26 Proc. roy. Soc. Med. Volume 68 January 1975
6
puborectalis, during prolonged straining efforts (this might affect not only the anterior rectal wall, but the posterior as well, and account for the increased incidence of midline posterior ulcers). Secondly, the anterior rectal wall may be forced into the upper end of the anal canal, and it has been pointed out earlier that solitary rectal ulcers are found most commonly in young people with powerful sphincters. The combined effects of these two mechanisms may be to cause direct trauma to the anterior wall, and possibly to induce temporary, but in the long run, damaging mucosal ischiemia. An isch3mic element would be supported to some extent by the fact that the sites where this peculiar histological picture are most commonly seen tend to be at positions remote from the blood supply; for example on a rectal valve, on the presenting part of a complete rectal prolapse, or on the tip of a prolapsing haemorrhoid. One patient would appear to give some support to the theory that an abnormal puborectalis is involved in the development of the syndrome. This was a woman of 24 who presented with a complete rectal prolapse in association with a lax pelvic floor. She was treated by postanal perineorrhaphy, in which the puborectalis was repaired behind the anorectal angle. Prior to the operation she had no rectal ulceration. Afterwards, however, she developed an unmistakeable ulcer with all the typical histological features, and it is tempting to suppose that there was a connexion between the newlyrestored puborectalis and the development of the ulcer. One other thing which still requires explanation is the fact that these ulcers may be found higher up in the rectum, and this may possibly be accounted for by the effectiveness or otherwise of rectal supporting tissues, the lateral ligaments in particular. In the case of a patient with the abnormally behaving puborectalis of the type described above, if the rectal support is normal, then as a result of prolonged straining he will only traumatize the anterior rectal wall lying immediately above the anal canal, producing an anterior mucosal prolapse, possibly with the histological features of the solitary ulcer syndrome. If rectal support is inadequate, then the rectal wall higher up may 'concertina' down allowing the anterior mucosa higher up to approach the traumatizing mechanism in the region of the puborectalis, so producing the typical solitary rectal ulcer. If both rectal support is poor and the sphincters are atonic and inhibit easily (Porter 1962) then we have the appropriate conditions for the development of a complete rectal prolapse, the presence of an ulcer depending on the degree of residual muscle tone.
Conclusion It may be that under the umbrella of the solitary rectal ulcer syndrome we are in fact describing a spectrum of conditions, ranging from anterior mucosal prolapse, possibly without frank ulceration, through the typical solitary ulcer higher up, to a complete rectal prolapse with an ulcer on its tip. All of these conditions show the same histological features, and would seem to be related to a breakdown in normal pelvic floor mechanisms. There is still a great deal to be learned about the subject, and only when the etiology is clearly established will it be possible to offer these patients a rational form of treatment. REFERENCES Allen M S jr (1966) Cancer 19,257-265 Cruveilhier J (1829-1842) Anatomie Pathologique du Corps Humain. Balliere, Paris; Vol 2 livre 25, p 4 Epstein S E, Ascar W 0, Ablow R C, Seaman W B & Lattes R (1966) American Journal of Clinical Pathology 45, 186-201 Floyd W F & Wails E W (1953) Journal ofPhysiology 122, 699-709 Haskell B & Rovner H (1965) Diseases ofthe Colon and Rectum 8, 333-336 Jalan K N, Brunt P W, Maclean N & Sirius W (1970) Scandinavian Journal of Gastroenterology 5, 143-147 Kerremans R (1969) Morphological and Physiological Aspects of Anal Continence and Defacation. Arscia, Brussels Madigan M R (1964) Proceedings of the Royal Society ofMedicine 57, 138-141 Madigan M R & Morson B C (1969) Gut 10, 871-881 Parks A G, Porter N H & Hardcastle J D (1966) Proceedings of the Royal Society of Medicine 59, 477 Phillips S F & Edwards D A W (1965) Gut 6, 396 Porter N H (1962) Annals of the Royal College of Surgeons of England 31, 379-404 Riek M, Halter F & Stirnemann H (1971) Schweizerische medizinische Wochenschrift 101, 758-759 Rutter K R P (1974) Proceedings ofthe Royal Society ofMedicine 67, 53-56
Mr A G Parks (St Mark's Hospital, London ECI V2PS) In the introduction to his short book entitled 'On Prolapsus of the Rectum' Frederick Salmon writes: 'I am inclined therefore to believe that some observations upon it, if founded upoA physiological reasoning, and supported by practical experience, may be of material utility to the profession.' By physiological reasoning, he meant, I think, an attempt to understand what is the cause of abnormality, the essential pathophysiology of the condition. I think that most of us on reading his book would not have been overimpressed with his physiological reasoning; nevertheless, according to the lights of his day, he was doing his best. The principle remains that we should also be trying to elucidate the basic pathophysiology of pelvic floor disorders
