eMedicine Specialties > Obstetrics and Gynecology > Obstetrical Complications

Malposition of the Uterus

Author: John P O'Grady, MD, MA, Professor of Obstetrics and Gynecology, Tufts University School of Medicine; Medical Director, Family Life Center and Mercy Perinatal Service, Mercy Medical Center; Attending Physician, Department of Obstetrics and Gynecology, Baystate Medical Center and St Elizabeth's Medical Center
Contributor Information and Disclosures

Updated: Jun 12, 2008

Introduction

Intermittent myometrial contractions and changes in uterine position are normal during pregnancy. Infrequently, various obstetric complications result from uterine malpositioning (retroversion or incarceration), inversion, and, in rare cases, prolapse, torsion, or herniation.

Uterine positioning and the practice of gynecology have a long and problematic history. In the 19th century, uterine retroversion in nonpregnant women was identified as a distinct abnormality held responsible for a wide range of clinical symptoms. Special devices and many surgical techniques were developed to either reposition the uterus or to hold it in its presumed correct location. These operations and manipulations were believed to be necessary for the maintenance or restoration of normal functioning.

In modern time, surgery for the correction of uterine retroversion in the absence of evidence of endometriosis or other specific pathologic conditions has fallen into disrepute. The reason has been the lack of scientific or experimental evidence supporting the effectiveness of these operations. Because of this situation, the performance of these once relatively common procedures has been markedly curtailed.

Uterine retroversion is now recognized as a normal variant of uterine positioning that, in most cases, does not result in symptoms. Among nonpregnant women, 1 of 5 have a retroverted uterus either as a normal variant of uterine position or as an acquired condition. However, when a pathology distorts the uterine contour (eg, m ü llerian anomaly, leiomyoma), or an inflammatory process has occurred in the past (eg, endometriosis with pelvic adhesions), the uterus may become fixed in a retroverted or retroflexed position and lose its normal mobility. Retroversion from any cause becomes an issue of clinical importance if it progresses to uterine incarceration once a pregnancy is established. Fixation of the uterus by adhesions is also a risk factor for the rare complication of uterine torsion.

Symptomatic uterine incarceration during an otherwise normal pregnancy is uncommon. Nonetheless, serious complications of this condition are possible. The literature on this subject, as well as most of the other conditions involving uterine malpositioning, consists mostly of case reports. Systematic studies have not been conducted.

Based on compiled data and the author's experience, several important clinical aspects concerning the diagnosis and management of uterine incarceration and potential complications of other acute and chronic types of uterine malpositioning are described in this article.

Uterine Retroversion or Incarceration

Frequency

During early pregnancy, uterine retroversion is a normal positional variant. Typically, first-trimester retroversion is intermittently present 10-20% of the time. If retroversion persists into the midtrimester, uterine incarceration is possible, but the likelihood of this complication is low. In only about 2% of uterine retroversions diagnosed during the first trimester does the condition progress to incarceration associated with urinary retention or other acute symptoms.

Accurate statistics concerning the prevalence of this disorder are not available, a situation true of many infrequently occurring obstetric complications. Most instances of retroversion or incarceration are not reported, and few publications beyond case reports are available for review. A rough estimate is that symptomatic incarceration occurs in 1 per 3000-6000 pregnancies.

Pathophysiology

Normal pelvic anatomy permits the fundus of the uterus to move relatively freely in the sagittal, vertical, oblique, and anteroposterior planes. In retroversion, the uterus is tipped posteriorly and may be fixed in this position by the presence of adhesions. Cases of marked retroversion with the uterine fundus positioned below the sacral promontory in the hollow of the pelvis lead to incarceration as the uterus enlarges during pregnancy. As the uterus becomes bigger, the fundus progressively moves posteriorly as it cannot escape from the cul de sac. As this occurs, the cervix is driven underneath and then behind the pubic symphysis. At some critical juncture of uterine size, tissue laxity, and other unknown factors, the uterus becomes entrapped. At this point, the fundus cannot easily exit the hollow of the sacrum or it is incapable of spontaneously rotating anteriorly past the sacral promontory (see Media file 1).

Entrapment usually occurs after the 12th week of gestation. However, it may occur earlier if special conditions such as a multiple gestation or a müllerian anomaly exist, or if a strategically located leiomyoma or adnexal tumor is present.

In cases involving a specific pathologic process, a variety of conditions are possible. These typically include the following entities:

• Müllerian abnormalities with a posterior uterine horn or a rudimentary horn
• Adnexal tumor or a fundal or posterior leiomyoma
• Adhesions due to endometriosis
• Adhesions due to previous pelvic inflammatory disease
• Adhesions due to previous surgery

As gestation advances, the incarceration worsens. Because the enlarging uterus cannot rotate anteriorly, it is wedged progressively firmly into the hollow of sacrum while the cervix exerts increasing pressure toward the urethra and/or bladder. Normal voiding eventually becomes difficult or impossible as progressive upward cervical pressure restricts normal funneling of the bladder outlet and obliterates the posterior uterovesical angle.

Clinical presentation

A review of patients' histories reveals that the principal risk factor for incarceration is multiparity (89% of cases). However, as incarceration is so infrequent, multiparity must coincide with a unique mixture of pelvic architecture, uterine positioning, and laxity of the supporting tissues to result in persisting retroflexion progressing to an entrapment. A history of previous retroversion or incarceration is often elicited in multiparous women with this disorder and an occasional case of prolapse will be noted. These observations suggest the importance of some specific, but currently unrecognized, predisposing factors of pelvic anatomy and tissue tonus in the etiology of retroversion/incarceration.

Recurrence is possible. Thus, women with a history of symptomatic incarceration should be evaluated frequently in the late first trimester and early second trimester to ensure that the uterus does not become fully incarcerated if it remains retroverted.

If early incarceration is suspected, prone positioning for sleep, intermittent knee-chest positioning, and, in a few patients, manipulations might be indicated. These interventions are described below.

When incarceration occurs, the acute symptoms mimic those of more common obstetric conditions. Yet, in most instances, the correct diagnosis is readily established by reviewing the clinical history and performing a pelvic examination. Conducting a real-time ultrasonic examination is confirmatory.

Uterine repositioning is usually easy and successful if the diagnosis is made early. However, if incarceration remains undiagnosed and progresses for a prolonged period, acute symptoms may develop. Uncommonly, the continuation of the pregnancy is threatened. Unfortunately, the principal symptoms of incarceration are nonspecific and this condition cannot be diagnosed based on patient history alone.

Common clinical symptoms include the following:

• Abdominal pain or pelvic pressure
• Uterine contractions or cramping
• Bowel dysfunction (eg, tenesmus, rectal pressure, constipation)
• Paradoxical urinary symptoms (eg, incontinence, frequency, and, eventually, retention)
• Vaginal bleeding (threatened spontaneous abortion)

In the differential diagnosis of pelvic pain and voiding difficulty in the late first trimester or early second trimester, the clinician should consider the possibility of uterine incarceration because the diagnosis is easy and early treatment is essential. Care is necessary because the signs and symptoms of incarceration are difficult to distinguish from those of normal pregnancy or other more frequent complications of late first-trimester or early second-trimester gestation (eg, threatened abortion, urinary tract infection). An episode of incarceration during a previous pregnancy on a woman's obstetric history is an important hint that recurrence is possible.

Diagnosis

The diagnosis of incarceration is established by performing a pelvic examination and pelvic sonography and by considering these data in combination with the characteristic clinical history. In the rare event of incarceration with sacculation first encountered late in pregnancy, an MRI study may prove helpful in establishing the correct diagnosis as uterine distortion, in these cases, is usually marked and the anticipated anatomic features are distorted. A common clue is a history of progressive difficulty with normal voiding that develops in the early midtrimester. Pelvic pain and/or pressure or uterine cramping usually accompanies the urinary symptoms. Vaginal spotting may also be present.

