Marc Polecritti, General Surgery Resident; Christopher J. Esper, Chief General Surgery Resident; William R. Henwood, Attending General Surgeon; Robert Marx, Attending General Surgeon; R. Zane Kelley, General Surgery Resident; Steven Hand, General Surgery Resident; Lee Farber, General Surgery Intern, Department of Surgery, University of Pittsburgh Medical Center?Horizon Hospital, Pittsburgh, PA
Marc Polecritti, DO
General Surgery Resident
Christopher J. Esper, DO
Chief General Surgery Resident
William R. Henwood, DO
Attending General Surgeon
Robert Marx, DO
Attending General Surgeon
R. Zane Kelley, DO
General Surgery Resident
Steven Hand, DO
General Surgery Resident
Lee Farber, DO
General Surgery Intern
Department of Surgery
University of Pittsburgh
Medical Center?Horizon Hospital
Stercoral perforation of the colon is a rare, life-threatening condition that has a high mortality rate and usually is diagnosed only during exploratory laparotomy. The condition results when a fecaloma causes pressure necrosis of the colon, leading to perforation of the bowel wall. The exact mechanism that causes fecalomas to form has yet to be defined clearly, but many factors, such as a history of constipation, are thought to contribute. The authors describe a case of multiple fecalomas in a patient who developed a stercoral perforation of the sigmoid colon.
Stercoral perforation of the colon is a rare surgical finding. To date, fewer than 100 cases have been reported in the literature. The first documented case was by Berry to the Pathological Society of London in 1894.1
Stercoral perforation results when pressure from a hard fecaloma leads to a perforated colonic ulcer with necrotic and inflammatory edges.2 This condition contrasts with idiopathic perforations, which are linear tears of the colon that do not exhibit inflammatory or ischemic components.3 According to Abella and Fernandez, a fecaloma is a localized accumulation of fecal matter, which stagnates and increases in volume until the colon becomes deformed.4 Fecalomas are denser than a fecal impaction, are often laminated, and can calcify, making them radio-opaque on radiological studies. The terms and have been used in the literature and are synonymous with fecaloma.
Stercoral perforation is a life-threatening condition that has an associated mortality rate of 35% for surgically treated cases and 47% for conservatively treated cases.5 We report a case of stercoral perforation that was managed successfully with resection of the perforated section of colon, creation of a Hartmann's pouch, and a proximal colostomy.
A 47-year-old woman presented to the emergency department because of diffuse, sharp, cramping abdominal pain, which began 3 days earlier. The pain initially was limited to the left lower quadrant, but it increased in severity during her first hospital day. Her last bowel movement also had occurred 3 days earlier, and she described it as being hard, leaving her feeling constipated and bloated. She reported no nausea, vomiting, fever, chills, or night sweats, but noted a recent loss of appetite.
The patient's medical history included a long history of intermittent constipation, depression, bipolar disorder, anxiety, muscle cramps, and two ectopic pregnancies. She had not undergone any previous investigations as to the cause of her intermittent constipation. Her current medications included olanzapine, naproxen, cyclobenzaprine, zolpidem, and quinine sulfate.
On initial evaluation, the patient had a temperature of 97.4°F, blood pressure of 146/75 mm Hg, a heart rate of 101 beats per minute, a respiratory rate of 18 breaths per minute, and an oxygen saturation of 94% on room air. Physical examination found abdominal distention and diffuse abdominal pain that was most severe in the left lower quadrant, with involuntary guarding and rebound tenderness on palpation. The patient had normoactive bowel sounds in all quadrants. Rectal examination revealed no palpable stool in the rectal vault and was hemoccult negative. Laboratory values on admission were notable for a leukocytosis of 24,000 mm3, with an increased number of bands of 9% on the differential and an increased platelet level to 601,000 mm3. Other aspects of the complete blood count and basic metabolic profile were within normal limits.
Computed tomography (CT) scans of the abdomen and pelvis with intravenous contrast were performed in the emergency department, which demonstrated free intraperitoneal air in the pelvis immediately adjacent to the sigmoid colon, a small amount of free fluid in the pelvis, and large collections of stool throughout the colon (Figure 1). The gallbladder and appendix appeared normal, with no evidence of colonic diverticula.
A presumptive diagnosis of perforated colon of uncertain etiology was made, and the patient was taken to the operating room for an exploratory laparotomy. The colon appeared diffusely distended, and free-flowing purulent fluid was encountered throughout the abdomen. Multiple hard fecalomas were palpated throughout the colon. Two fecalomas were free floating in the pelvis, both of which measured 4 cm in diameter. An approximately 3.5-cm irregular perforation was discovered at the rectosigmoid junction. A Hartmann?s procedure was performed, and a total of 15 fecalomas were expressed out of the proximal colon before formation of the end colostomy. The fecalomas ranged in size from 2 to 4 cm in diameter. The patient had an unremarkable postoperative recovery and was discharged to home on postoperative day 6.
