6.1 Introduction

The introduction of in vitro fertilization in the late 1970s lead to a continuous development of reproductive medicine with the introduction of innovative techniques to solve the various causes of couples’ sterility.

Infertility and sterility are caused by several etiopathogenetic factors, such as: genetic abnormalities, endocrine dysfunctions, thrombophilic disorders, autoimmune diseases, endometriosis, incompetent cervix, luteal phase defect, certain infections, and sperm DNA abnormalities.

The work up of patients affected by infertility and sterility includes congenital malformation (bicornuate, didelphic, septate, and unicornuate uterus) acquired defects (fibroids, adenomas, adhesions, and polyps) and chronic endometrial (CE) infection.

Suspected congenital malformations may emerge during transvaginal ultrasound procedures and are subsequently confirmed by diagnostic hysteroscopy. Acquired defects may also be suspected during transvaginal ultrasound, but their diagnosis is based on histological findings. On the other hand, hysteroscopy rather than ultrasound is needed to suspect CE with subsequent diagnosis being confirmed by histological findings. For this reason, hysteroscopy plays an important diagnostic role in uterine sterility factor [1].

6.2 Hysteroscopic Technique and Instruments

Current hysteroscopic techniques allow both diagnosis and treatment of uterine cavity diseases [2].

Traditional hysteroscopy was only a diagnostic technique considered as a painful procedure due to frequent vasovagal reaction. Often it required analgesia and was performed into operating room (Fig. 6.1) [3].

Technological improvement has resulted in hysteroscopy to become an operative outpatient procedure performed without analgesia.

Diagnostic hysteroscopy is now performed with a vaginoscopic approach, without speculum, using a saline solution at low pressure for distending the uterine cavity and a minihysteroscopy (3.5 mm or less in size) ensuring only minimal patients’ discomfort [4].

It has been shown that fiberoptic-hysteroscopes offer several advantages over the lens-based instruments (first of all they are more resistant) but they cannot yet match the image quality of a rod-lens-based telescope system [5].

Operative instruments have also been miniaturized (5F forceps and a bipolar coaxial electrode) allowing a “see-and-treat” approach [6] and many uterine cavity diseases (biopsy, polypectomy, synechiae, septum) can be treated by office hysteroscopy immediately after diagnosis using operative hysteroscopes sized 5 mm equipped with a 5F operative canal (Fig. 6.2) [7].

6.3 Asherman’s Syndrome

The presence of acquired intrauterine adhesions is known as Asherman’s syndrome (Figs. 6.3, 6.4, and 6.5). Potential causes include intrauterine retention of post-abortion or postpartum material and post-abortion curettage or endometrial infections [8].

Asherman’s syndrome may be totally asymptomatic or it may cause hypomenorrhea, secondary amenorrhea, pelvic pain, and hematometra. Intrauterine adhesions could cause infertility or pregnancy loss [9].

For the Asherman’s syndrome’s diagnosis, a combination of ultrasound (2D and 3D) and hysteroscopy is needed. It is mandatory to perform a mapping of synechiae to avoid inadvertent uterus perforation during hysteroscopy. The American Society for Reproductive Medicine (ASRM) identifies three different types of Asherman’s syndrome on the basis of: characteristics of the menstrual flow, type of synechiae, and portion of uterine cavity obliterated.

The gold standard treatment of Asherman’s syndrome is office hysteroscopy, which consists of a surgical adhesiolysis performed without general or regional anesthesia [10, 11]. IUD Foley catheter or Cook intrauterine splint can be used to recurrences of synechiae [12].

Approximately 70–90% of patients with hypomenorrhea or amenorrhea return to have a regular menses after hysteroscopic adhesiolysis showing an improvement of pregnancy rate and rate of live births [13].

6.4 Müllerian Anomalies

An impaired median fusion of Müllerian ducts during embryonic life causes anatomical abnormalities of the female genital tract, known as Müllerian anomalies. Müllerian anomalies are more prevalent in infertile than in sterile patients [14] and are associated with recurrent (41%) miscarriages [15].