In the differential diagnosis, the clinician must consider uterine leiomyomata, müllerian anomalies, and various other adnexal or pelvic tumors that either displace a normal uterus into an unusual position or distort its shape. Also to be considered are the rare functional and anatomic malformations of the uterus. These unusual disorders distort the normal uterine contour, and some, such as sacculation, may be the result of chronic retroversion/incarceration.

In cases of retroversion with incarceration, clinical examination usually yields the following striking findings:

• Acute anterior angulation of the vagina
• A cervix abutting firmly against or positioned well behind the pubic symphysis
• A soft, smooth, nontender mass filling the cul-de-sac
• An inability to palpate the uterus during abdominal examination or a uterine fundus too small for the known gestational age

In the midtrimester, the initial clinical suspicion is usually easily verified by means of real-time ultrasonography. The posteriorly located uterine fundus occupies the hollow of the sacrum, and the cervix is positioned anteriorly behind the pubic symphysis. Various uterine or adnexal tumors are also revealed during sonography. The possible diagnosis of a müllerian anomaly must also be considered.

Treatment

Possible therapies for retroversion with incarceration include the following:

• Bladder decompression by means of intermittent or indwelling catheter drainage
• Patient positioning (eg, intermittent knee-chest or all-fours positioning, sleeping prone)
• Manual uterine replacement: manipulation of the uterus into its usual anatomic position, with or without tocolysis and/or anesthesia
• Colonoscopic manipulation of the uterine fundus with the patient under anesthesia
• Application of specialized and rarely attempted techniques of replacement (eg, use of a mercury-filled Voorhees bag in the vagina, amniocentesis with manipulations or surgical exploration and replacement)

Bladder decompression and patient positioning

The best initial treatment for symptomatic midtrimester incarceration of a normal uterus is a trial of bladder decompression combined with a program of patient positioning. Such management relieves most cases.

Spontaneous voiding is often impossible and catheterization is usually required. If the bladder is distended, an indwelling catheter is inserted for 24-48 hours. If a urinary tract infection is present, appropriate treatment is initiated.

During the interval of bladder drainage, the patient is instructed to perform repositioning exercises on a frequent basis. These exercises consist of modified all-fours or knee-chest positioning done several times a day for 5-15 minutes, with intermittent Valsalva maneuvers. The patient is also instructed to sleep in the prone position. Spontaneous repositioning normally occurs with these steps alone.

Manipulation of the uterus

If the aforementioned outpatient maneuvers prove unsuccessful, manual uterine replacement is considered. After informed consent is obtained and ultrasonography is performed, a tocolytic agent (eg, terbutaline 0.250 mg administered subcutaneously) is electively given 15-20 minutes before reversion is attempted. Note that no data address the efficacy of tocolytic therapy in improving the success of uterine replacement; therefore, its use is elective. However, tocolytics are generally well tolerated by otherwise-healthy gravidas and, in the opinion of experienced practitioners, they facilitate the necessary manipulations.

Before the procedure begins, the woman is instructed to void, or, if a Foley catheter was placed, it is fully drained. An attendant is present to support and encourage the patient and to help prevent a fall. In the replacement procedure, a speculum is passed and the anterior lip of the cervix is grasped by using a long Allis clamp or another atraumatic clamp (see Media file 2).

The patient is then placed in the knee-chest or all-fours position. The surgeon inserts a finger into the vagina or rectum and applies pressure to the incarcerated fundus while simultaneously applying gentle but constant traction to the cervix. With this combined technique, the uterus should slowly rotate into its normal position. In theory, passing the fundus to either side of the sacral promontory, where more room is available, is probably best. In the author's experience, such refinements in technique are nearly impossible to achieve, and simple pressure combined with cervical traction suffices.

The maneuvers just described are usually easy to perform. This repositioning maneuver should be neither painful for the gravida nor difficult for the surgeon. Only mild-to-moderate force is appropriate for the replacement. Excessive force jeopardizes patient compliance, and it poses a risk of cervical injury due to the cervical grasping instrument. In addition, excessive force could theoretically damage the pregnancy by acutely distorting the uterus and obstructing uterine blood flow. In unusual instances, when both bladder drainage with repositioning and a trial of gentle manipulation fail to replace the uterus, other methods must be considered.

If simple replacement is not possible, another technique is the use of anesthesia combined with a tocolytic. To perform this method of uterine replacement, an epidural anesthetic is best. As an alternative, a general anesthetic could be given with a uterus-relaxing agent to avoid the need for a separate tocolytic drug. However, this approach is not recommended as it is too easy to apply excessive force and the manipulation of patient position is not possible.

To perform uterine replacement with anesthesia, the gravida is positioned in lateral recumbency. The epidural anesthetic is administered. Once a proper level is achieved, nitroglycerin 0.15-0.5 mg is given intravenously and titrated to effect, or a parenteral beta-mimetic (eg, terbutaline 0.15-0.25 mg administered intravenously or subcutaneously) is electively administered. Due to its rapidity of onset, short half life, and effectiveness, the authors favor the use of nitroglycerin.

After the tocolytic is administered, the anterior lip of the cervix is grasped with a long Allis clamp or another atraumatic clamp. Thereafter, cervical traction is combined with rectal pressure against the fundus in the same manner as previously described. This is usually performed in Sim position or in dorsal lithotomy.

Another technique involves the passage of a colonoscope to provide the upward force necessary to dislodge the entrapped fundus.

Use of real-time sonographic guidance during manipulation procedures is prudent. Successful replacement is verified by means of palpation and real-time ultrasonography.

Specialized and rarely attempted techniques

The literature includes case reports describing a number of techniques for uterine repositioning. These include unusual maneuvers, such as placement of a mercury-filled Voorhees bag in the vagina, along with other more complex methods. In the author's experience, these manipulations are not indicated.

In unusually advanced cases, amniotic fluid could be aspirated to reduce uterine volume. This procedure cannot be recommended save in the most difficult of circumstances.

Postprocedural care

After the procedure, repeat real-time ultrasonography should reveal normal fetal cardiac activity and fetal motion and the patient's original symptoms should resolve promptly. When replacement is successful by any technique, the patient is often instructed to continue to sleep in the prone position, to practice occasional knee-chest or all-fours positioning, or to use a pessary to keep the uterus correctly positioned. These manipulations are probably not necessary but are commonly recommended by various authors. As a general rule, reincarceration should not recur during the same pregnancy if the uterus has been fully released. No studies have been performed regarding either the efficacy or the necessity of any of these postreplacement treatments.

After any procedures to attempt uterine replacement, administration of Rh immunoglobulin is indicated in Rh-negative patients who are not isoimmunized.

With modern techniques of treatment, serious maternal problems due to retroversion or incarceration and consequential fetal complications should be rare. In rare cases of chronic uterine retroversion, ballooning out of the uterine wall (sacculation) may permit the uterus to expand abdominally. If this occurs, the pregnancy may progress even into the third trimester. In such instances, the correct diagnosis is established only when dystocia in labor ensues or when abdominal and/or pelvic examination reveals markedly unusual findings that lead to an MRI study. In the rare case that reaches the third trimester, the uterine malpositioning is fixed and cesarean delivery is required.

In the midtrimester, spontaneous abortion may occur because of incarceration alone, or it may follow manual uterine replacement. The risk of such loss is believed to be low. However, the extant literature consists of case reports and opinions and the true risk is not known. Because of this, before a midtrimester repositioning maneuver is performed, a frank discussion with the gravida is essential. Also, it is prudent to verify fetal cardiac activity and conduct as much of an anatomic survey of the fetus and draw any diagnostic biochemical tests for aneuploidy before any manipulations are attempted.

