Fetal Thrombotic Vasculopathy

  • Rebecca N. Baergen
Chapter

Abstract

The umbilical vessels insert onto the placental surface, branch, run within the chorionic plate, and then, at the periphery, turn abruptly toward the maternal surface, branching repeatedly to finally become villous capillaries. Blood is returned from the villous capillary loops to the umbilical cord by veins that merge into the umbilical vein. In the overwhelming majority of cotyledons, there is a 1:1 relation between artery and vein at the periphery, and each artery “supplies” a single cotyledon (placentone). It is remarkable that at least the larger arteries always cross over the veins on the placental surface. They can thus be readily identified by macroscopic examination, while histologically it is nearly impossible to make this distinction. It is interesting to note that the circumferential architecture of the placental surface vessels is asymmetrical. This is due to hemodynamic thinning where pressure in the vessels buckle and thin the superficial portions of the vessels, whereas the “fixed” portions resist this pressure. This phenomenon of thinning of the superficial aspect of chorionic vessels is also shared with cord vessels.

Keywords

Preeclampsia Rounded Thrombophilias Mucopolysaccharide Chorioamnionitis 

Selected References

  1. PHP5, pages 426–434.Google Scholar
  2. Baergen RN, Malicki D, Behling CA, et al. Morbidity, mortality and placental pathology in excessively long umbilical cords. Pediatr Dev Pathol 2001;4:144–153.CrossRefPubMedGoogle Scholar
  3. Boué DR, Stanley C, Baergen RN. Placental pathology casebook. J Perinatol 1995;15:429–431.PubMedGoogle Scholar
  4. De Sa DJ. Intimal cushions in foetal placental veins. J Pathol 1973;110:347–352.CrossRefGoogle Scholar
  5. Gogia N, Machine GA. Maternal thrombophilias are associated with specific placental lesions. Pediatr Dev Pathol 2008;11:424–429.CrossRefPubMedGoogle Scholar
  6. Heifetz SA. Thrombosis of the umbilical cord: analysis of 52 cases and literature review. Pediatr Pathol 1988;8:37–54.CrossRefPubMedGoogle Scholar
  7. Kaplan CG. Fetal and maternal vascular lesions. Semin Diagn Pathol 2007;24:14–22.CrossRefPubMedGoogle Scholar
  8. Kraus FT, Achen VI. Fetal thrombotic vasculopathy in the placenta. Cerebral thrombi, infarct, coagulopathy and cerebral palsy. Hum Pathol 1999;30:759–769.CrossRefPubMedGoogle Scholar
  9. Rayne SC, Kraus FT. Placental thrombi and other vascular lesions: classification, morphology, and clinical correlations. Pathol Res Pract 1993;189:2–17.PubMedGoogle Scholar
  10. Redline RW. Severe fetal placental vascular lesions in term infants with neurologic impairment. Am J Obstet Gynecol 2005;192:452–457.CrossRefPubMedGoogle Scholar
  11. Redline RW, Ariel I, Baergen RN, DeSa DJ, Kraus FT, Roberts DJ, Sander CM. Fetal vascular obstructive lesions: nosology and reproducibility of placental reaction patterns. Pediatr Dev Pathol 2004;7:443–452.CrossRefPubMedGoogle Scholar
  12. Redline RW, Pappin A. Fetal thrombotic vasculopathy: the clinical significance of extensive avascular villi. Hum Pathol 1995;26:80.CrossRefPubMedGoogle Scholar
  13. Sander CM. Hemorrhagic endovasculitis and hemorrhagic villitis of the placenta. Arch Pathol Lab Med 1980;104:371–373.PubMedGoogle Scholar
  14. Sander CM, Gilliland D, Flynn MA, et al. Risk factors for recurrence of hemorrhagic endovasculitis of the placenta. Obstet Gynecol 1997;89:569–576.CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Rebecca N. Baergen
    • 1
  1. 1.New York Presbyterian Hospital—Weill Medical College of Cornell UniversityNew YorkUSA

Personalised recommendations