**10. Placental infections**

**Figure 6.** Ultrasound color Doppler image of a chorioangioma diagnosed in the second trimester of pregnancy.

and a "grape-like" placental appearance, both mistaken clinically and macroscopically for a partial hydatidiform molar pregnancy [44]. The differential diagnosis is important, because it may result in termination of pregnancy. Still, the final diagnosis is made by means of placental histology. The disorder also has been reported to be associated with both intrauterine growth restriction (IUGR) and fetal death [45]. In many cases, the cause of fetal death is fetal vascular obstructive pathology, causing longstanding, severe fetal hypoxia, due to chorionic vessel thrombosis [46]. Beckwith-Wiedemann syndrome has been linked to placental mesenchymal dysplasia. Invasive testing is advisable to confirm a normal karyotype and exclude

The placenta represents a natural selective barrier between maternal and fetal blood circulations, and it is highly sensitive to the hyperglycemic environment. Consequently, adaptive changes of the structure and function appear. The histological findings are typical: villous immaturity, villous fibrinoid necrosis, chorioangiosis, and increased angiogenesis [48]. Chronic fetal hypoxia can occur due to placental changes associated with inflammation and oxidative stress. Potential intrauterine complications are growth restriction, premature labor, preeclampsia, risk of oxygen deprivation, low neonate body temperature, low blood sugar levels at birth,

Chorioangioma is a benign vascular tumor, found in approximately 1% of all pregnancies [50]. It was firstly described in 1798 by Clarke [51]. This pathology is a malformation of the primitive angioblastic tissue of the placenta perfused by the fetal circulation. It is rarely clinically significant and is usually discovered incidentally. Most of the chorioangiomas have small

partial molar pregnancy [47].

334 Congenital Anomalies - From the Embryo to the Neonate

**8. Diabetic placenta**

and stillbirth [49].

**9. Placental chorioangioma**

Most infections arise from several infective agents that may cross into the placenta from the maternal circulation [1]. These kinds of infections can be associated with a variety of developmental effects, from virtually insignificant to major maternal and fetal developmental complications. Placental examination by a pathologist should be considered in every case of preterm delivery, fetal tachycardia, maternal signs of endomyometritis (e.g., fever, uterine tenderness, leukocytosis, tachycardia), neonatal intensive care unit admission, malodorous placenta, retained placenta or postpartum hemorrhage, and stillbirth [54]. However, a specific infectious agent is rarely diagnosed by placental examination. Still, the placental histology may confirm the clinical diagnosis of an infectious etiology in some cases of nonreassuring fetal heart rate patterns or neonatal morbidity/mortality. The most common placental infections are:


• Toxoplasmosis implies a risk of placental colonization, depending on the volume of uteroplacental blood flow, on the maternal immunocompetence, and parasitemia. Placental infection, described by granulomatous villitis, cysts, plasma cell deciduitis, villous sclerosis, and chorionic vascular thrombosis, is more common with advancing gestational age at the time of maternal parasitemia [59].

of HM is usually benign, but it has a known potential to become malignant and invasive. The incidence of a HM is 1:1000–2000 [67]. Risk factors include extremes of maternal age (greater than 35 years old and less than 20 years old), a previous molar pregnancy, women with previous spontaneous abortions or infertility, dietary factors, and smoking [68]. The HM can be a *complete mole*, with the absence of the fetus, or a *partial mole* with an abnormal fetus or a fetal demise; rarely, a mole coexists with a normal pregnancy. In complete HM, 90% of cases the karyotype are 46XX diploid, while in partial HM, the karyotype is usually triploid 69XX [1]. The histopathological event of HM is considered to be a proliferation of the villous trophoblast, accompanied by swelling of the chorionic villi, resulting in high levels of human chorionic gonadotrophin (hCG) production (e.g., **Figure 7**) [68]. The location of the HM is the uterine cavity, with exceptionally rare cases located in the fallopian tubes or ovaries. Clinically, the most common symptom is the vaginal bleeding in the first trimester. Sometimes an association of hyperemesis (severe nausea and vomiting) or passage of vaginal tissue described as "grape-like clusters" or "vesicles" can be encountered. If not early diagnosed, other significant complications may appear, such as hyperthyroidism, including tachycardia and tremors and preeclampsia. Usually, on a physical exam, there is a uterine size discrepancy compared with the amenorrhea period, the uterus being larger in complete mole and smaller in partial mole [69]. The ultrasound exam finding is a heterogeneous mass in the uterine cavity, with multiple anechoic spaces

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http://dx.doi.org/10.5772/intechopen.75985

**Figure 7.** Image of post-hysterectomy uterus invaded by a hydatidiform mole in a 48-year-old patient.

• *Chlamydia psittaci*: can infect the placenta and can cause significant feto-maternal morbidity and mortality by an intense, acute intervillositis, perivillous fibrin deposition with villous necrosis, and large irregular basophilic intracytoplasmic inclusions within the syncytiotrophoblast [60, 61].
