Talk:Placenta - Abnormalities

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Cite this page: Hill, M.A. (2019, September 18) Embryology Placenta - Abnormalities. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Placenta_-_Abnormalities

2019

Heavy metals in maternal and cord blood in Beijing and their efficiency of placental transfer

J Environ Sci (China). 2019 Jun;80:99-106. doi: 10.1016/j.jes.2018.11.004. Epub 2018 Nov 14.

Abstract This study aimed to determine the effect of exposure to heavy metals in pregnant women in Beijing, China. We also evaluated the association of these heavy metals with birth weight and length of newborns. We measured the levels of 10 heavy metals, including lead (Pb), titanium (Ti), manganese (Mn), nickel (Ni), cadmium (Cd), chromium (Cr), antimony (Sb), stannum (Sn), vanadium (V), and arsenic (As), in 156 maternal and cord blood pairs. An inductively coupled plasma mass spectrometry method was used for measurement. Pb, As, Ti, Mn, and Sb showed high detection rates (>50%) in both maternal and cord blood. Fourteen (9%) mothers had blood Pb levels greater than the United States Center for Disease Control allowable threshold limit for children (50 μg/L). In prenatal exposure to these heavy metals, there was no significant association between any heavy metal and birth weight/length. Moreover, we estimated the placental transfer efficiency of each heavy metal, and the median placental transfer efficiency ranged from 49.6% (Ni) to 194% (Mn) (except for Cd and Sn). The level and detection rate of Cd in maternal blood were much higher than that in cord blood, which suggested that Cd had difficulty in passing the placental barrier. Prospective research should focus on the source and risk of heavy metals in non-occupationally exposed pregnant women in Beijing.

Copyright © 2018. Published by Elsevier B.V.

KEYWORDS: Cord blood; Heavy metal; Maternal blood; Newborn; Placental transfer efficiency PMID: 30952357 DOI: 10.1016/j.jes.2018.11.004


New  ICD-11 tables in preparation.

 ICD-11 KA02 Foetus or newborn affected by complications of placenta
KA02.1 Foetus or newborn affected by placental oedema or large placenta | KA02.2 Foetus or newborn affected by placental infarction | KA02.3 Foetus or newborn affected by placental insufficiency or small placenta | KA02.4 Foetus or newborn affected by placental transfusion syndromes


KA03 Foetus or newborn affected by complications of umbilical cord | KA04 Foetus or newborn affected by other abnormalities of membranes
JA8A Maternal care related to placental disorders
detailed list

 ICD-11
KA02 Foetus or newborn affected by complications of placenta

KA02.0 Foetus or newborn affected by placenta praevia - Placenta praevia exists when the placenta lies wholly or in part in the lower segment of the uterus. Diagnosis has evolved from the clinical I-IV grading system, and is determined by ultrasonic imaging techniques relating the leading edge of the placenta to the cervical os. Grade I is a low lying placenta, Grade II is a placenta that meets the edge of the cervical os, Grade III is a placenta that partially covers the os, and Grade IV is a placenta that completely covers the os.

KA02.1 Foetus or newborn affected by placental oedema or large placenta - A large placenta, also known as placentomegaly, is one that weighs greater than 750 g. Placentomegaly can be seen in the following conditions: fetal hydrops, maternal diabetes mellitus, Rh incompatibility, chronic infections (e.g. syphilis, cytomegalovirus), maternal anemia, or acute placental edema with acute chorioamnionitis.

KA02.2 Foetus or newborn affected by placental infarction - Placental infarction is the formation of localised areas of ischemic villous necrosis, usually due to vasospasm of the maternal circulation. The affected regions of the placenta are incompetent, and lead to placental insufficiency if the infarcts are severe.

KA02.3 Foetus or newborn affected by placental insufficiency or small placenta - Placental insufficiency is defined as the inability of the placenta to deliver a sufficient supply of oxygen and nutrients to the fetus, and therefore, is unable to sustain the growth of the developing baby until term. Placental insufficiency can result in intrauterine growth restriction (IUGR), pre-eclampsia, abruption, or preterm labour and delivery. A small placenta is defined as a placenta that weighs less that the lower limit of normal for the gestational period. A low placental weight can be the result of a maternal condition that is causing underperfusion of the placenta, such as pre-eclampsia or maternal hypertension. A small placenta may lead to IUGR, fetal malformations, or chromosomal anomalies.

KA02.4 Foetus or newborn affected by placental transfusion syndromes - Twin-to-twin transfusion syndrome (TTTS) occurs in monozygotic twins while they are in the uterus. It occurs when blood travels from one twin to the other, and the twin that loses blood is the donor twin, while the twin that receives blood is the recipient twin. Depending on the severity of the transfusion, both infants may experience problems, such as anaemia, paleness, and dehydration in the donor twin, and redness and an increased blood pressure in the recipient twin.

KA03 Foetus or newborn affected by complications of umbilical cord

KA03.0 Foetus or newborn affected by prolapsed cord - A prolapsed umbilical cord is when the cord enters the opening cervix and down into the birth canal during labour before the baby has left the uterus. The risk of prolapse is higher if the baby is lying in a transverse position, the mother has had more than one baby, an excess amount of amniotic fluid exists, there is preterm prelabour rupture of membranes, or if membranes are artificially ruptured.

KA03.1 Foetus or newborn affected by other compression of umbilical cord - A group of conditions characterized by findings in the fetus or newborn due obstruction of blood flow through the umbilical cord secondary to pressure from an external object or misalignment of the cord itself not classified elsewhere.

LB03 Structural developmental anomalies of umbilical cord

LB03.0 Allantoic duct remnants or cysts - Any condition caused by failure of the umbilical cord to correctly develop during the antenatal period. These conditions are characterized by cysts or remnants of allantoic tissue within the umbilical cord, the umbilicus, or the urachus.

LB03.1 Single umbilical cord artery - A single umbilical artery arising from the either the allantoic arterial system (Type I), or vitelline artery (Type II). And has been associated with renal abnormalities.

Foetus or newborn affected by abnormalities of umbilical cord length - KA03.20 Foetus or newborn affected by short umbilical cord - An umbilical cord greater than 2 SD in length below mean for the gestational age. At term, this is less than 35 cm. Often associated with fetal hypokinsesia. | KA03.21 Foetus or newborn affected by long umbilical cord - An umbilical cord greater than 2 SD in length above mean for the gestational age. At term, this is greater than 80 cm.

KA03.3 Foetus or newborn affected by vasa praevia - An obstetric complication characterized by fetal vessels crossing or running in close proximity to the internal orifice of the cervix (inner cervical os).

KA03.4 Foetus or newborn affected by traumatic injury of the umbilical cord


KA04 Foetus or newborn affected by other abnormalities of membranes

KA04.0 Foetus or newborn affected by chorioamnionitis - Chorioamnionitis is an infection of the placental tissues and amniotic fluid. It can lead to bacteremia in the mother, which is an infection of the blood, and this can cause preterm birth or infection in the newborn. Organisms which are usually responsible for chorioamnionitis include Escherichia coli (E. coli) and Group B streptococcus.

KA04.1 Foetus or newborn affected by amniotic Band Syndrome

JB63.00 Tuberculous placenta

KA80.2 Foetal blood loss from placenta

Maternal

JA8A Maternal care related to placental disorders - JA8A.0 Placental transfusion syndromes | JA8A.1 Malformation of placenta | JA8A.2 Morbidly adherent placenta

JA8B Maternal care related to placenta praevia or low lying placenta - JA8B.0 Placenta praevia specified as without haemorrhage | JA8B.1 Placenta praevia with haemorrhage

JA8C Maternal care related to premature separation of placenta

JB0B.0 Retained placenta without haemorrhage - A condition characterized by a placenta that has not been expelled from the uterus during the third stage of labour and up to 30 minutes following delivery, and without haemorrhage. This condition is caused by uterine atony, a trapped placenta, or a placenta accreta. This condition may lead to primary postpartum haemorrhage or infection.

