CASE REPORT
The Journal of TRAUMA威 Injury, Infection, and Critical Care
Clostridium difficile Pericarditis Complicating Pseudomembranous Colitis in a Trauma Patient Richard Koehler, MD, Mary Mone, RN, Edward Kimball, MD, Daniel Vargo, MD, Nick Lonardo, PharmD, and Richard Barton, MD J Trauma. 2003;55:771–773.
Clostridium difficile is a spore-forming, toxigenic bacillus that causes diarrhea and colitis, typically after the use of broad-spectrum antibiotics. It is reported to colonize roughly a quarter of hospitalized patients and can be cultured from environmental contamination in most health care facilities. C. difficile is most commonly associated with colonic infection, but a number of extracolonic manifestations have been reported. We report the first documented case of a patient with C. difficile pericarditis that presented as pericardial effusion and resultant tamponade in a patient hospitalized after multiple trauma. Institutional Review Board approval was obtained, as was informed patient consent providing permission for review and publication of this information.
CASE REPORT
A
previously healthy 47-year-old man was the restrained driver of an automobile that was struck broadside by a semitrailer. Oral intubation was performed at the scene and the patient was brought to our Level I trauma facility and admitted to the surgical intensive care unit. Injuries included subdural and subarachnoid hemorrhages; grade III liver laceration; multiple nondisplaced pelvic fractures, with a large hematoma in the right hemipelvis; and bilateral mandibular fractures, with an open fracture on the left. Initial resuscitation and stabilization were routine. The liver laceration and pelvic fractures were managed nonoperatively. The patient was started on intravenous clindamycin (900 mg every 8 hours) as prophylaxis at admission and on posttrauma day 3 underwent open reduction and internal fixation of the mandibular fractures. The patient’s condition improved and he was transferred to a general surgical floor on posttrauma day 8. Treatment with clindamycin was continued through postoperative day 10 (posttrauma day 13). On hospital day 12, the patient developed diarrhea and vague abdominal pain and
Submitted for publication June 26, 2003. Accepted for publication July 16, 2003. Copyright © 2003 by Lippincott Williams & Wilkins, Inc. From the Department of Surgery, University of Utah, Salt Lake City, Utah. Presented at the Southwestern Surgical Society, April 29 –May 3, 2001, Cancun, Mexico. Address for reprints: Richard G. Barton, MD, Department of Surgery, University of Utah, 3B313, School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132; email:
[email protected]. DOI: 10.1097/01.TA.0000088859.47719.C8
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distention, followed by hypotension, tachycardia, fever, hyperlactatemia (5.4 mmol/L), and an elevated white blood cell count (40.5 K/L), consistent with sepsis. A computed tomographic scan of the abdomen was obtained showing a massively dilated colon with colonic wall thickening (Fig. 1). The patient was transferred emergently to the surgical intensive care unit and placed on broad-spectrum antibiotics including metronidazole for suspected C. difficile enterocolitis. Despite aggressive volume resuscitation and hemodynamic and ventilatory support, the patient deteriorated and required a total abdominal colectomy with Brooke ileostomy for toxic megacolon. A stool sample obtained before surgery ultimately proved positive for C. difficile toxin, and the surgical pathology report confirmed the presence of ischemic necrosis with pseudomembrane formation consistent with toxic megacolon. Over the course of the following week, the patient remained febrile and became progressively tachycardic. Abdomen, pelvis, and thorax computed tomographic scans were obtained to rule out a septic focus and revealed ascites, bilateral pleural effusions, and a pericardial effusion (Fig. 2). Aspirates of the ascitic and pleural fluid proved to be sterile. With continued signs of hemodynamic instability, an urgent echocardiogram was obtained that revealed normal left ventricular systolic function but a moderate pericardial effusion that was compressing the right atrium and ventricle (Fig. 3). Ultrasound-guided pericardiocentesis was performed, with immediate hemodynamic improvement; approximately 700 mL of straw-colored fluid was obtained and sent for analysis. The initial laboratory analysis of the pericardial fluid revealed acute neutrophilic inflammation, with the anaerobic cultures growing gram-negative rods with spores, eventually identified as C. difficile. The patient was treated successfully with a 10-day course of metronidazole.1 The patient progressed through the remainder of the hospitalization and was eventually transferred to rehabilitation on postinjury day 49. On posttrauma day 80 and postpericardial effusion drainage day 57, the patient was discharged to home with a full recovery and no known sequelae.
DISCUSSION Clostridium difficile is a gram-positive, anaerobic, sporeforming bacillus, first described as “Bacillus difficilis” by Hall and O’Toole in a review article on the bacterial flora of 771
The Journal of TRAUMA威 Injury, Infection, and Critical Care
Fig. 1. Computed tomographic scan of the abdomen showing markedly inflamed colon and ascites.
