FOGSI FOCUS: Abnormal Placentation Jyotsna Suri, Alpesh Gandhi, Kanan Avinash Yelikar
INDEX
ABCDEFGHIJKLMNOPRSTUV
Page numbers followed by f refer to figure, fc refer to flowchart, b refer to box, and t refer to table.
A
Abnormal placentation, types of 1
Abruptio placentae 4, 8
Abruption 35
expectant management in 10
risk factors for 6b
Absent end diastolic flow 26f
Adaptation, failure of 23
Adeno-associated virus 29
Air pollution and social environment 24
Amniotic membranes 36f
Antepartum hemorrhage 4, 5fc, 7, 8, 11t, 19
causes of 4
fetal consequences of 6b
major 8
maternal consequences of 6b
minor 8
Aorta clamp 14, 14f
Assisted reproductive technology 4
Asymptomatic placenta previa 8
Autocrine 1
B
Bacterial infections 31
Battledore placenta 19
Bilobed placenta 18
Blastocyst implants 1
Blood flow, redistribution of 26f
C
Carbon dioxide accumulation 23
Cardiotocography 27
Central nervous system 33
Cervical intraepithelial neoplasia 4
Cervix 2
Cesarean delivery, steps of 15
Cesarean hysterectomy, steps of 15
Cesarean scar implantation 1
Cesarean section 1, 17
Chlamydia pneumoniae 31
Chorioangioma 21, 21f
clinical implications of 21
Chorioangiomatosis 21
Chorioretinitis 31
Chromosomal anomalies 45
Circummarginate placenta 20
Common placental infections 32t
Cord insertion, abnormalities of 19, 19f
Corticotropin-releasing hormone 44
Cytomegalovirus 2, 18, 29
D
Decidua 1
Dehiscent scar 2
Doppler indices, measurement of 25
Dr Alpesh Gandhi's principle 17
Ductus venosus 26f
E
Endocrine functions 18
Epstein-Barr virus 30
Estrogens 44
Extrachorial placentation 20
types of 20f
F
Fetal biometry, ultrasonography for 25
Fetal blood flow disruption 21
Fetal distress 4
Fetal erythroblastosis 1
Fetal growth restriction 19, 23, 35, 37
Fetal morbidity 1, 19
Fetal thrombotic vasculopathy 21
Fetal vasculature, abnormalities of 20, 21
Fetomaternal hemorrhage 7
Fluorescence in situ hybridization 37
Furcate cord insertion 19
G
General anesthesia 42
Genital tract 4
Gestational diabetes mellitus 45, 46
Glucocorticoids 45
Great obstetrical syndromes 23
H
Heart failure 26f
Hematomas 20
consequences of 20
types of 20f
Hemorrhage 4
postpartum 10, 19
Herpes simplex virus 30
Hormone 44, 45
Human chorionic gonadotropin 44
Human papillomavirus 29
Human placental growth hormone 44
Human placental lactogen 44
Hydrocephalus 31
Hypercapnia 23
Hyperemesis gravidarum 46
Hypertension 35
Hysterectomy 15
I
Infections 28
Inferior epigastric artery 13
Influence fetal growth 23
Insulin 45
Interpositional insertion 19
Intracranial calcification 31
Intraumbilical oxytocin injection 41
Intrauterine compensatory mechanisms 23
Intrauterine environment 45
Intrauterine fetal transfusion 28
Intrauterine growth restriction 33, 40, 46
J
Jaw, closeup of 14f
K
Kleihauer-Betke test 7
L
Last menstrual period 25
Late preterm gestations 11t
Leukemia inhibitor factor 1
Listeria monocytogenes 32
Luteinizing hormone 44
M
Malaria 31
and placenta 31
Maternal and fetal morbidity 2
Maternal blood flow disruption 20
Maternal diabetes mellitus 2
Maternal floor infarction 20
Maternal infections 24
Maternal nutrition 45
Maternal spiral arteries 1
Maternal vasculature, abnormalities of 20, 21
Membrane, abnormality of 37t
