Abstract and Introduction

Abstract

Technological advances in fiberoptics and endoscopy have resulted in the development of minimally invasive transcervical tubal catheterization procedures with the potential of improved diagnostic accuracy of tubal disease and transcervical treatment of proximal tubal obstruction (PTO) with reduced risks, costs and morbidity compared with surgical procedures. Fallopian tube recanalization can be performed with catheters, flexible atraumatic guidewires or balloon systems under endoscopic (falloposcopy/hysteroscopy/laparoscopy), sonographic, fluoroscopic or tactile guidance. Falloposcopy provides a unique possibility to accurately visualize and grade endotubal disease, characterize and document endotubal lesions, identify the segmental location of tubal pathology without complications, objectively classify the cause of PTO and guide future patient management. This is in contrast to the surgical and radiological gold standards, laparoscopy and hysterosalpingography, respectively, that are often associated with poor or misdiagnosis of PTO. Nonhysteroscopic transuterine falloposcopy using the linear eversion catheter is a successful, well-tolerated, outpatient technique with a good predictive value for future fertility. Hysteroscopic–falloposcopic–laparoscopic tubal aquadissection, guidewire cannulation, guidewire dilatation and direct balloon tubuloplasty may be used therapeutically to breakdown intraluminal adhesions or dilate a stenosis in normal or minimally diseased tubes with high patency and pregnancy rates. However, guidewire cannulation of proximally obstructed tubes yields much lower pregnancy rates compared with other catheter techniques, despite the high tubal patency rates. Laparo-hysteroscopic selective tubal catheterization with insufflation of oil-soluble radiopaque dye has been reported to be an effective treatment for infertility associated with endometriosis. The various disadvantages associated with fluoroscopic and sonographic techniques limit their application, despite the reportedly high patency and intrauterine pregnancy rates. Recanalization is contraindicated in florid infections and genital tuberculosis, obliterative fibrosis and long tubal obliterations that are difficult to bypass with the catheter, severe tubal damage, male subfertility and previously performed tubal surgery. Distal tubal obstruction is not amenable to catheter recanalization techniques. Tuberculosis, salpingitis isthmica nodosa, isthmic occlusion with club-changed terminal, ampullar or fimbrial occlusion, and tubal fibrosis have been cited as reasons for recanalization failure. In lieu of the poor pregnancy outcomes in patients with severe tubal disease and poor mucosal health following tubal recanalization, as well as poor available technical skills and results with microsurgery, in vitro fertilization and embryo transfer is a valid option in such women. Despite the high diagnostic and therapeutic power of falloposcopic interventions, technical shortcomings with falloposcopy must be overcome before the procedure gains widespread acceptance.

Rationale

Although proximal tubal obstruction (PTO), is a frequent finding on hysterosalpingography (HSG), approximately two-thirds of the Fallopian tubes resected for PTO reveal an absence of luminal occlusion.^[1] False-positive diagnosis of PTO ranges from 16 to 40%,^[2] and can be as high as 50%.^[3] The specific indications and limitations of Fallopian tube recanalization (FTR) makes a careful evaluation of the Fallopian tube prior to therapy an absolute requirement, underscoring the significance of endoscopy. The distinction between true pathologic occlusion, spasm or plugging and abnormalities of the mucosa is crucial in determining therapy,^[1] and the diagnostic test used has an important bearing on the selection of patients and, consequently, the results, further signifying the value of endoscopy.^[4] While outlining the various cannulation techniques available to diagnose and treat tubal pathology, this article will highlight the applications, efficiency and success of endoscopic FTR, and the place of tubal cannulation against the challenge of IVF.

