrosis, and one case of polyhydramnios and bowel calcifications. This last fetus died in utero at 32 weeks of gestation and no autopsy was performed. Of the remaining 10 fetuses, all were normal at birth with no sequelae from the calcifications. Koopman and Wladimiroff (1998) reported their experience with seven fetuses with intrahepatic hyperechogenic foci. One case of trisomy 18 was identified. Another case had associated encephalocele and unilateral renal agenesis. Outcome was normal in five fetuses with isolated intrahepatic findings. More recently, Simchen et al., (2002) performed a 10-year prospective study of the cause and outcome of 61 cases of fetal liver calcifications; 21 of 61 (35%) cases were isolated and 40 (65%) had additional abnormalities. Of the isolated cases, 1 had trisomy 21, 1 had parvovirus B19 infection, 4 were lost to follow-up, and the remaining 15 infants did well. Of the 40 cases with associated abnormalities, 9 had minor findings, such as echogenic bowel or growth restriction. In this group, two were lost to follow-up and seven infants did well. Of the group with major associated sonographic abnormalities (n = 31), 10 had abnormal karyotypes and 1 had cytomegalovirus (CMV) infection. There was 1 fetal demise and 18 pregnancies were terminated. The most frequently associated anomalies included central nervous system (n = 13), cardiac (n = 12), cystic hygroma (n = 12), skeletal (n = 11), and hydrops fetalis (n = 9). Importantly, these investigators found no differences regarding cause and outcome when stratifying their cases by parenchymal or surface calcification; startifying cases by isolated or with additional abnormalities was more informative (Simchen et al., 2002).