Placenta - Abnormalities

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Placental implantation abnormalities

The placenta is a mateno-fetal organ which begins developing at implantation of the blastocyst and is delivered with the fetus at birth. As the fetus relies on the placenta for not only nutrition, but many other developmentally essential functions, the correct development of the placenta is important to correct embryonic and fetal development.

Abnormalities can range from anatomical associated with degree or site of inplantation, structure (as with twinning), to placental function, placento-maternal effects (pre-eclampsia, fetal erythroblastosis) and finally mechanical abnormalities associated with the placental (umbilical) cord.

This current page lists some abnormalities associated with the placenta and also provides links to other resources. (See also Week 2 Abnormalities - Hydatidiform mole)

Placenta Links: Introduction | Lecture - Placenta | Practical - Placenta | Implantation | Villi Development | Trophoblast | Maternal Decidua | Endocrine | Cord | Membranes | Abnormalities | Stage 13 | Stage 22 | Histology | Vascular Beds | Blood Vessel Development | Stem Cells | Category:Placenta

Some Recent Findings

  • Hypoxic ischemic encephalopathy in newborns linked to placental and umbilical cord abnormalities[1] "Birth asphyxia and hypoxic ischemic encephalopathy (HIE) of the newborn remain serious complications. We present a study investigating if placental or umbilical cord abnormalities in newborns at term are associated with HIE. A prospective cohort study of the placenta and umbilical cord of infants treated with hypothermia (HT) due to hypoxic brain injury and follow-up at 12 months of age has been carried out. ...A velamentous or marginal umbilical cord insertion and histological abruption was associated with the risk of severe HIE. Velamentous or marginal umbilical cord insertion was found in 39% among HIE cases compared to 7% in controls." Neural System - Abnormalities
  • The branching pattern of villous capillaries and structural changes of placental terminal villi in type 1 diabetes mellitus[2] "In this paper, normal placental terminal villi and pathological villi of type 1 diabetic placentas were compared concerning the structure of villous stroma, spatial arrangement of villous capillary bed and quantitative assessment of capillary branching pattern. ...The quantitative assessment of capillary branching has shown that villous capillaries are more branched in diabetic placentas. It is concluded that type 1 maternal diabetes enhances the surface area of the capillary wall by elongation, enlargement of diameter and higher branching of villous capillaries and disrupts the stromal structure of terminal villi." Maternal Diabetes
  • Velamentous cord insertion caused by oblique implantation after in vitro fertilization and embryo transfer[3] "We present a case of a 36-year-old pregnant female after intracytoplasmic sperm injection. Ultrasonographic examination at 8 weeks' gestation revealed umbilical cord insertion with a viable fetus located on the septum membrane of dichorionic twin pregnancy near the anterior wall, while the other fetus was observed to have vanished. Next, this umbilical cord was seen to connect to the anterior wall and the placenta developed on the posterior wall later in the pregnancy. As a result, velamentous cord insertion with long membranous umbilical vessels developed at the time of delivery. The present case indicates that the assessment of the cord insertion site during the early gestation period is very important to predict any abnormality of the cord insertion site at the time of delivery. Furthermore, this case is valuable to understand the pathophysiological development of the placenta and velamentous cord insertion. "
More recent papers
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References listed on the rest of the content page and the associated discussion page (listed under the publication year sub-headings) do include some editorial selection based upon both relevance and availability.

