**4. Abnormalities of placenta**

### **4.1. Placenta succenturiata**

The accessory lobe is developed from the activated villi on the chorionic leave, may be placed at varying distances from the main placental margin. A leash of vessels connecting the main to the small lobe traverses through the membranes (**Figure 5**). In cases of absence of communicating blood vessels, it is called placenta spuria. The incidence of placenta succenturiata is about 3%. If the succenturiate lobe is retained, the following birth of the placenta may lead to:


**c.** preterm labor

It can be:

**4.4. Placenta extrachorialis**

There is increased chance of:

**b.** Hydrorrhea gravidarum **c.** Antepartum hemorrhage

**e.** Preterm delivery

**d.** Growth retardation of the baby

**f.** Retained placenta or membranes

**4.5. Morbidly adherent placenta**

the peritoneum or bladder.

**a.** Abortion

**d.** decreased birth weight of baby and placenta

the fetal vessels appear to terminate.

**1.** Circumvallate placenta: the fetal surface is divided into a central depressed zone surrounded by a thickened white ring which is usually complete. The ring is situated at varying distances from the margin of the placenta and is composed of a double fold of amnion and chorion with degenerated decidua (vera) and fibrin in between. Vessels radiate from

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**2.** Placenta marginata: a thin fibrous ring is present at the margin of the chorionic plate where

Morbidly adherent placenta, which includes placenta accreta, increta, and percreta, implies an abnormal implantation of the placenta into the uterine wall (**Figure 6**). The incidence of placenta accreta has increased significantly over the past several decades, with the main risk factors including prior cesarean section and placental previa. Sonographic markers of placenta accreta can be present as early as the first trimester and include a low uterine implantation of a gestational sac, multiple vascular lacunae within the placenta, loss of the normal hypoechoic retroplacental zone, and abnormality of the uterine serosa-bladder interface, among others.

**a.** Placenta accreta is an extremely rare form in which the placenta is directly anchored to the myometrium partially or completely without any intervening decidua. The probable cause is due to the absence of decidua basalis and poor development of the fibrinoid layer.

**c.** Placenta percreta: The placenta penetrates whole of the myometrium and may reach up to

**b.** Placenta increta: The placenta invades whole thickness of myometrium.

the cord insertion as far as the ring and then disappear from view.

**Figure 5.** Placental abnormalities.

*Treatment*: Whenever the diagnosis of missing lobe is made, exploration of the uterus and removal of the lobe under general anesthesia is to be done.

#### **4.2. Velamentous placenta**

Normally, the umbilical cord inserts into the middle of the placenta as it develops. In velamentous cord insertion, the umbilical cord inserts into the fetal membranes (chorioamniotic membranes) and then travels within the membranes to the placenta (between the amnion and the chorion). The exposed vessels are not protected by Wharton's jelly and hence are vulnerable to rupture (**Figure 5**). Rupture is especially likely if the vessels are near the cervix, in which case they may rupture in early labor, likely resulting in a stillbirth. Once it is diagnosed, baby should be delivered by cesarean section.

#### **4.3. Battledore placenta**

Umbilical cord may be attached in the center, off center, on the edge, or in the membranes of the placenta. Battledore placenta is a placenta in which the umbilical cord is attached at the placental margin. The shortest distance between the cord insertion and the placental edge is within 2 cm. The incidence of the battledore placenta is 7–9% in singleton pregnancies and 24–33% in twin pregnancies [4, 5]. Complications associated with the battledore placenta are:


#### **4.4. Placenta extrachorialis**

It can be:


There is increased chance of:

**a.** Abortion

*Treatment*: Whenever the diagnosis of missing lobe is made, exploration of the uterus and

Normally, the umbilical cord inserts into the middle of the placenta as it develops. In velamentous cord insertion, the umbilical cord inserts into the fetal membranes (chorioamniotic membranes) and then travels within the membranes to the placenta (between the amnion and the chorion). The exposed vessels are not protected by Wharton's jelly and hence are vulnerable to rupture (**Figure 5**). Rupture is especially likely if the vessels are near the cervix, in which case they may rupture in early labor, likely resulting in a stillbirth. Once it is diag-

Umbilical cord may be attached in the center, off center, on the edge, or in the membranes of the placenta. Battledore placenta is a placenta in which the umbilical cord is attached at the placental margin. The shortest distance between the cord insertion and the placental edge is within 2 cm. The incidence of the battledore placenta is 7–9% in singleton pregnancies and 24–33% in twin pregnancies [4, 5]. Complications associated with the battledore

removal of the lobe under general anesthesia is to be done.

nosed, baby should be delivered by cesarean section.