JA8A.2 Morbidly adherent placenta

JA43.0 Third-stage haemorrhage - A condition characterized by excessive loss of blood during the third stage of labour for a vaginal delivery. This condition is caused by uterine atony, trauma, retained placenta, or coagulopathy.

placenta abnormalities |  ICD-11
International Classification of Diseases - Structural developmental anomalies of the digestive tract 
 ICD-11
KA02 Foetus or newborn affected by complications of placenta

KA02.0 Foetus or newborn affected by placenta praevia - Placenta praevia exists when the placenta lies wholly or in part in the lower segment of the uterus. Diagnosis has evolved from the clinical I-IV grading system, and is determined by ultrasonic imaging techniques relating the leading edge of the placenta to the cervical os. Grade I is a low lying placenta, Grade II is a placenta that meets the edge of the cervical os, Grade III is a placenta that partially covers the os, and Grade IV is a placenta that completely covers the os.

KA02.1 Foetus or newborn affected by placental oedema or large placenta - A large placenta, also known as placentomegaly, is one that weighs greater than 750 g. Placentomegaly can be seen in the following conditions: fetal hydrops, maternal diabetes mellitus, Rh incompatibility, chronic infections (e.g. syphilis, cytomegalovirus), maternal anemia, or acute placental edema with acute chorioamnionitis.

KA02.2 Foetus or newborn affected by placental infarction - Placental infarction is the formation of localised areas of ischemic villous necrosis, usually due to vasospasm of the maternal circulation. The affected regions of the placenta are incompetent, and lead to placental insufficiency if the infarcts are severe.

KA02.3 Foetus or newborn affected by placental insufficiency or small placenta - Placental insufficiency is defined as the inability of the placenta to deliver a sufficient supply of oxygen and nutrients to the fetus, and therefore, is unable to sustain the growth of the developing baby until term. Placental insufficiency can result in intrauterine growth restriction (IUGR), pre-eclampsia, abruption, or preterm labour and delivery. A small placenta is defined as a placenta that weighs less that the lower limit of normal for the gestational period. A low placental weight can be the result of a maternal condition that is causing underperfusion of the placenta, such as pre-eclampsia or maternal hypertension. A small placenta may lead to IUGR, fetal malformations, or chromosomal anomalies.

KA02.4 Foetus or newborn affected by placental transfusion syndromes - Twin-to-twin transfusion syndrome (TTTS) occurs in monozygotic twins while they are in the uterus. It occurs when blood travels from one twin to the other, and the twin that loses blood is the donor twin, while the twin that receives blood is the recipient twin. Depending on the severity of the transfusion, both infants may experience problems, such as anaemia, paleness, and dehydration in the donor twin, and redness and an increased blood pressure in the recipient twin.

KA03 Foetus or newborn affected by complications of umbilical cord

KA03.0 Foetus or newborn affected by prolapsed cord - A prolapsed umbilical cord is when the cord enters the opening cervix and down into the birth canal during labour before the baby has left the uterus. The risk of prolapse is higher if the baby is lying in a transverse position, the mother has had more than one baby, an excess amount of amniotic fluid exists, there is preterm prelabour rupture of membranes, or if membranes are artificially ruptured.

KA03.1 Foetus or newborn affected by other compression of umbilical cord - A group of conditions characterized by findings in the fetus or newborn due obstruction of blood flow through the umbilical cord secondary to pressure from an external object or misalignment of the cord itself not classified elsewhere.

LB03 Structural developmental anomalies of umbilical cord

LB03.0 Allantoic duct remnants or cysts - Any condition caused by failure of the umbilical cord to correctly develop during the antenatal period. These conditions are characterized by cysts or remnants of allantoic tissue within the umbilical cord, the umbilicus, or the urachus.

LB03.1 Single umbilical cord artery - A single umbilical artery arising from the either the allantoic arterial system (Type I), or vitelline artery (Type II). And has been associated with renal abnormalities.

Foetus or newborn affected by abnormalities of umbilical cord length - KA03.20 Foetus or newborn affected by short umbilical cord - An umbilical cord greater than 2 SD in length below mean for the gestational age. At term, this is less than 35 cm. Often associated with fetal hypokinsesia. | KA03.21 Foetus or newborn affected by long umbilical cord - An umbilical cord greater than 2 SD in length above mean for the gestational age. At term, this is greater than 80 cm.

KA03.3 Foetus or newborn affected by vasa praevia - An obstetric complication characterized by fetal vessels crossing or running in close proximity to the internal orifice of the cervix (inner cervical os).

KA03.4 Foetus or newborn affected by traumatic injury of the umbilical cord


KA04 Foetus or newborn affected by other abnormalities of membranes

KA04.0 Foetus or newborn affected by chorioamnionitis - Chorioamnionitis is an infection of the placental tissues and amniotic fluid. It can lead to bacteremia in the mother, which is an infection of the blood, and this can cause preterm birth or infection in the newborn. Organisms which are usually responsible for chorioamnionitis include Escherichia coli (E. coli) and Group B streptococcus.

KA04.1 Foetus or newborn affected by amniotic Band Syndrome

JB63.00 Tuberculous placenta

KA80.2 Foetal blood loss from placenta

Maternal

JA8A Maternal care related to placental disorders - JA8A.0 Placental transfusion syndromes | JA8A.1 Malformation of placenta | JA8A.2 Morbidly adherent placenta

JA8B Maternal care related to placenta praevia or low lying placenta - JA8B.0 Placenta praevia specified as without haemorrhage | JA8B.1 Placenta praevia with haemorrhage

JA8C Maternal care related to premature separation of placenta

JB0B.0 Retained placenta without haemorrhage - A condition characterized by a placenta that has not been expelled from the uterus during the third stage of labour and up to 30 minutes following delivery, and without haemorrhage. This condition is caused by uterine atony, a trapped placenta, or a placenta accreta. This condition may lead to primary postpartum haemorrhage or infection.

JA8A.2 Morbidly adherent placenta

JA43.0 Third-stage haemorrhage - A condition characterized by excessive loss of blood during the third stage of labour for a vaginal delivery. This condition is caused by uterine atony, trauma, retained placenta, or coagulopathy.

placenta abnormalities |  ICD-11

Removed International Classification of Diseases ICD-10 information shown below.

XV Pregnancy Childbirth

O12 Gestational oedema and proteinuria without hypertension

[pregnancy-induced]

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

O13 Gestational hypertension without significant proteinuria

[pregnancy-induced]

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)

2018

Effect of site of placentation on pregnancy outcomes in patients with placenta previa

PLoS One. 2018 Jul 17;13(7):e0200252. doi: 10.1371/journal.pone.0200252. eCollection 2018.

Jing L1, Wei G1, Mengfan S1, Yanyan H1.

Abstract INTRODUCTION: We aimed to evaluate the site of placentation on the pregnancy outcomes of patients with placenta previa. METHODS: This retrospective study included 678 cases of placenta previa. Basic information and pregnancy outcome data were collected. Differences between the different placenta previa positions and pregnancy outcomes were compared using the chi-square and independent t tests. Logistic and multiple regression analyses were used to calculate the odds ratios (ORs) to determine the risk factors for PAS disorders and postpartum hemorrhage and evaluate the effect of placental attachment site on pregnancy outcomes. RESULTS: There was no significant difference between the PAS disorders rate and the incidence of complete placenta previa depending on the type of placentation; however, placental attachment site influenced the pregnancy outcome. Placental attachment to the anterior wall was associated with shorter gestational age, low birth weight, lower Apgar score, higher prenatal bleeding rate, increased postpartum hemorrhage, longer duration of hospitalization, and higher blood transfusion and hysterectomy rates compared to cases with lateral/posterior wall placenta. Placental attachment at the incision site of a previous cesarean section significantly increased the incidence of complete placenta previa and PAS disorders compared with placental attachment at a site without incision, but did not significantly influence pregnancy outcomes. Placental attachment to the anterior wall was an independent risk factor for postpartum hemorrhage in patients with placenta previa. Placental attachment to a previous incision site was an independent risk factor for PAS disorders. CONCLUSION: The site of placental attachment in patients with placenta previa has an important influence on the pregnancy outcome. When the placenta is located on the anterior wall, clinicians should pay attention to the adverse pregnancy outcomes and the possibility of massive postpartum hemorrhage. In cases of placental attachment to the uterine incision site, physicians should be highly vigilant regarding the occurrence of PAS disorders. PMID: 30016336 DOI: 10.1371/journal.pone.0200252


Complete Placenta Previa: Ultrasound Biometry and Surgical Outcomes

AJP Rep. 2018 Apr;8(2):e74-e78. doi: 10.1055/s-0038-1641163. Epub 2018 Apr 20.