Links: References | Discussion Page | Pubmed Most Recent

Search term: Placenta Abnormalities

Makiko Tachibana, Masahiro Nakayama, Shinobu Ida, Hiroyuki Kitajima, Nobuaki Mitsuda, Keiichi Ozono, Yoko Miyoshi Pathological examination of the placenta in small for gestational age (SGA) children with or without postnatal catch-up growth. J. Matern. Fetal. Neonatal. Med.: 2015;1-18 PMID: 25781499 Thomas E Ichim, Shuang Li, Hong Ma, Yuliya V Yurova, Julia S Szymanski, Amit N Patel, Santosh Kesari, Wei-Ping Min, Samuel C Wagner Induction of tumor inhibitory anti-angiogenic response through immunization with interferon Gamma primed placental endothelial cells: ValloVax™. J Transl Med: 2015, 13(1);441 PMID: 25779148 Richard J Levy Carbon Monoxide Pollution and Neurodevelopment: A Public Health Concern. Neurotoxicol Teratol: 2015; PMID: 25772154 Miriam Kamper, Clara C Manns, Julia A Plieschnig, Wolfgang J Schneider, N Erwin Ivessa, Marcela Hermann Estrogen enhances secretion of apolipoprotein B-100 containing lipoproteins by BeWo cells. Biochimie: 2015; PMID: 25765953 Mohamed Ahmed Mostafa AboEllail, Kenji Kanenishi, Nobuhiro Mori, Ako Kurobe, Toshiyuki Hata HDlive image of circumvallate placenta. Ultrasound Obstet Gynecol: 2015; PMID: 25754975

Search term: Placenta Previa

Sameera Ehtisham, Haleema Akhtar Hashmi Determinants of caesarean section in a tertiary hospital. J Pak Med Assoc: 2014, 64(10);1175-8 PMID: 25823160 Iwona Szymusik, Pawel Bartnik, Klaudia Wypych, Halszka Kolaczkowska, Katarzyna Kosinska-Kaczynska, Miroslaw Wielgos The association of first trimester bleeding with preterm delivery. J Perinat Med: 2015; PMID: 25822321 Diego Rossetti, Salvatore Giovanni Vitale, Giorgio Bogani, Agnese Maria Chiara Rapisarda, Ferdinando Antonio Gulino, Luigi Frigerio Usefulness of vessel-sealing devices for peripartum hysterectomy: a retrospective cohort study. Updates Surg: 2015; PMID: 25813428 Vijaya Kancherla, Sari Räisänen, Mika Gissler, Michael R Kramer, Seppo Heinonen Placenta previa and risk of major congenital malformations among singleton births in Finland. Birth Defects Res. Part A Clin. Mol. Teratol.: 2015; PMID: 25808834 Donna L D'Souza, John C Kingdom, Hagai Amsalem, John R Beecroft, Rory C Windrim, John R Kachura Conservative Management of Invasive Placenta Using Combined Prophylactic Internal Iliac Artery Balloon Occlusion and Immediate Postoperative Uterine Artery Embolization. Can Assoc Radiol J: 2015; PMID: 25797171

Placenta Shape

Circumvallate placenta

Placentas are generally round or oval in shape and can also be "irregular" (multilobate, "star") shapes. These irregular shaped placentas have been associated with lower birth weight for placental weight suggesting an altered function. [4]

Embryo Virtual Slides

Human Circumvallate Placenta

Circumvallate placenta 01.jpg

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Placenta Abnormal | Embryo Slides
Circumvallate placenta is an abnormally shaped placenta where the chorionic membranes are not inserted at the edge of the placenta, but are located inward from the margins toward the placental cord. The membranes are described as "doubled back" over the fetal surface of the placenta.

Placenta Weight

A recent Canadian study of 87,600 singleton births[5] has identified a number of risk factors for both high and low placental weight. Some factors are associated either before, after or both accounting for birthweight.

Low placental weight

  • chronic hypertension (before and after accounting for birthweight).
  • pre-eclampsia (before, but not after adjustment for birthweight).

High placental weight

  • anaemia (before and after adjustment for birthweight).
  • gestational diabetes (before and after adjustment for birthweight).
  • smoking (after adjustment for birthweight).
  • Placental and cord determinants include chorioamnionitis, chorangioma/chorangiosis, circumvallate placenta and marginal cord insertion.

Placenta Accreta

MRI Placenta accreta showing uterine bulging into the bladder.[6]

Abnormal adherence, with absence of decidua basalis. The incidence of placenta accreta also significantly increases in women with previous cesarean section compared to those without a prior surgical delivery.[7][8]

Ultrasound features:[9]

  1. Deficiency of retroplacental sonolucent zone
  2. Vascular lacunae
  3. Myometrial thinning
  4. Interruption of bladder line

Placenta Increta

Placenta Increta occurs when the placenta attaches deep into the uterine wall and penetrates into the uterine muscle, but does not penetrate the uterine serosa.

