Frederick A. Moore

Early enteral feeding, compared with parenteral, reduces postoperative septic complications. The results of a meta-analysis.

This two-part meta-analysis combined data from eight prospective randomized trials designed to compare the nutritional efficacy of early enteral (TEN) and parenteral (TPN) nutrition in high-risk surgical patients. The combined data gave sufficient patient numbers (TEN, n = 118; TPN, n = 112) to adequately address whether route of substrate delivery affected septic complication incidence. Phase I (dropouts excluded) meta-analysis confirmed data homogeneity across study sites, that TEN and TPN groups were comparable, and that significantly fewer TEN patients experienced septic complications (TEN, 18%; TPN, 35%; p = 0.01). Phase II meta-analysis, an intent-to-treat analysis (dropouts included), confirmed that fewer TEN patients developed septic complications. Further breakdown by patient type showed that all trauma and blunt trauma subgroups had the most significant reduction in septic complications when fed enterally. In conclusion, this meta-analysis attests to the feasibility of early postoperative TEN in high-risk surgical patients and that these patients have reduced septic morbidity rates compared with those administered TPN.

A genomic storm in critically injured humans

Critical injury in humans induces a genomic storm with simultaneous changes in expression of innate and adaptive immunity genes.

THE ABDOMINAL COMPARTMENT SYNDROME

1. ACS is caused by an acute increase in intra-abdominal pressure, usually as a result of intra-abdominal hemorrhage. 2. The most common and significant complications are respiratory and renal failure. 3. Abdominal decompression promptly reverses the complications of ACS. 4. Failure to recognize and treat ACS is inevitably fatal.

Post-injury Multiple Organ Failure: The Role Of The Gut

ABSTRACT— 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.

Prospective characterization and selective management of the abdominal compartment syndrome

BACKGROUND The abdominal compartment syndrome (ACS) is now recognized as a frequent confounder of surgical critical care following major trauma; however, few prospective data exist concerning its characterization, evolution, and response to decompression. METHODS Acutely injured patients with an injury severity scale (ISS) score >15 requiring emergent laparotomy and intensive care unit (ICU) admission were prospectively evaluated for the development of ACS. The syndrome was defined as an intra-abdominal pressure (IAP) >20 mm Hg complicated by one of the following: peak airway pressure (PAP) >40 cm H2O, oxygen delivery index (DO2I) <600 mL O2/min/m2, or urine output (UO) <0.5 mL/kg/hr. Physiologic response to decompression was similarly documented prospectively. RESULTS Over a 14-month period ending December 1995, 21 (14%) of 145 patients (ISS >15) requiring laparotomy and admitted to our surgical ICU developed ACS; mean age was 39 +/- 9 years; injury mechanism was blunt in 60%; ISS 26 +/- 6. At initial laparotomy, 67% underwent abdominal packing (57% for major liver injuries). Mean IAP was 27 +/- 2.3 mm Hg, and time from laparotomy to decompression was 27 +/- 4 hours; 24% were planned whereas the remaining were prompted by deteriorating organ function as defined above (cardiopulmonary in 43%; renal in 19%; both renal and cardiopulmonary in 14%). Following decompression, there was an increase in cardiac index, oxygen delivery, urine output, and static compliance while there was a decrease in pulmonary capillary wedge pressure, systemic vascular resistance, and peak airway pressure. CONCLUSIONS The abdominal compartment syndrome occurs in a significant number of severely injured patients, and it develops quickly (27 +/- 4 hours). Cardiopulmonary deterioration is the most frequent reason prompting decompression. Timely decompression of the ACS results in improvements in cardiopulmonary and renal function. These data support the use of the proposed ACS grading system for selective management of the syndrome.

Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure

BACKGROUND Primary abdominal compartment syndrome (ACS) is a known complication of damage control. Recently secondary ACS has been reported in patients without abdominal injury who require aggressive resuscitation. The purpose of this study was to compare the epidemiology of primary and secondary ACS and develop early prediction models in a high-risk cohort who were treated in a similar fashion. METHODS Major torso trauma patients underwent standardized resuscitation and had prospective data collected including occurrence of ACS, demographics, ISS, urinary bladder pressure, gastric tonometry (GAP(CO2) = gastric regional CO(2) minus end tidal CO(2)), laboratory, respiratory, and hemodynamic data. With primary and secondary ACS as endpoints, variables were tested by uni- and multivariate logistic analysis (MLA). RESULTS From 188 study patients during the 44-month period, 26 (14%) developed ACS-11 (6%) were primary ACS and 15 (8%) secondary ACS. Primary and secondary ACS had similar demographics, shock, and injury severity. Significant univariate differences included: time to decompression from ICU admit (600 +/- 112 vs. 360 +/- 48 min), Emergency Department (ED) crystalloid (4 +/- 1 vs. 7 +/- 1 L), preICU crystalloid (8 +/- 1 vs. 12 +/- 1L), ED blood administration (2 +/- 1 vs. 6 +/- 1 U), GAP(CO2) (24 +/- 3 vs. 36 +/- 3 mmHg), requiring pelvic embolization (9 vs. 47%), and emergency operation (82% vs. 40%). Early predictors identified by MLA of primary ACS included hemoglobin concentration, GAP(CO2), temperature, and base deficit; and for secondary ACS they included crystalloid, urinary output, and GAP(CO2). The areas under the receiver-operator characteristic curves calculated upon ICU admission are primary= 0.977 and secondary= 0.983. Primary and secondary ACS patients had similar poor outcomes compared with nonACS patients including ventilator days (primary= 13 +/- 3 vs. secondary= 14 +/- 3 vs. nonACS = 8 +/- 2), multiple organ failure (55% vs. 53% vs. 12%), and mortality (64% vs. 53% vs. 17%). CONCLUSION Primary and secondary ACS have similar demographics, injury severity, time to decompression from hospital admit, and bad outcome. 2 degrees ACS is an earlier ICU event preceded by more crystalloid administration. With appropriate monitoring both could be accurately predicted upon ICU admission.

