Posterior vaginal wall prolapse is one of the most common prolapses encountered by gynecological surgeons. What appears to be a straightforward condition to diagnose and treat surgically for physicians has proven to be frustratingly unpredictable with regard to symptom relief for patients. Functional disorders such as dyssynergic defecation and constipation are often attributed to posterior vaginal wall prolapse. Little scientific evidence supports this assumption, emphasizing that structure and function are not synonymous when treating posterior vaginal wall prolapse. Rectoceles, enteroceles, sigmoidoceles, peritoneoceles, rectal and intraanal intussusception, rectal prolapse, and descending perineal syndrome are all conditions that have an impact on the posterior vaginal wall. All too often these different anatomic conditions are treated with the same surgical approach, addressing a posterior vaginal wall bulge with a traditional posterior colporrhaphy. Studies that examine the correlation between stage of posterior wall prolapse and patient symptoms have failed to reliably do so. Surgical outcomes measured by prolapse staging appear successful, yet patient expectations are often not met. As increasing attention is being placed on patient satisfaction outcomes concerning surgical treatments, this fact will need to be addressed. Surgeons will have to clearly communicate what can and what cannot be expected with surgical repair of posterior vaginal wall prolapse.
Mrs Jones is referred for correction of her rectocele by her primary care physician. She is a 53 year old with a history of total vaginal hysterectomy in the remote past for menorrhagia. She reports increasing bowel symptoms for the last 10 years, stating she has irritable bowel, constipation predominant. She answers moderately to quite a bit to all questions on the Colorectal-Anal Distress Inventory-8 and Colorectal-Anal Impact bowel questionnaires. She has a body mass index of 33 kg/m 2 and has diabetes mellitus controlled with oral medications, has hypertension controlled on metoprolol, and takes an anticholinergic for a nervous bladder.
On physical examination, her Pelvic Organ Prolapse Quantification System (POPQ) demonstrates International Continence Society stage III posterior wall prolapse with Ap and Bp at +2, C = –4 with a total vaginal length of 9, Aa and Ba are –1, genital hiatus is 4, and perineal body is 4. She has an atrophic epithelium and a Brink score of 5. She would like to schedule surgery to fix her problems because she wants to be normal again. She hates feeling bloated, worrying about where a bathroom is, and having to push vaginally to empty her rectum.
Symptoms and initial evaluation of posterior wall prolapse
Reliably attributing definitive symptoms to posterior vaginal wall prolapse has proven difficult, leading to the conclusion that the only consistent symptom with posterior vaginal wall prolapse is its inconsistency. Bulging, pelvic pressure, perineal ballooning, vaginal splinting, perineal splinting, digitation, obstructed defecation syndrome (ODS), dyssynergic defecation, constipation, anismus, tenesmus, bleeding, or dyschezia are symptoms described with posterior compartment defects. Unfortunately, none of these symptoms is unique to a rectocele or cul-de-sac prolapse.
Studies have failed to reliably correlate symptoms with stage of posterior wall prolapse. Using validated bowel questionnaires, Colorectal-Anal Distress Inventory-8 and Colorectal-Anal Impact questionnaire scores did not increase with prolapse stage. This strongly suggests that prolapse alone does not or cannot explain the presence or absence of bowel symptoms. This reaffirms earlier work failing to show correlation between physical exam findings relating to the posterior vaginal wall and patient symptoms. Burrows et al reported on 352 women and failed to show any relationship between the POPQ and bowel symptoms, whereas Fialkow et al demonstrated more bowel symptoms with perineal descent of 2 cm but no difference with POPQ stage. The limitation of our physical examination in predicting symptoms is clear and not reassuring.
Adding physiological testing (anal manometry, pudendal terminal motor latencies, electromyography) to physical examination and imaging in patients, the authors concluded that there is no correlation between posterior vaginal wall prolapse with bowel symptoms or objective measures of anorectal function. The authors studying ODS symptoms and their relationship to rectocele concluded that rectoceles were not associated with increased severity of ODS symptoms, anorectal abnormalities, or pelvic floor dyssynergia. They further suggest that rectoceles may be the result of obstructed defecation rather than the cause. Their only positive finding was of splinting in patients with rectoceles compared with those without, 36.7% vs 0% ( P < .0001).
Splinting or digitation commonly reflects having to press on a bulge to help redirect the stool to the path of least resistance, the anal opening. Although this generally refers to pressing on a vaginal bulge, it has been used freely in the literature and may also include supporting the perineal body, rectal digitation, or pressure to the coccygeal or posterior levator area. Each of these scenarios may have very different clinical implications. Studies have suggested that splinting and feeling of stool trapping (bulge) are the 2 most common symptoms of posterior vaginal wall prolapse. However, this is not a consistent dependable finding when large groups of patients are studied. A weak correlation (r = 0.23) was reported between point Bp and the use of digital assistance, defined as vaginal splinting or rectal digitation/ disimpaction.
