2
If it is inert, why does it move? G. BASSOTTI Clinica di Gastroenterologia ed Epatologia, Dipartimento di Medicina Clinica e Sperimentale, Universita ` di Perugia, Italy 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 criteria 1 ) 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 hetero- geneity, STC has attracted the interest of researchers, and its pathophysiological basis has been extensively explored. 4 Several mechanisms of colonic motor dys- function 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 ÔinertiaÕ implies. However, it is unclear what proportion of STC demonstrates iner- tia. In this issue, Herve ´ and colleagues investigated a group of severely constipated patients, 8 and conclu- ded 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 constipa- ted patients, but the authorsÕ 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, electromyograph- ic or scintigraphic investigations) been used 12–15 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, Frex- inos 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 sti- mulation (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 med- ical 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. Address for correspondence Dr Gabrio Bassotti, Strada del Cimitero, 2/a, 06131 San Marco (Perugia), Italy. Fax: +39-075-584-7570; e-mail: [email protected] Neurogastroenterol Motil (2004) 16, 395–396 doi: 10.1111/j.1365-2982.2004.00512.x Ó 2004 Blackwell Publishing Ltd 395

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Page 1: If it is inert, why does it move?

If it is inert, why does it move?

G. BASSOTTI

Clinica di Gastroenterologia ed Epatologia, Dipartimento di Medicina Clinica e Sperimentale, Universita di Perugia, Italy

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 hetero-

geneity, STC has attracted the interest of researchers,

and its pathophysiological basis has been extensively

explored.4 Several mechanisms of colonic motor dys-

function 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 iner-

tia.

In this issue, Herve and colleagues investigated a

group of severely constipated patients,8 and conclu-

ded 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 constipa-

ted 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, electromyograph-

ic 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, Frex-

inos 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 sti-

mulation (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 med-

ical 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.

Address for correspondence

Dr Gabrio Bassotti, Strada del Cimitero,2/a, 06131 San Marco (Perugia), Italy.Fax: +39-075-584-7570; e-mail: [email protected]

Neurogastroenterol Motil (2004) 16, 395–396 doi: 10.1111/j.1365-2982.2004.00512.x

� 2004 Blackwell Publishing Ltd 395

Page 2: If it is inert, why does it move?

REFERENCES

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2 Lembo A, Camilleri M. Chronic constipation. N Engl

J Med 2003; 349: 1360–8.3 Knowles CH, Martin JE. Slow transit constipation: a

model of human gut dysmotility. Review of possibleaetiologies. Neurogastroenterol Motil 2000; 12: 181–96.

4 Bassotti G, Iantorno G, Fiorella S, Bustos-Fernandez L,Bilder CR. Colonic motility in man: features in normalsubjects and in patients with chronic idiopathic consti-pation. Am J Gastroenterol 1999; 94: 1760–70.

5 Rao SSC, Sadeghi P, Batterson K, Beaty J. Altered periodicrectal motor activity: a mechanism for slow transit con-stipation. Neurogastroenterol Motil 2001; 13: 591–8.

6 Hagger R, Kumar D, Benson M, Grundy A. Colonic motoractivity in slow-transit idiopathic constipation as identi-fied by 24-h pancolonic ambulatory manometry. Neuro-gastroenterol Motil 2003; 15: 512–22.

7 Bassotti G, Chistolini F, Battaglia E et al. Are colonicregular contractile frequency patterns in slow transitconstipation a relevant pathophysiological phenomenon?Digest Liver Dis 2003; 35: 552–6.

8 Herve S, Savoye G, Behbahani A, Leroi AM, Denis P,Ducrotte P. Results of 24-hour manometric recording ofcolonic motor activity with endoluminal instillation of

bisacodyl in patients suspected of having colonic inertia.Neurogastroenterol Motil 2004; 16: 397–402.

9 Watier A, Devroede G, Duranceau A et al. Constipationwith colonic inertia. A manifestation of systemic disease?Dig Dis Sci 1983; 28: 1025–33.

10 Verne GR, Hocking MP, Davis RH et al. Long-termresponse to subtotal colectomy in colonic inertia. J Gastr-

ointest Surg 2002; 6: 738–44.11 Zhao RH, Baig MK, Thaler KJ et al. Reduced expression of

serotonin receptor(s) in the left colon of patients withcolonic inertia. Dis Colon Rectum 2003; 46: 81–6.

12 Stivland T, Camilleri M, Vassallo M et al. Scintigraphicmeasurement of regional gut transit in idiopathic consti-pation. Gastroenterology 1991; 101: 107–15.

13 Bassotti G, Betti C, Pelli MA, Morelli A. Extensiveinvestigation on colonic motility with pharmacologicaltesting is useful for selecting surgical options in patientswith inertia colica. Am J Gastroenterol 1992; 87: 143–7.

14 Redmond JM, Smith GW, Barofsky I, Ratych RE, Golds-borough DC, Schuster MM. Physiological tests to predictlong-term outcome of total abdominal colectomy forintractable constipation. Am J Gastroenterol 1995; 90:748–53.

15 Shafik A, Shafik AA, el-Sibai O, Ahmed I. Colonic pacingin patients with constipation due to colonic inertia. Med

Sci Monit 2003; 9: CR191–6.16 Frexinos J. Inertie colique primitive: mythe ou realite?

Gastroenterol Clin Biol 1987; 11: 302–6.

396 � 2004 Blackwell Publishing Ltd

Editorial Neurogastroenterology and Motility