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Slow transit constipation: more than one disease?
  1. C Pehl1,
  2. T Schmidt1,
  3. W Schepp1
  1. 1Department of Gastroenterology, Hepatology, and Gastrointestinal Oncology, Bogenhausen Academic Teaching Hospital, Englschalkinger Str 77, 81925 Munich, Germany
  1. Correspondence to:
    C Pehl;
    Christian.pehl{at}extern.lrz-muenchen.de
  1. M A Kamm2,
  2. A V Emmanuel2
  1. 2St Mark's Hospital, Watford Road, Harrow HA1 3UJ, UK

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Emmanuel and Kamm reported on the response of behavioural treatment, biofeedback, in constipated patients (Gut 2001;49:214–19). Biofeedback is an established therapy for outlet obstruction due to paradoxical anal sphincter contraction.1 Beyond that, Emmanuel and Kamm demonstrated that slow transit constipation (STC) can also be improved by biofeedback with normalisation of the slow transit in most symptomatic responders. These results contrast with the common belief of STC as a manifestation of a panenteric disease, presumably of the enteric nervous system.

Disturbances of oesophageal motility, gastric emptying, small bowel transit, and gall bladder motility have been described.2 Dysmotility of the small intestine has been thoroughly investigated by manometry in STC patients3,4 Disturbed motility—for example, abnormal configuration or disturbed aboral migration of phase III of the migrating motor complex, bursts, and sustained uncoordinated activity—occur in up to 60% of these patients. In our recent study5 using long term small bowel manometry in 30 clinical STC patients, disturbed aboral migration of phase III was present in 47%, and bursts/sustained uncoordinated activity occurred in 33% of patients, respectively.

It is well established that these manometric findings are markers of a neuropathy of the myenteric plexus and occur in an identical way in patients with chronic intestinal pseudo-obstruction of neuropathic origin. Furthermore, treatment by colectomy has been reported to result in excellent long term outcome in 90% of patients with dysmotility limited to the colon whereas patients with generalised intestinal dysmotility experience a sustained relief in only 13%.6 It is hard to understand how these manifestations of neuropathy, especially in the myenteric plexus of the small intestine, can be successfully treated by biofeedback therapy.

An alternative explanation is that STC is an inhomogeneous group of different aetiologies. In transit studies, slow transit can be the result of a right sided or global delay (the “classical” finding in idiopathic STC), a left sided delay, or a rectal marker accumulation.7 In physiological evaluation, an overlap of slow transit and outlet obstruction can be seen in some patients.8 At least in healthy volunteers, voluntary suppression of defecation resulted in a marked prolongation of colonic transit.9

Of the 22 slow transit patients studied by Emmanuel and Kamm, seven had marker retention predominantly in the rectosigmoid, 13 had a paradoxical sphincter contraction as a marker of outlet obstruction, and seven could not expel a balloon during simulated defecation. In contrast, in our study of small bowel manometry in slow transit patients,5 all patients demonstrated a right sided or global delay and had no signs of outlet obstruction.

Thus the response of behavioural treatment, biofeedback, in constipated patients with slow transit might be influenced by the existence of more than one disease as a possible aetiology of STC. We are looking forward to seeing data on the response of biofeedback therapy in patients with STC with and without pathological small bowel manometry.

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Authors' reply

We thank Dr Pehl and colleagues for their interest in our paper (Gut 2001;49:214–19).

Our findings do not contrast with the belief that slow transit constipation is a condition associated with a panenteric disorder of function. Work from our own unit has previously demonstrated that approximately half of all patients with slow transit constipation have delayed gastric emptying and small bowel transit.1 Behavioural treatment, which includes biofeedback, is a holistic treatment which we believe has both central and peripheral effects. Our study on the effects of behavioural treatment (

) demonstrated enhanced activity of the autonomic nerves innervating the gut. Such a change in extrinsic nerve function might be expected to alter upper gut function as well as colonic function. In support of this, we have previously demonstrated that such treatment not only normalises colonic transit but also diminishes the sensation of bloating and abdominal pain.2

The existence of a panenteric disturbance of function, including the motor abnormalities described by Pehl et al, should not be interpreted as evidence of enteric neuropathology throughout the gut. Such disturbed function could also result from altered central autonomic control of a neurologically normal gut. We would disagree that these manometric findings are markers of neuropathy in patients with idiopathic constipation; they may be associated but causality has not been established.

Ultimately, the value of behavioural treatment can be judged best by careful prospective evaluation of patient symptoms and physiological function. Such assessment has demonstrated the benefit of such treatment, suggesting that disturbances of upper gut function and motility are often secondary and reversible.

We would also disagree that the long term results of colectomy are excellent. In our own experience of the long term results of colectomy,3 only 50% of patients had a good outcome, one third experienced diarrhoea, and 10% experienced recurrent constipation. Two thirds of patients continued to experience some pain.

We agree that not all patients with constipation are the same. Some have slow transit while in others transit is normal. There are probably some patients with underlying irreversible gut changes but our pathological techniques are not good enough to distinguish these patients from those who will respond to simple treatment. Therefore, for practical reasons, we suggest using simple treatments first and investigating patients who have failed treatment later.

We believe that too much emphasis should not be placed on different patterns of colonic delay, or the presence of disturbed pelvic floor function. We have shown that patients with different patterns of colonic delay, with or without pelvic floor contraction, respond equally to behavioural treatment.2 Too much emphasis has been placed on these physiological observations.

Small bowel manometry is invasive while behavioural treatment is non-invasive. We feel that manometry should therefore be reserved for patients in whom invasive treatment, such as surgery, is being contemplated after other treatments have failed. Even then we feel it does not have a proven role in predicting the outcome of surgery.

References

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