**4.2. Velamentous placenta**

**Figure 5.** Placental abnormalities.

6 Placenta

**4.3. Battledore placenta**

placenta are:

**a.** fetal distress

**b.** intrauterine growth restriction


#### **4.5. Morbidly adherent placenta**

Morbidly adherent placenta, which includes placenta accreta, increta, and percreta, implies an abnormal implantation of the placenta into the uterine wall (**Figure 6**). The incidence of placenta accreta has increased significantly over the past several decades, with the main risk factors including prior cesarean section and placental previa. Sonographic markers of placenta accreta can be present as early as the first trimester and include a low uterine implantation of a gestational sac, multiple vascular lacunae within the placenta, loss of the normal hypoechoic retroplacental zone, and abnormality of the uterine serosa-bladder interface, among others.


pregnancies and in female babies [6]. Chorioangiomas that are clinically evident are less common with an incidence between 1:3500 and 1:9000 births [6]. It is believed to arise by 16th day of fertilization, although there is no documentation of the tumor in the first trimester [7]. In the majority of cases, it is small or microscopic and of no clinical significance. If it increases in size >5 cm, then it may be associated with serious maternal and fetal complications (**Figure 7**) [6]. The pathogenesis of these neoplasms is controversial; however, they can originate from any part of the placenta excluding the trophoblastic tissues [8]. Three histological patterns of cho-

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• The angiomatous is the most common, with numerous small areas of endothelial tissue,

These lesions are sometimes classified as placental hamartomas rather than true neoplasia [10].

Large tumors probably act as arteriovenous shunts and cause complications. Maternal complications are preeclampsia, preterm labor, placental abruption, polyhydramnios, and postpartum hemorrhage [11]. The correlation of chorioangioma with hydramnios and preterm delivery is found to be significant among the various reported clinical complications. Fetal congestive heart failure may develop because of the increased blood flow through the low resistance vascular channels in the chorioangioma acting as an arteriovenous shunt. Other associated fetal complications are nonimmune hydrops, fetal demise, hemolytic anemia, congenital anomalies, fetal thrombocytopenia, cardiomegaly, intrauterine growth restriction, and neonatal death [12].

rioangiomas have been described: angiomatous, cellular, and degenerate [9];

• The cellular pattern has abundant endothelial cells within a loose stroma.

capillaries, and blood vessels surrounded by placental stroma.

• The degenerate pattern has calcification, necrosis, or hyalinization.

There is no malignant potential.

**Figure 7.** Chorioangioma of placenta.

**Figure 6.** Morbidly adherent placenta (A: Accrete, B: Increta, C: Percreta).

#### **4.6. Gestational trophoblastic disease/neoplasm**

Gestational trophoblastic disease is divided into molar and nonmolar tumors. Nonmolar tumors are grouped as gestational trophoblastic neoplasia. It is classified as:


#### **4.7. Chorioangioma of placenta**

Placental chorioangioma is the commonest benign tumor of the placenta. Its incidence is around 1% when examined microscopically and is seen more frequently in multiple pregnancies and in female babies [6]. Chorioangiomas that are clinically evident are less common with an incidence between 1:3500 and 1:9000 births [6]. It is believed to arise by 16th day of fertilization, although there is no documentation of the tumor in the first trimester [7]. In the majority of cases, it is small or microscopic and of no clinical significance. If it increases in size >5 cm, then it may be associated with serious maternal and fetal complications (**Figure 7**) [6].

The pathogenesis of these neoplasms is controversial; however, they can originate from any part of the placenta excluding the trophoblastic tissues [8]. Three histological patterns of chorioangiomas have been described: angiomatous, cellular, and degenerate [9];


These lesions are sometimes classified as placental hamartomas rather than true neoplasia [10]. There is no malignant potential.

Large tumors probably act as arteriovenous shunts and cause complications. Maternal complications are preeclampsia, preterm labor, placental abruption, polyhydramnios, and postpartum hemorrhage [11]. The correlation of chorioangioma with hydramnios and preterm delivery is found to be significant among the various reported clinical complications. Fetal congestive heart failure may develop because of the increased blood flow through the low resistance vascular channels in the chorioangioma acting as an arteriovenous shunt. Other associated fetal complications are nonimmune hydrops, fetal demise, hemolytic anemia, congenital anomalies, fetal thrombocytopenia, cardiomegaly, intrauterine growth restriction, and neonatal death [12].