Microbiological examination 38
Middle cerebral artery 26f
Multilobate placenta 18
Mycoplasma 38
N
Neonatal morbidity 1
Nitabuch's fibrinoid 1
Nitabuch's layer 2
O
Obesity 24
Opaque chorion 36f
Oxidative stress 24
P
Paracrine 1
Perivillous fibrin deposition 20
Placenta 1, 2, 18, 22, 23, 28, 30, 44
AAV and 29
abnormality of 37t
abnormally located 1
abruption 5t
adherent 1
circumvallate 20
CMV and 29
examination of 41
fenestrate 18
fetal surface of 35f
histopathological examination of 38
HPV and 29
HSV and 30
implantation abnormalities of 1
influences 45
low-lying marginal 1
maternal surface of 36f
membranacea 18
normal 35
percreta 15
ring-shaped 18
toxoplasma and 31
varicella and 30
vascular abnormalities of 22
Placenta accreta 2, 13
disorders 8
spectrum 13, 15, 16
disorders 2, 4, 17, 22, 40
diagnosis of 13
management of 14
Placenta accrete 15f
hysterectomy specimen of 15f
Placenta previa 1, 4, 5t, 8, 9fc
accreta 13
management of 9
risk factors for 6b
symptomatic 8
Placental abnormalities 35
types of 18
Placental abruption 9, 10
management of 10
termination in 10fc
Placental and cord examination, role of 35
Placental endocrinology 44
Placental function, mood disorders affecting 25
Placental hormones 44
clinical applications of 45
on pregnancy 45
Placental implantation 2
abnormal 1
Placental infections 28, 28t, 32
Placental insufficiency 23, 24
diagnosis of 25
etiopathogenesis of 24
pathophysiology of 23
Placental membrane abnormalities 22
Placental perfusion disorders 20, 21
Placental protein 46
Placental shape
abnormalities 2
and size 18
variants of 19
variants of 19f
Placental size abnormalities 2
Placental structure, variants of 20
Placental tissue, chromosomal examination of 37t
Placental transfusion syndromes 1
Placental tumor 21, 37f
Plasma protein A 45
Polycyclic aromatic hydrocarbons 24
Polymerase chain reaction 33, 37
Postpartum hemorrhage 40
Preeclampsia 1, 23, 45, 46
Pregnancy
hormone of 44
implantation of 1
plan of termination of 11
termination of 9, 9fc, 10, 11fc
Progesterone 44, 46
Prophylactic management 41
Protein kinase A 44
Protozoan infections 31
R
Rapid plasma regain 33
Renal disease 35
Retained placenta 40, 42
after birth 40
complications of 41
diagnosis of 41
management of 41
risk factors for 40, 40t
types of 40
Rh-incompatibility 2
S
Sexually transmitted disease 29
Spectrum 13
Spontaneous abortion 46
Stillbirth, unexplained 35
Subchorionic fibrin deposition 20
Syphilis 2
T
Third stage of labor, active management of 41
Thyroxine 45
Toxoplasma 31
gondii 31
Toxoplasmosis 31
Transparent amnion 36f
Treponema pallidum 32
U
Umbilical artery 26f
Umbilical cord
abnormality of 37t
inserts 35
Umbilical vein pulsations 26f
Ureaplasma 38
Uterine artery
Doppler 25
waveform, abnormal 25f
Uterine curettage 1
Uterine segment, lower 15f
Uterine surgery 1
Uterus, cut section of 15
V
Varicella 30
Varicella-zoster virus 30
Vasa previa 8, 10, 11, 11fc, 19
management of 11
Vascular endothelial growth factor 44
Vascular system, adaptation of 23
Velamentous insertion 19
Venereal disease research laboratory 33
Vessel umbilical cord 36f
Villous vascular lesions 21
Viral infections 28
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Chapter Notes