Placenta increta accounts for approximately 15-17% of all placenta abnormality cases.

Placenta previa and increta 02.jpg

Placenta Increta and Previa[10]

Placenta Percreta

MRI Surgery
Placenta percreta 04.jpg Placenta percreta 03.jpg
Placenta Percreta MRI[11] Surgical photograph
Showing the placenta extending through uterine wall (+) and covered by
thin serosal layer (arrow), no features of bladder invasion.

Placental villi penetrate myometrium and through to uterine serosa.

See clinical article on the laparoscopic management of placenta percreta. [12]

Placenta percreta 01.jpg

Placenta Percreta Histopathology[13]

Placenta Previa

historic model of Placenta Previa (praevia)

Historically, Paul Portal (1630-1703), a French physician[14], was the first to describe in 1685 a case of placenta previa in his "The Compleat Practice of Men and Women Midwives".

In this placental abnormality, the placenta overlies internal cervical os of uterus, essentially covering the birth canal. This condition occurs in approximately 1 in 200 to 250 pregnancies and risk factors include prior cesarean delivery, pregnancy termination, intrauterine surgery, smoking, multifetal gestation, increasing parity, and maternal age. A retrospective study of from 59,149 women of 724 pregnancies (1.2%) diagnosed with a complete or partial previa, identified no associated with fetal growth restriction.[15]

In the third trimester and at term, abnormal bleeding can require caesarian delivery and can also lead to Abruptio Placenta.

Ultrasound screening programs during 1st and early 2nd trimester pregnancies now include placental localization. Diagnosis can also be made by transvaginal ultrasound.

Placenta previa 01.jpg

Placenta previa MRI[11]

See also recent advances in the management of placenta previa. [16][8]

Ultrasound Placenta Previa

Placenta previa - anterior.jpg Placenta previa ultrasound 01.jpg
Anterior placenta position (upper arrow) in relation to cervix os (lower arrow). Posterior placenta position (arrow) in relation to cervix os (triangle).
Links: Ultrasound

Vasa Previa

Vasa previa (vasa praevia) placental abnormality where the fetal vessels lie within the membranes close too or crossing the inner cervical os (opening). This occurs normally in 1:2500-5000 pregnancies and leads to complications similar too those for placenta previa.[17][8]

Type II is defined as the condition where the fetal vessels are found crossing over the internal os connecting either a bilobed placenta or a succenturiate lobe with the main placental mass.[18]

There are suggestions that colour doppler ultrasound can be used to visualise the blood vessels in high-risk cases and if required elective caesarean performed at 35–36 weeks in cases diagnosed as vasa praevia.[19]

Two main associations:

  1. velamentous insertions (25–62%)
  2. vessels crossing between lobes in succenturiate or bilobate placentas (33–75%)

Some recent evidence of successful in utero laser ablation of type II vasa previa at 22.5 weeks of gestation.

Management of vasa previa

The following text is from a recent paper identifying the Canadian guidelines for the management of vasa previa.[20]

  1. If the placenta is found to be low lying at the routine second trimester ultrasound examination, further evaluation for placental cord insertion should be performed. (II-2B)
  2. Transvaginal ultrasound may be considered for all women at high risk for vasa previa, including those with low or velamentous insertion of the cord, bilobate or succenturiate placenta, or for those having vaginal bleeding, in order to evaluate the internal cervical os. (II-2B)
  3. If vasa previa is suspected, transvaginal ultrasound colour Doppler may be used to facilitate the diagnosis. Even with the use of transvaginal ultrasound colour Doppler, vasa previa may be missed. (II-2B)
  4. When vasa previa is diagnosed antenatally, an elective Caesarean section should be offered prior to the onset of labour. (II-1A)
  5. In cases of vasa previa, premature delivery is most likely; therefore, consideration should be given to administration of corticosteroids at 28 to 32 weeks to promote fetal lung maturation and to hospitalization at about 30 to 32 weeks. (II-2B)
  6. In a woman with an antenatal diagnosis of vasa previa, when there has been bleeding or premature rupture of membranes, the woman should be offered delivery in a birthing unit with continuous electronic fetal heart rate monitoring and, if time permits, a rapid biochemical test for fetal hemoglobin, to be done as soon as possible; if any of the above tests are abnormal, an urgent Caesarean section should be performed. (III-B
  7. Women admitted with diagnosed vasa previa should ideally be transferred for delivery in a tertiary facility where a pediatrician and blood for neonatal transfusion are immediately available in case aggressive resuscitation of the neonate is necessary. (II-3B)
  8. Women admitted to a tertiary care unit with a diagnosis of vasa previa should have this diagnosis clearly identified on the chart, and all health care providers should be made aware of the potential need for immediate delivery by Caesarean section if vaginal bleeding occurs. (III-B).