Comments

Etiology of retroversion

In nonpregnant women, if retroversion alone is the cause of symptoms, these are usually minimal. Pelvic pain and similar symptoms are principally due to coincidental pathology. Other causes of chronic pelvic pain in which retroversion may be present are discussed below. Evidence to show that isolated retroversion is responsible for abortion or infertility is lacking. When these conditions are encountered, another etiology must be sought.

See Medscape CME activity, Management of Chronic Pelvic Pain in Women Reviewed.

Uterine suspension procedures

Uterine suspension procedures have largely disappeared from gynecologic surgery. Exceptions are cases involving specific pathology when suspension is performed to help prevent the formation of new adhesions during healing. As an example, uterine suspension is frequently performed when retroversion is associated with endometriosis or tubal pregnancy or when the patient has undergone microsurgical tubal reconstruction procedures to treat infertility. However, uterine retroversion alone in an asymptomatic woman is not an indication for prophylactic uterine suspension or a similar procedure.

In nonpregnant women with uterine retroversion and chronic pelvic pain, uterine suspension does not invariably relieve symptoms. This is especially true when patients are monitored long term. Therefore, clinicians must act conservatively and critically review claims about the relief or lessening of abdominal-pelvic distress after any procedure or therapy to correct retroversion.

Atypical cases of retroversion in late pregnancy

The rare instances of retroversion that are diagnosed after the second trimester are difficult to manage. Similarly hard to treat are cases complicated by pelvic adhesions or cases due to congenital anomalies or permanent tumor-induced distortions in uterine shape. These situations require individualized treatment.

In many of these unusual or atypical cases, the correct diagnosis is often not made until the abdomen is opened for cesarean delivery or until laparotomy is performed to address a presumed abdominal catastrophe.

Multiple gestations

Multiple gestations, which now often occur in association with assisted reproductive technologies, are special cases. In this setting, the uterus can become incarcerated earlier in gestation than when only a single fetus is present. This change is presumably due simply to the increased size of the uterus. Therefore, if characteristic symptoms occur in women with known multiple gestations—even when the pregnancy has not reached 12 weeks of gestation—retroversion or incarceration should remain in the differential diagnosis.

The literature mentions few cases of incarceration of the uterus in spontaneously occurring multiple gestations. The apparently high incidence of retroversion or incarceration in early multiple gestations might be a new phenomenon due to some unrecognized effect of infertility treatment. Or, past incidences of incarceration among spontaneous multiple gestations might have been understated because of sampling or reporting errors. The answer remains unknown.

Persistent retroversion

In a few cases, the uterus remains retroverted and cannot be repositioned despite the administration of tocolysis and the use of regional anesthesia. The best management strategy in this setting is moot.

In an unknown number of such instances, the uterus will balloon into the upper abdomen by a process of progressive thinning of the superior segment of the posterior uterine wall. This process of progressive uterine distortion (sacculation) relieves the compression. However, sacculation cannot be assumed to occur without complication. In a fixed incarceration in the midtrimester the risks are pregnancy loss and uterine rupture yet the magnitude of these risks is unknown.

When the uterus is fixed posteriorly, the central issue is whether it is bound down by adhesions due to endometriosis, infection, or previous surgery. In the most unusual cases, surgical exploration of the pelvis may be required to determine the cause of the retroversion and, if possible, to return the uterus to its normal position. However, if the cause of the retroversion and/or incarceration is the presence of dense adhesions, surgery may injure the uterus or other pelvic structures, lead to hemorrhage and potentially threaten continuation of the pregnancy. Fortunately, such obstetric and surgical dilemmas are exceedingly rare. Of course, in such cases, treatment must be individualized.

Symptomatic retroversion with bladder outlet obstruction in the puerperium

Symptomatic retroversion with bladder outlet obstruction unusually will first occur in the puerperium. This is due to persisting uterine enlargement or subinvolution combined with flaccidity of the supporting tissues and other unknown causes. These cases are rare and are treated in the same manner as uterine incarceration occurring during pregnancy.

Counseling

The paucity of data concerning the risks associated with retroversion or incarceration during pregnancy makes counseling difficult. Patients should be informed that both symptomatic incarceration and efforts for its relief carry some risk of pregnancy loss.

In all cases, the fetal condition should be evaluated by both ultrasonographic review of fetal anatomy and by the drawing of biochemical tests for fetal normality. These data and their limitations should be discussed with the patient and family prior to attempting any manipulations.

If treatment is elected, begin with the simple and noninvasive procedures and/or manipulations, as they are often successful. The need to administer an anesthetic with a parenteral tocolytic to relieve symptomatic retroversion is, at best, uncommon.

Ultrasonography

Because of the general uncertainties, as noted, a real-time sonographic examination should proceed any intervention. This imaging study is done to reassure both the patient and practitioner, to verify the original diagnosis, to confirm that an anatomically normal and living fetus is present, and to verify that a mass or tumor is not the cause of the incarceration. The study is repeated after repositioning to confirm success of the procedure to verify the presence of an active fetus and normal amniotic fluid.

Other Syndromes of Pelvic Pain/Retroversion

In nonpregnant patients, the evaluation of chronic pelvic pain that accompanies uterine retroversion includes a consideration of 2 indistinct and somewhat suspect syndrome complexes: pelvic congestion syndrome (PCS) and Allen-Masters syndrome (AMS).

Allen-Masters syndrome, as originally described in 1955, includes the following 3 elements:

• History of obstetric pelvic trauma
• Uterine retroversion with a hypermobile cervix
• A tear or tears in the posterior serosa and subperitoneal fascia of the broad ligament

Symptoms attributed to AMS are multiple and include chronic pelvic pain, dyspareunia, and various menstrual disturbances.

Although the cause of AMS was originally ascribed to obstetric injuries, a symptom complex similar to that of AMS has also been attributed to endometriosis, independent of a history of obstetric trauma.

The classic approach to AMS consists of first visually establishing the diagnosis during laparotomy or laparoscopy. Any demonstrated peritoneal broad ligament defects are then either fulgurated or sutured.

Other surgical procedures have traditionally been performed at the same time. These procedures include shortening of the uterosacral ligaments, resection or obliteration of the pouch of Douglas, or other similar operations to cause the uterus to remain anteflexed.

In theory, repair of the tears in the posterior serosa and subperitoneal fascia of the broad ligament, along with the performance of ancillary procedures (eg, plication of the uterosacral ligament to return the uterus to the usual anterior position), are curative. This is a problematic syndrome with the pathophysiology ill defined. AMS remains a diagnosis of exclusion.

Pelvic congestion (Taylor) syndrome

Another possible diagnosis is PCS, or Taylor syndrome. This condition is characterized by menometrorrhagia and symptoms of continuous pelvic pain. On examination, the uterus is variably enlarged and soft, and some degree of tenderness is present. Uterine retroversion is again a common but not invariable finding. The cervix may be patulous or cyanotic. Among other treatment possibilities, both hysterectomy and vascular embolization have been used to manage PCS. The symptoms of this condition are nonspecific and poorly defined. Both this and the AMS are suspect diagnostic entities.

Rare mimics of uterine retroversion or incarceration

Several rare conditions can mimic uterine retroversion and incarceration.

• With müllerian anomalies, a uterus didelphys or an unconnected rudimentary horn can become positioned in the lower pelvis. This can cause the uterus to rotate or to become displaced anteriorly, mimicking classic retroversion/incarceration.
• A posterior uterine sacculation or herniation of the uterine wall can confuse the clinician as the normal anatomy is distorted.
• Tumors arising in the adnexa or myometrium can fill the pelvis and force the uterus anteriorly, rotating its position or distorting its shape. This process of tumoral displacement may result in symptoms of pressure or urinary dysfunction similar to those of simple incarceration.

In unusual or difficult cases, MRI can safely complement ultrasonography to help establish the correct diagnosis.

Uterine Torsion

Frequency

Uterine torsion is a rare condition in humans, and the extant papers are restricted to scattered case reports. Most cases of torsion are reported in the veterinary literature (see Table 1).

