David Mercer

Despite intensive investigation, the pathogenesis of post-injury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly suggests that the gastrointestinal tract (i.e., the gut) plays a pivotal pathogenic role. Since its inception in 1988, the Trauma Research Center (TRC) at the University of Texas-Houston Medical School (UTHMS) has focused its efforts on elucidating the role of the gut in post-injury MOF. On the basis of our observations and those of others, we believe that 1) shock with resulting gut hypoperfusion is an important inciting event, 2) the reperfused gut is a source of proinflammatory mediators that can amplify the early systemic inflammatory response syndrome (SIRS) and thus contribute to early MOF, 3) early gut hypoperfusion causes an ileus in both the stomach and small bowel that sets the stage for progressive gut dysfunction so that the proximal gut becomes a reservoir for pathogens and toxins that contribute to late sepsis-associated MOF, and 4) late infections cause further worsening of this gut dysfunction. Thus, the gut can be both an instigator and a victim of MOF. The purpose of this article is to provide the rationale behind these beliefs and to provide a brief overview of the ongoing research projects in the TRC at UTHMS.

OBJECTIVE: To assess the utility of triage guidelines for patients with cholelithiasis and suspected choledocholithiasis, incorporating selective use of magnetic resonance cholangiography (MRC) and endoscopic retrograde cholangiopancreatography (ERCP) before laparoscopic cholecystectomy (LC). SUMMARY BACKGROUND DATA: ERCP is the most frequently used modality for the diagnosis and resolution of choledocholithiasis before LC. MRC has recently emerged as an accurate, noninvasive modality for the detection of choledocholithiasis. However, useful strategies for implementing this diagnostic modality for patient evaluation before LC have not been investigated. METHODS: During a 16-month period, the authors prospectively evaluated all patients before LC using triage guidelines incorporating patient information obtained from clinical evaluation, serum chemistry analysis, and abdominal ultrasonography. Patients were then assigned to one of four groups based on the level of suspicion for choledocholithiasis (group I, extremely high; group 2, high; group 3, moderate; group 4, low). Group 1 patients underwent ERCP and clearance of common bile duct stones; group 2 patients underwent MRC; group 3 patients underwent LC with intraoperative cholangiography; and group 4 patients underwent LC without intraoperative cholangiography. RESULTS: Choledocholithiasis was detected in 43 of 440 patients (9.8%). The occurrence of choledocholithiasis among patients in the four groups were 92.6% (25/27), 32.4% (12/37), 3.8% (2/52), and 0.9% (3/324) for groups 1, 2, 3, and 4, respectively (P <.001). MRC was used for 8.4% (37/440) of patients. Patient triage resulted in the identification of common bile duct stones during preoperative ERCP in 92.3% (36/39) of the patients. Unsuspected common bile duct stones occurred in six patients (1.4%). CONCLUSIONS: The probability of choledocholithiasis can be accurately assessed based on information obtained during the initial noninvasive evaluation. Stratification of risks for choledocholithiasis facilitates patient management with the most appropriate diagnostic studies and interventions, thereby improving patient care and resource utilization.

BACKGROUND: Much is still unknown about the actual incidence of anesthesia-related cardiac arrest in the United States. METHODS: The authors identified all of the cases of cardiac arrest from their quality improvement database from 1999 to 2009 and submitted them for review by an independent study commission to give them the best estimate of anesthesia-related cardiac arrest at their institution. One hundred sixty perioperative cardiac arrests within 24 h of surgery were identified from an anesthesia database of 217,365 anesthetics. An independent study commission reviewed all case abstracts to determine which cardiac arrests were anesthesia-attributable or anesthesia-contributory. Anesthesia-attributable cardiac arrests were those cases in which anesthesia was determined to be the primary cause of cardiac arrest. Anesthesia-contributory cardiac arrests were those cases where anesthesia was determined to have contributed to the cardiac arrest. RESULTS: Fourteen cardiac arrests were anesthesia-attributable, resulting in an incidence of 0.6 per 10,000 anesthetics (95% CI, 0.4 to 1.1). Twenty-three cardiac arrests were found to be anesthesia-contributory resulting in an incidence of 1.1 per 10,000 anesthetics (95% CI, 0.7 to 1.6). Sixty-four percent of anesthesia-attributable cardiac arrests were caused by airway complications that occurred primarily with induction, emergence, or in the postanesthesia care unit, and mortality was 29%. Anesthesia-contributory cardiac arrest occurred during all phases of the anesthesia, and mortality was 70%. CONCLUSION: As judged by an independent study commission, anesthesia-related cardiac arrest occurred in 37 of 160 cardiac arrests within the 24-h perioperative period.

BACKGROUND: Shock is a prime inciting event for postinjury multiple organ failure (MOF), believed to induce a state of injurious systemic inflammation. In animal models of hemorrhagic shock, early (< 24 hours) changes in cytokine production are an index of the systemic inflammatory response syndrome. However, their predictive value in trauma patients remains to be fully elucidated. STUDY DESIGN: In a prospective observational pilot study of > 1 year at an urban Level I trauma center, serial (every 4 hours) serum cytokine levels were determined during a 24-hour period using multiplex suspension immunoassay in patients with major torso trauma (excluding severe brain injury) who met criteria for standardized shock resuscitation. Temporal cytokine expression was assessed during shock resuscitation in severe trauma patients to predict risk for MOF. MOF was assessed with the Denver score. RESULTS: Of 48 study patients (mean age 39 +/- 3 years, 67% men, 88% blunt mechanism, mean Injury Severity Score 25 +/- 2), MOF developed in 11 (23%). MOF patients had a considerably higher mortality (64% versus 3%) and fewer ICU-free days (3.5 +/- 2 versus 17.8 +/- 1.3 days) compared with non-MOF patients. Traditional predictors of MOF, including age (45 +/- 7 versus 38 +/- 3 years; p=0.21), Injury Severity Score (26 +/- 3 versus 25 +/- 2; p=0.67), admission hemoglobin (11.4 +/- 0.9 versus 12.1 +/- 0.5 g/dL; p=0.22), international normalized ratio (1.6 +/- 0.2 versus 1.4 +/- 0.06; p=0.17), and base deficit (9.0 +/- 2 versus 7.1 +/- 0.8; p=0.19), were not significantly different between MOF and non-MOF patients. Statistical analysis identified six candidate predictors of MOF: inducible protein 10, macrophage inflammatory protein-1beta, interleukin-10, interleukin-6, interleukin-1Ra, and eotaxin. CONCLUSIONS: These data provide insight into cytokine expression during traumatic shock that can enable earlier identification of patients at risk for development of MOF.