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.