Wortman AC1, Schaefer SL1, McIntire DD1, Sheffield JS1, Twickler DM1,2.

Abstract

Objective  To evaluate the relationship between surgical outcomes and ultrasound measurement of placental extension beyond the cervical os in women with placenta previa. Study Design  This is a retrospective cohort study of singleton pregnancies with placenta previa undergoing third-trimester ultrasound and delivering at our institution from 2002 through 2011. For study purposes, an investigator measured placental extension, defined as the placental distance from the internal os across the placenta continuing out to the lowest placental edge. If morbidly adherent placentation was suspected, women were excluded. Receiver operating characteristic (ROC) curves were developed for pertinent surgical outcomes, and multivariate analysis was performed to determine the placental extension with the best predictive discriminatory zone. Results  In total, 157 women had placenta previa, ultrasound, and delivery data: 86 (55%) had a placental extension of <40 mm, and 71 (45%) had a placental extension of ≥40 mm. Women with placental extension of ≥40 mm had increased surgical time, blood loss > 2,000 mL, blood transfusion, and rate of peripartum hysterectomy. After multivariate analysis, only peripartum hysterectomy and surgical time > 90 minutes remained significant, p ≤ 0.05 and p ≤ 0.01, respectively. Conclusion  In women with placenta previa, the placental extension ultrasound measurement of ≥40 mm is a predictor of adverse surgical outcomes. KEYWORDS: central previa; placenta previa; placental extension; surgical outcomes; ultrasound PMID: 29686936 PMCID: PMC5910059 DOI: 10.1055/s-0038-1641163

2016

Intrahepatic Persistent Right Umbilical Vein and Associated Outcomes: A Systematic Review of the Literature

J Ultrasound Med. 2016 Jan;35(1):1-5. doi: 10.7863/ultra.15.01008. Epub 2015 Dec 3.

Lide B1, Lindsley W1, Foster MJ1, Hale R1, Haeri S2.

Abstract

The aim of this study was to provide a comprehensive review of the current data surrounding an intrahepatic persistent right umbilical vein in the fetus, including associated anomalies and outcomes, and to assist practitioners in counseling and management of affected pregnancies. We performed a MEDLINE, Embase, Cochrane Central Register of Controlled Trials, and Northern Light database search for articles reporting outcomes on prenatally diagnosed cases of a persistent right umbilical vein. Each article was independently reviewed for eligibility by the investigators. Thereafter, the data were extracted and validated independently by 3 investigators. A total of 322 articles were retrieved, and 16 were included in this systematic review. The overall prevalence of an intrahepatic persistent right umbilical vein was found to be 212 per 166,548 (0.13%). Of the 240 cases of an intrahepatic persistent right umbilical vein identified, 183 (76.3%) were isolated. The remaining cases had a coexisting abnormality, including 19 (7.9%) cardiac, 9 (3.8%) central nervous system, 15 (6.3%) genitourinary, 3 (1.3%) genetic, and 17 (7%) placental/cord (predominantly a single umbilical artery). In summary, a persistent right umbilical vein is commonly an isolated finding but may be associated with a coexisting cardiac defect in 8% of cases. Therefore, consideration should be given to fetal echocardiography in cases of a persistent right umbilical vein. © 2016 by the American Institute of Ultrasound in Medicine. KEYWORDS: ductus venosus; obstetric ultrasound; persistent right umbilical vein; portal vein

PMID 26635256

2015

Society for Maternal-Fetal Medicine (SMFM) Consult Series #37: Diagnosis and Management of Vasa Previa

Am J Obstet Gynecol. 2015 Aug 17. pii: S0002-9378(15)00897-2. doi: 10.1016/j.ajog.2015.08.031. [Epub ahead of print]

Society for Maternal-Fetal Medicine (SMFM) Publications Committee. Electronic address: pubs@smfm.org, Sinkey RG, Odibo AO, Dashe J.

Vasa previa occurs when fetal blood vessels unprotected by the umbilical cord or placenta run through the amniotic membranes and traverse the cervix. If membranes rupture, these vessels may rupture, with resultant fetal hemorrhage, exsanguination, or even death. Prenatal diagnosis of vasa previa by ultrasound is approximately 98%. Approximately 28% of prenatally diagnosis cases result in emergent preterm delivery. Management of prenatally diagnosis vasa previa includes antenatal corticosteroids between 28-32 weeks of gestation, considerations for preterm hospitalization at 30-34 weeks of gestation, and scheduled delivery at 34-37 weeks of gestation. Copyright © 2015 Elsevier Inc. All rights reserved.

PMID 26292048

Placenta praevia: incidence, risk factors and outcome

J Matern Fetal Neonatal Med. 2015 Jun 4:1-4. [Epub ahead of print]

Kollmann M1, Gaulhofer J, Lang U, Klaritsch P.

Abstract

OBJECTIVE: Aim of this study was to evaluate the incidence, potential risk factors and the respective outcomes of pregnancies with placenta praevia. METHODS: Data were prospectively collected from women diagnosed with placenta praevia in 10 Austrian hospitals in in the province of Styria between 1993 and 2012. We analyzed the incidence, potential risk factors and the respective outcomes of pregnancies with placenta praevia. Differences between women with major placenta praevia (complete or partial placenta praevia) and minor placenta praevia (marginal placenta praevia or low-lying placenta) were evaluated. RESULTS: 328 patients with placenta praevia were identified. The province wide incidence of placenta praevia was 0.15%. Maternal morbidity was high (ante-partum bleeding [42.3%], post-partum hemorrhage [7.1%], maternal anemia [30%], comorbid adherent placentation [4%], and hysterectomy [5.2%]) and neonatal complications were frequent (preterm birth [54.9%], low birth weight <2500 g [35.6%], Apgar-score after five minutes <7 [5.8%], and fetal mortality [1.5%]. Women with major placenta praevia had a significant higher incidence of preterm delivery, birthweight <2500 g and Apgar-score after five minutes <7. CONCLUSIONS: Placenta praevia was associated with adverse maternal (34.15%) and neonatal (60.06%) outcome. The extent of placenta praevia was not related with differences regarding risk factors and maternal outcome. KEYWORDS: Incidence; maternal and neonatal outcome; placenta praevia; risk factors

PMID 26043298

http://informahealthcare.com/doi/abs/10.3109/14767058.2015.1049152

Sonography of placental abnormalities: a pictorial review

Emerg Radiol. 2015 May 2. [Epub ahead of print]

Rheinboldt M1, Delproposto Z.

Abstract

Often overlooked during routine ultrasound evaluation of a normal pregnancy, the placenta forms the biologic interface between the mother and fetus and is critical to fetal growth and development. Malformations in development, positioning, and vascularity can have profound implications for both maternal and fetal well-being. As such, a judicious inspection of the placenta is warranted as an integral part of every screening or emergent prenatal ultrasound. Herein, we present a pictorial review of a variety of placental pathologic conditions including abnormalities in positioning, adherence, vascularity, and hemorrhage as well as potential peri-placental masses and gestational trophoblastic disease, all of which are readily encountered in a busy emergency radiology practice.

PMID 25933509

Hypoxic ischemic encephalopathy in newborns linked to placental and umbilical cord abnormalities

J Matern Fetal Neonatal Med. 2015 Feb 25:1-6. [Epub ahead of print]

Nasiell J1, Papadogiannakis N, Löf E, Elofsson F, Hallberg B.

