Clostridium difficile Infections after Blunt Trauma: A Different Patient Population?

BACKGROUND The epidemiology of Clostridium difficile-associated infection (CDI) has changed, and it is evident that susceptibility is related not only to exposures and bacterial potency, but host factors as well. Several small studies have suggested that CDI after trauma is associated with a different patient phenotype. The purpose of this study was to examine and describe the epidemiologic factors associated with C. difficile in blunt trauma patients without traumatic brain injury using the Trauma-Related Database as a part of the "Inflammation and Host Response to Injury" (Glue Grant) and the University of Florida Integrated Data Repository. METHODS Previously recorded baseline characteristics, clinical data, and outcomes were compared between groups (67 C. difficile and 384 uncomplicated, 813 intermediate, and 761 complicated non-C. difficile patients) as defined by the Glue Grant on admission and at days seven and 14. RESULTS The majority of CDI patients experienced complicated or intermediate clinical courses. The mean ages of all cohorts were less than 65 y and CDI patients were significantly older than uncomplicated patients without CDI. The CDI patients had increased days in the hospital and on the ventilator, as well as significantly higher new injury severity scores (NISS), and a greater percentage of patients with NISS >34 points compared with non-CDI patients. They also had greater Marshall and Denver multiple organ dysfunction scores than non-CDI uncomplicated patients, and greater creatinine, alkaline phosphatase, neutrophil count, lactic acid, and PiO2:FiO2 compared with all non-CDI cohorts on admission. In addition, the CDI patients had higher glucose concentrations and base deficit from uncomplicated patients and greater leukocytosis than complicated patients on admission. Several of these changes persisted to days seven and 14. CONCLUSION Analysis of severe blunt trauma patients with C. difficile, as compared with non-CDI patients, reveals evidence of increased inflammation, immunosuppression, worse acute kidney injury, higher NISS, greater days in the hospital and on the ventilator, higher organ injury scores, and prolonged clinical courses. This supports reports of an increased prevalence of CDI in a younger population not believed previously to be at risk. This unique population may have specific genomic or inflammation-related risk factors that may play more important roles in disease susceptibility. Prospective analysis may allow early identification of at-risk patients, creation of novel therapeutics, and improved understanding of how and why C. difficile colonization transforms into infection after severe blunt trauma.

[1]  H. Baker,et al.  A genomic analysis of Clostridium difficile infections in blunt trauma patients , 2013, The journal of trauma and acute care surgery.

[2]  D. Schoenfeld,et al.  Benchmarking Outcomes in the Critically Injured Trauma Patient and the Effect of Implementing Standard Operating Procedures , 2012, Annals of surgery.

[3]  John D. Storey,et al.  A genomic storm in critically injured humans , 2011, The Journal of experimental medicine.

[4]  D. Mukamel,et al.  Increases in mortality, length of stay, and cost associated with hospital-acquired infections in trauma patients. , 2011, Archives of surgery.

[5]  V. Tam,et al.  A common polymorphism in the interleukin-8 gene promoter is associated with an increased risk for recurrent Clostridium difficile infection. , 2010, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[6]  R. Chinn,et al.  National point prevalence of Clostridium difficile in US health care facility inpatients, 2008. , 2009, American journal of infection control.

[7]  P. Efron,et al.  Clostridium difficile colitis. , 2009, The Surgical clinics of North America.

[8]  D. Musher,et al.  Nitazoxanide versus vancomycin in Clostridium difficile infection: a randomized, double-blind study. , 2009, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[9]  J. Cavaillon,et al.  Compensatory anti-inflammatory response syndrome , 2008, Thrombosis and Haemostasis.

[10]  T. Scalea,et al.  Clostridium difficile infection in critically injured trauma patients. , 2008, Surgical infections.

[11]  C. Kelly,et al.  Clostridium difficile--more difficult than ever. , 2008, The New England journal of medicine.

[12]  J. Bartlett,et al.  Clinical recognition and diagnosis of Clostridium difficile infection. , 2008, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[13]  M. Larocco,et al.  Association of interleukin-8 polymorphism and immunoglobulin G anti-toxin A in patients with Clostridium difficile-associated diarrhea. , 2007, Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association.

[14]  J. Minei,et al.  Inflammation and the Host Response to Injury, a Large-Scale Collaborative Project: patient-oriented research core--standard operating procedures for clinical care. II. Guidelines for prevention, diagnosis and treatment of ventilator-associated pneumonia (VAP) in the trauma patient. , 2006, The Journal of trauma.

[15]  G. Pawelec,et al.  Aging and innate immunity. , 2006, Immunity.

[16]  N. Weng Aging of the immune system: how much can the adaptive immune system adapt? , 2006, Immunity.

[17]  M. Larocco,et al.  A Common Polymorphism in the Interleukin 8 Gene Promoter Is Associated with Clostridium difficile Diarrhea , 2006, The American Journal of Gastroenterology.

[18]  Stuart Johnson,et al.  An epidemic, toxin gene-variant strain of Clostridium difficile. , 2005, The New England journal of medicine.

[19]  C. Kelly,et al.  Health care costs and mortality associated with nosocomial diarrhea due to Clostridium difficile. , 2002, Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.

[20]  F. Barbut,et al.  Epidemiology of Clostridium difficile-associated infections. , 2001, Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases.

[21]  M. Grotz,et al.  [Scoring multiple organ failure after severe trauma. Comparison of the Goris, Marshall and Moore scores]. , 2001, Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen.

[22]  W. Wiesmann,et al.  Lymphocyte activation after non‐thermal trauma , 2000, The British journal of surgery.

[23]  T. Menges,et al.  Changes in blood lymphocyte populations after multiple trauma: association with posttraumatic complications. , 1999, Critical care medicine.

[24]  J. Simes,et al.  Total parenteral nutrition and cancer clinical trials , 1986, Cancer.

[25]  J. Rodrigues,et al.  Clostridium difficile infection in general surgery patients; identification of high-risk populations. , 2010, International journal of surgery.

[26]  J. Gerberding,et al.  Severe Clostridium difficile-associated disease in populations previously at low risk--four states, 2005. , 2005, MMWR. Morbidity and mortality weekly report.

[27]  A. Sauaia,et al.  Early predictors of postinjury multiple organ failure. , 1994, Archives of surgery.