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The prolonged carriage of Clostridium difficile in Hirschsprung’s disease reported in this study1 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 seems to be the primary cause of pouchitis and the septic complications and anastomotic leaks complicating restorative proctocolectomy of ulcerative colitis.3 Anaerobes proliferate in a newly constructed pouch,4 and when pouchitis develops, these may include C difficile. This is consistent with the proposal that C difficile might be a marker of ischaemic colitis.5 Pseudomembranous enterocolitis and haemorrhagic necrotising enterocolitis complicating Hirschsprung’s might also be products of intestinal ischaemia.6
Objective evidence of chronic intestinal ischaemia might only be apparent in a 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 on 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 performing tonometry8; the partial pressure of the carbon dioxide-gap may not be 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
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Competing interests: None declared.
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