Infertility
Both partners should be seen and investigated together, as infertility may result from male or female factors and is often associated with a combination of both. At the completion of all investigations, about one quarter will be given a diagnosis of ‘unexplained infertility’. Long-term follow-up studies of couples with unexplained infertility have shown that 30–40% will conceive over a 7-year period after investigation. Many ‘unexplained’ cases involve women over age 35 years who may later be shown to have a poor response to ovarian stimulation and oocyte abnormalities if in vitro fertilization (IVF) is performed. Age, particularly female age, undoubtedly affects fertility. IVF success rates fall sharply for women age 35 or older (Table 17.1), and natural fertility appears to decline slowly but irrevocably from the late 20s onwards. The effect of age on the male is less pronounced, but older men exhibit more sperm abnormalities and DNA fragmentation.
Table 17.1
Female age and IVF outcomes in the UK (2007 and 2008)
| Under 35 | 35–37 | 38–39 | 40–42 | 43–44 | Over 44 | |
| 2007 | 32.3% | 27.7% | 19.2% | 11.9% | 3.4% | 3.1% |
| 2008 | 33.1% | 27.2% | 19.3% | 12.5% | 4.9% | 2.5% |
(Data sourced from www.HFEA.gov.uk.)
The relative incidence of causative factors will vary according to country and whether the problem is primary or secondary. Furthermore, in many couples there are multiple reasons for the infertility. Table 17.2 shows the pattern of causative factors of primary infertility in a Western population.
Table 17.2
| Diagnosis* | Primary infertile group (n = 167) N (%) | Secondary infertile group (n = 151) N (%) | P-value |
| Ovulation problems | 54 (32.3) | 35 (23.2) | 0.069 |
| Sperm quality problems | 49 (29.3) | 36 (23.8) | 0.268 |
| Blocked Fallopian tubes | 20 (12) | 21 (13.9) | 0.607 |
| Unexplained infertility | 49 (29.3) | 45 (29.8) | 0.928 |
| Endometriosis | 19 (10.7) | 15 (10) | 0.677 |
| Others | 23 (13.8) | 32 (21.2) | 0.081 |
*Women have reported more than one diagnosis.
Data derived from a Scottish general practice-based survey (Bhattacharya et al. 2009). Self-reported cause of infertility amongst women who reported a diagnosis (North East Scotland). The data reflect unsuccessful attempted conception for 12 months or longer and/or had sought medical help with conception.
History and examination
The history should include the following:
• Age, occupation and educational background of both partners.
• Number of years that conception has been attempted and the previous history of contraception.
• Previous conceptions of either partner in this or previous relationships.
• Details of any complications associated with previous pregnancies, deliveries and postpartum.
• Full gynaecological history including regularity, frequency and nature of menses, cervical smears, intermenstrual bleeding and vaginal discharge.
• Coital history, including frequency of intercourse, dyspareunia, post-coital bleeding, erectile or ejaculatory dysfunction
• History of sexually transmitted diseases and their treatment.
• A general medical history to include concurrent or previous serious illness or surgery, particularly in relation to appendicitis in the female or herniorrhaphy in the male; a history of undescended testes or of orchidopexy.
Examination of both partners should be considered, although examination of the male is unlikely to reveal anything of significance in the presence of a normal semen analysis, and of the woman may well be equally unremarkable if there is a normal high quality pelvic ultrasound. Azoospermic men should be examined for congenital bilateral absence of the vas deferens (CBAVD) which is associated with cystic fibrosis mutations.
Female infertility
Disorders of ovulation
• Type I – hypogonadal hypogonadism resulting from failure of pulsatile gonadotrophin secretion from the pituitary. This relatively rare condition can be congenital (as in Kallman’s syndrome) or acquired, for example, after surgery or radiotherapy for a pituitary tumour. Serum concentrations of luteinizng hormone (LH) and follicle-stimulating hormone (FSH) and oestradiol are abnormally low/ undetectable and menses will be absent or very infrequent.
• Type II – normogonadotropic anovulation, most commonly caused by polycystic ovary syndrome (PCOS; see Chapter 16). Serum concentrations of FSH will be normal and LH normal or raised. Serum anti-Müllerian hormone (AMH) will be elevated and there may also be elevation of serum testosterone or free androgen index.
• Type III – hypergonadotropic hypogonadism, frequently described as ‘premature ovarian failure’ describes cessation of ovulation due to depletion of the ovarian follicle pool before age 40 years. Serum gonadotrophin concentrations will be greatly raised and AMH low/undetectable, with postmenopausal (low) concentrations of oestradiol.
• Type IV – hyperprolactinaemia, with elevated serum prolactin and low/normal serum FH and LH. Frequently due to a pituitary microadenoma although it is important to rule out a space occupying macroadenoma using pituitary MRI or CT.
Anovulation is usually associated with amenorrhoea or oligomenorrhoea. Alterations in the menstrual cycle are commonly associated with periods of stress and also with excessive weight gain or obesity, worsening the impact of PCOS on ovulation, or at the other extreme, with anorexia nervosa or excessive exercise leading to hypogonadal (type I) anovulation.
Tubal factors
The Fallopian tube must first collect the ovum from its site of ovulation from the ruptured Graafian follicle and then transport the ovum to the ampullary segment, where fertilization occurs. The fertilized ovum must then be transported to the uterine cavity to arrive at the correct point in the menstrual cycle at which the endometrium becomes receptive to implantation (the ‘implantation window’). Tubal factors account for about 10–30% of cases of infertility: this figure varies considerably according to the population involved. Occasionally, congenital anomalies occur but the commonest cause of tubal damage is infection. Infection may cause occlusion of the fimbrial end of the tube, with the collection of fluid (hydrosalpinx) or pus (pyosalpinx) within the tubal lumen (Fig. 17.1).
Even in the presence of a patent tube, damage to the internal structure with depletion of cilia and impairment of tubal peristalsis may result in loss of tubal function.
