If it is inert, why does it move?

Abstract

Chronic constipation is a frequently experienced symptom, unfortunately there is no single definition even among health care workers. Some consensus documents (such as the Rome II criteria1) provided an opportunity for such a uniform definition, and these have been embraced, at least for research purposes. Three main forms of constipation may be identified: normal transit constipation, disorders of defecation or rectal evacuation (outlet obstruction), and slow transit constipation (STC).2 The latter is usually more severe, often refractory to medical treatment,3 and probably is a semantic umbrella under which there are patients with different severity. Notwithstanding this heterogeneity, STC has attracted the interest of researchers, and its pathophysiological basis has been extensively explored.4 Several mechanisms of colonic motor dysfunction have been documented.5-7 One form of STC is called colonic inertia (CI), a subtype that should constitute the extreme expression of colonic motility impairment, as the term ‘inertia’ implies. However, it is unclear what proportion of STC demonstrates inertia. In this issue, Hervé and colleagues investigated a group of severely constipated patients,8 and concluded that these subjects represented an heterogeneous cohort, that CI was present in 25% of cases, and that bisacodyl may be useful to evaluate whether there is residual propagated contractile activity that can be elicited in the colon. These results are already partly established in the literature on chronically constipated patients, but the authors’ main contribution is that they attempted to develop objective criteria for diagnosis of CI, based on manometric measurements. The proposed criteria are a combination of absence of high amplitude propagated contractions, lack of colonic response to eating and an overall reduction of colonic motility during a 24-h period. The validity of these recommended criteria requires further study. For example, delayed colonic transit time was less frequent in these patients compared with transit time in the other constipated patients (60%vs 76%). Moreover, 60% of patients classified as having CI using these criteria were able to have a contractile response to the endoluminal infusion of bisacodyl. There remains a significant problem in assessing such studies; there is no agreement in the definition of CI among authors: definitions may be based only on the assessment of delayed transit in the right colon,9 in the right and left colon,10 or the term is used as an equivalent of STC.11 Only rarely have more objective assessments (including manometric, electromyographic or scintigraphic investigations) been used12-15 Summarizing these observations in the current study and in the literature, it appears that most of these patients should be labelled as STC patients, whose colons are still able to respond (at least partially) to pharmacological stimulation. Several years ago, Frexinos proposed that true CI should be defined by the objective absence (or severe impairment) of colonic motility,16 as demonstrated by manometry and/or electromyography. It is probably time to embrace this advice and to develop criteria for true CI, to avoid further confusion. For instance, based on the literature, the following criteria would be reasonable: (i) severe constipation; (ii) delayed colonic transit (> 2 SD from upper normal limit); (iii) no evidence of evacuation disorder; (iv) manometric, electromyographic or scintigraphic evidence of absent or almost absent colonic motility, including propagated activity and response to meals; (v) no response to endoluminal pharmacological stimulation (e.g. bisacodyl) or response to parenteral neostigmine (1 mg intramuscular). Such criteria would help identify those patients whose constipation may be truly refractory to medical treatment or rescue, and in whom surgery is indicated and it is likely to be of benefit, as the term will really mean what it says: if it is inert, it does not move.