Abruptio Placenta

Represents interruption of the placenta by partial or complete separation, retroplacental blood clot formation and abnormal hemorrhage prior to delivery. There is significant perinatal mortality associated with abruptio placenta.[21]

Placenta Variants

Multilobed placenta succenturiata

Bilobed Placenta

Placenta with two equal-sized lobes connected by a thin bridge. No identified risks of this structure.

Bilobed placenta with velamentous cord insertion.jpg

Circumvallate placenta

Chorionic plate smaller than basal plate, edges rolled. Placental abruption and haemorrhage risks.

Placenta Membranacea

A rare placental abnormality where either all (diffuse placenta membranacea) or part (partial placenta membranacea) is covered by chorionic villi (placental cotyledons). Clinically the abnormality presents with vaginal bleeding, in the second or third trimester or during labor, due to an associated placenta previa.[22] Ultrasound has been used to detect this condition.[23]

Succenturiate placenta

Additional lobule separate from the main part of placenta. Risk of vessel rupture and placenta retention.

Links: Ultrasound

Chronic Intervillositis

(massive chronicintervillositis, chronic histiocytic intervillositis) Rare placental abnormality and pathology defined by inflammatory placental lesions, mainly in the intervillous space (IVS), with a maternal infiltrate of mononuclear cells (monocytes, lymphocytes, histiocytes) and intervillous fibrinoid deposition.

Chronic intervillositis of the placenta. Jacques SM, Qureshi F. Arch Pathol Lab Med. 1993 Oct;117(10):1032-5.

Placental Mesenchymal Dysplasia

Due to a similar "grape-like" placental appearance, this rare disorder placental mesenchymal stem villous hyperplasia has been mistaken both clinically and macroscopically for a partial hydatidiform molar pregnancy. The disorder also has a high incidence of both intrauterine growth restriction (IUGR) and fetal death.[24] The placental abnormality may be detected, but difficult to diagnose, by ultrasound.[25]

Current research suggests that placental cells may be originated from a mixed population of androgenetic (paternal-derived genome only) and biparental cells.[26] This means that chorionic villus sampling can provide a differential diagnosis between this and a partial mole.[27]


This condition is also known as gestational proteinuric hypertension and occurs in occurs in approximately 2 to 4% of all pregnancies. The pathogenesis of eclamptic convulsions remains unknown and women with a history of eclampsia are at increased risk of eclampsia (1-2%) and preeclampsia (22-35%) in subsequent pregnancies. "Magnesium sulfate is the drug of choice for reducing the rate of eclampsia developing intrapartum and immediately postpartum."(see Sibai BM. 2005).

Recent research using a large population study in Norway has shown a strong generational association such that daughters of women who had pre-eclampsia during pregnancy had more than twice the risk of pre-eclampsia themselves. The paper concludes "Maternal genes and fetal genes from either the mother or father may trigger pre-eclampsia. The maternal association is stronger than the fetal association. The familial association predicts more severe pre-eclampsia."[28]

Diabetic Placenta

Maternal Type 1 diabetes can alter placental vascular development. Effects may be due to either maternal hyperglycaemia or fatal hyperinsulinaemia with high glucose and insulin shown in other systems to alter vascularity, increasing vascular endothelial growth factor (VEGF), nitric oxide (NO) and protein kinase C (PKC).[29][30]

Features of the placental vessels include:

  • Increased angiogenesis
  • altered junctional maturity and molecular occupancy
  • increased leakiness

The placental terminal villi also show vascularity changes including both hypovascularity and hypervascularity. A recent study of the normal and diabetic placenta,[2] shows the diabetic placenta terminal villi were:

  • hypovascular villi - had a smaller diameter and a wavy course
  • hypervascular villi - had numerous capillaries, reduced stroma and were large in diameter.