Since 2013 the ESHRE/ESGE classification system has divided Müllerian anomalies into seven main classes (from U0 to U6), describing uterine anatomical deviations of the same embryological origin (Fig. 6.6). Anatomical varieties expressing different clinical significance, within main classes, have been divided into subclasses. Cervical and vaginal anomalies are classified independently into subclasses having clinical significance [16].

The most common Müllerian anomaly is the septate uterus, with the worse reproductive outcome and poor obstetrical outcomes, including malpresentation, preterm delivery, intrauterine growth restriction, placental abruption, and perinatal mortality. This is due to its own histological features presenting poorly vascularized fibrous tissue and subatrophic endometrium [17]. Before any surgical intervention, it is mandatory to perform an accurate differential diagnosis between septate, arcuate, and bicornuate uterus to avoid inadvertent fundal perforation (Fig. 6.7). The uterus with an abnormal fundal outline is a bicornuate uterus (external fundal indentation >1 cm) while arcuate and septate uterus have regular external profile. Septate, arcuate, and bicornuate uterus, all have a—larger o smaller—inner indentation and angle of the indentation: arcuate—depth <1 cm angle >90°, septate—depth >1.5 angle of the indentation <90°, bicornuate—endometrial cavity is similar to a partial septate uterus (Fig. 6.8 bis) [18].

To perform an accurate differential diagnosis between septate, arcuate, and bicornuate uterus, it is necessary to visualize both outline and innerline of the uterus. For this reason, the gold standard diagnostic technique is 3D ultrasound associated or not with hysteroscopy [19].

The hysteroscopic surgery under ultrasound guidance, performed in the operating room or in an office setting, is the gold standard technique to treat the septate uterus [20]. Proceeding from both sides, the septum is cut from the apex to the fund by cold scissors, unipolar or bipolar cautery, laser, or resectoscope until the cavity is flush with the fundic portion. Then hysteroscope/resectoscope can visualize both tubal ostia without colliding with the residue of the septum [21]. After septum incision, there is a risk of subsequent pregnancy-related uterine rupture, which may be due to an extreme septal excision, penetration of the myometrium, uterine perforation, or excessive use of cautery or laser energy [22]. Several studies compared resectoscopic and hysteroscopic technique [23–26]. The Versapoint technique is a safe and effective alternative to the resectoscope avoiding cervical dilation and cervical incompetence and lacerations, and lowering the risk of uterine perforation [27]. Some have expressed a preference for the use of cold scissors rather than bipolar Versapoint to avoid thermal and cautery damage to the cut edges [26].

Many IVF centers recommend removal of the septum before assisted reproductive treatment to reduce the risk of miscarriage.

6.5 Myomas

Common benign uterine findings during women’s fertile life are myomas, which consist of muscle cells circumscribed by a capsule. Macroscopically, they present the characteristic vortex appearance. According to their histological composition (fibrous or muscular), their consistency may vary from soft to hard and may present colliquated or calcified areas. Their growth is influenced by local growth factors, cytokines, estrogen, and progesterone [28].

Myomas may be totally asymptomatic or they may cause menorrhagia, pelvic pain, dysmenorrhea, bladder and bowel dysfunction (due to mass-effect), and infertility. Symptoms depend on number, size, and localization. Myomas are classified in submucosal, intramural, and subserosal according to their relationship with endometrium, myometrium, and uterine surface. The leiomyoma subclassification system of the Federation of Gynecology and Obstetrics (FIGO) classifies myoma into eight classes (from 0 to 7) according to their localization (Fig. 6.9). Submucosal myomas are classified in type 0 (Fig. 6.10) (100% intracavity), type 1 (>50% intracavity), and type 2 (<50% intracavity). Intramural myomas are classified into type 3 (in contact with endometrium) and type 4 (100% intramural). Type 5 includes intramural but <50% subserosal myomas, type 6 subserosal but <50% intramural. Subserosal peduncolate myomas are classified as type 7 [29].