Gross abnormalities of the umbilical cord: related placental histology and clinical significance.
OBJECTIVE
To evaluate umbilical cord abnormalities predisposing to mechanical cord compression and determine their relationship to adverse clinical outcomes and stasis-associated histologic changes in the placenta.


METHODS
Placental slides of 224 singleton pregnancies with gross cord abnormality (true knots, long cords, nuchal/body cords, abnormal cord insertion, hypercoiled cords, narrow cords with diminished Wharton's jelly), delivered on or after 28 weeks gestational age, and 317 gestational age-matched controls, were reviewed and specifically evaluated for the following histologic changes: (1) fetal vascular ectasia, (2) fetal vascular thrombosis, (3) and fetal thrombotic vasculopathy/avascular villi. These changes were analyzed in relation to both clinical information and findings at gross pathologic examination.


RESULTS
Gross cord abnormalities were associated with stillbirth, intrauterine growth restriction, non-reassuring fetal tracing, meconium-stained amniotic fluid, and increased rate of emergency Cesarean section. At microscopic evaluation, cases with gross cord abnormalities showed a statistically significant association with both ectasia and thrombosis in the fetal vasculature, as well as changes of fetal thrombotic vasculopathy in the terminal villi. When considering individual gross cord abnormalities, long cord and nuchal cord had the highest rates of thrombosis-related histopathology. Finally, cases with both abnormal cords and histologic thrombosis had significantly higher rates of adverse outcomes, including IUGR and stillbirth.


CONCLUSIONS
Gross cord abnormalities predispose the fetus to stasis-induced vascular ectasia and thrombosis, thus leading to vascular obstruction and adverse neonatal outcome, including IUGR and stillbirth. We recommend a thorough histopathologic evaluation of all placentas with gross cord abnormalities predisposing to cord compression.
Tantbirojn
P
P
Division of Women's and Perinatal Pathology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Saleemuddin
A
A
Sirois
K
K
Crum
C P
CP
Boyd
T K
TK
Tworoger
S
S
Parast
M M
MM
D000653:Amniotic Fluid / Q000737:chemistry; D001034:Apgar Score; D002585:Cesarean Section; D002823:Chorion / Q000098:blood supply / Q000473:pathology; D002824:Chorionic Villi / Q000098:blood supply / Q000473:pathology; D004108:Dilatation, Pathologic / Q000209:etiology / Q000473:pathology; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology; D005333:Fetus / Q000098:blood supply / Q000473:pathology; D006340:Heart Rate, Fetal; D006801:Humans; D053589:Nuchal Cord / Q000150:complications; D010920:Placenta / Q000098:blood supply / Q000473:pathology* / Q000503:physiopathology*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000209:etiology / Q000473:pathology; D011256:Pregnancy Outcome; D012307:Risk Factors; D050497:Stillbirth; D013927:Thrombosis / Q000209:etiology / Q000473:pathology; D014470:Umbilical Cord / Q000002:abnormalities* / Q000473:pathology*