PCOS (Polycystic Ovarian Syndrome):
Although earlier these two conditions that is PCOS and hyperandrogenaemia were considered distinct separate entities, it look us almost 60 yrs to understand that the two are infact linked by a common feature- hyperinsulinaemia and insulin resistance. In PCOS the full blown syndrome is that of hyperandrogenism, chronic anovulation and polycystic ovaries. We now know that approximately 75 per cent of anovulatory women of any cause have polycystic ovaries and 20 to 25 per cent of women with normal ovulation demonstrate ultrasound findings typical of polycystic ovaries. The currently accepted definition is chronic anovulation accompanied by hyperandrogenism and clinical manifestations including hirsutism, acne, elevated testosterone and androstenedione, androgen dependent alopecia and frequently but not always obesity.
There is widespread interest in the possibility that insulin resistance is the unifying pathogentic link between obesity, glucose intolerance, lipid abnormalities, hypertension and ischaemic heart disease- collectively called syndrome X. It has been suggested that in population studies only the fasting insulin level should be used as a marker of insulin resistance, particularly in subjects with abnormal glucose tolerance.
Sampson first described the disease formally in 1921. Then he proposed the hypothesis that the origin of peritoneal endometrial implants was tissue delivered by the retrograde menstruation. Retrograde menstruation is a nearly universal phenomenon among cycling women but it is not clear why endometrial tissue will implant and grow in the peritoneal cavity of only a subgroup of women. These endometrial cells can respond to ovarian hormones and therefore undergo cyclic menstrual changes with periodic bleedings. Several key steps are required to establish glands and stroma, attachment of endometrial cells to the peritoneum invasion into the mesothelium, and survival and growth of the ectopic tissue.
The history of endometriosis is reviewed in the light of today’s clinical and pathological knowledge of this disease. Prior to Sampson’s report in 1921, attention was focused on the enclosed type of endometriosis, sited deep in the pelvis and called adenomyosis externa. Sampson’s first hypothesis, that ruptures of an ovarian endometrioma caused superficial peritoneal endometriosis, was probably changed after this observation that the free, superficial peritoneal implants reacted like eutopic endometrium. These implants were recognized as implants from menstrual blood regurgitated into the pelvic cavity. Adenomyosis externa, ovarian endometrioma and peritoneal endometriosis then came to be regarded as the same disease. In the light of today’s knowledge, it may be important to remember this progressive understanding in the nosology of what is now universally called pelvic endometriosis.
Earlier studies suggested that 10 % to 30 % of women with endometriosis are infertile. A prospective study of infertile women and women undergoing tubal ligation demonstrated a higher incidence of endometriosis in infertile women around 48% against 5% in parous women.
Various prospective and retrospective studies have evaluated the efficacy of specific treatment over expectant management for restoration of fertility for endometriosis associated infertility.
These studies failed to demonstrate that treatment of minimal or mild endometriosis improves fecundity over expectant management alone. These observations, therefore, indicate that minimal or mild endometriosis may be a marker of a pathophysiologic process associated with subfertility and not necessarily the cause of infertility. In severe endometriosis, however, retrospective studies indicate higher pregnancy rates after surgical treatment compared with no treatment. This means that advanced disease does impair fertility. Hence it appears rational to evaluate the different treatment modalities associated with different stages of endometriosis.
Treatment employed for infertility patients with endometriosis can be divided into five categories: expectant management, medical therapy, conservative surgical excision, combination of surgical and medical treatment and treatment through assisted reproductive technologies.
Due to increased awareness and availability of sophisticated investigational modalities like ultrasound, Doppler, etc. and their regular and frequent use, the detection of the above- mentioned pathologies has definitely become easy. Most of the gynaecologists would agree to the fact that the incidence of detection of fibroids has gone significantly higher due to these transformations in the clinical practice. It is more surprising that a significant proportions of these are detected in patients otherwise asymptomatic, but seeking advice for the complaints like infertility.
Fibroids may reduce fertility by following mechanisms:
1) Significantly large fibroid distorting the proximal tubo-ovarian anatomy.
2) Intracavitary or submucous fibroids causing menstrual disturbances and obliterating the cavity.
3) Large intramural fibroids distorting the endometrial cavity thereby elongating absolute distance of sperm transport.
4) Submucous fibroids causing vascular compromise thereby affecting reproductive nourishment.
5) Submucous and intramural fibroids with larger cavitary component interfering with proper implantation thereby causing infertility or miscarriage.
6) Cervical fibroids alter the position of cervix and affect fertility.
7) Endocrine imbalance- this is a surprising clinical entity, which is encountered in clinical practice. Apart from the hyperestrogenic milieu in women with fibroids, it was found that 36 % of these women with fibroids and infertility had hyperprolactinaemia with or without galactorrhoea. This association was corroborated as it was found 29% pregnancy rate after laparoscopic myomectomy, with actual normalisation of prolactin level in these patients.
Leiomyoma (fibroids) can be managed either conservatively or surgically and sometimes by both in combination. More than 90% of the fibroids can be removed laparoscopically.
Myomectomy is necessary or truly indicated in cases associated or presenting with infertility in following situations:
1) Disturbed tubo-ovarian anatomy.
2) Intracavitary fibroids.
3) Significantly large, multiple intramural fibroids.
4) Cornual fibroid, pressing on the uterotubal junction.
5) Association of hormonal imbalance like raised elevated prolactin levels.
13 to 15 % of fibroids were submucous fibroids or intramural fibroids with significant intracavitory component.
Hysteroscopic myomectomy is a very technically demanding procedure the efficacy of this procedure is proven to be far superior to open or laparoscopic myomectomy due to the inherent and suturing the uterine musculature for the removal of fibroid.
Pelvic Inflammatory Disease (PID):
The portal of entry of microorganisms into the peritoneal cavity is via the endocervical canal from the vagina into the fallopian tubes and the pelvic cavity. It commonly occurs at the time of menstruation as bacteria gain access to the upper genital tract due to the loss of the cervical mucus plug and the trail provided by the retrograde menstrual flow into the fallopian tubes.
PID is frequently a complication of STD and like STD, is most commonly found in young sexually active females with a maximum incidence in the 20 to 40 year old age group. The most vulnerable group is sexually active girls under 20 years old.
PID can be managed by proper regimens of antibiotics and by hospitalization. All regimens used in outpatient treatment must be effective against a negative endocervical test does not preclude upper genital tract infection.