dynamic anomaly which may progress to an external rectal prolapse. A HRI may ..... Patton V, Wiklendt L, Arkwright JW, Lubowski DZ, Dinning PG. The effect of ...
A closer look at rectal intussusception and its relationship to fecal incontinence Gosselink MP1 & Joshi HM2 1. Department of Colorectal Surgery, Westmead Hospital, Sydney, New South Wales, Australia. 2. Department of Colorectal Surgery, University College London Hospitals Foundation Trust, London, United Kingdom Faecal incontinence can be a presenting symptom of a large number of conditions. Most patients are well-treated by conservative measures, however if symptoms persist, a trial of sacral neuromodulation seems to be a reasonable first line option for surgical therapy. This innovative technique has evolved to an attractive minimal invasive method for the treatment of faecal incontinence with good long-term results. Initially, it was thought that sacral neuromodulation was only effective in patients with intact external anal sphincter. However, recent evidence suggests that sacral neuromodulation can also be used in patients with external sphincter defect. Long-term efficacy of sacral neuromodulation can be maintained in about half of all patients screened with a Percutaneous Nerve Evaluation test (PNE) test (1). A positive response to the PNE test shows a positive predictive value for a good long-term response to the subsequent permanent implantation implant as high as 80% (2). No demographic or physiological factors have been identified as predictors for successful sacral neuromodulation. A recent study showed that patients with high-grade rectal intussusception (HRI) have lower success rate (69%) of PNE test stimulation than patients without HRI (85%) (3). Furthermore, long-term success of SNS implantation in screened patients without HRI was 52% compared to only 16% in patients with HRI. HRI appears to be one of the contributing factors in the multifactorial origin of faecal incontinence. Recently, Bloemendaal et al. found the presence of HRI in 49% of patients with ultrasound proven intact anal sphincters (4). Moreover, HRI adversely influences the outcome of patients undergoing pelvic floor retraining/biofeedback for faecal incontinence (5). Surgical correction of HRI has been shown to improve faecal incontinence in 56% to 90% of patients (6-8). The relationship between HRI and faecal incontinence is still poorly understood. Hawkins and coauthors showed a linear relationship between worsening symptoms of faecal incontinence and increasing grades of internal rectal prolapse (9). Some studies also revealed worsening of sphincter pressures with increasing grades of internal rectal prolapse, although this may be biased by weakening of the sphincters with age (4,10,11). According to these findings, HRI could be a dynamic anomaly which may progress to an external rectal prolapse. A HRI may cause stretching of the internal anal sphincter and as the prolapse abuts the internal sphincter, it may lead to inappropriate firing of the recto-anal inhibitory reflex, resulting in urge fecal incontinence. This might explain the mechanism and success of rectopexy and needs better evaluation perhaps by prolonged ambulatory manometry rather than the snapshot obtained by standard anorectal physiology. It is well established that an external rectal prolapse is associated with faecal incontinence and surgical treatment of this condition is recommended in most guidelines. There is no definitive evidence that a patient with any degree of rectal intussusceptions will ultimately progress to an external rectal prolapse. Wijffels et al. demonstrated a strong relationship between age and prolapse grade in a cohort of 531 patients, supporting the view of rectal intussusception as a precursor to occult rectal prolapse (12). In this study 148 patients (28%) had an external rectal prolapse. Hotauras et al. found only a weak association between age and prolapse grade in a large
series of 1014 patients (11). Surprisingly, not more than 88 patients (9%) presented with external rectal prolapse in this study. Furthermore, they estimated the progression rate in 36 patients who underwent serial proctograms. Patients with initial low-grade rectal intussusception progressed to HRI in 20% of cases within 2 years, whereas the progression from rectal intussusception to external rectal prolapse was as little as 4%. These rates could potentially increase over a longer time period. However another explanation might be the impact of lifestyle advice by the doctor, such as ceasing to strain and avoidance of hard stool, after the diagnosis of IRP on the further development of the prolapse. An isolated rectal prolapse is extremely rare. It has been demonstrated that most of patients with HRI have other types of pelvic floor prolapse, especially rectoceles in over 70% (13). The symptoms of faecal incontinence might be due to these co-existing prolapses, such as postdefaecatory incontinence because of a rectocele. A randomized trial comparing anterior Delorme’s procedure and rectopexy would elucidate the role of HRI versus rectocele on defaecation disturbances. The prolapse can be the tip of the iceberg, as suggested by Pescatori, necessitating treatment first of the concomitant occult disorders such as psychological distress and anismus (14). One must also consider the implication of continued straining, seen with chronic constipation or anismus, resulting in HRI. An interesting theory, supposed by Pucciani describes the evolutionary progress joining obstructed defaecation to faecal incontinence (15). According to this theory, many years of obstructed defecation may impair the pelvic floor structure, resulting to hypotonia of the pelvic floor and associated pudenal neuropathy, finally causing fecal incontinence. This pathway explains why fecal incontinence is a late sign of internal rectal prolapse. These prior theories suppose that HRI develops