Fig. 3. Echocardiogram showing pericardial effusion compressing the right atrium and ventricle.
meconium from 50 healthy newborn infants in 1935.2 It is now known to be a normal component of fecal flora in 1% to 4% of healthy adults, and it has also been reported to colonize roughly 17% of hospitalized patients.3,4 Since the first description of antibiotic-associated diarrhea and colitis in the late 1970s, C. difficile has been thought to be responsible for approximately 15% to 25% of all antibiotic-associated diarrheas and 50% to 70% of antibiotic-related colitis.5,6 The organism can be cultured as a contaminant from many surfaces in a hospital and is transmitted between patients by equipment and the hospital staff. Because of the relative pervasiveness of this organism, C. difficile is regarded as a significant and potentially lethal cause of infection in all patient populations. The spectrum of clinical presentations from this disease in hospitalized patients varies from the asymptomatic carrier to that of life-threatening toxicity. The systemic symptoms exhibited are primarily attributable to the circulating toxins from released
sepsis inflammatory mediators. The patients considered at highest risk for C. difficile include the immunocompromised, such as organ transplant or cancer patients; however, every patient is potentially at risk because of the exposure to the bacillus or because of any number of risk factors.1,4 Although broad-spectrum antibiotics are most often associated with Clostridium difficile enterocolitis, all antibiotics, including metronidazole, have been reported to cause this disease state. Clindamycin use has long been associated with pseudomembranous colitis; because of this, clindamycin indications are limited to serious infections caused by susceptible anaerobic bacteria.1,5 The use of clindamycin in this case for a class III contaminated open traumatic wound was appropriate, but the treatment duration of 13 days likely contributed to this complication.7 The mortality associated with C. difficile infections is reported to be 0.6% of patients with active infections (pseudomembranous colitis) and as high as 57% in patients requiring colectomy for toxic megacolon.8 Typically, C. difficile is associated with colonic manifestations, but it also has been implicated in a number of extraintestinal infections. Extracolonic C. difficile is an unlikely diagnosis and not well appreciated by many clinicians. Previously documented extracolonic infections include bacteremia, arthritis, peritonitis, necrotizing fasciitis, splenic abscess, and osteomyelitis.9 The timing of distant site infections is not well described but ranges from the time of antibiotic therapy to weeks later. A recent article notes that except for cases involving the small intestine and arthritis, most of the extracolonic cases were unrelated to previous antibiotic exposure, the reasons for which were unclear.10 This patient presentation involved sepsis from toxic megacolon with development of a pericardial fluid collection that cultured positive for C. difficile despite appropriate antibiotic therapy with intravenous metronidazole. The cardiac effusion was large enough to produce tamponade physiology requiring drainage. As this case demonstrates, the versatility of the C. difficile organism can be responsible for a variety of well-documented
Fig. 2. Computed tomographic scan of the thorax showing pericardial effusion and bilateral pleural effusions.
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Pericarditis Complicating Pseudomembranous Colitis clinical manifestations, ranging from diarrhea to toxic megacolon and sepsis, in addition to this newly reported extracolonic manifestation of infectious pericarditis. This clinical scenario is likely rare; however, in cases of C. difficile sepsis where systemic antibiotics, adequate fluid resuscitation, and surgical intervention fail to stabilize the patient, the diagnosis of infectious pericarditis with cardiac tamponade should be considered as a possible mechanism for hemodynamic instability.
REFERENCES Cleary RK. Clostridium difficile-associated diarrhea and colitis: clinical manifestations, diagnosis, and treatment. Dis Colon Rectum. 1998;41:1435–1449. 2. Hall IC, O’Toole E. Intestinal flora in newborn infants with a description of a new pathogenic anaerobe, bacillus difficilis. Am J Dis Child. 1935;49:390 – 402. 3. Kyne L, Warny M, Qamar A, Kelly C. Asymptomatic carriage of Clostridium difficile and serum levels of IgG antibody against toxin A. N Engl J Med. 2000;342:390 –397.
4.
5. 6.
7.
8.
1.
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9.
10.
Siemann M, Koch-Dörfler M, Rabenhorst G. Clostridium difficileassociated diseases: the clinical courses of 18 fatal cases. Intensive Care Med. 2000;26:416 – 421. Bartlett JG. Antibiotic associated diarrhea. Clin Infect Dis. 1992; 15:573–581. Fekety R. Guidelines for the diagnosis and management of Clostridium difficile associated diarrhea and colitis. Am J Gastroenterol. 1997;92:739 –750. Mangram AJ, Horan TC, Pearson ML, et al. Guideline for prevention of surgical site infection, 1999: Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol. 1999; 20:247–278. Dallal RM, Harbrecht BG, Boujoukas AJ, et al. Fulminant Clostridium difficile: an underappreciated and increasing cause of death and complications. Ann Surg. 2002;235:363–372. Feldman RJ, Kallich M, Weinstein MP. Bacteremia due to Clostridium difficile: case report and review of extraintestinal C. difficile infections. Clin Infect Dis. 1995;20:1560 –1562. Jacobs A, Barnard K, Fishel R, Gradon J. Extracolonic manifestations of Clostridium difficile infections: presentation of two cases and review of the literature. Medicine. 2001;80:88 – 101.
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