Specific changes included:

  • villous stroma - collagen envelope around capillaries looked thinner and the network of collagen fibers seemed less dense.
  • stromal cells - loss of desmin filaments.
  • villous capillaries - were more branched.

Links: Maternal Diabetes

Placental Chorioangioma

Chorioangiomas occur in approximately 1 percent of all placentas and are benign haemangiomas. Small chorioangiomas are generally not clinically significant, while large chorioangiomas have been associated with a range of fetal conditions (fetal anemia, thrombocytopenia, hydrops, hydramnios, intrauterine growth retardation) including prematurity and stillbirth.

Placental Chorioangioma Ultrasound
Placental chorioangioma ultrasound 01.jpg Placental chorioangioma ultrasound 02.jpg
Ultrasound scan placenta and chorioangioma Ultrasound blood flow in chorioangioma
Placental Chorioangioma
Placental chorioangioma 01.jpg Placental chorioangioma 02.jpg Placental chorioangioma 03.jpg

Example of a placental chorioangioma forming a yellowish, well-circumscribed firm mass (5 cm × 5 cm) connected by two vessels to the placenta. Histopathologic examination revealed a placental disc 15 cm × 17 cm × 13 cm, with a three-vessel umbilical cord that was attached peripherally and measured 9 cm × 1.5 cm. The weight of the placenta was 530 g. The tumor was confirmed to be a chorioangioma.[31]

Hydatidiform Mole

Hydatidiform Mole

Another type of abnormality is when only the conceptus trophoblast layers proliferates and not the embryoblast, no embryo develops, this is called a "hydatidiform mole" (HM), which is due to the continuing presence of the trophoblastic layer, this abnormal conceptus can also implant in the uterus. The trophoblast cells will secrete human chorionic gonadotropin (hCG), as in a normal pregnancy, and may appear maternally and by pregnancy test to be "normal". Prenatal diagnosis by ultrasound analysis demonstrates the absence of a embryo.

There are several forms of hydatidiform mole: partial mole, complete mole and persistent gestational trophoblastic tumor. Many of these tumours arise from a haploid sperm fertilizing an egg without a female pronucleus (the alternative form, an embryo without sperm contribution, is called parthenogenesis). The tumour has a "grape-like" placental appearance without enclosed embryo formation. Following a first molar pregnancy, there is approximately a 1% risk of a second molar pregnancy.

  • The incidence of hydatidiform mole varies between ethnic groups, and typically occurs in 1 in every 1500 pregnancies.
  • All hydatidiform mole cases are sporadic, except for extremely rare familial cases.
  • A maternal gene has been identified for recurrent hydatidiform mole (chromosome 19q13.3-13.4 in a 15.2 cM interval flanked by D19S924 and D19S890).[32]

Links: Hydatidiform Mole | Week 2 - Abnormalities

Mole Types

Complete mole - chromosomal genetic material from the ovum (egg) is lost, by an unknown process. Fertilization then occurs with one or two sperm and an androgenic (from the male only) conceptus (fertilized egg) is formed. With this conceptus the embryo (fetus, baby) does not develop at all but the placenta does grow but it is abnormal and forms lots of cysts and has no blood vessels. These cysts look like a cluster of grapes and that is why it is called a hydatidiform mole (grape like). A hydatidiform mole miscarries by about 16 to 18 weeks gestational age. Since the diagnosis can be made by ultrasound before that time, it is better for you to have an evacuation of the uterus (D & C) so that there is no undue bleeding and no infection. Human chorionic gonadotropin (hCG) will assist in making the diagnosis.

