Hysteroscopy Basic

Endometrial cycle and Hysteroscopy

The endometrium has the ability to experience cyclical changes in response to different hormonal stimuli that occur during the menstrual cycle. These changes are known as the endometrial cycle. The endometrial cycle is divided into three phases: the proliferative phase, the secretory phase and the menstrual phase.

1- The proliferative phase:

Starting from the end of the menstrual period to ovulation, ie, between the 4th to 14th day of the cycle. During this phase, egg development occurs and is mainly mediated by estrogen. The endometrium reaches a thickness of 1-3 mm. During this phase the endometrial lining grows due to development of the endometrial glands, the stroma and the vascular component.

2- The secretory phase:

Also known as the luteal phase begins at the time of ovulation up to menstruation, ie between the 14th to 28th days of the cycle. It is this phase the corpus luteum produces high levels of estrogen and progesterone. The endometrium reaches 5-6 mm thickness. The glands have some morphological changes and secretory activity becoming more tortuous and dilated. The endometrial spiral arteries are also developed.

3- The menstrual phase:

In the absence of pregnancy, a sudden decline of estrogen and progesterone production by the corpus luteum produces endometrial ischemia due to vasoconstriction of the spiral arteries between 1 to 24 hours before menstruation. After the period of vasoconstriction there is return of blood flow to the superficial layers of the endometrium, resulting in detachment only of the basal layer. During this phase, uterine contractions occur to facilitate the expulsion of endometrial tissue.

These changes occurring during the endometrial cycle, give the endometrium different hysteroscopic patterns typical of each phase, allowing the assessment of normal “hysteroscopic” endometrial cycle.

1- Proliferative phase:

The endometrium has a light pink color due to the presence of small vessels. The surface is smooth and glands are small and rounded, appearing as small and uniform dots. The endometrial notch is small and generally hemorrhagic.

2- Secretory phase:

The endometrium has a pale pink color. The surface is slightly wavy and irregular. The glands are larger, open and rose at the level of the superficial layer. The vessels disappear from the endometrial surface due to stromal edema. The endometrium reaches its maximum thickness at this stage, showing a deep avascular endometrial notch.

3- Menstrual phase:

The endometrium takes on a reddish color, with indentations and bleeding. In this phase there are alternating areas of detaching and well preserved endometrium.

Endometrial Hyperplasia

  Endometrial hyperplasia is an overgrowth of endometrial glands, with different shapes and sizes, which causes increased endometrial thickness which results in a greather gland / stroma ratio than observed in normal endometrium.

 The term endometrial hyperplasia includes different pathologies that have the  common feature to increased endometrial thickness. Some of these pathologies have virtually no potential for malignancy while others are clearly premalignant lesions. The pathological diagnosis is the key to the diagnosis of this entity.

 Little is known on the actual incidence of endometrial hyperplasia although it is estimated to affect about 8/1000 in asymptomatic menopausal patients and 15% of patients with postmenopausal bleeding.

 There are different classifications, perhaps the most accepted is that of the International Society of Gynecological Pathologists that defines the following types:

 1-Simple hyperplasia without atypia: Glandular dilatation and increased evidence glands and stroma.

 2-Complex hyperplasia without atypia: Great growth of the endometrial glands with little stroma. The distribution pattern is irregularly glandular.

 3-Simple hyperplasia with atypia: There are atypical cells present in the lining of the glands.

 4-Complex hyperplasia with atypia: pattern of complex hyperplasia with atypical cells in the lining of the glands.

  Endometrial exposure to high levels of estrogen in an unopposed continuous manner can lead to endometrial hyperplasia, this effect seems to be time and dose dependent. High levels of estrogen may be due to the presence of endogenous or exogenous estrogen. Endogenous in cases of anovulation, polycystic ovaries, some ovarian hormone producing tumors (granulosa cell, Brenner and tecoma) and exogenous such as in obesity and diabetes or in the case of continuous estrogen therapy without progestagenic opposition and in cases of tamoxifen use.

 We can consider endometrial hyperplasia as a precancerous lesion, being the most important prognostic factor for the presence or absence of epithelial atypia. Kurman et al published one of the most important studies describing the evolution of endometrial hyperplasia in which he observed that

 1.07% of simple hiperplasia without atypia, 3.4% of the complex hiperplasia without atypia, 8% of the simple hyperplasia with atypia and 23% of the complex with atypia would, if untretaed, progress to endemetrial cancer. There is also another study recently published that reports a 52% risk of progression of atypical hyperplasia to carcinoma.

 The median time of progression of hyperplasia without atypia to carcinoma has been established in about 10 years, whereas if there is atypia the progression occurs in about 4 years. The presence of atypia is key to the progression to carcinoma.

 The diagnosis of endometrial hyperplasia should be suspected in women with heavy and frequent menstrual bleeding or in women with abnormal uterine bleeding, especially if they have risk factors such as anovulation, obesity or are taking estrogen therapy. Endometrial hyperplasia produces abnormal uterine bleeding in both pre- and postmenopausal patients being the cause of 10% of abnormal uterine bleeding and 15% of postmenopausal metrorrhagia.

    Ultrasound: Transvaginal ultrasound allows the assessment, measuring the thickness of the endometrium in a midsagittal view. It has little value in the final diagnosis, but it is important in determining which women need further study. In postmenopausal women an endometrial thickness of 4 mm or less exclude endometrail pathology with a sensitivity of 90%.

    Hysteroscopy: It is considered the gold standard modality for the workup of the patient with abnormal uterine bleeding. It allows to perform endometrial biopsy under direct visualization. Unfortunately, it is difficult to differentiate between complex endometrial hyperplasia and endometrial adenocarcinoma. There is no consensus on the hysteroscopic appearance of endometrial hyperplasia.


    Endometrial biopsy: It can be performed by directed suction cannula while performing hysteroscopy. There is an excellent correlation between a sample collected by a suction cannula and the one collected by blind curettage. The endometrial biopsy should always be performed after the ultrasound to preserve the ultrasound image.


    The treatment of endometrial hyperplasia varies according to hystological type, patient’s age and desire to preserve fertility. The goal of treatment of hyperplasia without atypia is to control abnormal uterine bleeding and prevent progression to carcinoma (1 to 3%). Endometrial hyperplasia with atypia, has a significant higher risk of progression to carcinoma (17-53%) usually requires surgery.

  Endometrial hyperplasia without atypia: medroxyprogesterone acetate 10mg / day for 12-14 days per month for 3-6 months. Regression was observed in 80% of cases. Ovulation induction is an alternative for patients with endometrial hyperplasia without atypia who desire to conceive. Another option to consider is the insertion of levonorgestel IUD which compared with oral therapy, has been shown in multiple observational studies to have fewer side effects and higher regression rates. In a recent study, Orbo et al have shown that after 6 months of treatment, all patients in the group with Levonorgestrel IUD (6 patients were with atypical hiperplasia) had complete remission. While the rate of regression of the continuous oral progesterone group was 96% and 69% in the group of cyclic oral progesterone. In postmenopausal patients the use of 10 mg medroxyprogesterone acetate or megestrol acetate for 6 months is also an option.

  Endometrial hyperplasia with atypia: in the presence of atypica, since the risk of progression to endometrial cancer is high, hysterectomy is considered the treatment of choice. In women who wish to preserve fertility megestrol acetate 40 mg can be used with biopsy and ultrasound scan at 3 months. As an alternative, the use of levonorgestrel IUD has been proposed with biopsy control at 3 months.