The role of the gastrointestinal tract in postinjury multiple organ failure

Despite intensive investigation, the pathogenesis of postinjury multiple organ failure (MOF) remains elusive. Laboratory and clinical research strongly implicate that the gastrointestinal tract plays a pivotal role. Shock with resulting gut hypoperfusion appears to be one important inciting event. While early studies persuasively focused attention on bacterial translocation as a unifying mechanism to explain early and late sepsis syndromes that characterize postinjury MOF, subsequent studies suggest that other gut-specific mechanisms are operational. Based on our Trauma Research Center observations and those of others, we conclude that: 1) bacterial translocation may contribute to early refractory shock; 2) for patients who survive shock, the reperfused gut appears to be a source of proinflammatory mediators that may amplify the early systemic inflammatory response syndrome; and 3) early gut hypoperfusion sets the stage for progressive gut dysfunction such that the gut becomes a reservoir for pathogens and toxins that contribute to late MOF.

Distal Aortic Perfusion and Cerebrospinal Fluid Drainage for Thoracoabdominal and Descending Thoracic Aortic Repair: Ten Years of Organ Protection

Objective To report the long-term results of our experience using cerebrospinal fluid drainage and distal aortic perfusion in descending thoracic and thoracoabdominal aortic repair. Summary Background Data Repair of thoracoabdominal and thoracic aortic aneurysm by the traditional clamp-and-go technique results in a massive ischemic insult to several major organ systems. Ten years ago, we began to use distal aortic perfusion and cerebrospinal fluid drainage (adjunct) to reduce end-organ ischemia. Methods Between January 1991 and February 2003, we performed 1004 thoracoabdominal or descending thoracic repairs. Adjunct was used in 741 (74%) of 1004. Multivariable data were analyzed by Cox regression. Number needed to treat was calculated as the reciprocal of the risk difference. Results Immediate neurologic deficit was 18 (2.4%) of 741 with adjunct and 18 (6.8%) of 263 without (P < 0.0009). In high-risk extent II aneurysms, the numbers were 11 (6.6%) of 167 with adjunct, and 11 (29%) of 38 without. Long-term survival was improved with adjunct (P < 0.002). The long-term survival results persisted after adjustment for age, extent II aneurysm, and preoperative renal function. Conclusion Use of adjunct over a long period of time has produced favorable results; approximately 1 neurologic deficit saved for every 20 uses of adjunct overall. In extent II aneurysms, where the effect is greatest, this increases to 1 saved per 5 uses. Adjunct is also associated with long-term survival, which is consistent with mitigation of ischemic end-organ injury. These long-term results indicate that cerebrospinal fluid drainage and distal aortic perfusion are safe and effective adjunct for reducing morbidity and mortality following thoracic and thoracoabdominal aortic repair.

Vacuum-assisted wound closure provides early fascial reapproximation in trauma patients with open abdomens

BACKGROUND Damage control and decompressive laparotomies salvage severely injured patients who would have previously died. Unfortunately, many of these patients develop open abdomens. A variety of management strategies exist. The end result in many cases, however, is a large ventral hernia that requires a complex repair 6 to 12 months after discharge. We instituted vacuum-assisted wound closure (VAWC) to achieve early fascial closure and eliminate the need for delayed procedures. METHODS For 12 months ending June 2000, 14 of 698 trauma intensive care unit admissions developed open abdomens and were managed with VAWC dressing. This was changed every 48 hours in the operating room with serial fascial approximation until complete closure. RESULTS Fascial closure was achieved in 13 patients (92%) in 9.9 +/- 1.9 days, and 2.8 +/- 0.6 VAWC dressing changes were performed. There were 2 wound infections, no eviscerations, and no enteric fistulas. CONCLUSIONS Use of VAWC can safely achieve early fascial closure in more than 90% of trauma patients with open abdomens.

Secondary abdominal compartment syndrome is an elusive early complication of traumatic shock resuscitation.

BACKGROUND The term secondary abdominal compartment syndrome (ACS) has been applied to describe trauma patients who develop ACS but do not have abdominal injuries. The purpose of this study was to describe major trauma victims who developed secondary ACS during standardized shock resuscitation. METHODS Our prospective database for standardized shock resuscitation was reviewed to obtain before and after abdominal decompression shock related data for secondary ACS patients. Focused chart review was done to confirm time-related outcomes. RESULTS Over the 30 months period ending May 2001, 11 (9%) of 128 standardized shock resuscitation patients developed secondary ACS. All presented in severe shock (systolic blood pressure 85 +/- 5 mm Hg, base deficit 8.6 +/- 1.6 mEq/L), with severe injuries (injury severity score 28 +/- 3) and required aggressive shock resuscitation (26 +/- 2 units of blood, 38 +/- 3 L crystalloid within 24 hours). All cases of secondary ACS were recognized and decompressed within 24 hours of hospital admission. After decompression, the bladder pressure and the systemic vascular resistance decreased, while the mean arterial pressure, cardiac index, and static lung compliance increased. The mortality rate was 54%. Those who died failed to respond to decompression with increased cardiac index and did not maintain decreased bladder pressure. CONCLUSIONS Secondary ACS is an early but, if appropriately monitored, recognizable complication in patients with major nonabdominal trauma who require aggressive resuscitation.