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Am Surg. 2002 Jan;68(1):62-4.
Stercoral perforation of the sigmoid colon: report of a rare case and its possible association with nonsteroidal anti-inflammatory drugs.

Patel VG, Kalakuntla V, Fortson JK, Weaver WL, Joel MD, Hammami A.

Department of Surgery, Morehouse School of Medicine, South Fulton Medical Center, Atlanta, Georgia 30310-1495, USA.

Stercoral perforation of the colon is a rare phenomenon with fewer than 90 cases reported in the literature to date. The pathogenesis of stercoral ulceration is thought to result from ischemic pressure necrosis of the bowel wall caused by a stercoraceous mass. Stercoral perforation in more than 90 per cent of cases involves the sigmoid or rectosigmoid colon with associated fecal mass causing localized mucosal ulceration and bowel wall thinning due to localized pressure effect. We report the case of a 45-year-old woman who presented with a 12-hour history of epigastric pain. Significant comorbidities included systemic lupus erythematosus, sarcoidosis, hypertension, and previous history of congestive heart failure. The patient was also on prednisone and a nonsteroidal anti-inflammatory drug for joint pains. On physical examination the patient had signs of generalized peritonitis. Chest X-ray showed significant free air under the diaphragm. Emergency laparotomy revealed localized perforation over the antimesenteric border of the sigmoid colon with associated stercoral mass at the site of perforation. A segmental resection of the sigmoid colon with end colostomy (Hartmann's procedure) was performed. The patient made an uneventful recovery. Stercoral perforation is often a consequence of chronic constipation; however, there are other predisposing factors as the condition is rare compared with the frequency of severe constipation. One of the hypotheses includes the association of nonsteroidal anti-inflammatory drugs (NSAIDs) with stercoral perforation of the colon. Our case report lends support to this association with NSAID use; thus there need to be greater awareness and caution when using NSAIDs in chronically constipated patients.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12467320&dopt=Abstract

Dis Colon Rectum. 2002 May;45(5):593-600.
Role of nitric oxide in the colon of patients with slow-transit constipation.

Tomita R, Fujisaki S, Ikeda T, Fukuzawa M.

Department of Surgery, Nippon Dental University Hospital, Tokyo, Japan.

PURPOSE: The cause of dysmotility in patients with slow-transit constipation is unknown. Nitric oxide has recently been shown to be a neurotransmitter in the nonadrenergic, noncholinergic inhibitory nerves of the human gut. To clarify the physiologic significance of nitric oxide in the colon of patients with slow-transit constipation, we investigated the enteric nerve responses in lesional and normal bowel segments derived from patients with slow-transit constipation and patients who underwent colon resection for colonic cancers. METHODS: Twenty-six preparations were taken from colonic lesions in eight patients with slow-transit constipation (2 men; age, 23 to 69 (mean, 44.8) years). Forty-two preparations were taken from the normal colons of 14 patients with colonic cancer (8 men; age, 40 to 66 (mean, 52.4) years). A mechanographic technique was used to evaluate in vitro muscle responses to electric field stimulation before and after treatment with various autonomic nerve blockers, NG-nitro-L-arginine, and L-arginine. RESULTS: The colons of patients with slow-transit constipation were more strongly innervated by nonadrenergic, noncholinergic inhibitory nerves than were normal colons (P <0.05). Nitric oxide was found to act on both normal and slow-transit constipation colons. The colons of patients with slow-transit constipation were more strongly innervated by nitric oxide nerves than were normal colons (P < 0.01). Responses to electric field stimulation were the same in each case among the normal colons and were also the same in each case among the slow-transit constipation colons. CONCLUSION: These findings suggest that an increase of nitric oxide mediates nonadrenergic, noncholinergic inhibitory nerves and plays an important role in the dysmotility observed in the colons of patients with slow-transit constipation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12004206&dopt=Abstract

Dis Colon Rectum. 2002 May;45(5):641-9.
Rectal wall properties in patients with acute and chronic spinal cord lesions.

Krogh K, Mosdal C, Gregersen H, Laurberg S.

Surgical Research Unit, Department of Surgery L, Section AAS, University Hospital of Aarhus, Denmark.

PURPOSE: Most patients with spinal cord injuries suffer from constipation or fecal incontinence. This study was designed to observe rectal wall properties and the rectoanal inhibitory reflex in patients with acute and chronic spinal cord injury. METHODS: Rectal wall properties were studied by rectal impedance planimetry, a method for simultaneous registration of pressure and rectal cross-sectional area during distention. Twenty-five patients with spinal cord injury (14 with supraconal lesions and 11 with conal/cauda equina lesions) were studied one to four weeks after injury, and 17 were available for follow-up after 6 to 14 months. Results were compared with 15 healthy volunteers. RESULTS: Rectal tone was significantly higher (P < 0.05) than normal in patients with acute and chronic supraconal lesions but significantly lower (P < 0.05) in patients with acute and chronic conal/cauda equina lesions. The proportion of subjects with single giant rectal contractions was significantly higher than normal (33 percent) after acute supraconal spinal cord injury (77 percent; P = 0.02) but not after acute conal/cauda equina lesions (45 percent; P = 0.69). Phasic giant contractions only occurred in patients with spinal cord injury (once or more in 8 of 25 patients), but they were not correlated with the level of the lesion. Rectal tone and the number of giant rectal contractions did not change significantly from the acute to the chronic phase of spinal cord injury. The amplitude of the rectoanal inhibitory reflex at distention pressures of 5 and 10 cm H2O was significantly lower than normal in patients with acute and chronic conal/cauda equina lesions (acute, -5 and 44 percent vs. 37 and 82 percent (P < 0.05); chronic, 6 percent (P < 0.05) and 66 percent (P = NS)) but not in patients with supraconal spinal cord injury (acute, 32 and 83 percent; chronic, 61 and 85 percent (all P = NS)). CONCLUSION: Rectal tone is stimulated by the sacral spinal cord but inhibited by supraspinal centers within the central nervous system. Likewise, rectal contractility is inhibited by supraspinal centers, and the rectoanal inhibitory reflex is stimulated by the sacral spinal cord. Alterations caused by either type of spinal cord lesion are present after one to four weeks and do not change significantly within the first year.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12004214&dopt=Abstract

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