**Figure 7.** Chorioangioma of placenta.

**4.6. Gestational trophoblastic disease/neoplasm**

**Figure 6.** Morbidly adherent placenta (A: Accrete, B: Increta, C: Percreta).

**a.** Hydatidiform mole

**b.** Gestational trophoblastic neoplasia

**e.** Placental site trophoblastic tumor **f.** Epithelioid trophoblastic tumor

**4.7. Chorioangioma of placenta**

**i.** Complete

**c.** Invasive mole

**d.** Choriocarcinoma

**ii.** Partial

8 Placenta

Gestational trophoblastic disease is divided into molar and nonmolar tumors. Nonmolar

Placental chorioangioma is the commonest benign tumor of the placenta. Its incidence is around 1% when examined microscopically and is seen more frequently in multiple

tumors are grouped as gestational trophoblastic neoplasia. It is classified as:

Antenatal ultrasound examination has made diagnosis and follow up possible before delivery. In the present case, the placental tumor was not diagnosed in the ultrasound documentation rather polyhydramnios was reported. Doppler ultrasound examination is the gold standard in primary diagnosis of hemangioma. But unfortunately, we could not conduct Doppler USG in the present case as delivery was imminent. Magnetic resonance imaging (MRI) is used only in suspicious cases, while the computed tomography (CT) technique has a limited role in the diagnosis of the placental angioma, mainly because of the high radiation risk and poor tissue differentiation.

[6] Guschmann M, Henrich W, Dudenhausen JW. Chorioangiomas-new insights into a well-known problem. II. An immuno-histochemical investigation of 136 cases. Journal

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[7] Bracero LA, Davidian M, Cassidy S. Chorioangioma: Diffuse Angiomatous Form. 1993- 09-18-11. Available from: https://www.hindawi.com/journals/criog/2012/913878

[8] Elsayes KM, Trout AT, Friedkin AM, Liu PS, Bude RO, Platt JF. Imaging of the placenta: A multimodality pictorial review. RadioGraphics. 2009;**29**(5):1371-1391 [PubMed] [9] Marchetti AA.A consideration of certain types of benign tumors of the placenta. Surgery,

[10] Kuhnel P. Placental chorioangioma. Acta Obstetricia et Gynecologica Scandinavica.

[11] Patil M. Placental chorangioma, A rare cause of Pre-Eclampsia. Global Journal for Research Analysis. 2013;**2**(5):197-198. ISSN No: 2277-8160. Available from: https://www.

[12] Kodandapani S, Shrestha A, Ramkumar V, Rao L. Chorioangioma of placenta: A rare placental cause for adverse fetal outcome. Case Reports in Obstetrics and Gynecology.

[13] Wanapirak C, Tongsong T, Sirichotiyakul S, Chanprapaph P. Alcoholization: The choice of intrauterine treatment for chorioangioma. Journal of Obstetrics and Gynaecology

[14] Quintero RA, Reich H, Romero R, Johnson MP, Gonçalves L, Evans MI. In utero endoscopic devascularization of a large chorioangioma. Ultrasound in Obstetrics and

[15] Hosseinzadeh P, Shamshirsaz AA, Javadian P, Espinoza J, Gandhi M, Ruano R, et al. Prenatal therapy of large placental chorioangiomas: Case report and review of the litera-

ture. AJP Reports. Oct 2015;**5**(2):e196-e202. DOI: 10.1055/s-0035-1558829

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researchgate.net/publication/292060070

Research. 2002;**28**(2):71-75

Gynecology. 1996;**8**(1):48-52

2012;**2012**. Article ID 913878. DOI: 10.1155/2012/913878

1933;**13**:143-145

Chorioangioma with complications before fetal viability requires interventions. Alcohol injection, laser coagulation of feeding vessels, and microcoil embolization of the feeding vessels are described for women with fetal complications like hydrops [13, 14]. Large chorioangioma associated with polyhydramnios leads to high perinatal morbidity and mortality. Polyhydramnios is treated with therapeutic amniocentesis and maternal indomethacin therapy [12]. Steroid administration for acceleration of fetal lung maturity before 34 weeks is indicated. If complications appear late in pregnancy, delivery is the choice. A recent literature review concluded that further studies are needed to refine the appropriate selection criteria that will justify the risk of invasive in utero therapy for chorioangiomas [15].