Table 1. Presenting Signs and Symptoms of Uterine Torsion According to the Degree of Uterine Rotation (as reported by Jensen, 2002) 

Open table in new window

*Some cases include more than 1 sign or symptom.

† Hypertonic uterus, PROM, pre-eclampsia, uterine rupture, etc

The earliest reported age for uterine torsion during pregnancy is the 6th gestational week; the latest is the 43rd week. The rare cases of torsion diagnosed at term are almost invariably discovered during the first stage of labor as a result of acute maternal or fetal problems that lead to exploratory surgery.

Pathophysiology

In uterine torsion, the uterus twists more than 45° around its long axis at the junction between the cervix and the corpus. The extent of the torsion is most often 180°. However, cases involving twists of 60-720° have also been described.

Dextrorotation is the most common finding. This is the normal orientation of the myometrial fibers. In rare situations, the torsion is of a sufficient degree to interfere with uterine circulation. This results in acute maternal symptoms or threatens fetal survival by directly restricting blood flow or by inducing an abruptio placentae.

In most instances, the cause of uterine torsion is obscure and no specific pathology is identified. Structural abnormalities of the uterus or adnexa are, however, demonstrated in at least 20% of cases.

Entities reportedly associated with torsion include the following:

• Abnormal fetal presentation (eg, a transverse lie)
• Distortion in uterine shape due to uterine leiomyomas
• Müllerian anomalies
• Pelvic adhesions
• Large ovarian neoplasms that distort the shape or position of the uterus
• Congenital weakness at the junction of the cervix and uterine corpus
• External cephalic version procedures
• Sudden maternal movements, as may occur during automobile accidents or, most rarely, during normal activity
• Long or rigid cervix or structural weakness at the junction of the cervix and the uterine corpus (possibly after a prior cesarean delivery)
• Abnormal pelvic architecture
• Hydramnios
• Multiple gestation
• Hyperactive fetus
• Interstitial pregnancy
• Unknown and/or idiopathic factors

Although many of the associations and predispositions listed above are common findings during pregnancy, torsion is rare. This observation suggests that additional factors must also be present in some unique concatenation for symptomatic torsion to occur. Such factors include certain unique maternal movements, postures, or positions; irregular contractions of the abdominal muscles; changes in myometrial tone; functional variations in the size, position, and mobility of the bladder and rectum; fetal movements; and possibly even segmental uterine contractions.

Clinical presentation

Although uterine torsion can be asymptomatic, most women with torsion present with complaints. The most common presenting symptoms are abdominal pain of acute onset, nonspecific gastrointestinal distress, and urinary dysfunction. The range of the associated symptoms is both wide and nonspecific, and they mimic those of other conditions much more common than torsion.

Gastrointestinal symptoms include nausea, vomiting, diarrhea, abdominal distention, and tenderness. Urinary symptoms can include urgency, frequency, nocturia, oliguria, and hematuria. Other reported symptoms are vaginal bleeding, hypertonic uterine contractions, or premature rupture of membranes. Much less frequent are maternal cardiovascular collapse (syncope) or abruptio placentae.

If the torsion occurs at term, obstructed labor is possible, or an acutely abnormal electronic fetal monitoring tracings may develop.

Diagnosis

The clinical challenge of uterine torsion lies in its elusive diagnosis. In most case reports, the correct diagnosis was rarely established before surgical exploration. However, MRI has recently been used to make the diagnosis prior to exploratory surgery.

Jensen described several clinical findings characteristic of uterine torsion.¹

• On surgical exploration, uterine rotation about the vertical axis is observed in association with marked venous engorgement and edema of the parametrial tissues.
• On abdominal examination, the round ligament is palpably stretched across the maternal abdomen
• On pelvic examination, the uterine artery is perceived as pulsating anteriorly.
• On speculum examination, the vagina and/or the cervical canal is distorted.

Uterine torsion is a rare obstetric complication. Nonetheless, because of its associated risks, torsion should be included in the differential diagnosis when severe but nonspecific abdominal pain occurs during pregnancy. Torsion is also a consideration, albeit a remote one, when dystocia is present or when acute fetal jeopardy develops during labor.

Mistaking torsion for a nonsurgical entity or another medically managed obstetric complication is potentially disastrous. Unfortunately, as a brief review of the reported signs and symptoms indicates, acute torsion mimics more common obstetric problems. Common prompts to surgery are maternal symptoms suggesting bowel obstruction, uterine rupture, obstructed labor or abruptio placentae. Exploration is usually performed to investigate acute maternal distress and a nonreassuring fetal heart-rate pattern, conditions that permit little time for extensive evaluation. For these reasons, the correct diagnosis is rarely established before laparotomy.

Treatment

Given the unique circumstances, establishing standard guidelines for management at the time of surgical exploration is impossible. However, several management points should be considered. At exploration, any contributing pathology of the uterus or adnexa is removed, if possible. Whether the pregnancy should continue is unclear and depends upon the gestational age and the clinical setting. The risk of repeat torsion or other potentially serious complications is simply not known. Also uncertain are whether any procedures should be performed to fix the uterus in its usual anatomic position at the time of surgery and, if so, which procedure to attempt.

In general, treatment of torsion depends on the gestational age. When torsion is discovered during exploratory surgery before the period of presumed fetal survival (ie, before 23-24 wk), promptly returning the uterus to the normal position is the principal therapy. In the various clinical case reports, especially if the uterus was not emptied, plication of the round ligaments was commonly performed. While no systemic studies have been conducted, during the operation, a uterus-stabilizing procedure should be considered to offset the recurrence of torsion. If the pregnancy continues, steroids should be administered after the 24th or 25th week.

When the fetus is beyond the 34th week at the time of diagnosis, the best approach is cesarean delivery at the time of the original laparotomy procedure. In the interval between the limit of fetal viability at 23-24 weeks and the 34th week, or in the rare instance when the diagnosis is established by means MRI or other study before laparotomy, ideal management is not established. Here, care must again be individualized to balance the unknown risk of recurrence or a maternal and/or fetal complication against the immediate risk of prematurity.

In several reported cases of torsion, the degree of rotation was so severe that detorsion was not possible and the hysterotomy incision made at the time of cesarean delivery could only be performed on the posterior uterine wall. Some surgeons described these posterior incisions as inadvertent, whereas others deliberately performed them when efforts to rotate the uterus to its normal position proved unsuccessful. A number of case reports relate that the uterus could not be rotated into the normal position until it was emptied.

Too few reports are available to permit accurate assessment of the long-term sequelae of delivery through a posterior hysterotomy incision. It seems reasonable to first attempt to rotate the uterus into the normal position. If detorsion is impossible, the posterior surgical approach is used. A transverse incision is best; it is curved upward in a manner mimicking that of the usual anterior-wall procedure.

As noted earlier, in a number of case reports of torsion, prophylactic plication of the round ligaments by various techniques was performed after delivery of the fetus. The intent is stabilizing the uterus to prevent the recurrence of torsion in the puerperium. The effectiveness of this treatment is unknown. In the unique situation of detorsion when the uterus is not emptied, the benefit of placation is not established. In the latter setting, as round ligament procedures are probably risk free and may be of some benefit, they are recommended.

In summary, if uterine torsion is discovered during laparotomy, the surgeon should initially search for a pathologic process responsible for the malrotation (eg, uterine distortion due to leiomyomas). If delivery is required, the type of myometrial incision should be individualized. A posterior-wall hysterotomy might be required. An elective uterine fixation procedure may be performed after the baby is delivered and probably should be performed if delivery is not accomplished at the time of the original exploration.

Comments

Abruptio placentae

While infrequent, abruptio placentae is associated with acute torsion. In theory, direct compression of the uterine veins, and perhaps the ovarian veins, due to the rotation of the uterus increases vascular pressure with the placental cotyledons. This effect predisposes to placental separation. Whether this mechanism is correct is speculative. Regardless of the exact pathophysiology, there is a clear the association between abruptio and episodes of acute torsion.