Partial mole - three sets of chromosomes instead of the usual two and this is called triploidy. With such a pregnancy the chromosomal (genetic) material from the ovum (egg) is retained and the egg is fertilized by one or two sperm. Since with partial mole there are maternal chromosomes there is a fetus but because of the three sets of chromosomes this fetus is always grossly abnormal and will not survive. (Text modified from: International Society for the Study of Trophoblastic Diseases,see also JRM Gestational Trophoblastic Disease)

Tumour Growth

Like any tumour, unless removed there is a risk of progression:

Stage I: Tumor confined to uterus (non-metastatic)
Stage II: Tumor involving pelvic organs and/or vagina
Stage III: Tumor involving lungs, with or without involving pelvic structures and/or vagina
Stage IV: Tumor involving distant organs

Placental Mesenchymal Dysplasia

Due to a similar "grape-like" placental appearance, this rare disorder has been mistaken both clinically and macroscopically for a partial hydatidiform molar pregnancy. This disorder also has a high incidence of intrauterine growth restriction (IUGR) and fetal death.

Twin Pregnancy Mole

Hydatidiform mole and co-existent healthy fetus is a very rare condition with only 30 cases documented in detail in the literature.[33]

Links: International Society for the Study of Trophoblastic Diseases | Sydney Gynaecological Oncology Group Gestational Trophoblastic Disease | The Journal of Reproductive Medicine Gestational Trophoblastic Disease (1998) | Dana-Farber Cancer Institute Gynecologic Oncology Program

Cord Abnormalities

Velamentous Cord Insertion[34]

Velamentous Cord Insertion

(velamentous insertion) Clinical term for describing a placental abnormality where the placental cord inserts into the chorion laeve (placental membranes) away from the edge of the placenta. The placental vessels can also diverge as they traverse between the amnion and chorion before reaching the placenta.The placental vessels are therefore unprotected by Wharton's jelly where they traverse the membranes before they come together into the umbilical cord. This can cause hemorrhage if the vessels are damaged when the membranes are ruptured prior to birth. The condition is more common in monozygotic twins (15%) and triplets.

Velamentous cord insertion, with a low uterine body implantation site, has also been shown to affect fetal heart rate.[35]

Bilobed placenta with velamentous cord insertion.jpg

A bilobed placenta with velamentous cord insertion.

Cord Vessel Number

Placental cord ultrasound 02.jpg
Cord with one artery and one vein

Cord Knotting

Placental cord true knot
There are few abnormalities associated with umbilical cord development, other that abnormally short or long cords, which in most cases do not cause difficulties.

In some cases though, long cords can wrap around limbs or the fetus neck, which can then restrict blood flow or lead to tissue or nerve damage, and therefore effect develoment.

Cord knotting can also occur (1%) in most cases these knots have no effect, in some cases of severe knotting this can prevents the passage of placental blood.

Umbilical cord torsion

Placenta- umbilical cord torsion.jpg Rare umbilical cord torsion, even without knot formation can also affect placental blood flow, even leading to fetal demise.[36]

Cord Length

Fetal Erythroblastosis

This disease is also called Haemolytic Disease of the Newborn, an immune problem from fetus Rh+ /maternal Rh-, leakage from fetus causes anti-Rh antibodies, which is then dangerous for a 2nd child.


Placental Infections

Listeria maternal-fetal barrier

Several infective agents may cross into the placenta from the maternal circulation, as well as enter the embry/fetal circulation. The variety of bacterial infections that can occur during pregnancy is as variable as the potential developmental effects, from virtually insignificant to a major developmental, abortive or fatal in outcome.

Placental Malaria

Pregnant women have an increased susceptibility to malaria infection. Malarial infection of the placenta by sequestration of the infected red blood cells leading to low birth weight and other effects. There are four types of malaria caused by the protozoan parasite Plasmodium falciparum (main), Plasmodium vivax, Plasmodium ovale, Plasmodium malariae). This condition is common in regions where malaria is endemic with women carrying their first pregnancy (primigravida).

Links: Abnormal Development - Malaria

Placental Herpesvirus

A recent paper has identified using an in vitro model that human herpesvirus 8 (HHV-8) can infect the placenta[37]

Cytomegalovirus Placentitis

Clinical term for the cytomegalovirus infection of the placenta.

