The incidence of this phenomenon is approximately 1%, ranging broadly from 0.05% in unselected low-risk population, to 3% to 4% among women with a short cervix and preterm birth, climbing to 8% in women with recurrent midtrimester pregnancy losses.^2,3,4,5 As is the case for other poorly defined and selectively reported situations, the distribution is wide and depends on the studied population, the precise criteria for diagnosis, and coexisting risk factors.

The cervix is mostly fibrous tissue, composed of 85% extracellular matrix comprising collagen, elastin, desmosine, hydroxyproline, and a smaller cellular component of muscle tissue.⁶ The cervix’s key role is to retain the fetus in the womb until term and then to undergo massive transformation to assist the baby on its way out during labor. Cervical weakness may be the result of several insults, alone or combined, progressive or abrupt, which can be of a biochemical-functional or biomechanical-anatomical nature, as well as genetics, infectious, or inflammatory contributions. It is not an all-or-none phenomenon^7,8 but rather a continuum affected by multiple structural and functional pathologies, not necessarily always leading to the same clinical outcome.

During a normal pregnancy, the cervical content changes, with increased water content and less collagen.⁹ Equivalent, although preterm, processes occur in the pathologically weak cervix. Incompetent cervices have a higher amount of muscle tissue¹⁰ and a smaller proportion of elastic tissue components.¹¹ Such biochemical events lead the cervix to function inappropriately, losing its primary role, to remain closed throughout gestation to retain the fetus in utero until term. This can also be demonstrated functionally in biopsies of midtrimester incompetent cervices showing that, although the amount of collagen was normal, the collagenolytic activity was high, with evidence for low tissue strength and high extensibility, most probably reflecting amplified collagen turnover, resulting in a greater proportion of freshly synthesized, biomechanically weaker, collagen.¹² In addition to these changes, genetic variations in collagen-related genes, such as polymorphisms in the collagen-1α1 gene¹³ and the transforming growth factor-beta1 gene, also play a role in the mechanism.¹³ Moreover, infection susceptibility and loss of protection from ascending vaginal infection, mediated predominantly by cervical mucus, probably has a supporting role in the weakening of the cervix and the subsequent aggravation of the related complications.¹⁴

Congenital or acquired structural or functional abnormalities of the uterine cervix or the uterus itself can all predispose a patient to cervical insufficiency.^{15,16,17,18,19,20} Of note, much of the literature differentiates poorly between the outcomes of preterm labor and cervical insufficiency, and other studies only explore preterm birth and not cervical insufficiency. Therefore, caution is advised when interpreting the results of studies regarding cervical insufficiency and its potential risk factors.

Obtaining a full and detailed medical history on the presence or absence of risk factors is an important part of the evaluation in women with suspected cervical insufficiency, as it may support the diagnosis in borderline clinical scenarios and contribute to the decision on the appropriate treatment. However, if only risk factors are present and without a definitive diagnosis of cervical insufficiency, there is no indication for treatment, by either cerclage, progesterone, or any other modality.

The typical presentation of cervical insufficiency will be a history of a previous single or recurrent pregnancy loss of a live fetus (although mostly nonviable at birth) occurring spontaneously during the second trimester, typically between 16 and 24 weeks’ gestation.

The classic preceding description will be of an asymptomatic, or at least mildly symptomatic, advanced cervical effacement and dilatation, without additional features of labor such as contractions or bleeding. If symptoms are indeed described, they can be pelvic pressure, abdominal cramps or pain, and deviant vaginal discharge, by either volume, color, or consistency. The symptoms are often present several days before actual pregnancy loss and may be accompanied by progressive cervical shortening, which may or may not have been detected when sonography was performed.

Some instances of cervical insufficiency make the diagnosis extremely difficult and challenging. For example, in advanced stages of the expulsion of the fetus, symptoms may increase, making it sometimes impossible to differentiate in retrospect whether the process was indeed and truly asymptomatic or not. Similarly, if the cervix is dilated for a prolonged time and the membranes are exposed to the unsterile vagina, an infection may have developed. Therefore, excluding confounders—ie, labor, abruption, and chorioamnionitis—will be impossible. Moreover, the diagnosis of an historical insufficiency is often confounded by a lack of objective measures and inappropriate documentation. The caregiver may fail to document or remember events and a possible differential diagnosis. In addition, the patient herself will often have a selective, memory-biased, report of the trauma.

Naturally, if one encounters the events in real time assigning a diagnosis of cervical insufficiency with an appropriate description and recommendations in the medical record will be very helpful for both the patient and her caregivers for future gestations.

The diagnosis is based on a combination of obstetrical history and transvaginal ultrasound measurement of cervical length. Among women with a previous preterm birth prior to 37 or 34 weeks’ gestation, who are asymptomatic or mildly
symptomatic, the diagnosis is made when a transvaginal ultrasound detects a short cervical length, defined below 25 mm.²¹ The ultrasound may be performed on routine follow-up or upon suspicious symptoms. Sonographic surveillance of cervical length is advised every 2 to 4 weeks, up until 24 weeks to allow placement of cerclage if shortening is detected, or up until 32 to 34 weeks to administer antenatal corticosteroids, if significant shortening is detected. In addition to routine cervical length assessment, the cervix should be measured if suspicious symptoms, including mild abdominal pain or cramps, pelvic pressure, and changed vaginal secretion, of cervical insufficiency arise, as had been previously described.

Importantly, physical examination is usually insufficient to diagnose women with ultrasound-defined cervical insufficiency, as the cervix is palpated without effacement and dilation until below 10 mm in a transvaginal ultrasound.²²

Physical examination defines this subtype alone if advanced cervical dilation and/or effacement is either viewed via speculum or palpated via vaginal examination. During examination the fetal membranes are exposed, reaching to the external cervical os or prolapsing beyond it. As for the other types, these women are either asymptomatic or mildly symptomatic.