7
Section ofProctology
in addition to treating the patient empirically to give the best relief possible with currently available methods. Rectal prolapse is such a dramatic state of affairs that we tend to view it in isolation. The symptoms are so unpleasant: the patient's life is made miserable by the prolapsed mass, the mucous discharge and the associated incontinence, so we tend to proceed speedily to the most effective operative technique currently in vogue. Our aim here is to focus our minds on the abnormalities in the pelvis and pelvic floor which may be responsible. It is also desirable to try to link this situation with the less dramatic abnormalities of pelvic floor physiology, such as the descending perineum syndrome and the solitary ulcer syndrome. That some primary anatomical rather than physiological factor is at work is suggested by the sex ratio which is about 20 female to 1 male. The first thought to cross one's mind is that rectal prolapse is the consequence of childbirth, a late result of injury to the pelvic floor. This hypothesis is, however, nullified by a consideration of the parous/non-parous ratio. The number of nulliparn in the rectal prolapse family, as it were, greatly exceeds those in the general population. Indeed, paradoxically, it would appear that childbirth protects a woman from rectal prolapse. When we examine patients with this condition we find usually (though not always) a marked drop of the pelvic floor coupled with patulous sphincters. At operation there is always a pelvic peritoneal pouch with apparently little tissue to support the rectum. The question immediately arises as to which is the primary defect, the weak sphincter muscles or the inadequacy of rectal supportive tissue. Does the weak pelvic floor allow descent of the pelvic contents with the development of a deep peritoneal pouch? Or does the prolapse occur due to fascial weakness, but the repeated stretching of the anal canal cause sphincter weakness? It is interesting to note that there is both weakness of the internal and external sphincters. Is there ever a separation of the various aspects of rectal prolapse? Do we see the deep pelvic pouch with prolapse, or gross sphincter weakness without prolapse? In the elderly, one not infrequently finds a very deep pelvic pouch without any symptom of prolapse, so that this by itself cannot be the culprit. Similarly, one sees sphincter weakness of such a degree that the patient is completely incontinent, yet there is no complete procidentia; so this alone is not the cause. Perhaps there are several factors which must coexist before prolapse will occur. Mr Porter in his survey of St Mark's cases found a very high incidence of excessive straining on deftcation.
Perhaps the most distressing feature of this condition for the patient is the incontinence. It was found that 60% of the St Mark's patients had a severe degree of incontinence before rectopexy. After operation only 30% were incontinent, still an unacceptable figure. Fortunately we can now help most of these patients by repairing the sphincters and levator muscles behind the anal canal. This restores the anorectal angle and narrows the sphincters to such a degree that about 75% of such patients will be restored to an acceptable life. We may therefore have to deal with several abnormalities seriatim before we can get a person so afflicted back to a normal mode of life. The speakers have described some aspects of normal and abnormal pelvic floor situations which particularly interest them and which have a bearing on the pathogenesis of rectal prolapse. There has been no major breakthrough. My hope, however, is that these papers will stimulate us to think, and that, as a result of Salmon's two foundations, that is, physiological reasoning and the observation of practical experience, the breakthrough will ultimately come.
27
The following papers were also read: The Mechanism of Rectal Evacuation Dr J J Misiewicz (Central Middlesex and St Mark's Hospitals,
London) The Pelvic Floor Abnormality in Rectal Prolapse Mr Nigel Porter
(Brighton)
Meeting 8-10 March 1974 A joint meeting was held with the Societe Nationale Frangaise de Proctologie in Paris.
Meeting 20-31 May 1974 A joint meeting was held with the American Society of Colon and Rectal Surgeons and the Section of Colonic and Rectal Surgery of the Royal Australasian College of Surgeons in Washington DC from 20-25 May, followed by a meeting in Mexico City with the Sociedad Mexicana de Cirugia del Recto y Colon from 27-31 May.
