Introduction

The fallopian tube has many active roles in the process of reproduction. As the fallopian tube provides the environment in which fertilization and early development take place, these events may have a significant effect on all the subsequent events of the pregnancy. The role of the fallopian tube in the process of natural conception begins when the oocyte is released by the ruptured ovarian follicle and is picked up by the fimbrial end of the fallopian tube. It also facilitates the final maturation of sperm, which have passed through the uterus. Both the sperm and oocytes are transported within the fallopian tube to the site of fertilization and meet within well-defined, species-dependent time limits. Fertilization takes place at the ampullary–isthmic junction, and the pre-embryo is transported to the uterine cavity at the optimum time for implantation. Significantly, the sperm and pre-embryo, which differ antigenically from the mother, are not attacked by the immune system. The mechanisms by which all these complex processes are controlled are not well understood.

Ovum and embryo transport is probably the result of an interaction between the egg/embryo and the muscle contractions, ciliary activity and flow of tubal secretions. The relative importance of these factors is debatable, although there is evidence that ciliary activity plays a dominant role in gamete and embryo transport (Lyons et al 2006). Both myosalpingeal and ciliary activity are affected by a diverse range of chemical, biological and hormonal agents, including ovarian steroids, sympathomimetic agents, prostaglandins and angiotensin II (Jansen 1984, Saridogan et al 1996, Mahmood et al 1998).

Fallopian tubes probably act as sperm reservoirs, and this role may be essential for maintaining a certain number of sperm at the site of fertilization and preventing polyspermy by reducing the number of sperm available for fertilization. Sperm interaction with the tubal epithelium and secretions may also play an important role in the preparation of sperm for fertilization (Saridogan and Djahanbakhch 2009).

Tubal secretions contain proteins that derive from the plasma and also some specific substances synthesized within the oviduct itself (Maguiness et al 1992a). Both tubal proteins and the physical contact between the gametes and the tubal epithelium may play a role in gamete function (i.e. capacitation), fertilization and early embryo development (Djahanbakhch et al 1994, Kervancioglu et al 2000).

Aetiology of Tubal Disease

Tubal disease is usually defined as tubal damage caused by pelvic infection such as pelvic inflammatory disease or tuberculosis, endometriosis, surgery or salpingitis isthmica nodosa, with varying degrees of tubal damage or obstruction, sometimes involving the adjacent ovary and the pelvic peritoneum, and adhesion formation. As a result, patients with tubal damage suffer from infertility and/or pelvic pain. This definition does not cover functional defects of the fallopian tube, as our ability to describe tubal disease is currently limited to demonstrating its patency and macroscopic normality. Tubal disease is accountable for 30–40% of cases of female infertility.

Salpingitis

Most salpingitis is the result of an ascending infection from the lower genital tract, caused primarily by Chlamydia trachomatis and Neisseria gonorrhoeae (see Chapter 61, Pelvic inflammatory disease, and Chapter 62, Sexually transmitted infections, for more information). These micro-organisms cause mucopurulent endocervicitis, and break down major cervical barriers, such as the mucus plug that protects the endometrium and upper genital tract, and permits ascending infection. Other pathogens such as Streptococcus sp., Escherichia coli and anaerobes ascend through the breached barrier and reach the upper genital tract (Rice and Schachter 1991). In a significant proportion of cases, no aetiological agent is identified; this suggests that a range of other aetiological agents have a role, but the identification of novel organisms is difficult to ascertain because of the limited availability of diagnostic tests. Serological evidence has associated Mycoplasma genitalium with pelvic inflammatory disease (Simms and Stephenson 2009).

In the majority of patients, salpingitis is due to a sexually transmitted infection. In other cases, iatrogenic manoeuvres such as insertion of an intrauterine device, termination of pregnancy, hysterosalpingography or curettage can spread a cervical infection into the uterus and tubes. In a small proportion of women, pelvic infection may be secondary to gastrointestinal infections such as perforated appendicitis. Mycobacterium tuberculosis is still seen in developing countries; however, migration to developed countries has resulted in a significant increase in the number of tuberculosis notifications since the 1980s (Rose et al 2001).

Acute salpingitis causes loss of ciliated cells and distal occlusion of the fallopian tubes. Some of the deciliation may be recovered later, but subsequent immune response following the acute phase causes permanent scarring, loss of mucosal folds and flattening of the mucosa (Lyons et al 2006). Distal occlusion of the tubes together with chronic inflammatory process could result in fluid collection in the lumen of the fallopian tube, leading to hydrosalpinges. Pelvic peritonitis during the acute phase may be followed by adhesions around the fallopian tubes and ovaries, distorting the pelvic anatomy. Perihepatic inflammation may cause ‘violin-string’ adhesions known as ‘Fitz–Hugh–Curtis syndrome’ (Figures 24.1–24.3).

