Inversio Uteri

01Pathophysiology

Uterine inversion occurs when the uterine fundus folds inward and descends through the endometrial cavity toward or beyond the cervix. Think of it as a sock being turned inside out. The process begins when the fundus, weakened by the placental implantation site, is pulled or pushed downward. This happens most often during the third stage of labor when excessive traction is applied to the umbilical cord before the placenta has fully separated, or when fundal pressure (Crede maneuver) is applied to a relaxed, atonic uterus.

The reason patients develop shock that appears disproportionate to the visible blood loss is twofold. First, the inversion itself causes significant hemorrhage because the placental bed is now exposed and the uterus cannot contract effectively around the bleeding vessels when it is inverted. Second, and critically for exam purposes, traction on the peritoneal structures and the round and broad ligaments triggers a parasympathetic (vasovagal) response, producing neurogenic shock with bradycardia and hypotension. This combination of hemorrhagic and neurogenic mechanisms explains why a patient may appear far more unstable than the amount of visible bleeding would suggest.

The fundal placental implantation is the single most important predisposing anatomical factor. When the placenta attaches at the fundus, the thinnest part of the myometrium at the implantation site becomes the weakest point, making it susceptible to inversion under traction or pressure forces. Additionally, conditions in the placenta accreta spectrum (accreta, increta, percreta) create abnormally adherent placentation that, when traction is applied, pulls the entire fundal wall downward rather than allowing the placenta to shear off cleanly.

02Classification and Clinical Manifestation

By Degree of Inversion

Classification by Timing

The clinical manifestation follows a recognizable triad: postpartum hemorrhage, severe pelvic pain, and a palpable or visible fundal mass with absence of the fundal contour on abdominal exam. In acute inversion, the patient often presents with sudden cardiovascular collapse immediately after cord traction or placental delivery, and this rapid hemodynamic deterioration is the key distinguishing feature from simple uterine atony.

03Diagnostic Workup

Uterine inversion is a clinical diagnosis. The best initial test is a thorough physical examination, which in most acute cases is both the first and the only diagnostic step needed. The classic finding on vaginal examination is a smooth, round, dark red or bluish mass in the vaginal canal, often with the placenta still attached. Simultaneously, abdominal palpation reveals the absence of the normal fundal contour, replaced by a cup-shaped depression or dimple at the expected fundal location.

The scenario where imaging becomes relevant is in incomplete (first-degree) inversion, where the fundus has not descended through the cervix and the clinical picture may be mistaken for a retained placenta, uterine atony, or cervical fibroid. In this setting, bedside ultrasound showing the characteristic "target sign" on transverse view (the inverted endometrium surrounded by myometrium) or indentation of the fundal contour on longitudinal view can confirm the diagnosis.

An important exam point: do not delay treatment to obtain imaging studies. If the clinical picture is consistent with uterine inversion (postpartum hemorrhage, absent fundus, visible or palpable mass), proceed directly to manual repositioning. Imaging is a tool for unclear cases, not a prerequisite for intervention.

04Management and Treatment

The next best step when you recognize uterine inversion is simultaneous resuscitation and manual reduction. Do not wait for the patient to be fully stabilized before attempting the Johnson maneuver, because the longer the uterus remains inverted, the more edematous and congested it becomes, and the harder reduction will be.

Discontinue oxytocin immediately. This is a commonly tested point. While oxytocin is the standard treatment for postpartum hemorrhage from uterine atony, in uterine inversion it is harmful because it causes the cervical ring to contract around the inverted fundus, trapping the uterus in its inverted position.

Administer a tocolytic agent to relax the uterus before or during the reduction attempt. Terbutaline 0.25 mg subcutaneously or intravenously is the most commonly cited agent. If the patient is already in the operating room, halogenated anesthetic agents (sevoflurane) provide excellent uterine relaxation. Nitroglycerin 50-200 mcg IV is another rapid-onset option.

Do not detach the placenta before attempting reduction. If the placenta is still attached to the inverted fundus, leave it in place. Premature placental removal exposes the raw placental bed to open hemorrhage without the ability of the uterus to contract and achieve hemostasis. Reduce first, then manage the placenta.

Once the uterus is successfully repositioned, immediately restart uterotonics (oxytocin infusion) to maintain uterine tone and prevent recurrence. The operator should keep a hand in the uterine cavity briefly to maintain the fundal position until the uterus firms up with oxytocin.

If manual reduction fails after adequate tocolysis and multiple attempts, proceed to surgical correction. The Huntington procedure (gradual upward traction on the round ligaments via laparotomy) is the standard first-line surgical approach. If the cervical constriction ring prevents reduction even with traction, the Haultain procedure adds a posterior longitudinal incision through the constriction ring to release it before repositioning the fundus.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common way students lose points on uterine inversion questions is by treating it like uterine atony. Both present with postpartum hemorrhage, and the reflexive answer for postpartum hemorrhage is uterine massage and oxytocin. However, giving oxytocin in the setting of uterine inversion worsens the condition by tightening the cervical ring. The vignette will contain the critical clue: the fundus is not palpable on abdominal exam, and there is a mass in or beyond the vagina. If the question mentions "unable to palpate the fundus" or "smooth round mass at the introitus," that is the signal to switch from the atony algorithm to the inversion algorithm.

Another frequently tested concept is the correct sequence of management. Students often want to remove the placenta first or obtain imaging before acting. The correct sequence is: recognize the inversion clinically, stop oxytocin, give a tocolytic, perform the Johnson maneuver with the placenta still in situ, and only after successful reduction remove the placenta and restart uterotonics. Questions that test "next best step" are looking for you to choose manual repositioning, not ultrasound, not placental removal, and not oxytocin.

The disproportionate shock is another pearl that test-writers exploit. If a vignette describes a patient with cardiovascular collapse after delivery but the visible blood loss seems modest, consider uterine inversion and its neurogenic (vasovagal) component contributing to the hemodynamic picture. This "shock out of proportion to blood loss" is a classic exam phrasing designed to point you toward this diagnosis.

Finally, remember the role of terbutaline versus oxytocin in this context. In almost every other postpartum hemorrhage scenario, oxytocin is the answer. Uterine inversion is the notable exception where a tocolytic (terbutaline, nitroglycerin, or halogenated anesthetics) is the correct pharmacologic choice for facilitating treatment.