6
puborectalis, during prolonged straining efforts (this might affect not only the anterior rectal wall, but the posterior as well, and account for the increased incidence of midline posterior ulcers). Secondly, the anterior rectal wall may be forced into the upper end of the anal canal, and it has been pointed out earlier that solitary rectal ulcers are found most commonly in young people with powerful sphincters. The combined effects of these two mechanisms may be to cause direct trauma to the anterior wall, and possibly to induce temporary, but in the long run, damaging mucosal ischiemia. An isch3mic element would be supported to some extent by the fact that the sites where this peculiar histological picture are most commonly seen tend to be at positions remote from the blood supply; for example on a rectal valve, on the presenting part of a complete rectal prolapse, or on the tip of a prolapsing haemorrhoid. One patient would appear to give some support to the theory that an abnormal puborectalis is involved in the development of the syndrome. This was a woman of 24 who presented with a complete rectal prolapse in association with a lax pelvic floor. She was treated by postanal perineorrhaphy, in which the puborectalis was repaired behind the anorectal angle. Prior to the operation she had no rectal ulceration. Afterwards, however, she developed an unmistakeable ulcer with all the typical histological features, and it is tempting to suppose that there was a connexion between the newlyrestored puborectalis and the development of the ulcer. One other thing which still requires explanation is the fact that these ulcers may be found higher up in the rectum, and this may possibly be accounted for by the effectiveness or otherwise of rectal supporting tissues, the lateral ligaments in particular. In the case of a patient with the abnormally behaving puborectalis of the type described above, if the rectal support is normal, then as a result of prolonged straining he will only traumatize the anterior rectal wall lying immediately above the anal canal, producing an anterior mucosal prolapse, possibly with the histological features of the solitary ulcer syndrome. If rectal support is inadequate, then the rectal wall higher up may 'concertina' down allowing the anterior mucosa higher up to approach the traumatizing mechanism in the region of the puborectalis, so producing the typical solitary rectal ulcer. If both rectal support is poor and the sphincters are atonic and inhibit easily (Porter 1962) then we have the appropriate conditions for the development of a complete rectal prolapse, the presence of an ulcer depending on the degree of residual muscle tone.
Conclusion It may be that under the umbrella of the solitary rectal ulcer syndrome we are in fact describing a spectrum of conditions, ranging from anterior mucosal prolapse, possibly without frank ulceration, through the typical solitary ulcer higher up, to a complete rectal prolapse with an ulcer on its tip. All of these conditions show the same histological features, and would seem to be related to a breakdown in normal pelvic floor mechanisms. There is still a great deal to be learned about the subject, and only when the etiology is clearly established will it be possible to offer these patients a rational form of treatment. REFERENCES Allen M S jr (1966) Cancer 19,257-265 Cruveilhier J (1829-1842) Anatomie Pathologique du Corps Humain. Balliere, Paris; Vol 2 livre 25, p 4 Epstein S E, Ascar W 0, Ablow R C, Seaman W B & Lattes R (1966) American Journal of Clinical Pathology 45, 186-201 Floyd W F & Wails E W (1953) Journal ofPhysiology 122, 699-709 Haskell B & Rovner H (1965) Diseases ofthe Colon and Rectum 8, 333-336 Jalan K N, Brunt P W, Maclean N & Sirius W (1970) Scandinavian Journal of Gastroenterology 5, 143-147 Kerremans R (1969) Morphological and Physiological Aspects of Anal Continence and Defacation. Arscia, Brussels Madigan M R (1964) Proceedings of the Royal Society ofMedicine 57, 138-141 Madigan M R & Morson B C (1969) Gut 10, 871-881 Parks A G, Porter N H & Hardcastle J D (1966) Proceedings of the Royal Society of Medicine 59, 477 Phillips S F & Edwards D A W (1965) Gut 6, 396 Porter N H (1962) Annals of the Royal College of Surgeons of England 31, 379-404 Riek M, Halter F & Stirnemann H (1971) Schweizerische medizinische Wochenschrift 101, 758-759 Rutter K R P (1974) Proceedings ofthe Royal Society ofMedicine 67, 53-56
Mr A G Parks (St Mark's Hospital, London ECI V2PS) In the introduction to his short book entitled 'On Prolapsus of the Rectum' Frederick Salmon writes: 'I am inclined therefore to believe that some observations upon it, if founded upoA physiological reasoning, and supported by practical experience, may be of material utility to the profession.' By physiological reasoning, he meant, I think, an attempt to understand what is the cause of abnormality, the essential pathophysiology of the condition. I think that most of us on reading his book would not have been overimpressed with his physiological reasoning; nevertheless, according to the lights of his day, he was doing his best. The principle remains that we should also be trying to elucidate the basic pathophysiology of pelvic floor disorders