Our gastrointestinal colleagues rarely attribute the anatomic findings of rectocele and/or enterocele to their symptomatic patients with constipation or defecatory disorders. They systematically work through constipation algorithms, first addressing medical issues that result in constipation, pharmacological causes, and dietary issues. Functional constipation as defined by the Rome III criteria must meet criteria for the last 3 months with symptom onset at least 6 months prior to diagnosis (see Table ).
| Diagnostic criteria b |
|---|
| 1. Must include 2 or more of the following |
| a. Straining during at least 25% of defecations |
| a. Lumpy or hard stool at least 25% of defecations |
| a. Sensation of incomplete emptying at least 25% of defecations |
| a. Sensation of anorectal obstruction/blockage at least 25% of defecations |
| a. Manual maneuvers to facilitate at least 25% of defecations (digital evacuation or support of the pelvic floor) |
| a. Fewer than 3 defecations per week |
| 2. Loose stool are rarely present without the use of laxatives |
| 3. Insufficient criteria for irritable bowel syndrome |
a Reproduced, with permission, from Bharucha et al.
b Criteria were fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis.
A full review of constipation and its treatment are beyond the scope of this paper, and the reader is referred to the 2013 American Gastroenterological Association guidelines and technical bulletin concerning constipation. Following the initial work up, the American Gastroenterological Association recommends assessment of colonic transit to classify patients into 3 subgroups (slow transit constipation [STC], normal transit constipation, or defecatory disorders). These may exist alone or together. Up to 50% of patients with defecatory disorders also have STC, demonstrating the multidimensional nature of these problems. Functional defecatory disorders are further defined by the Rome III criteria as patients meeting the criteria for constipation plus at least 2 of the following:
- (1)
evidence of impaired evacuation, based on balloon expulsion test or imaging.
- (2)
inappropriate contraction of pelvic floor muscles (ie, anal sphincter or puborectalis) or less than 20% relaxation of basal resting sphincter pressure by manometry, imaging, or electromyography.
- (3)
inadequate propulsive forces assessed by manometry or imaging.
Dyssynergic defecation is one type of functional bowel disorder (number 2 mentioned in the list previously) and can serve as an example of the complexity of these conditions. This is evaluated by manometric testing and further broken down into 4 subtypes based on the propulsive force generated and anal sphincter function.
Surgery for defecatory disorders is considered for anatomic defects only if this evaluation is normal. Surgeons caring for patients with defecatory dysfunction often take the opposite approach. Surgery often becomes the primary treatment if an anatomic defect is present and the gastrointestinal workup is performed only if surgery fails to improve patient symptoms. Randomized studies have been done demonstrating the efficacy of biofeedback therapy in these patients and challenging surgery as a first-line therapy. Hicks et al argues that any patient being considered for surgery for rectocele and symptoms of ODS (including dyssynergic defecation) should first undergo biofeedback due to a 71.1% response rate.
Symptoms of enterocele are even more unreliable because clinicians cannot agree on what an enterocele is. Wexner and colleagues classify enteroceles as primary (mutiparity, advanced age, constipation, obesity, increased intraabdominal pressure) or secondary occurring after surgical procedure, an example being hysterectomy. Nichols describes 4 different types of enterocele (congenital, pulsion, traction, and iatrogenic), whereas others have described a defect in the fascial tissue of the posterior wall that allows direct contact of peritoneum with vaginal epithelium.
Defining it as a cul-de-sac herniation extending down the posterior vaginal wall is incorrect. The cul-de-sac in asymptomatic nulliparas frequently extends more than 5 cm below the posterior fornix. This length plus the length of the dorsal perineal membrane adds up to the total vaginal length. The defect in the posterior wall connective tissue was dispelled in a histological study that failed to demonstrate a fascial vaginal wall layer and secondly found no evidence that cul-de-sac peritoneum came into direct contact with vaginal epithelium.
As with anterior wall prolapse that is almost always associated with apical prolapse, enteroceles are likewise a problem with vaginal apical support and vaginal axis disturbances. With the dysfunctional levators, the required support of the levator plate is no longer present and the vault may take on a more vertical orientation. This allows the cul-de-sac and its contents to come in direct contact with the posterior vaginal wall during increases in intraabdominal pressure.
In addition, perineal descent is associated with overall poor levator function and global pelvic floor descent. As the levator drops, a more vertical vaginal axis is produced, eliminating the flap valve mechanism between the posterior vagina and levator plate. Perineal descent was first reported first by Parks et al in 1966, and the differences between controls and patients can be striking. Clinically this descent is seen as a ballooning perineal body dropping below the ischial tuberosities. Radiologically, perineal descent is described as > 3 cm of movement or located > 3 cm below the ischial tuberosities. Although vaginal axis shifts may happen because of levator dysfunction, the point is also emphasized with performance of surgical procedures that alter the vaginal axis. Burch procedures predispose a patient to developing an enterocele in 13-32% of the cases by shifting the vaginal axis more anteriorly.