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Abnormal Placental Implantation: An OverviewCHAPTER 1

Ashok Kumar,
Charmila Ayyavoo,
Munjal Jayeshkumar Pandya,
Divya KV
 
INTRODUCTION
Implantation of pregnancy is a crucial step for a successful outcome. It occurs in the endometrium around 6–7 days after the conception. Blastocyst implants in the upper portion of the uterus by apposition to the endometrium and subsequent invasion into the endometrium. The proliferative trophoblast on the anchoring villi then invades endometrium and inner one-third of myometrium and maternal spiral arteries. Nitabuch fibrinoid is maintained in the interface of the placenta and decidua. Placenta normally implants in the upper segment on the posterior wall in two-thirds cases and on the anterior wall in one-third. Placental implantation abnormalities (PIA) comprise a large group of disorders associated with maternal, fetal and neonatal morbidity. They exhibit varying degree of severity. Implantation abnormalities of placenta lead to a group of disorders which cover several entities: placental shape abnormalities, abnormally located placenta (site) and morbidly adherent placenta, maternal vascular malperfusion due to deficient remodeling of the maternal spiral arteries,1–2 resulting in placento-maternal effects (preeclampsia, fetal erythroblastosis), velamentous cord insertion and other mechanical abnormalities associated with the placental (umbilical) cord and placental transfusion syndromes like twin-to-twin transfusion syndrome.
 
ETIOPATHOGENESIS
A number of etiologies have been proposed. Abnormality of decidualization either by trauma or deficiency of decidua is one of them. Others include abnormal interaction between decidua and the invasive extravillous trophoblast, leading to a failure of maternal tissues to restrain the invading trophoblast.3–4 Anti-invasive factor deficiency in the areas of decreased decidualization favors the matrix metalloproteinase activity promoting tissue invasion. An imbalance in the paracrine or autocrine regulation between the deficient decidualized endometrium and the invasive trophoblasts is also a contributing factor.5–6
 
RISK FACTORS
Any factor that can lead to damage to endometrium and its scarring is an important risk factor for abnormal placental implantation. Risk factors include prior cesarean section, uterine surgery, uterine curettage, previous pregnancy affected by abnormal placentation, endometriosis, endometrial ablation, manual removal of placenta, uterine anomalies.7–8
 
TYPES OF ABNORMAL PLACENTATION
  1. Low—lying marginal placenta: Low—lying placenta ends 2 cm of the internal cervical os but does not cover it. Low—lying placentas are most frequently diagnosed ultrasonographically in the second trimester and resolve by the third trimester.
  2. Placenta previa: Placenta previa is defined as a placenta with complete or partial obstruction of the internal cervical os. It is a major cause of antepartum hemorrhage and has been associated with severe maternal morbidity with risk of disseminated intravascular coagulation and emergency hysterectomy.9 In the fetus, acute and massive bleeding from placenta previa has been associated with fetal brain damage.10
    The lower segment of the uterus has increased vascularity due to placenta previa and decreased contractility. Therefore there is increased risk of bleeding in antenatal as well as in postpartum period. The placenta previa warrants multidisciplinary management which may sometimes result in a cesarean hysterectomy and maternal mortality.
  3. Cesarean scar implantation: Cesarean scar implantation refers to the placental implantation within the scar of a prior cesarean delivery. Factors such as β3 and leukemia—inhibitor factor (LIF), have been shown to be overexpressed in the site of abnormal implantation in a cesarean scar site when compared with the remaining uterine cavity which enhances endometrial receptivity.11 The placental implantation may occur in a dehiscent 2scar and when this happens, it has worst prognosis, probably due to the thinning of the myometrium noted in areas of a dehiscent scar.12
  4. Placenta accreta spectrum disorders: Placenta accreta spectrum disorders (PAS) is an umbrella term encompassing similar entities with varying degree of severity. Depending on the depth of invasion, it could be placenta accreta, increta and percreta. Invasive trophoblast is present in varying number in the basal Nitabuch's layer manifesting in subclinical form of adherent placenta and these patients have delayed placental delivery, manual removal, or disruption. There is an increased risk for development of clinical apparent placenta accreta in a subsequent pregnancy.13 Individual management for delivery is determined with identification of prenatal risk of accreta placentation in patients with a low-lying placenta/previa and a history of prior cesarean delivery.
  5. Placental shape abnormalities: Abnormal placental shapes such as bilobed placenta, placenta succenturiata, placenta membranacea could lead to abnormal placental implantation. Vasa previa is associated with velamentous insertions (25–62%) and vessels crossing between lobes in succenturiate or bilobate placentas (33–75%).
  6. Placental size abnormalities: Placentomegaly (weight more than 750 g) are associated with fetal hydrops, Rh-incompatibility, maternal diabetes mellitus, chronic infections (e.g., syphilis, cytomegalovirus), maternal anemia, or acute placental edema with acute chorioamnionitis. Underperfusion of the placenta, such as preeclampsia or maternal hypertension is associated with low placental weight and lead to fetal growth restriction, fetal malformations or chromosomal anomalies.
Sometimes, complications of umbilical cord such as cord prolapse, cord compression, true knots also affect the fetus and newborn outcome.
Placental implantation abnormalities carry a greater risk of maternal and neonatal morbidity. PIAs contribute to 8.7% of preterm births as well as neonatal intensive care unit admissions and a number of maternal complications.2 Transabdominal ultrasound is the primary technique used to rule—out abnormal placentation. Accurate prenatal diagnosis of abnormal placentation is paramount for optimal management, ensuring that the patient is treated at tertiary center by multidisciplinary approach.14 However, the clinicians must focus on their goal to identify patients who can be expectantly managed till term and those who require inpatient management or early delivery.2 Every hospital must have a clear protocol, policy, and procedure of a team to manage all cases of PIAs.15
 
