The etonogestrel implant is a single-rod progestin contraceptive placed subdermally in the inner upper arm for long-acting (three years) reversible contraception in women (figure 1). It was originally marketed under the brand name Implanon, but was subsequently modified and marketed as Nexplanon (figure 2). Implanon and Nexplanon are bioequivalent.
Accumulating evidence supports the safety, efficacy, and acceptability of this contraceptive method [1,2]. In 2009, 0.8 percent of current contraceptors used an etonogestrel implant, up from 0.4 percent in 2002 . Contraception is the only approved indication for the etonogestrel implant, although it has been studied for use in progestin-responsive disorders, such as endometriosis .
STRUCTURE AND PHARMACOKINETICS
The implant consists of a 40 mm by 2 mm semi-rigid plastic (ethylene vinyl acetate) rod containing 68 mg of the progestin etonogestrel (the 3-keto derivative of desogestrel). Etonogestrel is slowly released over at least three years, initially at 60 to 70 mcg/day, decreasing to 35 to 45 mcg/day at the end of the first year, to 30 to 40 mcg/day at the end of the second year, and then to 25 to 30 mcg/day at the end of the third year .
Unlike Implanon, the Nexplanon rod is radio-opaque so it can be detected by x-ray and thus does not require magnetic resonance imaging (MRI) for locating an impalpable implant. In addition, the redesigned applicator makes subdermal insertion easier and failed insertion unlikely because the new cap will not open if the implant is not in the needle and a finger pressure activated lever ensures that the trocar completely discharges the contraceptive implant under the skin.
MECHANISM FOR CONTRACEPTION
Progestins cause changes in cervical mucus and tubal motility that are unfavorable to sperm migration, thus inhibiting fertilization. At high doses, progestins also inhibit gonadotropin secretion, thereby inhibiting follicular maturation and ovulation. This dual effect allows contraceptive efficacy to be maintained even though ovulation is not consistently inhibited in implant users toward the end of the three-year period of use. Although progestins suppress endometrial activity, which makes the endometrium unreceptive to implantation, this is less important since the major mechanisms of contraceptive action prevent fertilization.