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Fecal impaction and systemic inflammatory response syndrome in a young male with cerebral palsy.

Abstract: Symptoms of fecal impaction extend from constipation, anorexia, nausea, vomiting and abdominal pain, to full blown sepsis. We present the case of a patient with cerebral palsy and mental retardation, who presented to the Emergency Department with a 3-day history of diffuse abdominal pain and fecal incontinence. Evaluation revealed severe fecal impaction. The patient developed systemic inflammatory response syndrome (SIRS), with negative workup for underlying etiology. He responded well to digital disimpaction and antibiotics. Our case illustrates the serious sequelae of fecal impaction, which should be considered in patients with neurologic disorders and SIRS.

Key Words: fecal impaction, fecal incontinence, systemic inflammatory response syndrome.


Constipation and fecal incontinence are common symptoms in patients with neurologic disorders. (1) Gastrointestinal complications of constipation include stercoral ulceration, rectal prolapse, intestinal obstruction, megacolon, and fecal incontinence. (2,3) We present a case of systemic inflammatory response syndrome (SIRS), attributed to fecal impaction.

Case Report

The patient is a 34-year-old man who presented to the Emergency Department with a 3-day history of severe, diffuse, crampy abdominal pain and anorexia, associated with fever, chills, two episodes of vomiting and oliguria.

The patient's personal history was positive for cerebral palsy, mental retardation, and chronic constipation requiring laxatives. He was status post ventriculoperitoneal shunt insertion. He was maintained on phenytoin, valproic acid, and phenobarbital. The physical examination was remarkable for fever (39.2[degrees]C), BP 90/50 mm Hg, tachycardia (112 bpm), tachypnea (22 breaths/min), diffuse abdominal tenderness and a severely deformed and rotated thorax. Digital rectal examination revealed severe fecal impaction.

Laboratory studies revealed a white count of 16,600 (90 segmented neutrophils); hemoglobin of 15.1 g/dL and a hematocrit of 46; BUN of 45 mg/dL; and creatinine of 1.6 mg/dL. Liver function tests, electrolytes, and coagulation profile were within normal limits. CRP was 6. Urine analysis was normal. Phenytoin, valproic acid, and phenobarbital levels were within normal limits. Blood cultures were negative. Stools for Wright stain and occult blood were negative.

Chest x-ray showed loss of volume of the right lobe, with a clear left lung, deformed chest wall and a dorsal rotoscoliosis. Abdominal films revealed a large fecaloma in the rectum with associated colonic and small bowel dilation (Fig. 1). Plain CT scan of abdomen and pelvis showed significant dilation of the rectum with large fecaloma associated with dilation of the colon, small bowel and stomach (Fig. 2). Digital disimpaction was done followed by water enemas and oral polyethylene glycol solution. The patient was also started empirically on ciprofloxacin and metronidazole. He made an unremarkable recovery. In view of the patient's overall condition and resolution of his symptoms, colonoscopy was not performed.


Constipation and fecal incontinence are common symptoms in patients with traumatic spinal cord injuries, spinal bifida, multiple sclerosis, diabetic polyneuropathy, Parkinson's disease, stroke, and cerebral palsy. (1) The factors that may contribute to fecal impaction include impaired mental function, immobility, rectal hyposensitivity, weak straining, use of constipating drugs, and dietary inadequacies. (4) In the special case of cerebral palsy, disruption of the neural modulation of the colon motility as well as alteration of the motor behavior of muscles of the anorectal region are responsible for the defecation problem. (5)

Typical symptoms of fecal impaction are anorexia, nausea, vomiting and abdominal pain. Paradoxical diarrhea and incontinence may occur. Urinary problems of frequency, retention, and overflow incontinence are also thought to be commonly caused by the mechanical effects of fecal impaction. In fact, the continuous seepage of moist bacteria-laden mucus and stool also fosters the development of decubitus ulceration. Infections of the urinary tract may also be caused by contamination, obstruction, or the direct passage of bacteria from the intestine to the bladder ("enterorenal syndrome"). (6)

