It has been estimated that about 1 million women develop PID annually in the United States. Less than one-third of these women present with an acute pelvic infl ammatory disease. The remaining cases usually go undetected until the woman presents with symptoms of infertility. In fact, more that 60% of patients who undergo surgery or in vitro fertilization and embryo transfer (IVF/ET) for the treatment of infertility secondary to pelvic inflammatory disease, do not have a history of previously diagnosed acute PID.
Acute PID may present as an acute illness with fever with severe lower abdominal pain. In this, the most dramatic presentation of PID, there is frequently a nonirritating yellow or blood stained vaginal discharge. Pain is typically severe enough to prompt urgent medical attention.
Subacute PID is more common and less severe. Its presentation is so gradual that it often goes unnoticed until superimposed acute PID occurs, or chronic incapacitating symptoms prompt the woman to seek medical attention because it has gone on long enough to become chronic.
Chronic PID is the result of untreated or unsuccessfully managed acute or subacute PID. The most common form of PID, it isn’t detected until symptoms of pelvic pain, heavy and painful menstrual periods, pain with intercourse (dyspareunia) and infertility trigger an evaluation that discovers extensive pelvic scar tissue.
Sexually Transmitted PID caused by Gonorrhea or Chlamydia are by far the most common causes of PID. The infections can rapidly invade via the cervix and uterus into the fallopian tube(s). These pencil length passages are highly specialized to promote the active passage of sperm traveling up from the uterus to meet up with an egg released by the ovary. After fertilization, which typically occurs near the site of egg release, the resulting embryo will slowly travel back to uterus—a journey that normally takes about 5 days.
The fallopian tubes are lined with cells whose function is to protect and nurture eggs, sperm and embryos during their journey. At their ends, the fallopian tubes have small delicate finger-like projections (fimbriae) that draw close to, envelop, and “pick-up” the eggs from the ovaries at the time of ovulation. Inflammation due to Chlamydia Trachomatis or Neisseria Gonorrhea damages and often permanently destroys the specialized lining of the fallopian tubes. In severe cases, it can result in fusion of the fimbriae, thereby blocking the ends of the tubes and compromising their mobility and their potential to facilitate timely passage of eggs, sperm and embryos.
Pus that has accumulated inside the tubes often passes into the pelvic cavity, producing peritonitis and resulting in the formation of scar tissue (adhesions) which further disrupts normal pelvic anatomy as well as the relationship between the tubes and the ovaries. This
may prevent the fallopian tubes from collecting the eggs during ovulation. In cases where the ends of the fallopian tubes are blocked, pus may collect and distend the tubes. The pus is usually absorbed over time and replaced by clear, straw-colored fluid. The resulting occluded, fluid-filled, distended, and often functionless fallopian tube is referred to as a hydrosalpinx.
Sexually transmitted PID almost invariably affects both fallopian tubes. Even in cases where a dye x-ray test (hysterosalpingogram) or laparoscopy (a procedure where a telescope-like instrument is passed through the belly button to visualize the pelvic structures) indicates that only one fallopian tube has been infected, the other tube is almost invariably involved. A new procedure called tuboscopy (where a thin fiber-optic telescope is passed into the fallopian tube(s) to evaluate the inner structure has confirmed that the tubes of PID victims, who seemingly have normal pelvic anatomy, often have internal scarring and/or adhesion. This could account for the low success rate seen with tubal reparative surgeries and the high ectopic pregnancy rate (8-15%) in PID patients who subsequently conceive.
Most fertility specialists would agree that IVF is the treatment of choice for almost all forms of tubal infertility. One exception that is commonly cited involves surgical reversal of tubal ligation. It is correctly argued that the chance of having a baby being born within a year of such surgery is about 50%. Those who favor surgical tubal reversal over IVF in such cases often site the national IVF birth rate of 25% as an argument in favor of this position. However, in selective IFV centers of excellence, where the anticipated birth rate following a singe attempt at IVF in women under 40 years is almost double the national average, and the birth rate following three IVF attempts is in the order of 80%, this recommendation is outdated.
Surgery to unblock fallopian tubes or clear adhesions resulting from an inflammatory process due to infections with gonorrhea or Chlamydia is truly an exercise in futility. The chance of pregnancy occurring following such an undertaking is less than 2% per month, and less than 25% in three years. We concur with a recent opinion by the Chairman of Gynecology and Obstetrics at UCLA, that in the modern context, infertility surgery for fallopian tubes damaged by inflammation should be considered an “anachronism”.
Given the high incidence of ectopic pregnancy following tubal surgery (20-25%), the fact that surgery requires hospitalization for a number of days, general anesthesia, associated pain, and a signifi cant risk of post-operative complications make tubal surgery less appealing. Furthermore, greater than 70% of the women that choose tubal surgery ultimately need IVF anyway. To make matters worse, some women have undergone more than one attempt at surgical tubal restoration. Since second and third attempts at surgery are even less likely to result in a pregnancy than the first attempt, such practice is worse than unwise.
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