Timing of diagnosis and maternal/fetal risk

Because potentially serious sequelae are possible, establishing the correct diagnosis of uterine torsion early, before complications ensue, is the challenge for clinicians. In his literature review, Jensen reported 19 maternal losses from torsion. He identified as important risk factors the degree of torsion (>180º) and the period of gestation (>20 wk).¹ The same risk factors were also identified by Piot.² These data, limited as they have been derived over many years, provide a rough indication of the high-risk cases. While maternal mortality from this condition is now rare in modern practice, Guie has reported a case ending in maternal death, reminding clinicians of the potential risk.³

When one considers these data, one must remember that the statistics were derived by the compilation of case reports transpiring over years at many different institutions. Therefore, these reported risks are almost certainly not representative of maternal risks in modern, fully equipped hospitals with current diagnostic equipment. Nonetheless, these data are a reminder that serious sequelae of torsion are possible, especially when diagnosis is delayed.

Documentation and counseling

In many if not most cases, patient counseling is, by necessity, retrospective. Because of the potential for complications and because the diagnosis is usually not established until an emergency surgical exploration is performed, full documentation in the medical record is mandatory. The patient's chart should reflect the steps taken during evaluation and diagnosis, as well as the basis for intraoperative decisions concerning the fate of both the pregnancy and the uterus.

Uterine Herniation

Frequency

Herniation of the uterus through an abdominal wall defect (also known as incisional hernia or umbilical hernia of pregnancy) is, at best, an uncommon condition. According to Saha, fewer than 20 cases have been reported in the medical literature.⁴ Most often, anterior uterine herniation develops when there is a prior abdominal wall defect, usually from prior surgery. Most cases have been reported from the nonindustralized world.

Presentation

The clinical presentation is striking. Usually during the midtrimester, the uterus prolapses into the hernia sac via anterior anteflexion.⁵ The protrusion of the abdomen is remarkable. Necrosis or ulceration of overlying skin is also possible.

Pathophysiology

Marked attenuation of the abdominal wall with diastasis recti and weakening of the fascia permit the uterus to deviate anteriorly and pass into the hernial sac. Varying degrees of this condition exist. In the most extreme cases, the fundus of the uterus passes through the rectus muscles and entirely outside of the abdominal wall resulting in a mass (uterus, peritoneum, skin) that extends at virtually a right angle from the maternal abdomen. There is normally a history of prior abdominal surgery or cesarean delivery via a midline incision or a prior, unrepaired umbilical hernia.
 
A number of potentially serious complications including spontaneous abortion, strangulation/incarceration, abruptio placentae, uterine rupture, and intrauterine death have been reported in association with these hernias. The constant pressure of the uterus against the hernia sac may also result in ulceration of the overlying skin.

Diagnosis

The diagnosis is confirmed by a combination of simple palpation and real time ultrasound scanning.

Treatment

As noted, both incarceration and serious complications are possible with this disorder. If possible, the uterus should be reduced through the hernia. In advanced cases, replacement may prove impossible. As the condition is so rare, treatment must be individualized. Activity restriction, abdominal binding, and close observation are the mainstays of management.

Herniorrhaphy has been performed during pregnancy but definitive repair of the abdominal wall defect is normally conducted only following delivery. The abdominal wall is often so attenuated that extensive repair with a permanent mesh is required.   

Uterine Inversion

Frequency

Postpartum partial or complete uterine inversion is an uncommon but potentially life-threatening obstetric complication.

Uterine inversion may occur in the immediate postpartum period or, less frequently, during the puerperium. Inversions are usually described as recent/acute (<30 d after delivery) or chronic (>30 d after delivery). Within the category of recent inversion, a distinction is made between acute and subacute varieties. Acute inversions occur within the first 24 hours after delivery, whereas inversions occurring more than 24 hours after delivery but before the 30th postpartum day are termed subacute.

Uterine inversion is reported to occur at a rate of 1 case per 2000-23,000 deliveries. This wide range reflects differences in recording methods in patient populations and perhaps in routine obstetric techniques. As examples of recent literature, in the 24-year series reported by Baskett involving 125,081 deliveries, the incidence was 1 in 3737 for vaginal deliveries and 1 in 1860 for cesarean deliveries.⁶ In the series described by Hussain et al⁷ and Shah-Hosseini⁸ et al, puerperal inversions occurred in 1 in 1584 and 1 in 4345 deliveries, respectively, while Abouleish⁹ reported an incidence of 1 in 3643. This condition, while uncommon, is far from rare.

So few reports describe gynecologic inversion that its incidence cannot be estimated accurately. Rare nonobstetric inversion usually occurs due to prolapsing uterine tumors.

Pathophysiology

The pathophysiology of puerperal inversion requires that a portion of the otherwise normal uterine fundus indents toward or prolapses through the dilated cervix after the baby is delivered. To initiate an inversion, relaxation of the lower uterine segment must combine with the simultaneous downward movement of the fundus. To completely invert the uterus, this process must be accompanied by uterine contractions occurring at precisely the right moment and of sufficient force to drive the prolapsing fundus through the patulous exocervix.

Terminology for the severity of an inversion is based on 2 clinical features: (1) the extent of prolapse in relation to the cervix and (2) how far down the birth canal the resultant mass extends (see Table 2).

Table 2. Degrees of Uterine Inversion

Open table in new window

• Idiopathic factors
• Excessive cord traction or a short umbilical cord
• Intrapartum fundal pressure (Credé maneuver)
• Placenta accreta, increta, or percreta
• Fundal implantation of the placenta
• Chronic endometritis
• Fetal macrosomia
• Trials of vaginal birth after cesarean delivery (VBAC)
• Myometrial weakness or uterine sacculation
• Precipitate labor
• Acute tocolysis with nitroglycerin or other potent tocolytic drugs
• Cesarean delivery

The principal factors that predispose to puerperal inversion are a fundally implanted placenta, flaccidity of the myometrium around the implantation site, and a dilated cervix. In some cases, the presence of a short cord and/or mismanagement of the third stage with imprudent cord traction undoubtedly contribute to inversion. However, the classic claim of meddlesome midwifery as the cause of inversion is insufficient to explain all reported cases, and it may not be a factor in most. Some inversions have occurred without cord traction and may even occur at cesarean delivery via the myometrial incision after the neonate is born but before the placenta is removed. This process has once surprised the author. Postpartum uterine flaccidity, fundal placental implantation, and some degree of cord traction are ubiquitous. However, inversion is so infrequent a complication that a number of otherwise common factors must act in concert to permit it to occur.

Clinical presentation

The diagnosis of uterine inversion is established clinically, except in rare cases. Classic observations include early-onset postpartum hemorrhage and the sudden appearance of a vaginal mass followed by various degrees of maternal cardiovascular collapse. Postpartum hemorrhage is usually the most striking symptom and initially commands the clinician's attention.

In the classic case, the initial, dramatic event is the sudden and disconcerting protrusion of a large, dark-red, polypoid mass through the vagina either accompanying or immediately following the delivery of the placenta. The characteristic appearance of the inverted uterus protruding externally is both surprising and startling and immediately establishes the correct diagnosis. In approximately 60-70% of cases, the placenta remains attached (at least initially) at the moment of inversion.

In about half of all complete inversions, some degree of acute maternal cardiovascular decompensation occurs. As a general rule, the extent of the observed bleeding varies depending on the degree of prolapse. A characteristic comment in case reports is that the extent of shock is more than that attributable to the observed blood loss alone.

