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Year : 2017  |  Volume : 2  |  Issue : 2  |  Page : 17-20

Perspectives on stercoral perforation

Department of Surgery, University of Buea, Buea, S.W. Region, Cameroon

Date of Web Publication23-May-2017

Correspondence Address:
Elroy Patrick Weledji
Department of Surgery, University of Buea, Buea, S.W. Region
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijssr.ijssr_7_17

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Stercoral perforation results from ischemic necrosis of the colonic wall by a fecaloma. The cause is multifactorial and the diagnosis is usually made only at laparotomy. There is high mortality from fecal peritonitis and Hartmann's procedure in the ill and toxic elderly patient carries the lowest mortality.

Keywords: Impaction, ischemia, perforation, stercoral

How to cite this article:
Weledji EP, Nana TC. Perspectives on stercoral perforation. IJS Short Rep 2017;2:17-20

How to cite this URL:
Weledji EP, Nana TC. Perspectives on stercoral perforation. IJS Short Rep [serial online] 2017 [cited 2019 Jan 18];2:17-20. Available from: http://www.ijsshortreports.com/text.asp?2017/2/2/17/206755

  Introduction Top

Stercoral perforation is a relatively neglected medical and surgical problem in the frail and elderly, which was first described by Berry in 1894.[1] It is a rare but an important phenomenon, and in more than 90% of cases it involves the narrow, high-pressure, and slower transit sigmoid or rectosigmoid colon.[2] It is a life-threatening situation with high mortality because spillage of feces would lead to fecal peritonitis.[2],[3]

The cause is multifactorial but the pathogenesis of stercoral ulceration is thought to result from ischemic pressure necrosis of the bowel wall by a dehydrated stercoraceous mass. This is because an increased intraluminal pressure in the colon from any reason interferes with mucosal perfusion. The intraluminal pressure exceeds the capillary perfusion pressure of the bowel walls leading to pressure necrosis especially on the antimesenteric border. It usually reveals itself as a localized, covert perforation over the less vascularized antimesenteric border of the sigmoid colon with an associated stercoral mass at the site of the perforation.[3],[4] The etiology may include hardened feces (fecaloma) which may form in longstanding constipation, sigmoid diverticular disease, pregnancy, hypothyroidism, proximal to an end colostomy, or other diseases which cause obstruction of transit such as Hirschsprung's disease, Chagas disease, carcinoma, vasculitides (connective tissue diseases, e.g., scleroderma, systemic lupus erythematosus), toxic colitis, and megacolon.[5],[6],[7],[8],[9],[10] They may be associated with medications such as nonsteroidal anti-inflammatory drugs, prednisolone, antidepressants, heroin, and opioids.[11],[12],[13],[14] Although it is well documented that many medications have the side effects of constipation, several studies in the literature suggest a direct link between medications and subsequent stercoral perforation.[3] Because of the low level of clinical suspicion, stercoral perforation is usually diagnosed only at laparotomy. Hartmann's procedure (resection of the perforation with the proximal colon brought out as an end colostomy and the distal end either closed off or brought out as a mucous fistula) demonstrates the lowest mortality risk for a stercoral perforation of the sigmoid colon.[15] Exteriorization of the perforation alone carries a mortality risk of 43%, with the risk increasing to 57% after closure of the perforation with a proximal colostomy.[2],[16],[17] Sepsis, malnutrition, or a further fecaloma upstream in an unprepared bowel will predispose to the breakdown of a simple closure of the perforation or a primary anastomosis.[2],[18],[19] Not only does the sigmoid colon generate fairly high pressures, but also more importantly, the marginal artery is absent in the sigmoid colon, which is thus prone to ischemia if it is used for anastomosis.[20]