Presenting signs may be confusing to the physician. Temperatures as high as 39.5[degrees]C (103[degrees]F), dysrhythmias, and tachypnea caused by the impaired motility of the diaphragm have all been reported with fecal impaction. (7-9) Laboratory abnormalities associated with impactions are nonspecific. Leukocytosis in which levels reach 15,000 per cubic millimeter may occur. (7) Electrolyte abnormalities, such as hyponatremia, or hypokalemia, may be associated with impaction. Stool that is positive for blood may reflect the mucosal irritation of an impaction. (7)


When a fecal impaction is suspected but the rectal examination is negative, plain abdominal radiography to look for fecaloma or signs of obstruction, such as colonic dilation and unusual air-fluid levels in the small bowel is indicated. (6,7,10,11) The cecum suffers the brunt of obstruction by virtue of its distensibility, and the closer the obstruction lies to the cecum, the larger the number of air-fluid levels in the small bowel.


Our patient developed typical symptoms of fecal impaction, including abdominal pain, anorexia, and nausea. He also developed fecal incontinence, oliguria and prerenal azotemia secondary to decrease fluid intake and gastrointestinal losses. The peculiarity in our case is that the patient had parameters in line with the diagnosis of SIRS. These included:

1. General parameters: fever (>38.3[degrees]C); heart rate > 90 bpm; tachypnea > 30 bpm

2. Inflammatory parameters: leukocytosis (WBC > 16 000/[micro]L); plasma CRP > 2 SD above the normal value

3. Hemodynamic parameters: arterial hypotension; acute oliguria; creatinine rise >0.0.5 mg/dL

The 1992 statement from the American College of Chest Physicians/Society of Critical Care Medicine (ACCP/SCCM) Consensus Conference introduced into common parlance the term "systemic inflammatory response syndrome" (SIRS). The term provides a reference for the complex findings that result from a systemic activation of the innate immune response, regardless of cause. The statement hypothesized that SIRS is triggered by localized or generalized infection, or sterile inflammatory processes. SIRS is considered to be present when patients have more than one of the following: body temperature > 38[degrees]C or < 36[degrees]C; heart rate > 90 bpm/min; hyperventilation evidenced by respiratory rate > 20/min or PaC[O.sub.2] < 32 mm Hg; WBC > 12,000 cells/[micro]L or < 4,000/[micro]L. (12) The 2001 Society of Critical Care Medicine/European Society of Intensive Care Medicine/The American College of Chest Physicians/American Thoracic Society/ Surgical Infection Society (SCCM/ESICM/ACCP/ATS/SIS) International Sepsis Definitions Conference (13) concluded that the 1992 consensus definitions are too widely considered to be of utility in diagnosing a cause of the syndrome, since the systemic inflammatory response can be triggered by a variety of infectious and noninfectious causes.

In fact, while the clinical manifestations of systemic inflammation are wide, the biochemical features may be more consistent. Investigators have detected elevated circulating levels of interleukin-6, adrenomedullin, soluble CD14, soluble endothelial cell/leukocyte adhesion molecule-1, macrophage inflammatory protein 1 [alpha], extraphospholipase A2, and C-reactive protein in patients meeting the 1992 SIRS criteria. In the future, if supported by further epidemiologic data, it may be possible to use purely biochemical and/or immunologic inflammatory response markers. It may be that inflammation is present when the circulating concentration of IL-6, procalcitonin, or CRP is increased. No large prospective studies currently support such a conclusion. (14)

Our patient developed SIRS with a negative workup for underlying infectious etiology. To our knowledge, this is the second case of constipation resulting in SIRS. However, in the reported case by Hagen and Jones, (14) group G streptococcal bacteremia was identified. Watsky et al (15) suggested a greater role for breaching of the anatomic mucosal or epithelial barriers to infection rather than a specific immune defect in the pathogenesis of this bacteremia. It is possible that our patient could have had a transient group G streptococcal bacteremia or any other bacteremia not detected by blood cultures, with no clinically evident source of infection. Other possible causes of the inflammatory response can be the metabolic alteration associated with bowel obstruction, or the breaching of the anatomic mucosal or epithelial barriers to exotoxins produced by altered flora.

