Motility Disorders In Diverticular Disease. M. Kreis. Ludwig-Maximilians Universität München Klinikum Großhadern, Chirurgische Klinik

Transcription

1 Motility Disorders In Diverticular Disease. M. Kreis Ludwig-Maximilians Universität München Klinikum Großhadern, Chirurgische Klinik

2 Pathophysiology Diet? Age? Diverticula Disposition? Constipation? Toxines? (Mercury?) Motility?

3 Morphology of Sigmoid Diverticula Diverticula Muscle layer Pressure Mucosa

4 Hypothesis for the pathogenesis of diverticular disease The formation of diverticula is triggered by a motility disorder with subsequent exceedingly high pressures in the sigmoid colon.

5 Specific questions: Are there elevated pressure and / or altered patterns of motility in diverticular disease? If so, which are the specific conditions that are associated with this disturbed motility? Is there a generalized motility disorder or is it limited to the sigmoid colon? Is the motility altered following treatment such as surgery or modified diet? Are alterations in motility primary or secondary to diverticular disease?

6 Techniques to record colonic motility I

7 Parameters for the evaluation of colonic motility 1. Colonic motility index 2. High amplitude propagated contractions Stimuli a) Standard meal / gastro-colonic response b) Cholinergic drugs, e.g. neostigmine

8 Definition of the colonic motility index pressure time Colonic motility index = (3 A/O (width x height) x C/B))

9 High amplitude propagated contraction (example) pressure time

10 Gastro-colonic reflex/ colonic motility after standard meal Standard meal Channel 1 (proximal) Channel 2 50 mmhg 15 min Channel 3 Channel 4 (distal) Kasparek et al. Surgery 2004; 136:

11 Effect of neostigmine on colonic motility Manometry 1 Baseline motility Motility after 5µg/kg Neostigmine i.v. Proximal barostat bag Manometry 2 Manometry 3 Distal barostat bag Manometry 4 5 ml 50 mmhg 20 minutes 20 minutes Kreis et al. Surgery 2001; 130:

12 Basal conditions: differences in motility index between diverticular disease and normal controls. Study Controls (n) Diverticular Disease (n) P-value Parks and Connell (15) 470 (25) n.s. Attisha and Smith (9) 343 (29) n.s. Trotman and Misiewicz 1988 Not given (13) Not given (6) p<0.02 Katschinski et al / (13) 282 / (15) n.s.

13 Motility studies in patients with diverticula: subgroups* Disease Description Asymptomatic diverticular disease (Diverticulosis / ADD) Colon diverticula without symptoms Symptomatic diverticular disease Uncomplicated (SUDD) Symptomatic and complicated (SCDD) Symptomatic colon diverticula (left lower quadrant abdominal pain) Complicated colon diverticula (hemorrhage, peridiverticulitis, fistulas, bowel obstruction) *Cortesini C et al. Dis Colon Rectum 1991; 34:

14 Motility studies in subgroups of patients with diverticula under basal conditions Motility index (mean/sem) * * N=30 N=30 N=30 N=55 Controls ADD SUDD SCDD P<0.001 Cortesini C et al. Dis Colon Rectum 1991; 34:

15 Response to a meal (gastro-colic reflex): differences in motility index between diverticular disease and normal controls. Study Controls (n) Diverticular Disease (n) P-value Parks and Connell (15) 820 (25) n.s. Attisha and Smith (9) 740 (29) Trotman and Misiewicz 1988 Not given (13) Not given (6) p<0.002 Katschinski et al / (13) 391 / (15) n.s.

16 Motility studies in subgroups of patients with diverticula following a meal (gastro-colic response) Motility index (mean/sem) * * N=30 N=30 N=30 N=55 Controls ADD SUDD SCDD P<0.001 Cortesini C et al. Dis Colon Rectum 1991; 34:

17 Response to a the acetylcholine inhibitor neostigmine Study Controls following neostigmine Diverticular disease following neostigmine P-value For Comparison of both groups Attisha and Smith (p< (p< vs.before Neostigmine) vs. before neostigmine) Weinreich * 0.05 *526 in patients with asymptomatic Diverticulosis (n.s. vs. Controls)

18 Motility patterns in diverticular disease / controls patients: 10.3 ± 2.7 HAPC / subject / day controls: 5.5 ± 0.8 HAPC / subject / day patients: Amplitude 118 ± 3.4 mmhg controls: Amplitude 110 ± 7.0 mmhg patients: Duration 13.6 ± 0.5 sec controls: Duration 14.0 ± 0.9 sec P<0.05 n.s. n.s. but: 18.4% of HAPCs in patients with diverticular disease were abnormal i.e. showing retropropagation, while none occurred in controls. Bassotti et al. Dis Colon Rectum 2000; 44:

19 Representative recording of HAPCs in a patient with diverticular disease Transverse colon Descending colon Sigmoid colon Bassotti et al. Dis Colon Rectum 2000; 44:

20 Alterations in motility are confined to the descending and sigmoid colon Overall Motility Index Patients Controls P-value (24 hours) Transverse 2481± ± Descending ± ± Sigmoid ± ± Bassotti et al. Dis Colon Rectum 2000; 44:

21 Effect of myotomy on motility of the sigmoid colon in patients with diverticular disease 3000 before myotomy after myotomy Motility index * * 0 Basal meal neostigmine Attisha and Smith Br J Surg, 1969; 56:

22 Effect of myotomy on sigmoid motility in patients with diverticular disease representative recording following neostigmine Attisha and Smith Br J Surg, 1969; 56:

23 Efffect of high fiber diet on motility of the sigmoid colon in patients with diverticular disease before myotomy after myotomy Motility index * * 0 basal meal Hodgson J, Br Med J 1972; 3:

24 Specific questions / answers I Are there elevated pressure and / or altered patterns of motility in diverticular disease? Symptomatic diverticular are associated with increased intraluminal pressures, particularly following a meal and neostigmine, and retrograde HAPCs. Is there a generalized motility disorder or is it limited to the sigmoid colon? There is no generalized motility disorder, as motility in the transverse colon is unchanged.

25 Specific questions / answers II Is the motility altered following treatment such as surgery or modified diet? Yes, it may be back to normal. Are alterations in motility primary or secondary to diverticular disease? Patients with asymptomatic diverticular frequently do not show any alterations in motility of the sigmoid colon which suggests that altered motility occurs secondary to diverticular disease.