A earlier histological study[38] identified fixed connective tissue cells predominantly infected cell type in placental tissue. In addition, endothelial cells, macrophages and in some cases trophoblast infection. While a more recent in vitro study[39] suggests that all villi cell types are likely to be infected.

Links: Abnormal Development - Viral Infection

Placental Membranes

There are few documented abnormalities associated with feral membranes (chorion, amnion). Ultrasound measurement of abnormal yolk sac size/shape in early embryonic development has been suggested as an indicator of early gestational loss. The most common literature described abnormalities are those associated with abnormal vasularization of the chorion.


ICD Code: O41.1 Infection of amniotic sac and membranes Amnionitis Chorioamnionitis Membranitis Placentitis

The best known environmental effect is infection of chorion and/or amnion referred to as chorioamnionitis.[40]

Chronic chorioamnionitis histology.jpg

Chronic Chorioamnionitis Histology[41]

  • Stage 1 ((a, b) inflammation showing infiltration of lymphocytes limited to the chorionic trophoblast layer (a). CD3 immunostaining demonstrates that the majority of these cells are T cells (b).
  • Stage 2 (c, d) inflammation is characterized by infiltration of lymphocytes into the chorioamniotic connective tissue layer ((Stain - Haematoxylin Eosin), c), which are largely CD3+ T cells (d).

Links: Bacterial Infection | Placental Membranes

Placental Pathology

The following pathology information from[42].

Chronic Villitis

This condition can occur following placental infection leading to maternal inflammation of the villous stroma, often with associated intervillositis. The inflammation can lead to disruption of blood flow and necrotic cell death.

Massive Chronic Intervillositis

(MCI) The maternal blood-filled space is filled with CD68-positive histiocytes and an increase in fibrin, occuring more commonly in the first trimester.

Meconium Myonecrosis

The prolonged meconium exposure leads to toxic death of myocytes of placental vessels (umbilical cord or chorionic plate).


A fetal malignancy that leads to an enlarged placenta, with tumor cells in the fetal circulation and rarely in the chorionic villi.


(protein C or S deficiency, factor V Leiden, sickle cell disease, antiphospholipid antibody) This condition can generate an increased fibrin/fibrinoid deposition in the maternal or intervillous space, this can trap and kill villi.

International Classification of Diseases

XV Pregnancy Childbirth

O12 Gestational oedema and proteinuria without hypertension


  • O12.0 Gestational oedema
  • O12.1 Gestational proteinuria
  • O12.2 Gestational oedema with proteinuria

O13 Gestational hypertension without significant proteinuria


Incl.: Gestational hypertension NOS Mild pre-eclampsia

O14 Gestational hypertension with significant proteinuria

[pregnancy-induced] Excl.: superimposed pre-eclampsia (O11)

  • O14.0 Moderate pre-eclampsia
  • O14.1 Severe pre-eclampsia
  • O14.2 HELLP syndrome Combination of hemolysis, elevated liver enzymes and low platelet count
  • O14.9 Pre-eclampsia, unspecified

O15 Eclampsia

Incl.: convulsions following conditions in O10-O14 and O16 eclampsia with pregnancy-induced or pre-existing hypertension

  • O15.0 Eclampsia in pregnancy
  • O15.1 Eclampsia in labour
  • O15.2 Eclampsia in the puerperium
  • O15.9 Eclampsia, unspecified as to time period Eclampsia NOS

  • Abruptio placentae (641.2)
  • Placenta previa (641.0, 641.1)
  • Postpartum hemorrhage (666.0–666.2)


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Gali Garmi, Raed Salim Epidemiology, etiology, diagnosis, and management of placenta accreta. Obstet Gynecol Int: 2012, 2012;873929 PMID: 22645616 | Obstet Gynecol Int. Khaled M Elsayes, Andrew T Trout, Aaron M Friedkin, Peter S Liu, Ronald O Bude, Joel F Platt, Christine O Menias Imaging of the placenta: a multimodality pictorial review. Radiographics: 2009, 29(5);1371-91 PMID: 19755601

J S Abramowicz, E Sheiner In utero imaging of the placenta: importance for diseases of pregnancy. Placenta: 2007, 28 Suppl A;S14-22 PMID: 17383721


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