7
Section ofProctology
in addition to treating the patient empirically to give the best relief possible with currently available methods. Rectal prolapse is such a dramatic state of affairs that we tend to view it in isolation. The symptoms are so unpleasant: the patient's life is made miserable by the prolapsed mass, the mucous discharge and the associated incontinence, so we tend to proceed speedily to the most effective operative technique currently in vogue. Our aim here is to focus our minds on the abnormalities in the pelvis and pelvic floor which may be responsible. It is also desirable to try to link this situation with the less dramatic abnormalities of pelvic floor physiology, such as the descending perineum syndrome and the solitary ulcer syndrome. That some primary anatomical rather than physiological factor is at work is suggested by the sex ratio which is about 20 female to 1 male. The first thought to cross one's mind is that rectal prolapse is the consequence of childbirth, a late result of injury to the pelvic floor. This hypothesis is, however, nullified by a consideration of the parous/non-parous ratio. The number of nulliparn in the rectal prolapse family, as it were, greatly exceeds those in the general population. Indeed, paradoxically, it would appear that childbirth protects a woman from rectal prolapse. When we examine patients with this condition we find usually (though not always) a marked drop of the pelvic floor coupled with patulous sphincters. At operation there is always a pelvic peritoneal pouch with apparently little tissue to support the rectum. The question immediately arises as to which is the primary defect, the weak sphincter muscles or the inadequacy of rectal supportive tissue. Does the weak pelvic floor allow descent of the pelvic contents with the development of a deep peritoneal pouch? Or does the prolapse occur due to fascial weakness, but the repeated stretching of the anal canal cause sphincter weakness? It is interesting to note that there is both weakness of the internal and external sphincters. Is there ever a separation of the various aspects of rectal prolapse? Do we see the deep pelvic pouch with prolapse, or gross sphincter weakness without prolapse? In the elderly, one not infrequently finds a very deep pelvic pouch without any symptom of prolapse, so that this by itself cannot be the culprit. Similarly, one sees sphincter weakness of such a degree that the patient is completely incontinent, yet there is no complete procidentia; so this alone is not the cause. Perhaps there are several factors which must coexist before prolapse will occur. Mr Porter in his survey of St Mark's cases found a very high incidence of excessive straining on deftcation.
Perhaps the most distressing feature of this condition for the patient is the incontinence. It was found that 60% of the St Mark's patients had a severe degree of incontinence before rectopexy. After operation only 30% were incontinent, still an unacceptable figure. Fortunately we can now help most of these patients by repairing the sphincters and levator muscles behind the anal canal. This restores the anorectal angle and narrows the sphincters to such a degree that about 75% of such patients will be restored to an acceptable life. We may therefore have to deal with several abnormalities seriatim before we can get a person so afflicted back to a normal mode of life. The speakers have described some aspects of normal and abnormal pelvic floor situations which particularly interest them and which have a bearing on the pathogenesis of rectal prolapse. There has been no major breakthrough. My hope, however, is that these papers will stimulate us to think, and that, as a result of Salmon's two foundations, that is, physiological reasoning and the observation of practical experience, the breakthrough will ultimately come.
27
The following papers were also read: The Mechanism of Rectal Evacuation Dr J J Misiewicz (Central Middlesex and St Mark's Hospitals,
London) The Pelvic Floor Abnormality in Rectal Prolapse Mr Nigel Porter
(Brighton)
Meeting 8-10 March 1974 A joint meeting was held with the Societe Nationale Frangaise de Proctologie in Paris.
Meeting 20-31 May 1974 A joint meeting was held with the American Society of Colon and Rectal Surgeons and the Section of Colonic and Rectal Surgery of the Royal Australasian College of Surgeons in Washington DC from 20-25 May, followed by a meeting in Mexico City with the Sociedad Mexicana de Cirugia del Recto y Colon from 27-31 May.
