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The prolonged carriage of Clostridium difficile in Hirschsprung's
disease reported in this study (1) raises the possibility that
Hirschsprung's might indeed be a product of intestinal ischaemia that
develops in utero and might persist thereafter as chronic intestinal
ischaemia possibly because of persistent vascular abnormalities (2).
Chronic ileal ischaemia appears to be the primary cause of...
Chronic ileal ischaemia appears to be the primary cause of pouchitis
and the septic complications and anastomotic leaks complicating
restorative proctocolectomy of ulcerative colitis (3). Anerobes
proliferate in a newly constructed pouch (4) and when pouchitis develops
these may include C difficle. This is consistent with the proposal that C
difficile might be a marker of ischaemic colitis (5). Pseudomembranous
enterocolitis and hemorrhagic necrotizing enterocolitis complicating
Hirschsprung's might also be products of intestinal ischaemia(6).
Objective evidence of chronic intestinal ischaemia might only be
apparant in an stress test, notably gastric exercise tonometry in the
adult(7). If, however, histopathic hypoxia is a contributing factor, as is
likely with any inflammatory disease superimposed upon the Hirschsprung's,
it should be evident from tonometric measurements performed at rest. It
would be advisable to include the intramucosal pH as an end-point in
perfroming tonometry (8) for the PCO2-gap may not increased in these
circumstances (9). From our experience with chronic gastric ischaemia
enteral feeding even with cold water might be conveniently used as a
stress test in infants. This may not be without risk in the critically
ill in whom histotoxic or cytopathic hypoxia might be present(10,11).
1. SP Hardy, R Bayston, and L Spitz
Prolonged carriage of Clostridium difficile in Hirschsprung's disease
Arch Dis Child 1993; 69: 221-224
2. Taguchi T, Suita S, Hirata Y, Hirose R, Yamada T, Toyohara T.
Abnormally shaped arteries in the intestine of children with
Hirschsprung's disease: etiological considerations relating to ischemic
J Pediatr Gastroenterol Nutr. 1994 Feb;18(2):200-4.
3. Kienle P, Weitz J, Reinshagen S, Magener A, Autschbach F, Benner
A, Stern J, Herfarth C. Association of decreased perfusion of the
ileoanal pouch mucosa with early postoperative pouchitis and local septic
complications. Arch Surg. 2001 Oct;136(10):1124-30.
4. Smith FM, Coffey JC, Kell MR, O'Sullivan M, Redmond HP, Kirwan WO.
A characterization of anaerobic colonization and associated mucosal
adaptations in the undiseased ileal pouch.
Colorectal Dis. 2005 Nov;7(6):563-70.
5. Fiddian-Green RG. Clostridium difficile colitis: a marker for
CMAJ. 2004 Nov 23;171(11):1325-6
6. Urushihara N, Kohno S, Hasegawa S. Pseudomembranous enterocolitis
and hemorrhagic necrotizing enterocolitis in Hirschsprung's disease. Surg
7. Otte JA, Geelkerken RH, Oostveen E, Mensink PB, Huisman AB,
Kolkman JJ. Clinical impact of gastric exercise tonometry on diagnosis and
management of chronic gastrointestinal ischemia.
Clin Gastroenterol Hepatol. 2005 Jul;3(7):660-6.
8. Fiddian-Green RG, Stanley JC, Nostrant T, Phillips D. Chronic
gastric ischemia. A cause of abdominal pain or bleeding identified from
the presence of gastric mucosal acidosis. J Cardiovasc Surg (Torino). 1989
9. Fink MP, Cohn SM, Lee PC, Rothschild HR, Deniz YF, Wang H, Fiddian
-Green RG Effect of lipopolysaccharide on intestinal intramucosal
hydrogen ion concentration in pigs: evidence of gut ischemia in a
normodynamic model of septic shock.
Crit Care Med. 1989 Jul;17(7):641-6.
10. Melis M, Fichera A, Ferguson MK. Bowel necrosis associated with
early jejunal tube feeding: A complication of postoperative enteral
Arch Surg. 2006 Jul;141(7):701-4.
11. Schloerb PR, Wood JG, Casillan AJ, Tawfik O, Udobi K. Bowel
necrosis caused by water in jejunal feeding.
JPEN J Parenter Enteral Nutr. 2004 Jan-Feb;28(1):27-9.