Our patient improved remarkably after digital disimpaction followed by water enemas, along with antibiotics. Reviewing the literature, we did not come across any study that looked at whether digital disimpaction is sufficient to resolve SIRS. This remains an issue to be answered by further workup, looking at the mechanisms of impaction and the effects of digital disimpaction per se.

Our case illustrates the serious sequelae of fecal impaction, which should be considered in patients with neurologic disorders and SIRS. Furthermore, SIRS may be a prelude to full blown sepsis and multiorgan failure.


1. Krogh K, Christensen P, Laurberg S. Colorectal symptoms in patients with neurological diseases. Acta Neurol Scand 2001;103:335-343.

2. Wald A. Constipation and fecal incontinence in the elderly. Gastroenterol Clin North Am 1990;19:405-418.

3. Schnelle JF, Leung FW. Urinary and fecal incontinence in nursing homes. Gastroenterology 2004;126:S41-S47.

4. Camilleri M, Bharucha AE. Gastrointestinal dysfunction in neurologic disease. Semin Neurol 1996;16:203-216.

5. Park ES, Park CI, Cho SR, et al. Colonic transit time and constipation in children with spastic cerebral palsy. Arch Phys Med Rehabil 2004;85: 453-456.

6. Breda G, Bianchi GP, Bonomi U, et al. Faecal stasis and bacteriuria: experimental research in rats. Urol Res 1975;2:155-157.

7. Gurll N, Steer M. Diagnostic and therapeutic considerations for fecal impaction. Dis Colon Rectum 1975;18:507-511.

8. Wright BA, Staats DO. The geriatric implications of fecal impaction. Nurse Pract 1986;11:53-66.

9. Young RW. The problem of fecal impaction in the aged. J Am Geriatr Soc 1973;21:383.

10. Gupta KL. Intestinal obstruction due to constipation in the elderly. Br J Clin Pract 1983;37:155-156.

11. Hughes JJ, Neuffer FH. Diagnostic imaging of postoperative fecal impaction. Ala J Med Sci 1986;23:420-422.

12. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992;20:864-874.

13. Levy MM. Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference. Intensive Care Med 2003;29:530-538.

14. Hagen MD, Jones J. Group G streptococcal bacteremia in a chronically constipated adolescent. South Med J 1987;80:1056-1057.

15. Watsky KL, Kollisch N, Densen P. Group G streptococcal bacteremia: the clinical experience at Boston University Medical Center and a critical review of the literature. Arch Intern Med 1985;145:58-61.
For myself I am an optimist--it does not seem to be much use being
anything else.
--Sir Winston Churchill

Ihab I. ElHajj, MD, Lara M. El-Zahabi, MD, Haitham Abdul-Baki, MD, and Kassem A. Barada, MD

From the Department of Internal Medicine, American University of Beirut Medical Center (AUBMC), Beirut, Lebanon.

Reprint requests to: Kassem Barada, MD, Associate Professor of Medicine, Department of Internal Medicine, AUBMC, 110 32090 Beirut, Lebanon. Email:

Accepted January 16, 2006.


* Constipation and fecal impaction are common symptoms in patients with neurologic disorders (traumatic spinal cord injuries, spina bifida, multiple sclerosis, diabetic polyneuropathy, Parkinson's disease, stroke, and cerebral palsy).

* Factors that may contribute to fecal impaction include impaired mental status, immobility, rectal hyposensitivity, weak straining, use of constipating drugs, and cerebral palsy.

* Symptoms of fecal impaction vary. They include abdominal pain, nausea, vomiting, anorexia, paradoxical diarrhea and incontinence, urinary problems of frequency, retention, and overflow incontinence.

* Fecal impaction can lead to systemic inflammatory response syndrome and in some cases to bacteremia.

* Treatment of fecal impaction include digital disimpaction, water enemas, and in some cases antibiotics.
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Title Annotation:Case Report
Author:Barada, Kassem A.
Publication:Southern Medical Journal
Geographic Code:1USA
Date:May 1, 2006
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