Abstract

Abstract Objective: 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. Materials and methods: 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. The study population included 41 infants treated for HT whose placentas were submitted for histopathological analysis. Main outcome measures were infant development at 12 months, classified as normal, cerebral palsy, or death. A healthy group of 100 infants without HIE and normal follow-up at 12 months of age were used as controls. Results: A velamentous or marginal umbilical cord insertion and histological abruption was associated with the risk of severe HIE, OR = 5.63, p = 0.006, respectively, OR = 20.3, p = 0.01 (multiple-logistic regression). Velamentous or marginal umbilical cord insertion was found in 39% among HIE cases compared to 7% in controls. Conclusions: Placental and umbilical cord abnormalities have a profound association with HIE. A prompt examination of the placentas of newborns suffering from asphyxia can provide important information on the pathogenesis behind the incident and contribute to make a better early prognosis. KEYWORDS: Hypoxic ischemic encephalopathy; newborns; placenta; umbilical cord; velamentous/marginal insertion

PMID 25714479


2014

Three-dimensional sonographic assessment of placental volume and vascularization in pregnancies complicated by hypertensive disorders

J Ultrasound Med. 2014 Mar;33(3):483-91. doi: 10.7863/ultra.33.3.483.

de Almeida Pimenta EJ1, Silva de Paula CF, Duarte Bonini Campos JA, Fox KA, Francisco R, Ruano R, Zugaib M.

Abstract

OBJECTIVES: The purpose of this study was to evaluate the association between placental volumes, placental vascularity, and hypertensive disorders in pregnancy. METHODS: A prospective case-control study was conducted between April 2011 and July 2012. Placental volumes and vascularity were evaluated by 3-dimensional sonographic, 3-dimensional power Doppler histographic, and 2-dimensional color Doppler studies. Pregnant women were classified as normotensive or hypertensive and stratified by the nature of their hypertensive disorders. The following variables were evaluated: observed-to-expected placental volume ratio, placental volume-to-estimated fetal weight ratio, placental vascular indices, and pulsatility indices of the right and left uterine and umbilical arteries. RESULTS: Sixty-six healthy pregnant women and 62 pregnant women with hypertensive disorders were evaluated (matched by maternal age, gestational age at sonography, and parity). Placental volumes were not reduced in pregnancy in women with hypertensive disorders (P > .05). Conversely, reduced placental vascularization indices (vascularization index and vascularization-flow index) were observed in pregnancies complicated by hypertensive disorders (P < .01; P < .01), especially in patients with superimposed preeclampsia (P = .04; P = .02). A weak correlation was observed between placental volumes, placental vascular indices, and Doppler studies of the uterine and umbilical arteries. CONCLUSIONS: Pregnancies complicated by hypertensive disorders are associated with reduced placental vascularity but not with reduced placental volumes. These findings are independent of changes in uterine artery Doppler studies. Future studies of the prediction of preeclampsia may focus on placental vascularity in combination with results of Doppler studies of the uterine arteries. KEYWORDS: 3-dimensional power Doppler sonography; 3-dimensional sonography; Doppler study; arterial hypertension; obstetric ultrasound; placental size; placental vascularity; placental volume; preeclampsia; pregnancy; umbilical arteries; uterine arteries

PMID 24567460

http://www.jultrasoundmed.org/lookup/pmid?view=long&pmid=24567460

The placenta in toxicology. Part IV: Battery of toxicological test systems based on human placenta

Toxicol Pathol. 2014;42(2):345-51. doi: 10.1177/0192623313482206. Epub 2013 Apr 2.

Göhner C1, Svensson-Arvelund J, Pfarrer C, Häger JD, Faas M, Ernerudh J, Cline JM, Dixon D, Buse E, Markert UR.

Abstract

This review summarizes the potential and also some limitations of using human placentas, or placental cells and structures for toxicology testing. The placenta contains a wide spectrum of cell types and tissues, such as trophoblast cells, immune cells, fibroblasts, stem cells, endothelial cells, vessels, glands, membranes, and many others. It may be expected that in many cases the relevance of results obtained from human placenta will be higher than those from animal models due to species specificity of metabolism and placental structure. For practical and economical reasons, we propose to apply a battery of sequential experiments for analysis of potential toxicants. This should start with using cell lines, followed by testing placenta tissue explants and isolated placenta cells, and finally by application of single and dual side ex vivo placenta perfusion. With each of these steps, the relative workload increases while the number of feasible repeats decreases. Simultaneously, the predictive power enhances by increasing similarity with in vivo human conditions. Toxic effects may be detected by performing proliferation, vitality and cell death assays, analysis of protein and hormone expression, immunohistochemistry or testing functionality of signaling pathways, gene expression, transport mechanisms, and so on. When toxic effects appear at any step, the subsequent assays may be cancelled. Such a system may be useful to reduce costs and increase specificity in testing questionable toxicants. Nonetheless, it requires further standardization and end point definitions for better comparability of results from different toxicants and to estimate the respective in vivo translatability and predictive value. KEYWORDS: choriocarcinoma; human toxicology.; placenta; placenta explant; placenta perfusion; trophoblast

PMID 23548605

The placenta in toxicology. Part III: Pathologic assessment of the placenta

Toxicol Pathol. 2014;42(2):339-44. doi: 10.1177/0192623313482207. Epub 2013 Mar 26.

Cline JM1, Dixon D, Ernerudh J, Faas MM, Göhner C, Häger JD, Markert UR, Pfarrer C, Svensson-Arvelund J, Buse E. Author information

Abstract This short review is derived from the peer-reviewed literature and the experience and case materials of the authors. Brief illustrated summaries are presented on the gross and histologic normal anatomy of rodent and macaque placentas, including typical organ weights, with comments on differences from the human placenta. Common incidental findings, background lesions, and induced toxic lesions are addressed, and a recommended strategy for pathologic evaluation of placentas is provided. KEYWORDS: macaca; mus; placenta; primate pathology; rodent pathology; toxicology.

PMID 23531795

The placenta in toxicology. Part II: Systemic and local immune adaptations in pregnancy. PMID 23531796

The placenta in toxicology. Part I: Animal models in toxicology: placental morphology and tolerance molecules in the cynomolgus monkey (Macaca fascicularis). PMID:23548606

Accuracy of ultrasonography and magnetic resonance imaging in the diagnosis of placenta accreta

PLoS One. 2014 Apr 14;9(4):e94866. doi: 10.1371/journal.pone.0094866. eCollection 2014.

Riteau AS1, Tassin M2, Chambon G2, Le Vaillant C3, de Laveaucoupet J4, Quéré MP5, Joubert M6, Prevot S7, Philippe HJ3, Benachi A2. Author information

Abstract

PURPOSE: To evaluate the accuracy of ultrasonography and magnetic resonance imaging (MRI) in the diagnosis of placenta accreta and to define the most relevant specific ultrasound and MRI features that may predict placental invasion. MATERIAL AND METHODS: This study was approved by the institutional review board of the French College of Obstetricians and Gynecologists. We retrospectively reviewed the medical records of all patients referred for suspected placenta accreta to two university hospitals from 01/2001 to 05/2012. Our study population included 42 pregnant women who had been investigated by both ultrasonography and MRI. Ultrasound images and MRI were blindly reassessed for each case by 2 raters in order to score features that predict abnormal placental invasion. RESULTS: Sensitivity in the diagnosis of placenta accreta was 100% with ultrasound and 76.9% for MRI (P = 0.03). Specificity was 37.5% with ultrasonography and 50% for MRI (P = 0.6). The features of greatest sensitivity on ultrasonography were intraplacental lacunae and loss of the normal retroplacental clear space. Increased vascularization in the uterine serosa-bladder wall interface and vascularization perpendicular to the uterine wall had the best positive predictive value (92%). At MRI, uterine bulging had the best positive predictive value (85%) and its combination with the presence of dark intraplacental bands on T2-weighted images improved the predictive value to 90%. CONCLUSION: Ultrasound imaging is the mainstay of screening for placenta accreta. MRI appears to be complementary to ultrasonography, especially when there are few ultrasound signs.

