PATHOPHYSIOLOGY AND RISK FACTORS
An appreciation of risk factors
for ectopic pregnancy leads to a timely diagnosis with improved maternal
survival and future reproductive potential.
Inflammation has been implicated
in the role of tubal damage that predisposes to ectopic pregnancies.
Inflam-matory processes, such as salpingitis
and salpingitis isth-mica nodosa, may
also play a role. Acute pathology, suchas chlamydial
infection, causes intraluminal inflamma-tion and subsequent fibrin
deposition with tubal scarring. Despite negative cultures, persistent
chlamydial antigens can trigger a delayed hypersensitivity reaction with
con-tinued scarring. Whereas endotoxin-producing Neisseriagonorrhoeae causes virulent pelvic inflammation with a
rapidclinical onset, chlamydial inflammatory response is indo-lent and peaks at
7 to 14 days.
Although pregnancy after
sterilization is rare, when it does occur, there is a substantial risk that the
pregnancy will be ectopic. Most forms of contraception
decrease the number of intrauterine pregnancies, thereby increasing the
relative (but not absolute) incidence of ectopic pregnancy. Oral contraceptives
prevent ovulation, significantly reduc-ing pregnancies in all locations.
Intrauterine devices do not increase the overall risk of ectopic pregnancy.
Abor-tion does not predispose to ectopic pregnancy, although associated
infection may do so.
A history of infertility,
independent of tubal disease, and ovulation induction also appear to be risk
factors in ectopic pregnancy. Additional risk factors include smok-ing, prior
tubal surgery, diethylstilbestrol exposure, and advanced age.
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