  What are the Possible Explanations for Stercoral Perforation? Top

First, fecal impaction in constipation or in sigmoid diverticular disease especially in the elderly is a predisposing factor for stercoral perforation. Hyperelastosis and altered collagen structure in the colon wall related to aging and disordered motility contribute.[21],[22] Segmentation of the narrow sigmoid colon predisposes to high intraluminal pressure with characteristic protrusion of the mucosa (“false diverticulum”) at weak points where the terminal arterial branches penetrate the circular muscle adjacent to the tenia. An inactive lifestyle and the increased intraluminal pressure associated with a low-fiber diet together increase the incidence of diverticular disease in the elderly. Diverticula frequently contain inspissated feces, and muscle hypertrophy and thickening of the pericolic fat are commonly observed in the adjacent bowel.[6] Obstruction of a diverticular ostium promotes bacterial proliferation in a sealed space with the risk of abscess formation. Inflammatory change in the diverticula (diverticulitis) is the common course of clinical symptoms usually encountered in the older age groups. Acute inflammation may progress to pericolic abscess formation and even to free perforation into the peritoneal cavity (acute peritonitis).[19] The development of fistulae between the colon and adjacent organs, especially the bladder, is not uncommon. Chronic diverticulitis leads to fibrous thickening of the colonic wall with some degree of intestinal obstruction, and the lesion may be mistaken macroscopically for carcinoma.[6]

Second, ischemic change may develop in the large bowel proximal to obstructive lesions, especially carcinoma or an obstructing hernia. In low intestinal obstruction, the absorptive area of the gut proximally is extensive, and depletion of water and electrolytes is often delayed. Ultimately, however, dehydration due to vomiting does take place and the vomitus becomes brown and foul-smelling – fecal or stercoral vomit. The dominant and dangerous factor in this form of obstruction is distension of the gut with fluid and with gas mainly derived from swallowed air. Prolonged increase of intraluminal pressure impairs the viability of the bowel wall, with subsequent diffusion of toxic bacterial products into the peritoneal cavity where they are absorbed and produce toxemia and death.[23] Relief of distension by intubation is thus critically important until surgical intervention can be undertaken. In partial chronic obstruction, prolonged intermittent gut distension leads to hypertrophy of the bowel muscle proximal to the obstructive lesion. The raised intraluminal pressure may interfere with mucosal blood flow and an ischemic enterocolitis, sometimes with pseudomembrane formation and frank ulceration. Furthermore, the pressure of fecal accumulation impairs mucosal viability and predisposes to bacterial invasion which leads to the formation of mucosal exudate and ultimately to mucosal breakdown and ulceration. This “stercoral” ulceration can take place at some distance proximal to the obstruction and sometimes can lead to perforation and fecal peritonitis.[24] The effects of a distal chronic colonic stricture or a slow-growing distal scirrhous colonic carcinoma are aggravated if the regurgitation of fecal material proximally is prevented by an all too competent ileocecal valve (closed loop obstruction). The problem here is not strangulating obstruction but intramural ischemia of the cecum due to stretching causing patchy necrosis. In this situation, stercoral ulceration is likely to occur and the cecum may rupture. According to the law of Laplace (2T = PR, where P is the transmural pressure, T is the wall tension, and R is the radius of a sphere), tension (in this case in the wall of the colon) is proportional to the radius and is therefore higher in the cecum which is the widest point of the colon than elsewhere. Thus, the cecum takes the brunt of the distension with imminent perforation if the cecal diameter is >15 cm.[23],[24]

Third, the common external hernias usually contain a loop of small intestine although in the larger ones, large bowel (sigmoid colon) or other structures may also be present. The most serious result of hernia is strangulation, i.e., obstruction of the blood flow (initially venous then arterial) to the herniated gut. This may occur by the addition of a fresh loop of bowel to the sac or by accumulation of feces and gas in a herniating colon and thus increasing the bulk of the contents. Strangulation may thus develop even when the hernia is first formed as when a portion of bowel is being forced into a tight aperture not uncommon in a femoral hernia.[25] Forced reduction may thus precipitate stercoral perforation and peritonitis or mucosal ischemia with resultant stricture formation – “intestinal stenosis of Garre,” noticed after repair of the hernia.[26]