PMID 24733409

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0094866

Risk factors for high and low placental weight

Paediatr Perinat Epidemiol. 2014 Mar;28(2):97-105. doi: 10.1111/ppe.12104. Epub 2013 Dec 20.

McNamara H1, Hutcheon JA, Platt RW, Benjamin A, Kramer MS. Author information

Abstract BACKGROUND: Placental weight is an independent predictor of adverse perinatal outcome. However, risk factors for high and low placental weight are poorly understood. The objective of this study was to identify maternal, placental, and umbilical cord determinants of placental weight, before and after accounting for birthweight. METHODS: This cohort study of 87,600 singleton births at the Royal Victoria Hospital in Montreal, Canada assessed the relationship between maternal, placental, and umbilical cord characteristics and placental weight (standardised for sex and gestational age). We separately examined risk factors for high (z-score >+1) and low (z-score <-1) placental weight. Multivariable logistic regression was used to study associations after adjusting for confounders and further adjusting for birthweight. RESULTS: Chronic hypertension was associated with low placental weight {relative risk (RR) 2.1 [95% confidence interval (CI) 1.8, 2.4] and 1.8 [95% CI 1.5, 2.1] before and after accounting for birthweight}, while pre-eclampsia was associated with low placenta weight before, but not after adjustment for birthweight. Anaemia and gestational diabetes were linked with high placental weight (RRs 1.2-1.4, respectively) before and after adjustment for birthweight, while smoking was linked with high placental weight only after adjustment for birthweight (RR 1.4 [95% CI 1.3, 1.5]). Placental and cord determinants of high placental weight included chorioamnionitis, chorangioma/chorangiosis, circumvallate placenta, marginal cord insertion, and other cord abnormalities. CONCLUSIONS: The broad range of risk factors for high placental weight suggests multiple aetiologic pathways. Future work should seek to understand the pathways by which the placenta adapts to unfavourable intrauterine conditions, which may provide insights into potential therapies. © 2013 John Wiley & Sons Ltd. KEYWORDS: birthweight, epidemiologic determinants, placenta, reference values

PMID 24354883


2013

Prenatal sonography can predict degree of placental invasion

Ultrasound Obstet Gynecol. 2013 Nov;42(5):518-24. doi: 10.1002/uog.12451. Epub 2013 Oct 9.

Chalubinski KM1, Pils S, Klein K, Seemann R, Speiser P, Langer M, Ott J.

Abstract

OBJECTIVE: To evaluate whether the maximum degree of placental invasion (placenta accreta, increta or percreta) can be predicted with ultrasound imaging, using criteria developed in our department. METHODS: This was a retrospective study of all 232 patients at risk for placental invasion who were part of a routine screening program for placental invasion from January 2001 to January 2011. The whole placenta was scanned in a systematic manner using both gray-scale ultrasound and color-flow mapping. Sonographic findings were compared with the clinical outcome during and after delivery and the histomorphological examination of the placenta. RESULTS: Placental invasion was suspected by ultrasound in 40 (17.2%) patients and was clinically/histopathologically confirmed in a total of 35 (15.1%) patients. The sensitivity, specificity and positive and negative predictive values of ultrasound for placental invasion were 91.4% (95% CI, 77.6-97.0%), 95.9% (95% CI, 92.2-97.9%), 80.0% (95% CI, 65.2-89.5%) and 98.4% (95% CI, 95.5-99.5%), respectively. No case of placenta increta (n = 7) or percreta (n = 17) was diagnosed as showing normal placentation or placenta accreta on ultrasound, giving an overall accuracy for the differentiation between normal placentation/placenta accreta and placenta increta/percreta of 100%. CONCLUSION: Our data suggest that prediction of the degree of placental invasion is possible using prenatal ultrasound, with high overall accuracy. Copyright © 2013 ISUOG. Published by John Wiley & Sons Ltd. KEYWORDS: antenatal; placenta accreta; placental invasion; predictive value; ultrasound

PMID 23471888

http://onlinelibrary.wiley.com/doi/10.1002/uog.12451/abstract;jsessionid=7A4C8D61CC3B363A42E82CEDFDEB8F98.f04t03


2012

Epidemiology, etiology, diagnosis, and management of placenta accreta

Obstet Gynecol Int. 2012;2012:873929. Epub 2012 May 7.

Garmi G, Salim R. Source Department of Obstetrics and Gynecology, Emek Medical Centre, 18101 Afula, Israel.

Abstract

Placenta accreta is a severe pregnancy complication and is currently the most common indication for peripartum hysterectomy. It is becoming an increasingly common complication mainly due to the increasing rate of cesarean delivery. Main risk factor for placenta accreta is a previous cesarean delivery particularly when accompanied with a coexisting placenta previa. Antenatal diagnosis seems to be a key factor in optimizing maternal outcome. Diagnosis can be achieved by ultrasound in the majority of cases. Women with placenta accreta are usually delivered by a cesarean section. In order to avoid an emergency cesarean and to minimize complications of prematurity it is acceptable to schedule cesarean at 34 to 35 weeks. A multidisciplinary team approach and delivery at a center with adequate resources, including those for massive transfusion are both essential to reduce neonatal and maternal morbidity and mortality. The optimal management after delivery of the neonate is vague since randomized controlled trials and large cohort studies are lacking. Cesarean hysterectomy is probably the preferable treatment. In carefully selected cases, when fertility is desired, conservative management may be considered with caution. The current review discusses the epidemiology, predisposing factors, pathogenesis, diagnostic methods, clinical implications and management options of this condition.

PMID 22645616

http://www.hindawi.com/journals/ogi/2012/873929/

Prenatal hypoxic-ischemic insult changes the distribution and number of NADPH-diaphorase cells in the cerebellum

PLoS One. 2012;7(4):e35786. Epub 2012 Apr 23.

Savignon T, Costa E, Tenorio F, Manhães AC, Barradas PC. Source Departamento de Farmacologia e Psicobiologia, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Brazil.

Abstract

Astrogliosis, oligodendroglial death and motor deficits have been observed in the offspring of female rats that had their uterine arteries clamped at the 18(th) gestational day. Since nitric oxide has important roles in several inflammatory and developmental events, here we evaluated NADPH-diaphorase (NADPH-d) distribution in the cerebellum of rats submitted to this hypoxia-ischemia (HI) model. At postnatal (P) day 9, Purkinje cells of SHAM and non-manipulated (NM) animals showed NADPH-d+ labeling both in the cell body and dendritic arborization in folia 1 to 8, while HI animals presented a weaker labeling in both cellular structures. NADPH-d+ labeling in the molecular (ML), and in both the external and internal granular layer, was unaffected by HI at this age. At P23, labeling in Purkinje cells was absent in all three groups. Ectopic NADPH-d+ cells in the ML of folia 1 to 4 and folium 10 were present exclusively in HI animals. This labeling pattern was maintained up to P90 in folium 10. In the cerebellar white matter (WM), at P9 and P23, microglial (ED1+) NADPH-d+ cells, were observed in all groups. At P23, only HI animals presented NADPH-d labeling in the cell body and processes of reactive astrocytes (GFAP+). At P9 and P23, the number of NADPH-d+ cells in the WM was higher in HI animals than in SHAM and NM ones. At P45 and at P90 no NADPH-d+ cells were observed in the WM of the three groups. Our results indicate that HI insults lead to long-lasting alterations in nitric oxide synthase expression in the cerebellum. Such alterations in cerebellar differentiation might explain, at least in part, the motor deficits that are commonly observed in this model.

PMID 22540005

The branching pattern of villous capillaries and structural changes of placental terminal villi in type 1 diabetes mellitus

Placenta. 2012 Feb 6. [Epub ahead of print]

Jirkovská M, Kučera T, Kaláb J, Jadrníček M, Niedobová V, Janáček J, Kubínová L, Moravcová M, Zižka Z, Krejčí V. Source Institute of Histology and Embryology, First Faculty of Medicine, Charles University in Prague, Albertov 4, CZ-12801 Prague 2, Czech Republic.