One theory to explain this observation is that stretching of the broad ligament or compression of the ovaries as they are drawn together results in a parasympathetic reflex, which contributes to the acute symptoms (neurogenic shock). However, estimated blood losses at the time of delivery or of any obstetric hemorrhage are notoriously inexact. Moreover, a clinician's retrospective estimate of the true blood loss may be far from accurate. Therefore, the apparently sudden and often unanticipated shock may be simply an artifact of observation and inaccurate estimation of the actual volume of the hemorrhage.

Whatever the mechanism, ie, simple blood loss, neurogenic reflex, or a combination thereof, prompt uterine replacement combined with vigorous fluid resuscitation including blood transfusion as required, reverses the hypotension.

With partial inversions, the findings from manual examination are unique. Initial findings from physical examination can easily mislead the clinician to believe that a uterine or pelvic tumor is present. In terms of the anatomy, the adnexa are compressed together in the midline along with the partially inverted fundus, which is itself entrapped in the lower segment of the uterus. On abdominopelvic examination, this globular and somewhat irregular, central pelvic mass approximates the size of a 22- to 24-week pregnancy. Several findings from clinical examination assist in making the correct diagnosis.

In the incomplete type, the inversion remains in the vagina, with the fundus only partially inverted but having passed through the cervix. In this circumstance, the most obvious diagnostic clue is the clinician's inability to palpate the uterine fundus during abdominal palpation or the inability to visualize or palpate the cervix during pelvic examination.

Unfortunately, inability to locate the cervix can have other causes. In simple severe atony, heavy bleeding may preclude observation of the cervix, and the uterus may be so flaccid that it is difficult to palpate, especially if the mother is obese. Therefore, neither nonvisualization of the cervix nor inability to palpate the uterine fundus is a pathognomonic sign of inversion.

If the inversion is retained entirely within the uterus and if it has not passed through the cervix into the birth canal, establishing the correct diagnosis is even more difficult. Although hemorrhage may be present, the cervix is palpable and it usually can be visualized. Fortunately, such partial inversions are very uncommon. Even in this situation, findings from abdominal palpation are strikingly atypical, and the correct diagnosis is easily and rapidly established by means of bedside real-time sonographic examination.

Due to the potential complexities of presentation, prompt ultrasonographic scanning is the most helpful technique in uncertain cases. If accompanying hemorrhage or shock is sufficiently alarming to prompt immediate surgical exploration, the correct diagnosis may be established only at laparotomy.

Chronic uterine inversion

Chronic inversion is unusual. The literature reports cases discovered as late as 14 weeks' postpartum. This condition manifests with a variety of vague symptoms, including persistent vaginal bleeding or discharge, as well as symptoms of low back pain or pelvic pressure. Such symptoms may also be accompanied by malaise or low-grade temperature elevation. At least once case was complicated by a mesenteric vein thrombosis.¹⁰ Again, the pathophysiology is not understood. This diagnosis is difficult to establish on clinical grounds alone. Here again, real-time ultrasonography is especially helpful. Most of these late cases will require surgical procedures for replacement.

Diagnosis

The following entities are included in the differential diagnosis of uterine inversion:

• Prolapse of a uterine tumor or a large cervical polyp
• Passage of previously unsuspected secundines or a succenturiate lobe
• Gestational trophoblastic disease
• Foreign body in the vagina
• Occult laceration of the genital tract
• Severe uterine atony
• Unanticipated delivery of a second twin
• Uterine rupture

In the unusual case in which the correct diagnosis is not apparent on direct observation or after bimanual examination, real-time ultrasonography is performed. In cases of inversion, a normal uterine fundus is not visualized on longitudinal midline scans. Findings that strongly suggest the correct diagnosis include a large, homogeneous mass apparently contiguous with the uterus; the inability to identify a normal appearing fundus; and a peculiar, globular uterine contour.

Treatment

• Summon nursing assistance and another surgeon.
• Begin fluid resuscitation with 2 large-bore intravenous lines. Promptly administer 1 L or more of an isotonic salt solution (Ringer's lactate).
• Submit specimens to the laboratory to prepare for possible transfusion of blood or blood products. Also send samples to determine baseline values of the following:
  • Hemoglobin concentration
  • Hematocrit
  • Coagulation factors (eg, prothrombin time, activated partial thromboplastin and time, level of fibrinogen)
• Insert a Foley catheter.
• Immediately summon an anesthesiologist.

Treat aggressively

• Administer oxygen.
• Order the appropriate surgical equipment, and instruct assistants to prepare the operating room for possible laparotomy.
• Once in the operating room, administer tocolytics to promote uterine relaxation. These drugs may include one of following:
  • Nitroglycerin 0.250-0.500 mg given intravenously over 1-2 minutes (preferred)
  • Terbutaline 0.100-0.250 mg given slowly intravenously
  • Magnesium sulfate 4-6 g administered intravenously over 20 minutes (less effective and not recommended as initial treatment)
• Attempt prompt replacement of the uterus.
  • Begin with a trial of manual replacement per vagina. Conducted with adequate uterine relaxation, this maneuver is highly likely to be successful.
  • If manual replacement fails, promptly perform laparotomy to achieve surgical replacement unless the clinician is trained in one of the vaginal surgical approaches. During laparotomy, general anesthesia with a uterine-relaxing agent is best, especially if a parenteral tocolytic was not previously given or if it appears to have failed.

Repair

• Manually replace uterus (techniques discussed below).
• Suture lacerations of the birth canal and any surgical incisions in the cervix or vagina.
• Perform uterine massage after replacement of the uterus.
• Administer uterotonics. These drugs may include one of the following:
  • Methylergonovine maleate (Methergine; Novartis Pharmaceuticals Corporation, East Hanover, NJ) 0.2 mg given intramuscularly every 30 minutes for up to 3 times, as needed
  • Oxytocin 40-60 IU/L in an isotonic, balanced salt solution (eg, Ringer lactate) given as a constant infusion
  • Prostaglandin 15-methyl F2alpha (carboprost tromethamine, Hemabate; Pharmacia & Upjohn Company, Division of Pfizer, New York, NY) 0.25 mg given intramuscularly every 30 minutes up to 3 times, as needed
  • Misoprostol 0.4 mg orally or buccally every 2 hours as needed, or, as an alternative, 0.8-1.0 mg per rectum given once
• Closely monitor the patient for several hours after the uterus is replaced to detect spontaneous reinversion.

The best technique for rapid uterine replacement is controversial. In theory, manipulating the genital organs and restretching the pelvic viscera in the presence of some degree of neurologic shock could potentiate shock. As a practical matter, however this risk is inconsequential. Long clinical experience indicates that the best management is always rapid manual replacement, preferably by vagina manipulation. The longer the delay, the greater the risk for blood loss and maternal cardiovascular collapse and its serious sequelae. Also, as the delay lengthens, the lower uterine segment and/or cervix increasingly contracts, rendering the prolapsed fundus more edematous than before. Thus, delay simply makes replacement progressively more difficult.

Because most deliveries now take place in labor rooms, this site is probably the most frequent venue for trials of immediate replacement if the placenta has separated. However, depending on the circumstances and on whether the placenta remains attached, a reasonable delay may be prudent. During this time, help is recruited (eg, from an anesthesiologist, nurses, assistants), laboratory tests are ordered, assistance from the blood bank is ensured, aggressive fluid resuscitation is started, and the parturient is transported to an operating room. There, the uterine inversion may be reduced by means of the traditional vaginal approach or a surgical procedure, as described later.

Nonsurgical replacement techniques

Once the correct diagnosis is made, the surgeon should act with celerity. Uterine replacement may be surprisingly easy when performed early, and the resort to the various complex manipulations to return the uterus to its correct anatomic position may be avoided. As discussed below, a potential exception to this rule of immediate action is the case of inversion when the placenta remains attached to the uterus.