because of progressive floor insufficiency. Traditionally, the aetiology of rectal prolapse has been associated with obstetric related trauma resulting in pelvic floor weakness. However, this condition can occur women who never had children, men and even children, suggesting genetic or epigenetic considerations in the development of rectal prolapse. A possible explanation in these groups of patients might be a difference in collagen distribution, elastin metabolism or a connective tissue disorder. An interesting study done by Joshi et al. found a reduction in the amount of Fibulin-5 protein in the extracellular matrix and mRNA by fibroblasts in young males with rectal prolapse compared with age matched controls, but no differences in females (16) . Production of elastin is unique among connective tissue proteins in that elastin biosynthesis is normally limited to augment the pelvis during pregnancy and to facilitate labour. The reason why this pregnancy gene is switched on in men is unknown. The observation that fibulin-5 expression is decreased in young men might explain the significantly higher recurrence rate after prolapse surgery in men compared with women reported in the literature (17,18) There truly is imperfect understanding of the relationship between anatomy and function of the posterior compartment, and how much the symptoms of faecal incontinence can be attributed to the posterior compartment prolapse, especially in patients with intact pelvic floor. It has been suggested that HRI induces a mild or even subclinical inflammation of the mid-lower rectum (4). Solitary rectal ulcers are a known symptom of HRI, leading to pain, tenesmus, incomplete evacuation, mucus discharge, perianal blood loss and faecal incontinence and rectopexy has been shown to benefit patients suffering from a solitary ulcer. One could imagine an inflammatory response to be at least contributory to the symptoms of urge incontinence in HRI; a “prolapse induced proctitis”, even though this hypothesis is not supported by histological evidence. Recently, a study by Kramer et al. showed muscular and neuronal defects in 90% of the rectal specimens in patient with HRI treated by stapled transanal rectal resection (19). They hypothized that HRI
formation initiates a vicious circle of progressive structural damage caused by shearing forces and ischemia, resulting in loss of function. The acquired structural damage leads to impairment of rectal function, which may persist despite operative repair of the HRI. Tsunoda et al. achieved successful anatomical correction in 26 patients with HRI, which was confirmed by postoperative evacuation proctography (20). However, clinical success was achieved in only 67% of patients with faecal incontinence, implying that the successful anatomical correction may not necessarily lead to sufficient improvement for HRI. Although the persistent or recurrent symptoms of faecal incontinence might be due to co-existing pelvic floor disorders, they may also be attributed to progression of the underlying disorder causing physiologic changes that surpass the otherwise effective repair. Mishra and co-authors offered sacral neuromodulation in 52 patients with persistent symptoms of faecal incontinence without recurrent/persistent prolapse after laparoscopic ventral rectopexy. Successful test stimulation was obtained in 94 percent of patients. (21). After a follow-up of 11 months, a reduction in incontinence score of at least 50% was observed in 59% of patients. Although the exact working mechanism of SNS remains unclear, several possible mechanisms such as improved sphincter function, alteration of rectal sensation, modulation of colonic motility by increased retrograde activity, as well as a central cerebral modulation have been proposed (22). Therefore, SNS is likely to modulate all nerve fibres within the sacral plexus including somatic fibres to external anal sphincter and pelvic floor, autonomic fibres to the internal anal sphincter and colon, and afferent sensory fibres from anus and rectum. According to a recent study by Patton et al. sacral neuromodulation causes an increase in retrograde motor patterns in the distal colon (23). These retrograde motor patterns act as a ‘brake’, and their absence or diminished frequency may allow colonic content to move more rapidly into the rectum, resulting in faecal incontinence if weakened pelvic floor muscles are present. This mechanism of action of sacral neuromodulation might be possibly blocked by the presence of high-grade internal rectal prolapse. This might explain the higher success rate on sacral neuromodulation in patients without HRI compared to patients with HRI (3). Therefore it might be worthwhile correcting rectal abnormalities first before proceeding to sacral neuromodulation rather than performing sacral nerve neuromodulation as the first line of treatment in this group of patients. What our editorial reiterates is the complexity of faecal incontinence treatment. No present therapy for faecal incontinence has perfect results however it appears conclusive that HRI has some role in the development of faecal incontinence. Diagnostic workup of faecal incontinence should include thorough evaluation of anatomy, with imaging of the defecation process to evaluate underlying aberrant anatomy, including HRI. The most appropriate surgical approach for HRI is still controversial. Correcting anatomy by for example laparoscopic ventral rectopexy, might be not enough. Treatment of occult concomitant pelvic floor disorders, subsequent sacral nerve stimulation or even an operation to remove the distal part of the insensitive and dysfunctional rectum might be necessary. A clearer comprehension of the pathophysiology responsible for faecal incontinence and HRI is relevant on different levels. It may allow an approach tailored to each patient’s needs and expectations.
References
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