Definition/Context/Significance:

This common disorder is most commonly due to ascension of birth-canal organisms through the cervix into the overlying amnionic membranes. A histo-pathological diagnosis of acute chorioamnionitis (ACA) implies much more than an inconsequential, possibly labor-producing acute WBC infiltrate involving only the small disc of membranes situated over the dilating cervical opening: our threshold for diagnosis is the visualization of acute inflammatory cells infiltrating into the stroma of the chorionic roof of the placental plate (invading the under-surface...the "underneath aspect"...the deep aspect of the fetal, shiny surface of the placental plate). If the infection spreads to a worse degree, involving blood vessels (phlebitis, vasculitis, funicular vasculitis) or even through vessels into umbilical cord stroma (funisitis), it is worth having information in the record as to degree of ACA. ACA occurs in 20% of placentae with only 25% of that 20% showing signs/symptoms.¹⁵ Ascending-route etiology is due to one or more of: vaginal anaerobes (such as Gardnerella vaginalis), vaginal aerobes (such as Group B Strep.), mycoplasma organisms, chlamydia organisms, or parasites (trichomonads), or fungi (such as Candida).¹⁴ When ACA also induces villous edema, there is a stronger correlation with neonatal morbidity and mortality.¹⁶

Especially when there is an anatomical defect compromising the cervix or causing risk of cervical incompetence (cervical scar; anomalous os; previous LEEP surgery for dysplasia of the cervix), ACA is likely to recur. If social or socio-economic circumstances predispose to vaginal pathogens or decreased antimicrobial activity of amniotic fluid¹⁵, ACA is more likely to recur; so, knowledge of the diagnosis on the original pregnancy allows an opportunity to clinically intercede on subsequent pregnancies, possibly preventing the well-known association of ACA with premature labor and delivery and possible consequences there-of.

Neurological sequelae, from minor milestone delays to cerebral palsy, would appear to be related to (not acute) subacute and/or chronic fetal vascular insufficiencies.² Even so, and though the topic is controversial, the newest edition of a leading textbook cautions, "A great deal of attention has been focused on the consequences of intra-uterine and intra-partum infections. At worst, some well-defined infections can result in abortion, stillbirth, prematurity, or multiply handicapped, severely disabled children who are mentally retarded, blind, deaf, or suffer from numerous other congenital malformations. In addition to this obvious and identified toll, many more subtle, late sequelae, including learning disabilities, school failure, and especially deafness, are being identified in children whose infections were asymptomatic at birth. The social and financial burden posed by the support of these children is enormous, not to mention the long-term grief and emotional cost to the families involved."¹⁶ From the standpoint of the infant, the absence of chorioamnionitis is an important finding¹⁶, negativity essentially excluding ascending infection during the first 48 hours of life. Though it would be difficult to routinely rapidly issue pathology reports as to positive or negative, infants having positive placentas are at increased risk to develop sepsis and die in the neonatal period¹⁶; if treated, most treatments will have been initiated according to clinical parameters.

My daughter's two children both had placentae with "bad" ACA under the microscope and no evidence of it at the bedside (clinically negative)...both children (now 12 & 16) are developing excellently. So, a pathology diagnosis of ACA simply helps the baby's physician know what the situation was as the baby started life in this world!

References:

1. see the bibliography refernec numbers with this page.

(file published September 26, 1994; posted on-line August 2002; addition 4 October 2009)