Fourth, ischemic disease may be more focal in distribution with focal lesions occurring in the small or large bowel due to disease of small blood vessels, for example, arteritis of rheumatoid arthritis, polyarteritis nodosa, or systemic lupus erythematosus.[9],[10] Another cause of focal ischemia is inadequate perfusion of intestinal arteries especially to the splenic flexure of the large bowel which is a watershed zone vulnerable to hypoperfusion during the episodes of generalized circulatory embarrassment or by surgical operations such as aortic aneurysm repair and anterior resection.[27],[28] It is important when mobilizing the blood supply at the splenic flexure to preserve the terminal two branches of the left colic artery which act as a support for the marginal artery at this point. The effect which depends on the duration of the hypoperfusion varies from slight mucosal damage with an episode of rectal bleeding to necrosis of the mucosa and submucosa followed by healing with scarring and stricture formation, to inflammation from intestinal commensal bacteria (ischemic colitis), to full-thickness necrosis of the colonic wall with subsequent gangrene and perforation.[4],[23] Ischemic enterocolitis is applied to multiple randomly distributed foci of ischemic damage involving both the large and small intestines which may occur in congestive cardiac failure, uremia, endotoxic or posttraumatic, and shock. The exact mechanisms are unknown but spasm of intestinal vessels complicating hypotension or disseminated intravascular coagulation may be involved.[4] A variant of this condition is encountered in newborn infants – neonatal necrotizing enterocolitis, in which premature infants are especially affected, and hypoxia during the neonatal period is suggested as an important factor although clostridia infection may be contributory.[3],[4]