Introduction

Pathophysiology of PTO

Tubal disease is the cause of subfertility in approximately 30% of women and 10–25% of these are due to PTO. PTO has been a diagnostic and therapeutic dilemma since its recognition more than 100 years ago.^[5] It can occur in either the intramural segment or the uterotubal junction, and is the result of tubal spasm or transient occlusion by mucus plugs in up to 40% of women.^[6] Figure 1 depicts a HSG plate showing a bilateral cornual block. Proximal, distal and peritubal damage can be caused by a number of pathologic processes, such as inflammation, endometriosis and surgical trauma.^[3] PTO has been associated with the presence of pathologic microflora in the oviducts of 36.6% women, as confirmed by bacteriological examination of tubal fluid.^[7] Inflammatory etiology seems to be important in isthmic tubal occlusion, and in many cases, chlamydial infection may be the chronic irritant, which also causes muscular hypertrophy leading to salpingitis isthmica nodosa.^[8] Induced abortion, uterine curettage, pelvic inflammatory disease and intrauterine devices may all influence PTO infertility.^[9]

Figure 1.

Enlarge

Hysterosalpingogram Plate Showing a Bilateral Cornual Block.

Hypothesis for the Genesis of PTO

The small caliber, thick muscular wall and reduced proportion of ciliated cells in the epithelium of the proximal tube predispose this tubal segment to blockage. Increased muscle tone, reduced ciliary activity and increased tubal secretions at the uterotubal junction (UTJ) and the isthmus during the estrogen-dominant phase of the cycle can result in stasis of the tubal luminal contents and functional obstruction of the proximal tube. This event may biologically serve to delay the zygote in the ampulla for nutritional and developmental benefits. With relaxation of the UTJ musculature, increased ciliary activity and a reduction in tubal secretions, this functional proximal tube obstruction should normally be completely reversed during the progesterone-dominant phase of the menstrual cycle. Failure to do so may result in prolonged stasis of uterine material and, therefore, initially partial (tubal spasm) and then, in a given time, complete anatomical obstruction of the narrow intramural tubal lumen.^[10] Calcification of this obstructing material can follow.^[11] Fibrosis may represent a nonspecific final response to chronic injury of the transmural and isthmic segments of the oviduct,^[12] following which, tubal damage has become irreversible.

Classification of PTO. Proximal tubal obstruction has been classified into nodular (salpingitis isthmica nodosa or endometriosis), non-nodular (true fibrotic occlusion) and so-called ‘pseudo’ occlusion (detritus, polyps or hypoplastic tubes).^[13] Falloposcopic observations of endotubal isthmic plugs reveal a cast of debris-containing aggregates of histiocytic-like cells of endometrial stromal or mesothelial origin, or white to yellow mucus-like fragments of unknown physiological or pathophysiological significance.^[11] Histological examinations of excised tubal segments reveal tubal abnormalities, such as obliterative fibrosis, salpingitis isthmica nodosa, endometriosis, chronic salpingitis, chronic tubal inflammation and tuberculosis in varying frequencies ( Table 1 ). Obliterative fibrosis has been observed as the most common histologic tubal abnormality by both Wiedemann et al.^[14] and Fortier and Haney ^[12] followed by salpingitis isthmica nodosa. The highest incidence of salpingitis isthmica nodosa was reported by Punnonen et al. (60%), ^[8] while the highest incidence of chronic tubal inflammation was reported by Zhang et al. (70.59%).^[9] On the basis of their observations on the pathologic spectrum of UTJ, Fortier and Haney demonstrated that there are multiple distinct histologic patterns and intra-abdominal findings that do not predict the histology of the UTJ pathology.^[12]

Proximal tube obstruction is the most treatable since it often occurs because of the accumulation of mucus or debris, which forms an impacted plug in the interstitial or proximal isthmic portion of the tube.^[11] Until recently a domain of microsurgery,^[15] the long-standing surgical corrective approach to treat tubal occlusion has been replaced by noninvasive tubal recanalization methods in selected patients with endoluminal damage.^[16] FTR is a minimally invasive procedure used to open blocked Fallopian tubes in patients with a history of infertility and confirmed PTO. There are several techniques to recanalize proximally obstructed tubes ( Box 1 ). However, the following discussion will focus on the endoscopic techniques for FTR.