CONCLUSION
Maternal and fetal morbidity and mortality are associated with placental implantation abnormalities and multidisciplinary approach is required to achieve successful outcome. Clinical clues such as vaginal bleeding or the use of ultrasound to evaluate the cervix and placenta might be able to predict catastrophic complications. Secondly, as a public health concern, with the rising cesarean delivery rates there is also an increase in PIA. Almost all cases of PIA are delivered prematurely to avoid complications. Therefore, the next step is not only to individualize management of PIA but to alert clinicians that decreasing the primary cesarean delivery rate will in turn decrease the overall contribution of PIA to preterm delivery.
REFERENCES
  1. Norwitz ER. Defective implantation and placentation: laying the blueprint for pregnancy complications. Reprod Biomed Online. 2006;13:591–9.
  1. Vahanian SA, Vintzileos AM. Placental implantation abnormalities: a modern approach. Curr Opin Obstet Gynaecol. 2016;28:477–84.
  1. Winship A, Cuman C, Rainczuk K, Dimitriadis E. Fibulin-5 is upregulated in decidualized human endometrial stromal cells and promotes primary human extravillous trophoblast outgrowth. Placenta. 2015;36:1405–11.
  1. Takahashi H, Ohkuchi A, Kuwata T, Usui R, Baba Y, Suzuki H, et al. Endogenous and exogenous miR-520c-3p modulates CD44-mediated extravillous trophoblast invasion. Placenta. 2017;50:25–31.
  1. Sharma S, Godbole G, Modi D. Decidual control of trophoblast invasion. Am J Reprod Immunol. 2016;75:341–50.
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  1. Faiz AS, Ananth CV. Etiology and risk factors for placenta previa: an overview and meta-analysis of observational studies. J Matern Fetal Neonatal Med. 2003;13:175–90.
  1. Furuta K, Tokunaga S, Furukawa S, Sameshima H. Acute and massive bleeding from placenta previa and infants’ brain damage. Early Hum Dev. 2014;90:455–8.
  1. 3 Qian ZD, Weng Y, Wang CF, Huang LL, Zhu XM. Research on the expression of integrin β3 and leukaemia inhibitory factor in the decidua of women with cesarean scar pregnancy. BMC Preg Childbirth. 2017;17:84.
  1. Kaelin Agten A, Cali G, Monteagudo A, Oviedo J, Ramos J, Timor-Tritsch I. The clinical outcome of cesarean scar pregnancies implanted “on the scar” versus “in the niche”. Am J Obstet Gynecol. 2017;216:510.
  1. Linn RL, Miller ES, Lim G, Ernst LM. Adherent basal plate myometrial fibers in the delivered placenta as a risk factor for development of subsequent placenta accreta. Placenta. 2015;36:1419–24.
  1. Shamshirsaz AA, Fox KA, Erfani H, Clark SL, Salmanian B, Baker BW, et al. Multidisciplinary team learning in the management of the morbidly adherent placenta: outcome improvements over time. Am J Obstet Gynecol. 2017;216:612.
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