Ogilvie Syndrome as a Postoperative Complication

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Abstract
IN 1948, OGILVIE1 described 2 cases of massive colonic dilation in the absence of mechanical obstruction. Both of his patients suffered from unsuspected malignant disease in the region of the celiac axis and semilunar ganglia. Ogilvie concluded that the nervous supply to the colon was affected by these tumors and that the neurological derangement led to a colonic "pseudo-obstruction." Multiple case reports have been published since that time; however, the actual mechanism that causes the colon to dilate in the absence of obstruction remains obscure. Most current research supports the theory that Ogilvie syndrome is secondary to large-bowel parasympathetic dysfunction. This theory has been supported by the successful use of parasympathomimetic agents in the treatment of Ogilvie syndrome. Agents that increase parasympathetic tone have been shown to resolve pseudo-obstruction without colonic decompression or surgical manipulation.2 Turegano-Fuentes et al3 demonstrated complete resolution of Ogilvie syndrome with the use of neostigmine methylsulfate in 12 of 18 patients.

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