Figure 24.1 Laparoscopic view of a pelvis after pelvic inflammatory disease. There is a ‘curtain’ of adhesions covering the pelvic organs.

Figure 24.2 Laparoscopic photograph of perihepatic adhesions: Fitz–Hugh–Curtis syndrome.

Figure 24.3 Laparoscopic appearance of bilateral hydrosalpinges as a result of previous inflammatory disease.

Diagnosis

Assessment of the fallopian tube should normally determine patency, a normal external and internal appearance, the ability to transport gametes and the embryo, and provision of an environment for the early steps of reproduction to occur. It is possible that, apart from the obvious need for tubal patency to allow passage of gametes, factors that affect the gametes and embryo, the effectors of tubal transport, the cilia, flow of tubal fluid and tubal contractions appear to constitute a higher-order system in which intact function of each may not be needed to achieve pregnancy (Verdugo 1986). However, dysfunction of this higher-order system may be the reason for unsuccessful tubal surgery even when tubal patency has been achieved. Similarly, a functional disorder of this system may account for subfertility in some cases of unexplained infertility. Currently, tubal function is determined by demonstrating patency and normal appearance at laparoscopy.

The methods commonly used to determine tubal patency are hysterosalpingography (HSG), laparoscopy and hysterosalpingo contrast sonography (HyCoSy). The first two methods have been used for many years, whereas HyCoSy is a relatively new technique. All these methods have some degree of false-negative and false-positive results in determining tubal patency. A comparison of HSG and laparoscopy showed that complete agreement of tubal patency was found in 80.2% of cases (Maguiness et al 1992b). Laparoscopy has the ability to identify peritubal adhesions, endometriosis, polycystic ovaries, and other pelvic and intra-abdominal pathology. However, it is usually performed under general anaesthesia and does not give information about the uterine cavity. In general, these methods are considered complementary investigations, offering very important information (Figures 24.4–24.6). Laparoscopy also allows the surgeon to operate on abnormalities detected such as pelvic adhesions and endometriosis, provided that they have the relevant experience and the patient’s consent has been obtained preoperatively.

Figure 24.4 Hysterosalpingogram of a patient with bilateral hydrosalpinges.

Figure 24.5 Tubal cornual block. Irregular vessels seen on the peritoneum surface as a result of previous inflammation (arrow).

Figure 24.6 Hysterosalpingogram of a patient with bilateral tubal block (arrows).

The internal appearance of the fallopian tubes can be assessed by salpingoscopy. Salpingoscopy is the transabdominal examination of the tubal lumen by introducing an endoscope through the fimbrial end. Rigid endoscopes with a diameter of 2.8 mm allow excellent visualization of the infundibulum and ampulla as far as the ampullary–isthmic junction. The presence of minor intratubal lesions is not necessarily incompatible with fertility (Maguiness and Djahanbakhch 1992); however, loss of mucosal folds and intratubal fibrosis are significant. Nowadays, salpingoscopic assessment of the tubal lumen is recommended by some groups before tubal surgery for hydrosalpinges (Puttemans et al 1998). De Bruyne et al (1989) proposed a classification of ampullary findings in hydrosalpinges: grades 1 and 2 refer to normal salpingoscopic findings, grade 3 (intermediate group) refers to focal adhesions, and grades 4 and 5 refer to severe adhesions and loss of mucosal folds.

Transvaginal hydrolaparoscopy and fertiloscopy approaches utilize the advantages of laparoscopy but with a less invasive approach (Gordts et al 1998, Watrelot et al 1999). Transvaginal hydrolaparoscopy is the endoscopic examination of pelvic structures through the posterior vaginal fornix after instilling saline into the pouch of Douglas. This allows tubal patency to be checked, in addition to assessment of the pelvis for other pathology. Fertiloscopy includes salpingoscopy, microsalpingoscopy and hysteroscopy for complete examination of the female reproductive tract. These procedures can be performed under local anaesthesia or sedation.

Selective transcervical salpingography and tubal catheterization can be done in cases where it is doubtful that there is cornual obstruction (Ataya and Thomas 1991). Mucus plugs and debris can be mobilized, and a tube that was apparently obstructed can be ‘opened’ following such a procedure.

Treatment

The treatment of tubal disease in the infertile patient includes selective salpingography with tubal cannulation, surgery and in-vitro fertilization-embryo transfer (IVF-ET). In comparison with the other two options, IVF is now widely used for the majority of patients with tubal disease. However, it is relatively expensive, labour intensive and carries risks of multiple pregnancy and ovarian hyperstimulation syndrome (see Chapter 22, Assisted reproduction treatments, for more information).