Cervical Insufficiency

Introduction

• Description: Cervical insufficiency is characterized by the asymptomatic dilation of the internal os during pregnancy. This generally leads to the dilation of the entire cervical canal during the second trimester with the subsequent risk for rupture of the membranes, expulsion of the fetus, or both. Most often, this occurs before 24 weeks gestation.

• Prevalence: 1/54 to 1/1842 pregnancies (as a result of uncertain diagnostic criteria); it accounts for 10%–25% of all mid-trimester pregnancy losses; appears to be declining.

• Predominant Age: Reproductive age.

• Genetics: No genetic pattern. Single nucleotide polymorphisms were found in a small sample of patients with cervical insufficiency. These included rs2586490 in collagen type I alpha 1 chain ( COL1A1 ), rs1882435 in collagen type IV alpha 3 chain ( COL4A3 ), rs2277698 in metallopeptidase inhibitor 2 ( TIMP2 ), and rs1800468 in transforming growth factor beta 1 ( TGFB1 ).

Etiology and Pathogenesis

• Causes: Iatrogenic (most common); damage from cervical dilation at the time of dilation and curettage (D&C) or other manipulation or damage caused by surgery (conization). Congenital tissue defect, uterine anomalies (uterus didelphys), obstetric lacerations, in utero exposure to diethylstilbestrol (DES).

• Risk Factors: In utero exposure to DES (rare now), uterine anomalies, connective tissue disorders (eg, Ehlers–Danlos syndrome).

Signs and Symptoms

• History of second-trimester pregnancy loss accompanied by the spontaneous rupture of the membranes without labor or rapid, painless, preterm labor. Some authors argue that there must be multiple losses to establish the diagnosis.

• Prolapse and ballooning of the fetal membranes into the vagina without labor.

Diagnostic Approach