Abstract

Maternal diabetes is associated with changes of the placental structure. These changes include great variability of vascularity manifested by strikingly hypovascular as well as hypervascular terminal villi. 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. Formalin fixed and paraffin embedded specimens of 14 normal and 17 Type 1 diabetic term placentas were used for picrosirius staining, vimentin and desmin immunohistochemistry and confocal microscopy. 3D models of villi and villous capillaries were constructed from stacks of confocal optical sections. Hypervascular as well as hypovascular villi of diabetic placenta displayed changed structure of villous stroma, i.e. the collagen envelope around capillaries looked thinner and the network of collagen fibers seemed less dense. The desmin immunocytochemistry has shown that stromal cells of hypervascular as well as hypovascular villi appeared nearly or completely void of desmin filaments. In comparison with normal villi, capillaries of hypovascular villi had a smaller diameter and displayed a markedly wavy course whereas in hypervascular villi numerous capillaries occurred in reduced stroma and often had a large diameter. 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. Copyright © 2012 Elsevier Ltd. All rights reserved.

PMID 22317894

2011

Velamentous cord insertion caused by oblique implantation after in vitro fertilization and embryo transfer

J Obstet Gynaecol Res. 2011 Nov;37(11):1698-701. doi: 10.1111/j.1447-0756.2011.01555.x. Epub 2011 Jun 9.

Hasegawa J, Iwasaki S, Matsuoka R, Ichizuka K, Sekizawa A, Okai T. Source Department of Obstetrics and Gynecology, Showa University School of Medicine, Tokyo, Japan. hasejun@oak.dti.ne.jp

Abstract

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. © 2011 The Authors. Journal of Obstetrics and Gynaecology Research © 2011 Japan Society of Obstetrics and Gynecology.

PMID 21651650

http://onlinelibrary.wiley.com/doi/10.1111/j.1447-0756.2011.01555.x/full

2010

Placental surface shape, function, and effects of maternal and fetal vascular pathology

Placenta. 2010 Nov;31(11):958-62. doi: 10.1016/j.placenta.2010.09.005. Epub 2010 Oct 8.

Salafia CM, Yampolsky M, Misra DP, Shlakhter O, Haas D, Eucker B, Thorp J. Source Placental Analytics, LLC, 93 Colonial Avenue, Larchmont, NY 10538, USA. Carolyn.salafia@gmail.com Abstract GOAL: In clinical practice, variability of placental surface shape is common. We measure the average placental shape in a birth cohort and the effect deviations from the average have on placental functional efficiency. We test whether altered placental shape improves the specificity of histopathology diagnoses of maternal uteroplacental and fetoplacental vascular pathology for clinical outcomes. MATERIALS AND METHODS: 1225 Placentas from a prospective cohort had chorionic plate digital photographs with perimeters marked at 1-2 cm intervals. After exclusions of pre-term (n = 202) and velamentous cord insertion (n = 44), 979 (95.7%) placentas were analyzed. Median shape and mean perimeter were estimated. The relationship of fetal and placental weight was used as an index of placental efficiency termed "β". The principal placental histopathology diagnoses of maternal uteroplacental and fetoplacental vascular pathologies were coded by review of individual lesion scores. Acute fetal inflammation was scored as a "negative control" pathology not expected to affect shape. ANOVA with Bonferroni tests for subgroup comparisons were used. RESULTS: The mean placental chorionic shape at term was round with a radius estimated at 9.1 cm. Increased variability of the placental shape was associated with lower placental functional efficiency. After stratifying on placental shape, the presence of either maternal uteroplacental or fetoplacental vascular pathology was significantly associated with lower placental efficiency only when shape was abnormal. CONCLUSIONS: Quantifying abnormality of placental shape is a meaningful clinical tool. Abnormal shapes are associated with reduced placental efficiency. We hypothesize that such shapes reflect deformations of placental vascular architecture, and that an abnormal placental shape serves as a marker of maternal uteroplacental and/or fetoplacental vascular pathology of sufficiently long standing to impact placental (and by extension, potentially fetal) development. Copyright © 2010 Elsevier Ltd. All rights reserved.

PMID 20933281

Chorioamnionitis: a multiorgan disease of the fetus?

J Perinatol. 2010 Oct;30 Suppl:S21-30. Gantert M, Been JV, Gavilanes AW, Garnier Y, Zimmermann LJ, Kramer BW. Source Department of Obstetrics and Gynecology, Klinikum Osnabrück, Osnabrück, Germany.

Abstract

The bacterial infection of chorion and amnion is a common finding in premature delivery and is referred to as chorioamnionitis. As the mother rarely shows symptoms of a systemic inflammation, the course of chorioamnionitis is frequently asymptomatic and chronic. In contrast, the fetal inflammatory response syndrome represents a separate phenomenon, including umbilical inflammation and increased serum levels of proinflammatory cytokines in the fetus. Ascending maternal infections frequently lead to systemic fetal inflammatory reaction. Clinical studies have shown that antenatal exposure to inflammation puts the extremely immature neonates at a high risk for worsening pulmonary, neurological and other organ development. Interestingly, the presence of chorioamnionitis is associated with a lower rate of neonatal mortality in extremely immature newborns. In the following review, the pathogeneses of inflammation-associated perinatal morbidity are outlined. The concept of fetal multiorganic disease during intrauterine infection is introduced and discussed.

PMID 20877404

Recurrent hydatidiform moles

Eur J Obstet Gynecol Reprod Biol. 2010 May;150(1):3-7. Epub 2010 Feb 19.

Williams D, Hodgetts V, Gupta J. Source Department of Clinical Genetics, Birmingham Women's Hospital, Edgbaston, Birmingham B15 2TG, United Kingdom. Abstract Hydatidiform moles (HMs) are abnormal conceptions of excessive trophoblast development resulting in abnormal human pregnancies with no embryo and cystic degeneration of the chorionic villi. Prompt diagnosis, treatment and follow-up of patients using assays for betahCG from centres that specialise in this condition enable early diagnosis of potential malignant change. Hydatidiform moles occur quite frequently and although recurrence is rare, women who have experienced one molar pregnancy should be aware that they are at an increased risk of a further molar pregnancy in comparison to other women in the general population. For some women multiple molar pregnancies occur. In these women the recurrent molar pregnancies may be non-familial, referred to as recurrent molar hydatidiform moles in this article, or may result from an inherited predisposition, which we refer to as familial recurrent hydatidiform moles. We use the term familial biparental hydatidiform moles (FBHMs) for cases in which the parental contribution to the moles has been investigated and found to be biparental. It is important to recognise, however, that in some apparently non-familial cases, the absence of female siblings, or the absence of female siblings who have tried to conceive, may not allow the inherited nature of the molar pregnancies to manifest in more than one woman and be obviously familial. This review considers our current understanding about the aetiology of HMs and explores the mechanisms of both types of recurrent hydatidiform moles. It highlights the role that genetics can play in determining the origin of multiple molar pregnancies, which should be considered essential in providing women with accurate advice about their risk of recurrence, so allowing them to make appropriate reproductive choices. Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.

PMID 20171777

2009

Placental weight relative to birth weight and long-term cardiovascular mortality: findings from a cohort of 31,307 men and women

Am J Epidemiol. 2009 Sep 1;170(5):622-31. doi: 10.1093/aje/kwp182. Epub 2009 Jul 28.

Risnes KR1, Romundstad PR, Nilsen TI, Eskild A, Vatten LJ.

Abstract

Birth weight is inversely associated with risk of adult cardiovascular disease, and evidence exists that fetal adaptation to challenges in the intrauterine environment may adversely affect long-term cardiovascular health. The placenta is in a key position to mediate such effects because adequate placental function is necessary for delivery of nutrients, oxygen, and hormones to the fetus. This prospective population study based on data from the hospital birth charts of 31,307 Norwegian men and women born between 1934 and 1959 assessed whether placental weight relative to birth weight was associated with risk of death from cardiovascular disease in adulthood. During 45 years of follow-up, 382 people died from cardiovascular disease (median age, 51.3 years). Results showed that the placenta-to-birth-weight ratio was positively associated with cardiovascular disease mortality; the sex- and cohort-adjusted hazard ratio for the highest versus the lowest third was 1.38 (95% confidence interval: 1.07, 1.77). The authors concluded that a disproportionately large placenta relative to birth weight was associated with increased risk of cardiovascular disease death. This finding suggests that placental function is important in the association of intrauterine factors with cardiovascular disease later in life. PMID 19638481

Guidelines for the management of vasa previa

J Obstet Gynaecol Can. 2009 Aug;31(8):748-60.