In 1945, O'Sullivan described a method for correcting partial inversion by using simple hydrostatic pressure. In this technique, warm sterile water or isotonic sodium chloride solution is rapidly instilled into the vagina through a tube while the introitus is blocked with either an instrument (eg, vacuum extractor) or the obstetrician's forearm or fist. The instilled fluid progressively distends the vaginal wall and forces the fundus upward to restore it to its original position. Some clinicians favor a trial of this procedure in selected patients because of its simplicity, but it is not a popular method.

With the advent of potent tocolytics, the technique of manual replacement has been greatly simplified and a variant of the manipulations Johnson originally described in 1949 is currently the treatment of choice. In this procedure, after the administration of the tocolytic and an analgesic, the operator's hand is placed in the vagina, with the palm cupping the inverted fundus. The uterus is then firmly and promptly lifted upward in the pelvic curve through the pelvis and into the abdominal cavity to the level of the umbilicus. This manipulation forces the uterine ligaments to stretch. When the inverted mass is pushed upward, the uterus typically reverts promptly, and the fundus returns to its anatomic position. If reversion is successful, the uterus is held in place for several minutes. Parenteral uterotonics are then administered to firm the myometrium (see Media file 3).

To facilitate uterine replacement, terbutaline, nitroglycerin, and, less frequently, magnesium sulfate have been successfully used as uterine relaxants with or without concomitant general anesthesia. In the period immediately following successful replacement, doses of uterotonics are serially administered to prevent reinversion, offset secondary atony, and control hemorrhage.

If the placenta has not separated before the replacement operation is attempted, the most prudent approach is to leave it undisturbed until the patient is in the operating room and an anesthetic or tocolytic is given. Immediate removal of the placenta without successful uterine replacement simply increases blood loss. Furthermore, in the uncommon event of placenta accreta, placenta increta, or placenta percreta, removal proves either difficult or impossible. In this setting, efforts at removal markedly increase blood loss and wastes valuable time.

Unfortunately, the degree of abnormal placental adherence cannot be established until removal is attempted, and then it is too late to avoid a sudden and severe hemorrhage. Therefore, if inversion occurs and the placenta is still attached, the best plan is to wait for the relatively safe environment of the operating room rather than attempt an immediate and perhaps incomplete placental removal in an ill-equipped setting. Exceptions to this general rule exist in clinical settings when access to equipment or surgical assistance is limited.

Surgical techniques

If 2 or more attempts at manual replacement are unsuccessful despite adequate tocolysis and analgesia, a surgical procedure is indicated. An abdominal approach for uterine replacement is favored. A vaginal technique has also been described, but it has few adherents.

In the vaginal procedure, the bladder is dissected from the cervix, and the anterior lip of the cervix and the anterior wall of the uterus are incised to the extent necessary to permit replacement. After the uterus is repositioned, the uterine wall and cervical defects are repaired in layers. Such transvaginal procedures are specifically not recommended except when done by especially trained surgeons or by those working under the immediate supervision of a properly experienced surgeon.

The favored transabdominal technique is a modification of the procedure Huntington originally described in 1921. Deep general anesthesia is first induced with an agent that promotes uterine relaxation. Laparotomy is performed. The inversion site is marked by the peculiar sight of the round ligaments passing down into the pelvis at the anatomic site normally occupied by the uterus.

To perform inversion, the surgeon grasps the round ligaments with atraumatic clamps (eg, Babcock clamp) and applies gentle upward traction. The operator pulls the round ligament up into the peritoneal cavity, and, as the ligament advances, it is immediately grasped more distally with a second clamp. This process is akin to pulling on a rope, hand over hand. This maneuver is repeated alternatively on one side and the other until the fundus is completely restored to it normal configuration.

If available, a second operator facilitates the procedure by applying upward pressure from below. As the uterus begins to revert, the lower segment can be squeezed like a tube of toothpaste to accelerate the process. As in the manual replacement technique, uterotonics are administered as soon as the uterus has returned to its normal shape.

In the unusual instance that the Huntington operation is unsuccessful, the more extensive Haultain procedure is required. This is usually necessary only when inversion is chronic or when tocolysis fails to adequately relax the lower segment. With this technique, a posterior longitudinal hysterotomy incision is performed. This widens the lower uterine segment and facilitates replacement of the uterus. The posterior uterine wall is incised to avoid inadvertent injury to the bladder that might occur with an anterior approach. Thereafter, upward traction is applied to the round ligaments, as in the Huntington procedure, until the uterus resumes its normal position. The myometrial defect is then repaired in layers. Once the uterus has been replaced, the placenta is removed. If an accreta or one of the more severe forms of placental adherence is present, the best approach is hysterectomy.

Regardless of the procedure used, immediate uterine atony is common after repositioning, and prompt reinversion may occur. Close observation for this complication is mandatory. Also recommended is the administration of 15-methyl F2alpha prostaglandin (Hemabate; Pharmacia & Upjohn Company), high-dose oxytocin, parenteral methylergonovine maleate (Methergine; Novartis Pharmaceuticals Corporation), or misoprostol per rectum. If magnesium sulfate was administered as a tocolytic, calcium can be administered parenterally to reverse the tocolytic effect.

The administration of antibiotics has been advocated when inversion occurs. This guidance is based on the theory that the various manipulations for replacement predispose the patient to develop an infection. The risk is probably small, but it is unknown. Many clinicians administer prophylactic doses of a broad-spectrum, first-generation cephalosporin or a similar drug after repositioning. No data concerning the need for such treatment are available. The decision to treat this condition or not is left to the discretion of the senior surgeon.

Comments

A chance observation in mice by Yokoi and coworkers hints at the possibility of a genetic propensity for inversion that might have implications for human medicine. In specially bred mice, females homozygous for a gene locus that codes for deficiencies in melanocytes, mast cells, and osteoclasts had a remarkably high incidence of postpartum uterine inversion (86%). In some of these mice, the uterus was inverted with the placenta still implanted.¹²

After a series of subsequent cross-mating studies, the maternal genotype (not that of either the father or the fetus) was determined to be the important component in coding for this inversion risk. The results of this unusual experiment hinted that specific genes code for abnormal uterine tone during the immediate puerperium. Thus, an apparent functional disorder of the myometrium predisposes the individual rodents to develop puerperal inversion by means of an unknown mechanism. These data open genetic predisposition as a new area for future investigation.

Uterine Prolapse

Frequency

Uterine prolapse during gestation is an infrequent clinical problem, though moderate degrees of descensus are common before pregnancy, especially in multiparas. If not severe, pregnancy-associated prolapse often partially or completely resolves in the midtrimester as the fundus grows and the uterus becomes an abdominal organ, drawing the cervix upward. In such cases, symptomatic prolapse usually recurs in the third trimester, or, on occasion, it is first observed at this time.

The incidence of prolapse during pregnancy is not accurately known. Only case reports are available in the literature. All reviewers concur that this is a highly uncommon, if not rare, condition in the United States. More cases occur in obstetric practice in the developing world, where advanced multiparity and obstetric injuries are relatively common. However, no firm data are available for review. By contrast, in gynecologic practice, prolapse is a common condition, especially among multiparous menopausal women.

Pathophysiology

The female pelvic viscera are best considered to be suspended from above and supported from below. To maintain the pelvic organs in their proper position, their suspensory and support structures must remain intact and interact. This joint function depends on the integrity of the muscular, fascial, and neurologic components of these various tissues. Substantial injury to one or more of these systems can result in a loss of support and result in a degree of prolapse that may prove permanent.

A complex of musculoconnective tissue forms a web of support for the pelvic organs. The upper suspensory structures for the uterus are a complex of pseudoligamentous tissues that are traditionally and loosely termed the pelvic ligaments. These sheets of connective tissue accompany vascular structures into the pelvis and surround the cervix and other pelvic structures. Included among these suspensory connective tissues are the pubovesical, cardinal, and uterosacral ligaments. The lower supports for the uterus are musculofascial structures, including the urogenital diaphragm and the pelvic diaphragm, which principally consists of the levator ani muscle and its divisions. The urogenital diaphragm is a complex of muscular structures and accompanying connective tissue that radially extends from the central perineal body to attach to various bony and ligamentous sites in the pelvis.