Older procedures that used the round ligament to support the uterus had the same effect and eliminated the flap valve mechanism exposing the posterior vaginal wall to intraabdominal forces. Instead of closing the cul-de-sac, it is now open and its contents free to bulge into the posterior vaginal wall. The small bowel is most often involved, but contents may be sigmoid colon, omentum, or a peritoneocele.
Symptoms from an enterocele are nonspecific and depend on the interaction of the prolapse within the pelvis. A small bowel that significantly presses on the anterior rectum may activate rectal wall distension receptors from the outside rather than the inside. The signal to the patient is the same, regardless of how the receptors are stimulated, and rectal distension leads to an urge to defecate. If the rectal distension is due to external pressure from the enterocele, tenesmus may result. The patient strains to empty when there is no stool to be evacuated. This may start the cascade of rectal intussusception, which now further distends the rectum, this time stimulating the rectal distension receptors from the inside. This leads to more urge and over time may lead to overt rectal prolapse as the patient continues to strain to empty stool that is not there. The complexity of these symptoms cannot be explained by physical examination alone, and functional studies may help define the true pathophysiology.
For our patient, symptoms were further clarified and initial therapy begun. Her constipation was addressed with a detailed high-fiber diet and increase in her water intake. She was to start slowly on the fiber working up to the recommended 35 g a day over a period of time. Her bladder was addressed with elimination of bladder irritants, increased water, vaginal estrogen, and pelvic floor strengthening. Her anticholinergic medication was also stopped to eliminate a confounder for constipation. At 6 weeks, she reported improved stool consistency, improved bladder function, and decreased vaginal irritation. However, she still strained at defecation, did not feel like she emptied, and reported needing rectal digitation and vaginal stenting to assist in defecation. Failure to respond to conservative management, the need for rectal digitation, and concern over possible STC resulted in ordering a dynamic cystocolpoproctogram (DCP) and transit study.
Imaging studies
Various imaging studies are available to aid in the diagnosis of pelvic floor disorders and include fluoroscopic defecography or its more thorough variation, dynamic cystocolpoproctography, magnetic resonance imaging (MRI) defecography, and ultrasound defecography. Transit studies can be combined with these.
Functional (dynamic) studies are superior to static studies and allow for complete relaxation of the levator muscles resulting in maximal prolapse. Not routinely obtained, these studies are used when the patient complaints do not agree with the findings on physical examination. These studies provide objective evidence of what may only be inferred and often undiagnosed by physical examination alone. No technique has proven superior to the other; however, cost and patient comfort with upright defecatory sequences may give DCP a slight edge. Enteroceles, sigmoidoceles, rectal intussusception, rectal-anal intussusception, rectal prolapse, and solitary rectal ulcer syndrome are often missed by physical examination alone and functional issues such as dyssynergic defecation or obstructed defecation require a functional evaluation for their diagnosis.
Numerous radiological prolapse classification schemes using different reference points have been proposed. These include the pubococcygeal line (PCL), the midpubic line, the anorectal junction, the H and M lines, and others. Each has its proponents but none have reliably correlated with the POPQ examination, making meaningful communication between clinicians difficult. Each also uses different protocols with regard to organ opacification, type and consistency of contrast and whether there is systematic emptying of the pelvic organs of their contrast.
The last point is a major issue and one often overlooked in these studies. It has to do with the concept of competition for the space. There is a defined area provided by the levator hiatus for prolapse. Clinicians should not be fooled by seeing only the first organ to occupy this space. Often a large rectocele may occupy this space, hiding other prolapse. Once the rectocele is emptied, a large enterocele or other prolapse is often identified. The same is true of other organs and may include the bladder, sigmoid colon, small bowel, or rectum. Whichever organ gets there first, will occupy the space and other prolapse is not identified until that organ is emptied completely ( Figure 1 ).
The functional nature of these studies allows for real-time observation of things like intussusception, and different patterns of organ interaction may be seen. For example, a large enterocele may actually be seen descending and compressing a large rectocele helping it empty. An enterocele may be seen pushing into the anterior rectal wall, starting the process of intussusception.
A classification of enteroceles has been proposed, typing classifying them as type A to C. Type A occurs when the small bowel descends below the PCL with strain but returns above the line after straining with no compression of the rectal ampulla or only compression from above with no obstruction. Type B is diagnosed when the enterocele descends below the PCL with strain through the rectovaginal space and compresses the rectal ampulla at the end of evacuation ( Figure 2 ). Type C is the most significant and occurs with descent of the small bowel below the PCL, extending to the perineal body through the rectovaginal space to compress and rectal ampulla at the beginning of defecation. Although the clinical significance of these different types is still being evaluated, type B was associated with abnormal perineal descent and anterior rectoceles, whereas type C was associated with obstructive defecation. The patient may be able to describe this only as difficulty with evacuation when the pathophysiology of these prolapses is complex and differs.