The pathology report described a 3-cm rent in the sigmoid colon on the antimesenteric side, with gross and histologic features of mucosal erosion, ulceration, and transmural necrosis. The margins of the specimen displayed severe inflammation with focal submucosal hemorrhage and fibropurulent exudates of the subserosa and serosal surface (Figure 2).
The definition of stercoral perforation was expanded on by Maurer and colleagues, who conducted one of the largest single-institution studies on this condition.6 The diagnostic criteria of stercoral perforation given by these authors that applied to our case include the following: (1) a round or ovoid antimesenteric colonic perforation larger than 1 cm in diameter; (2) the presence of fecalomas within the colon that protrude through the perforation site or lie within the abdominal cavity; and (3) microscopic evidence of pressure necrosis or ulcer and chronic inflammatory reaction around the perforation site. The aim of applying these criteria is to isolate true cases of stercoral perforation from colonic perforation caused by other processes, such as diverticulitis, inflammatory bowel disease, idiopathic perforation, and trauma.
The pathophysiology of stercoral perforation is thought to result from bowel distension around the fecaloma, which causes intraluminal pressure to increase to a point that exceeds the capillary perfusion pressure within the bowel wall.7 This process results in focal ischemia, necrosis, ulceration, and, ultimately, perforation.
Because of the relatively diminished blood flow at the antimesenteric border of the sigmoid and rectosigmoid colon, it is the most common site of perforation. Several factors appear to contribute to the prevalence of the ischemia with subsequent perforations in the sigmoid and rectosigmoid regions. Fecal material becomes progressively more dehydrated as it travels toward the anus, allowing fecalomas to form most commonly in the left colon. The blood supply distal to the mid-transverse colon is more susceptible to ischemia. The sigmoid and rectosigmoid regions possess the narrowest diameter of the entire colon and must withstand the highest intraluminal pressures, ranging between 5 and 100 cm of H2O.7
The cause of stercoral perforation is multifactorial. In all true cases of stercoral perforation, the colonic mucosa adjacent to the localized ischemic area surrounding the perforation is histologically normal tissue. There is no evidence of an underlying infectious process, inflammatory bowel disease, mesenteric ischemia, or toxic megacolon in the adjacent mucosa. A history of chronic or recent constipation appears to be a common contributing factor; however, a review by Serpell and Nicholls noted only 61% of the reported cases had a significant history of constipation.7 Our patient noted a history of intermittent constipation, and her last bowel movement had occurred 3 days before she presented to the emergency department.
The one universal component in patients with stercoral perforation is the formation of a fecaloma. The exact mechanism that causes fecalomas to develop in patients with or without a history of constipation has yet to be clearly defined. It has been suggested that factors such as dysmotility, partial luminal obstruction, previous barium administration, or the use of medications that can exacerbate constipation may play a role. It is well known that many medications have constipation as a side effect, including opioids, antidepressants, aluminum-based antacids, and nonsteroidal anti-inflammatory drugs. At least six case reports in the literature suggest a direct link between medications and subsequent stercoral perforation. Two of these describe constipated patients who were abusing opioids (one methadone and the other heroin).8,9 Four cases suggest a link between the use of nonsteroidal antiinflammatory drugs and stercoral perforation.10,11 One report suggests that the inhibition of prostaglandin synthase activity may disrupt the cytoprotective effect, compromising intestinal integrity and resulting in increased susceptibility to transmucosal migration of luminal toxins.10 This process may make the bowel more susceptible to perforation. Our patient was taking naproxen and olanzapine, both of which are known to cause constipation.
Several surgical treatment options for stercoral perforation have been described, including colectomy, exteriorization and colostomy, closure of the perforation with proximal colostomy, and resection with colostomy.12 Serpell and Nicholls reported mortality rates of 32% after resection and exteriorization, 43% after exteriorization of the perforation alone, and 57% after closure of the perforation with proximal colostomy.7 Our patient underwent resection of the perforated section of colon, creation of a Hartmann's pouch, and proximal colostomy. The distal transverse colon and descending colon possessed multiple large fecalomas, which were removed individually before creation of the colostomy. Failure to check for and remove these more proximal fecalomas would subject the patient to a much higher chance of recurrence.
Stercoral perforation of the colon is a rare condition that is often diagnosed at the time of surgery. Stercoral perforation should be suspected in any patient with a history of chronic constipation who develops acute abdominal pain. Acute presentations may require exploratory laparotomy for both diagnosis and treatment. Although many patients suffer from constipation, it seldom progresses to stercoral perforation of the colon. When stercoral perforation is recognized, patients need to be treated urgently to avoid the high mortality rate associated with this condition. Further studies are needed to uncover what causes fecalomas to develop so that their formation can be prevented and stercoral perforations can be avoided.
Choose the best answer for each of the following questions.