Conditions that result in both reversible and permanent injuries to the maternal pelvic supports include dystocia in labor, vaginal delivery, obstetric lacerations, multiparity, age, genetic propensity, and, perhaps, the mode of delivery. Passage of the baby through the birth canal produces most of the damage. Descent of the presenting part elongates the levator ani muscle complex by up to 50% and traumatizes the pelvic nerves by stretch and direct pressure. Various spontaneous lacerations or episiotomy extensions account for additional injuries to perineal structures. Thus, important pelvic connective tissues are often simply torn, lacerated, denervated, or otherwise disrupted by the process of parturition.

The issue is not whether vaginal delivery results in injuries to the pelvic support tissues. The question is the degree of the injury and the extent to which spontaneous postpartum healing or specific muscle-strengthening exercises performed in the puerperium may ameliorate this damage.

The etiology of uterine prolapse during pregnancy is multifactorial. It requires a combination of previous traumatic injuries to the upper fascial suspensory system, damage to the muscular supporting structures of the pelvic diaphragm, and a degree of neurogenic myopathy or nerve injury at various levels, likely in combination with overstretching or laceration of the musculoconnective tissues of the pelvic floor.

Although multiparity, dystocia, instrumental delivery, and lacerations of the birth canal are routine obstetric events, uterine prolapse during pregnancy is notable for its rarity. This observation indicates that some combination of pregravid structural injury to the support and suspension system, constitutional or hereditary weaknesses in the connective tissues, and the pressure and hormonal effects of an established pregnancy must occur to result in this uncommon complication.

Clinical presentation

Signs and symptoms associated with uterine prolapse may include the following:

• Pelvic pressure or discomfort
• Lower back pain
• Urinary tract infection
• Paradoxical urinary tract symptoms (eg, acute retention, incontinence)
• Preterm membrane rupture
• Preterm labor
• Cervicitis, vaginitis, vaginal discharge
• Bleeding due to mucosal ulcerations or cervicitis
• Vaginal or perineal mass
• Constipation

Diagnosis

Establishing the diagnosis is not a challenge. On examination, the clinician observes unusual cervical descent, accompanied by variable protrusion of the anterior and posterior vaginal walls. In advanced cases, inflammation of the cervix, and occasionally even ulceration of the vaginal mucosa, is present. Protrusion of the cervix is partially ameliorated when the gravida assumes a horizontal position.

Uterine distortion due to tumors such as large leiomyomas or other masses, prolapse of a cervical or endocervical tumor, or a müllerian anomaly must be considered in the differential diagnosis.

Results from physical examination and ultrasonographic study should promptly establish the correct diagnosis.

Treatment

Aspects of treatment are as follows:

• Restrict activity.
• Aggressively treat cervicitis or soft tissue erosions of the birth canal.
• Conduct a trial of a pessary.
• Treat associated urinary tract infections.
• Determine the fetal fibronectin value.
• Administer corticosteroids to enhance fetal pulmonic maturity.
• Serially assess fetal growth, and sonographically verify normality of fetal anatomy.
• If appropriate, conduct ultrasound. 

Although treatment with a pessary may be successful early in gestation, it usually fails by the onset of the third trimester. Thereafter, restriction of activity becomes the principal means of management, along with symptomatic treatment for cervicitis or urinary tract infection and close clinical observation for obstetric complications. Close clinical observation of patients in this situation is mandatory.

Prolapse is uncommon, but an unfortunate and all-too-common associated problem is the high incidence of obstetric complications. These are principally complications related to premature rupture of the membranes, preterm labor, and, eventually, preterm delivery.

The appropriate postpartum recommendation is unclear. A pessary may be tried. Patient counseling, interim contraception, sterilization, and hysterectomy with vault suspension are to be considered. Successful pregnancies after mesh-supported uterine suspensions have been reported, but the numbers are few.

Comments

Serious complications

A number of serious complications are reported in association with prolapse during pregnancy. However, the number of cases is small, and they do not represent the entire population of women with this disorder. After pregnancy ends, symptomatic prolapse may confidently be anticipated to recur in these women. Again, firm data on this point are not available.

Among nonpregnant women, hysterectomy with vault suspension is usually required to definitively repair advanced degrees of prolapse. The necessary procedure depends on the severity of the problem and on the individual's pelvic anatomy.

Possibility of vaginal delivery

A surprising observation is that vaginal delivery is often possible in cases of pregnancy-related prolapse. However, a word of caution is appropriate. A possible vaginal trial must be reevaluated if severe cervicitis or edema is present, especially when insufficient time remains to permit adequate antepartum treatment.

Cervical inflammation and its treatment

Cervical inflammation is an invariable finding. The biochemical effects of infection and the resultant inflammatory response are possibly etiologic in the oft-reported complications of membrane rupture and preterm labor. Prompt and adequate treatment of cervicitis and close attention to any concomitant urinary tract infection are prudent. However, treatment of these infections does not necessarily reduce the risk of premature rupture of membranes or preterm labor.

In the common condition of midtrimester bacterial vaginosis and cervicitis, antibiotic therapy has minimal effect on preventing prematurity or early membrane rupture. By the time the severe inflammation that characterizes a prolapsed cervix during pregnancy develops, the various promoters of early inappropriate uterine activity may already been elaborated. If so, they render antibiotic therapy ineffectual in the prevention of prematurity.

Other management steps may be taken. Testing for fetal fibronectin helps in estimating the risk of early delivery, which can alert both the patient and the clinician that the immediate risk of preterm delivery is increased. If prolapse is diagnosed after the 24th week and before the 33rd week, steroid treatment to enhance fetal lung maturity should also be considered.

Other than use of a pessary, treatment of cervicitis or urinary tract infection, and activity restriction, a possible future treatment for pregnant women with prolapse might be the parenteral or intravaginal administration of progesterone.

Data indicate that prophylactic progesterone therapy reduces the incidence of preterm labor. Once labor ensues, this treatment is ineffective. Therefore, patients at risk must be identified, and therapy should be started before the signs and symptoms of labor begin. At present, no data address the effectiveness of progesterone therapy in pregnant women with uterine prolapse and cervicitis. An absence of effect might be anticipated; the chronic cervical infection may render a progesterone block ineffective.

Multimedia

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Media file 1: Uterine retroversion and incarceration progressing to sacculation as pregnancy advances.

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Media file 2: Uterine retroversion-incarceration has occurred. Depicted is the technique of manual uterine replacement with the patient in the knee-chest position.

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Media file 3: Uterine inversion. Image depicts the technique of manual replacement. Note the potential incision of the posterior uterine wall if surgical replacement is required.

Keywords

malpositioning of the uterus, uterine malposition, uterine retroversion, retroflexed uterus, uterine incarceration, uterine prolapse, uterine torsion, puerperal uterine inversion, inverted uterus, postpartum hemorrhage, pelvic adhesions, endometriosis, ovarian cancer, ovarian cysts, leiomyomas, uterine leiomyoma (fibroid), uterine tumors, ovarian tumors, pelvic congestion syndrome, PCS, Taylor syndrome

Allen-Masters syndrome, AMS, mullerian anomalies, müllerian anomaly, mullerian duct abnormalities, chronic pelvic pain, pelvic discomfort, pelvic pressure, female reproductive tract, chronic salpingitis, adnexal tumors, disturbances in menstruation, dyspareunia, infertility, spontaneous abortion, constipation, urinary difficulty, urinary retention, pelvic inflammatory disease

The authors and editors of eMedicine are pleased to note the contributions of previous authors Christian S Pope, DO, and Zaya Darouian in the development and writing of the original article. The intense effort of Carolyn J Taugher in the preparation of the current revision is also gratefully acknowledged.

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