[Article in English, French] Gagnon R, Morin L, Bly S, Butt K, Cargill YM, Denis N, Hietala-Coyle MA, Lim KI, Ouellet A, Raciot MH, Salem S; Diagnostic Imaging Committee, Hudon L, Basso M, Bos H, Delisle MF, Farine D, Grabowska K, Menticoglou S, Mundle W, Murphy-Kaulbeck L, Pressey T, Roggensack A; Maternal Fetal Medicine Committee. Source The Society of Obstetricians and Gynaecologists of Canada (SOGC), Montreal, QC.

Abstract OBJECTIVES: To describe the etiology of vasa previa and the risk factors and associated condition, to identify the various clinical presentations of vasa previa, to describe the ultrasound tools used in its diagnosis, and to describe the management of vasa previa. OUTCOMES: Reduction of perinatal mortality, short-term neonatal morbidity, long-term infant morbidity, and short-term and long-term maternal morbidity and mortality. EVIDENCE: Published literature on randomized trials, prospective cohort studies, and selected retrospective cohort studies was retrieved through searches of PubMed or Medline, CINAHL, and the Cochrane Library, using appropriate controlled vocabulary (e.g., selected epidemiological studies comparing delivery by Caesarean section with vaginal delivery; studies comparing outcomes when vasa previa is diagnosed antenatally vs. intrapartum) and key words (e.g., vasa previa). Results were restricted to systematic reviews, randomized control trials/controlled clinical trials, and observational studies. Searches were updated on a regular basis and incorporated into the guideline to October 1, 2008. Grey (unpublished) literature was identified through searching the websites of health technology assessment and health technology assessment-related agencies, clinical practice guideline collections, clinical trial registries, and from national and international medical specialty societies. VALUES: The evidence collected was reviewed by the Diagnostic Imaging Committee and the Maternal Fetal Medicine Committee of the Society of Obstetricians and Gynaecologists of Canada (SOGC) and quantified using the evaluation of evidence guidelines developed by the Canadian Task Force on Preventive Health Care. BENEFITS, HARMS, AND COSTS: The benefit expected from this guideline is facilitation of optimal and uniform care for pregnancies complicated by vasa previa. SPONSORS: The Society of Obstetricians and Gynaecologists of Canada. SUMMARY STATEMENT: A comparison of women who were diagnosed antenatally and those who were not shows respective neonatal survival rates of 97% and 44%, and neonatal blood transfusion rates of 3.4% and 58.5%, respectively. Vasa previa can be diagnosed antenatally, using combined abdominal and transvaginal ultrasound and colour flow mapping; however, many cases are not diagnosed, and not making such a diagnosis is still acceptable. Even under the best circumstances the false positive rate is extremely low. (II-2).

RECOMMENDATIONS:

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). Republished in Int J Gynaecol Obstet. 2010 Jan;108(1):85-9.

PMID 19772710

2008

In vitro and in vivo human herpesvirus 8 infection of placenta

PLoS One. 2008;3(12):e4073. Epub 2008 Dec 30.

Di Stefano M, Calabrò ML, Di Gangi IM, Cantatore S, Barbierato M, Bergamo E, Kfutwah AJ, Neri M, Chieco-Bianchi L, Greco P, Gesualdo L, Ayouba A, Menu E, Fiore JR. Source Laboratory of Molecular Medicine, University of Foggia, Foggia, Italy.

Abstract

Herpesvirus infection of placenta may be harmful in pregnancy leading to disorders in fetal growth, premature delivery, miscarriage, or major congenital abnormalities. Although a correlation between human herpesvirus 8 (HHV-8) infection and abortion or low birth weight in children has been suggested, and rare cases of in utero or perinatal HHV-8 transmission have been documented, no direct evidence of HHV-8 infection of placenta has yet been reported. The aim of this study was to evaluate the in vitro and in vivo susceptibility of placental cells to HHV-8 infection. Short-term infection assays were performed on placental chorionic villi isolated from term placentae. Qualitative and quantitative HHV-8 detection were performed by PCR and real-time PCR, and HHV-8 proteins were analyzed by immunohistochemistry. Term placenta samples from HHV-8-seropositive women were analyzed for the presence of HHV-8 DNA and antigens. In vitro infected histocultures showed increasing amounts of HHV-8 DNA in tissues and supernatants; cyto- and syncitiotrophoblasts, as well as endothelial cells, expressed latent and lytic viral antigens. Increased apoptotic phenomena were visualized by the terminal deoxynucleotidyl transferase-mediated deoxyuridine nick end-labeling method in infected histocultures. Ex vivo, HHV-8 DNA and a latent viral antigen were detected in placenta samples from HHV-8-seropositive women. These findings demonstrate that HHV-8, like other human herpesviruses, may infect placental cells in vitro and in vivo, thus providing evidence that this phenomenon might influence vertical transmission and pregnancy outcome in HHV-8-infected women.

PMID 19115001


Placental pathology, a survival guide

Arch Pathol Lab Med. 2008 Apr;132(4):641-51.

Roberts DJ. Source Department of Pathology, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02115, USA. djroberts@partners.org Abstract Placental pathology continues to be an underutilized, undertaught, and inadequately handled surgical subspecialty. The requests for placental pathology are soaring, due partly to demands from obstetricians and to the litigious environment in which they practice, and to improved obstetrical care leading to pregnancies in medically challenging situations. Evaluation of the placenta requires a good understanding of the questions and issues concerning both the fetus/infant and the mother. Information from placental pathology can be critical in early neonatal care and in reproductive planning for the family, and it can provide risk assessment for neurologic outcome of the infant. A comfortable interaction among the obstetric staff, mothers, and pathologists often obviates need for legal intervention in unexpected pregnancy outcomes. Some critical pathologic features that involve maternal and fetal management are illustrated herein. A template for gross examination and a few critical histopathologic diagnostic features with clincopathologic correlation are included.

PMID 18384216


Modeling the variability of shapes of a human placenta

Placenta. 2008 Sep;29(9):790-7. Epub 2008 Jul 31.

Yampolsky M, Salafia CM, Shlakhter O, Haas D, Eucker B, Thorp J. Source Department of Mathematics, University of Toronto, 40 St. George Street, Toronto, Ontario, Canada M5S2E4. yampolsky.michael@gmail.com

Abstract

BACKGROUND: Placentas are generally round/oval in shape, but "irregular" shapes are common. In the Collaborative Perinatal Project data, irregular shapes were associated with lower birth weight for placental weight, suggesting variably shaped placentas have altered function. METHODS: (I) Using a 3D one-parameter model of placental vascular growth based on Diffusion Limited Aggregation (an accepted model for generating highly branched fractals), models were run with a branching density growth parameter either fixed or perturbed at either 5-7% or 50% of model growth. (II) In a data set with detailed measures of 1207 placental perimeters, radial standard deviations of placental shapes were calculated from the umbilical cord insertion, and from the centroid of the shape (a biologically arbitrary point). These two were compared to the difference between the observed scaling exponent and the Kleiber scaling exponent (0.75), considered optimal for vascular fractal transport systems. Spearman's rank correlation considered p<0.05 significant. RESULTS: (I) Unperturbed, random values of the growth parameter created round/oval fractal shapes. Perturbation at 5-7% of model growth created multilobate shapes, while perturbation at 50% of model growth created "star-shaped" fractals. (II) The radial standard deviation of the perimeter from the umbilical cord (but not from the centroid) was associated with differences from the Kleiber exponent (p=0.006). CONCLUSIONS: A dynamical DLA model recapitulates multilobate and "star" placental shapes via changing fractal branching density. We suggest that (1) irregular placental outlines reflect deformation of the underlying placental fractal vascular network, (2) such irregularities in placental outline indicate sub-optimal branching structure of the vascular tree, and (3) this accounts for the lower birth weight observed in non-round/oval placentas in the Collaborative Perinatal Project.

