Cervical Incompetence and Cerclage - 3 - Significance of the Internal Cervical Os
Some of the potential risk factors for cervical incompetence include past obstetrical and family history of premature delivery and cervical incompetence, maternal obesity, congenital uterine abnormalities, uterine fibroids, previous uterine surgery (e.g., D&C, removal of uterine septum, myomectomy), previous cervical surgery, multiple gestation, traumatic vaginal delivery, recurrent vaginal infections, connective tissue disorders (e.g., Ehlers-Danlos syndrome and Marfan's syndrome), polycystic ovary syndrome/insulin resistance, and perhaps diabetes. There is debate that a ‘short cervix’ by itself may increase the risk for cervical insufficiency, but if the cervical connective tissue is normal and there is no loss of integrity at the internal cervical os, this seems to be a weak call in many instances.
Whether there is an underlying connective tissue abnormality of the cervix, pathologic activation of the cascade of biochemical events that leads to remodeling of the cervical connective tissue, or simply a congenital or acquired anatomical abnormality of the internal cervical os, the most pathognmonic and sentinel event occurring with cervical incompetence is progressive loss of integrity at the internal cervical os. Cervical change that anticipates labor starts from the inside and progresses outward. Premature cervical ‘remodeling’ can lead to this loss of integrity at the internal os, but it is also often seen in conjunction with congenital uterine malformations (Mullerian defects) that affect midline structures (such as the cervix) and as the consequence of trauma during operative procedures, the most common being D&C. I emphasize this point, because I am a firm believer in the laws of physics with regard to cervical incompetence and its progression, even prior to the connective tissue remodeling (‘ripening’) that will eventually occur once the cervix has been stretched from within.
Let me elaborate on this in the way I explain it to patients: The internal cervical os is supposed to remain closed and basically contiguous with the rest of the inner surface of the uterus – distributing the weight of the baby and fluid over that entire surface area. If the internal os has been damaged and is not closed, or if other factors decrease the resistance at that anatomic site allowing it to begin to open, the tendency will be to simply continue to open, and as that progresses, it actually takes less pressure to continue that process with time. We are talking simple physics here, the same principle that holds when we drive a wedge into a log to split it. It’s hard to get started and then eventually it just gives way.
All women who wear spiked heels should know the reason for this. If you concentrate all the weight of your body, say 150 lbs, on a heel that measures say .2 x .2 inches that translates into a weight of 3750 lbs per square inch! That’s why spiked heels can punch holes in flooring. If we apply that same thinking to pregnancy and the entire volume of the uterus is focused on a weak point, a defective and slightly opened internal cervical os, the tendency is to enlarge that opening and eventually squeeze the membranes into the cervical canal – an event we call cervical funneling – just like squeezing a water balloon through a small opening. The important thing to recognize is that we CAN detect loss of integrity at the internal os during pregnancy by ultrasound and evaluate the configuration of the cervical canal as it begins to distend with membranes and amniotic fluid BEFORE this is readily apparent by clinical symptoms or obvious changes evaluable by vaginal examination of the patient. And this sometimes gives us an opportunity to intervene in a way that can prolong and preserve a pregnancy that might have otherwise been lost or accompanied by extreme prematurity and its attendant morbidity....