Short abstract

  • Stercoral perforation is a relatively neglected surgical problem
  • Life-threatening situation with high mortality from fecal peritonitis
  • Result from ischemic pressure necrosis of the colonic wall by a fecaloma
  • Stercoral perforation is usually diagnosed only at laparotomy
  • Hartmann's procedure in the ill and toxic elderly patient carries the lowest mortality.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Berry J. Dilatation and rupture of the sigmoid flexure short report. BMJ 1894;1:301.  Back to cited text no. 1
Serpell JW, Nicholls RJ. Stercoral perforation of the colon. Br J Surg 1990;77:1325-9.  Back to cited text no. 2
Tokunaga Y, Hata K, Nishitai R, Kaganoi J, Nanbu H, Ohsumi K. Spontaneous perforation of the rectum with possible stercoral etiology: Report of a case and review of the literature. Surg Today 1998;28:937-9.  Back to cited text no. 3
Dubinsky I. Stercoral perforation of the colon: Case report and review of the literature. J Emerg Med 1996;14:323-5.  Back to cited text no. 4
Bharucha AE, Wald A, Enck P, Rao S. Functional anorectal disorders. Gastroenterology 2006;130:1510-8.  Back to cited text no. 5
Simpson J, Scholfield JH, Spiller RC. Pathogenesis of colonic diverticula. Br J Surg 2002;89:546-54.  Back to cited text no. 6
Costales AB, Agarwal AK, Chauhan SP, Refuerzo JS, Taub EA. Stercoral perforation of the colon during pregnancy: A case report and review of the literature. AJP Rep 2015;5:e25-9.  Back to cited text no. 7
Serpell JW, Sen M, Giddins G, Nicholls RJ, Bradfield WJ. Stercoral perforation of the colon proximal to an end colostomy. Postgrad Med J 1991;67:299-300.  Back to cited text no. 8
Ferrari BT, Ray JE, Robertson HD, Bonau RA, Gathright JB Jr. Colonic manifestations of collagen vascular diseases. Dis Colon Rectum 1980;23:473-7.  Back to cited text no. 9
Regan PT, Weiland LH, Geall MG. Scleroderma and intestinal perforation. Am J Gastroenterol 1977;68:566-71.  Back to cited text no. 10
Patel VG, Kalakuntla V, Fortson JK, Weaver WL, Joel MD, Hammami A. Stercoral perforation of the sigmoid colon: Report of a rare case and its possible association with nonsteroidal anti-inflammatory drugs. Am Surg 2002;68:62-4.  Back to cited text no. 11
Hollingworth J, Alexander-Williams J. Non-steroidal anti-inflammatory drugs and stercoral perforation of the colon. Ann R Coll Surg Engl 1991;73:337-9.  Back to cited text no. 12
Haley TD, Long C, Mann BD. Stercoral perforation of the colon. A complication of methadone maintenance. J Subst Abuse Treat 1998;15:443-4.  Back to cited text no. 13
Tessier DJ, Harris E, Collins J, Johnson DJ. Stercoral perforation of the colon in a heroin addict. Int J Colorectal Dis 2002;17:435-7.  Back to cited text no. 14
Rothenberger DA, Mayoral J, Deen K. Obstruction and perforation. In: Williams NS, editor. Colorectal Cancer, Clinical Surgery International. Vol. 20. Edinburgh: Churchill Livingstone; 1996. p. 123-33.  Back to cited text no. 15
Guyton DP, Evans D, Schreiber H. Stercoral perforation of the colon. Concepts of operative management. Am Surg 1985;51:520-2.  Back to cited text no. 16
Durrans D, Redmond EJ, Marshman L. Stercoral perforation of the colon. Br J Surg 1991;78:1148.  Back to cited text no. 17
Kim YW, Kwon HJ, Kim IY. Stercoral perforation of the colon in sigmoid colostomy patients: Two case reports. Int J Surg Case Rep 2013;4:1038-40.  Back to cited text no. 18
Hinchey EJ, Schaal PG, Richards GK. Treatment of perforated diverticular disease of the colon. Adv Surg 1978;12:85-109.  Back to cited text no. 19
Constantinides VA, Tekkis PP, Athanasiou T, Aziz O, Purkayastha S, Remzi FH, et al. Primary resection with anastomosis vs. Hartmann's procedure in nonelective surgery for acute colonic diverticulitis: A systematic review. Dis Colon Rectum 2006;49:966-81.  Back to cited text no. 20
Pare P, Ferrazzi S, Thompson WG, Irvine EJ, Rance L. An epidemiological survey of constipation in Canada: Definitions, rates, demographics, and predictors of health care seeking. Am J Gastroenterol 2001;96:3130-7.  Back to cited text no. 21
Kang JY, Hoare J, Tinto A, Subramanian S, Ellis C, Majeed A, et al. Diverticular disease of the colon – On the rise: A study of hospital admissions in England between 1989/1990 and 1999/2000. Aliment Pharmacol Ther 2003;17:1189-95.  Back to cited text no. 22
Dexter SP, Monson JR. Large bowel obstruction. In: Monson J, Duthie G, O'Malley K, editors. Surgical Emergencies. Osney Mead, Oxford OX20EL: Blackwell Science; 1999.  Back to cited text no. 23
Lalla R, Enquist I, Oloumi M, Velez FJ. Stercoraceous perforation of the right colon. South Med J 1989;82:80-2.  Back to cited text no. 24
Browse N. Hernia. In: Browse N, editor. An Introduction to the Symptoms and Signs of Surgical Disease. London: Edward Arnold; 1990.  Back to cited text no. 25
Weledji EP, Nana T, Aminde LN. Atypical small bowel obstruction following hernia repair: A case of intestinal stenosis of Garré. J Surg Acad 2013;3:16-8.  Back to cited text no. 26
Weledji EP, Mokake MD, Sinju M. Segmental resection with primary anastomosis is not always safe in splenic flexure perforation. BMC Res Notes 2015;8:415.  Back to cited text no. 27
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