PMID 18674815

Chorioamnionitis and increased galectin-1 expression in PPROM --an anti-inflammatory response in the fetal membranes?

Am J Reprod Immunol. 2008 Oct;60(4):298-311.

Than NG, Kim SS, Abbas A, Han YM, Hotra J, Tarca AL, Erez O, Wildman DE, Kusanovic JP, Pineles B, Montenegro D, Edwin SS, Mazaki-Tovi S, Gotsch F, Espinoza J, Hassan SS, Papp Z, Romero R. Source Perinatology Research Branch, NICHD/NIH/DHHS, Wayne State University/Hutzel Women's Hospital, 3990 John R, Box 4, Detroit, MI 48201, USA. nthan@med.wayne.edu Abstract PROBLEM: Galectin-1 can regulate immune responses upon infection and inflammation. We determined galectin-1 expression in the chorioamniotic membranes and its changes during histological chorioamnionitis. METHOD OF STUDY: Chorioamniotic membranes were obtained from women with normal pregnancy (n = 5) and from patients with pre-term pre-labor rupture of the membranes (PPROM) with (n = 8) and without histological chorioamnionitis (n = 8). Galectin-1 mRNA and protein were localized by in situ hybridization and immunohistochemistry. Galectin-1 mRNA expression was also determined by quantitative reverse transcriptase polymerase chain reaction. RESULTS: Galectin-1 mRNA and protein were detected in the amniotic epithelium, chorioamniotic fibroblasts/myofibroblasts and macrophages, chorionic trophoblasts, and decidual stromal cells. In patients with PPROM, galectin-1 mRNA expression in the fetal membranes was higher (2.07-fold, P = 0.002) in those with chorioamnionitis than in those without. Moreover, chorioamionitis was associated with a strong galectin-1 immunostaining in amniotic epithelium, chorioamniotic mesodermal cells, and apoptotic bodies. CONCLUSION: Chorioamnionitis is associated with an increased galectin-1 mRNA expression and strong immunoreactivity of the chorioamniotic membranes; thus, galectin-1 may be involved in the regulation of the inflammatory responses to chorioamniotic infection.

PMID 18691335

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2784815/

2007

Association of caesarean delivery for first birth with placenta praevia and placental abruption in second pregnancy

BJOG. 2007 May;114(5):609-13. Epub 2007 Mar 12.

Yang Q1, Wen SW, Oppenheimer L, Chen XK, Black D, Gao J, Walker MC.

Abstract OBJECTIVE: To quantify the risk of placenta praevia and placental abruption in singleton, second pregnancies after a caesarean delivery of the first pregnancy. DESIGN: Retrospective cohort study. SETTING: Linked birth and infant mortality database of the USA between 1995 and 2000. POPULATION: A total of 5,146,742 singleton second pregnancies were available for the final analysis after excluding missing information. METHODS: Multiple logistic regressions were used to describe the relationship between caesarean section at first birth and placenta praevia and placental abruption in second-birth singletons. MAIN OUTCOME MEASURES: Placenta praevia and placental abruption. RESULTS: Placenta praevia was recorded in 4.4 per 1000 second-birth singletons whose first births delivered by caesarean section and 2.7 per 1000 second-birth singletons whose first births delivered vaginally. About 6.8 per 1000 births were complicated with placental abruption in second-birth singletons whose first births delivered by caesarean section and 4.8 per 1000 birth in second-birth singletons whose first births delivered vaginally. The adjusted odds ratio (95% CIs) of previous caesarean section for placenta praevia in following second pregnancies was 1.47 (1.41, 1.52) after controlling for maternal age, race, education, marital status, maternal drinking and smoking during pregnancy, adequacy of prenatal care, and fetal gender. The corresponding figure for placental abruption was 1.40 (1.36, 1.45). CONCLUSION: Caesarean section for first live birth is associated with a 47% increased risk of placenta praevia and 40% increased risk of placental abruption in second pregnancy with a singleton.

PMID 17355267

The Black-White disparity in pregnancy-related mortality from 5 conditions: differences in prevalence and case-fatality rates

Tucker MJ, Berg CJ, Callaghan WM, Hsia J.

Division of Reproductive Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, Ga 30341-3724, USA. Comment in:

Am J Public Health. 2007 Sep;97(9):1541; author reply 1541. Abstract OBJECTIVES: We sought to determine whether differences in the prevalences of 5 specific pregnancy complications or differences in case fatality rates for those complications explained the disproportionate risk of pregnancy-related mortality for Black women compared with White women in the United States. METHODS: We used national data sets to calculate prevalence and case-fatality rates among Black and White women for preeclampsia, eclampsia, abruptio placentae, placenta previa, and postpartum hemorrhage for the years 1988 to 1999. RESULTS: Black women did not have significantly greater prevalence rates than White women. However, Black women with these conditions were 2 to 3 times more likely to die from them than were White women. CONCLUSIONS: Higher pregnancy-related mortality among Black women from preeclampsia, eclampsia, abruptio placentae, placenta previa, and postpartum hemorrhage is largely attributable to higher case-fatality rates. Reductions in case-fatality rates may be made by defining more precisely the mechanisms that affect complication severity and risk of death, including complex interactions of biology and health services, and then applying this knowledge in designing interventions that improve pregnancy-related outcomes.


Placenta- umbilical cord torsion.jpg


J Clin Pathol. 2004 Aug;57(8):785-92.

Best practice no 178. Examination of the human placenta

J Clin Pathol. 2004 Aug;57(8):785-92.

Hargitai B, Marton T, Cox PM. Source No 1 Department of Obstetrics and Gynecology, Semmelweis University Budapest, Baross u. 27, 1088 Budapest, Hungary.

Abstract

The human placenta is an underexamined organ. The clinical indications for placental examination have no gold standards. There is also inconsistency in the histological reports and the quality is variable. There is great interobserver variability concerning the different entities. Although there are still grey areas in clinicopathological associations, a few mainstream observations have now been clarified. The histopathological examination and diagnosis of the placenta may provide crucial information. It is possible to highlight treatable maternal conditions and identify placental or fetal conditions that can be recurrent or inherited. To achieve optimal benefit from placental reports, it is essential to standardise the method of placenta examination. This article summarises the clinical indications for placenta referral and the most common acknowledged clinicopathological correlations.

PMID 15280396


Fetal environment

Indian J Radiol Imaging. 2008 Nov;18(4):326-44.

Kinare A.

Department of Ultrasound, K.E.M. Hospital, Jehangir Hospital, Pune, India. Abstract The intrauterine environment has a strong influence on pregnancy outcome. The placenta and the umbilical cord together form the main supply line of the fetus. Amniotic fluid also serves important functions. These three main components decide whether there will be an uneventful pregnancy and the successful birth of a healthy baby. An insult to the intrauterine environment has an impact on the programming of the fetus, which can become evident in later life, mainly in the form of cardiovascular diseases, diabetes, and certain learning disabilities. The past two decades have witnessed major contributions from researchers in this field, who have included ultrasonologists, epidemiologists, neonatologists, and pediatricians. Besides being responsible for these delayed postnatal effects, abnormalities of the placenta, umbilical cord, and amniotic fluid also have associations with structural and chromosomal disorders. Population and race also influence pregnancy outcomes to some extent in certain situations. USG is the most sensitive imaging tool currently available for evaluation of these factors and can offer considerable information in this area. This article aims at reviewing the USG-related developments in this area and the anatomy, physiology, and various pathologies of the placenta, umbilical cord, and the amniotic fluid.

PMID: 19774194 http://www.ncbi.nlm.nih.gov/pubmed/19774194

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747450/?tool=pubmed

(good placental abnormalities ultrasound images)

Historic References

Portal P. The Compleat Practice of Men and Women Midwives: Or the True Manner of Assisting a Woman in Child-bearing. Paris, 1685. (English translation, London: J Johnson; 1763: 143-4)