Understanding endometriosis, and pelvic pain starts with understanding the menstrual anatomy and the hormones of menstruation, the neural pathways related to organs involved with endometriosis implants. Pelvic pain originates from the layer covering the organs, and their connecting structures, namely the peritoneum. Additionally pain also be due to dysfunction of the organ deeply infiltrated and involved by endometriosis. The mechanism of pain caused by endometriosis is extremely complex and completely not understood. Endometriosis is the most common cause of pelvic pain in women in their menstrual years, and pelvic pain is the most common symptom of endometriosis. While most women experience mild cramps, not all cramps are painful. Those women with endometriosis, however, experience excessively painful cramps with their menstruation that may progressively worsen in severity and duration as well as heavier menstrual flow. Cramps, or pelvic discomfort and pelvic distress in sustained version, could be described as dull, or sharp stabbing, twisting, penetrating, or pulsating. In the initial implantation stages of endometriosis, before deep infiltration or invasion, the pain is nonspecific and very commonly associated with gastro-intestinal symptoms. These symptoms are nausea, vomiting, bloating, gas, fluid retention, diarrhea. In the later stages when fibrosis and nodule formation progress into invasion and infiltration, severe symptoms of constipation, and painful bowel movement, painful intercourse.
Pain is another way of expressing sustained discomfort and along with uterine cramps, may be associated with intercourse, bowel movement, and joints. Endometriosis pain is always pelvic in location and overlap with menstruation. Uterus at the end of menstrual sustained cramps, a killer in nature, secondary to contraction of the uterus as well as heavy bleeding.
Every month the uterine lining called endometrium, sheds in the absence of conception. Endometrium consists of swollen glands and blood vessels to accommodate pregnancy. The uterus must contract to expel this debris through its opening called cervix. Uterine contractions may be laborious to dilate the cervix due to tightness and lengthiness of the cervix. A deficiency in the prostaglandins may also play a role in this process. Other factors causing incomplete and ineffective emptying of the endometrial cavity are uterine anomalies such as intrauterine septum, arcuate cavity, and rudimentary horn. When the endometrial cavity and its menstrual debris is deposited into the inner peritoneal cavity through the tubal openings, the process is called the retrograde menstruation also known as menstrual reflux or regurgitation. While most women experience this process, the volume of the menstrual debris could be excessive in the amount due to factors causing heavy periods. In young girls, and adolescents coagulopathies such as Von Villa Brand disease, thrombocytopenia, factor 8 Laden must be ruled out. Endometrial polyps, fibroids submucosal and adenomyosis develop from uterine muscle tissue and the must be considered in women of later age with any type abnormal uterine bleeding. Heavy menstrual bleeding with pain is called menorrhagia and dysmenorrhea respectively, and point the uterus mainly as the source of pelvic pain.
Debris of the refluxed endometrial contains not only glands and intense blood vessel network but also stem cells from the junction of muscle layer and endometrium. Debris is usually dissolved and eradicated by immune system cells within the peritoneal fluid. In the case of endometriosis, however, menstrual debris survive as deposited on the peritoneal lining of the pelvis. The peritoneum has nerve endings as well as capillary blood supply that reach its surface layer. What start as intense irritation of the peritoneal surface layer eventually lead to inflammation, a battleground for the immune system cells trying to reject and eliminate the implanted deposits.
The basic mechanism explaining the foundation of endometriosis pain is the peritoneal inflammation. Therefore dysmenorrhea, painful period are mainly due to uterine cramps, accompanying pelvic pain is due to irritation, and inflammation of the peritoneum. As the implanted lesions settle down and begin to be hormonally responsive to estrogen similar to what happens in the endometrium, the so-called foci of mini periods is trapped within the thin peritoneal layer. Monthly reoccurrence of the same inflammatory process leads to thickening and disfiguring of the peritoneum due to scar formation that is called fibrosis. It is the fibrosis that set the stage for the more advanced disease the deeply infiltrating endometriosis of the bowel, bladder, ureter, and endometrioma of the ovary. The infiltrative process into much deeper tissues of the bigger nerves, ligaments connecting to the bones of pelvis define the end stage of the endometriosis disease process called frozen pelvis.