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Total parenteral nutrition (TPN) decreases intestinal IgA and levels of Th2 cytokines, interleukin (IL)-4, and IL-10 within the supernatants of intestinal homogenates. These cytokines are known to stimulate IgA production in vitro by cells of the gut-associated lymphoid tissue (GALT). Glutamine (GLN) supplementation of TPN normalizes GALT mass and cytokine levels. Because intestinal homogenates contain mucosa which itself is a source of cytokines, it was unclear whether cytokines change within the GALT itself. This study investigates dietary effects on IL-4 and IL-10 cytokine mRNA expression within isolated GALT lamina propria cells after lipopolysaccharide (LPS) stimulation. Prospective randomized experimental trials were used in this study. Fifty-nine mice were randomized to chow, intravenous TPN (IV-TPN), intragastric TPN (IG-TPN), complex enteral diet (CED), or 2% GLN-supplemented TPN (GLN-TPN). In experiment 1, animals were fed chow, IV-TPN, IG-TPN, or CED for 5 days and received intraperitoneal LPS (100 microg/kg BW), and then were sacrificed 1 h later. Intestine was harvested for GALT lamina propria. Total RNA was extracted from lamina propria cells and cytokine mRNA for IL-4, and IL-10 was measured by reverse transcriptase polymerase chain reaction. IgA levels of intestinal washing were also measured with ELISA. In experiment 2, mRNA for IL-4 and IL-10, and intestinal IgA levels were measured in mice fed chow, IV-TPN, or GLN-TPN as in experiment 1. Both IL-4 and IL-10 mRNA expression decreased significantly in IV-TPN mice compared to chow or CED feeding. IG-TPN resulted in IL-10 mRNA expression significantly lower than chow or CED but significantly better than IV-TPN. GLN preserved IL-4 and IL-10 mRNA levels, which correlated with intestinal IgA levels. Route and type of nutrition as well as GLN influence message for the Th2 type IgA-stimulating cytokines, IL-4 and IL-10, within the primary site of GALT IgA production, the lamina propria.

Magnesium (Mg) deficiency, commonly diagnosed as hypomagnesemia based upon low serum Mg concentrations, is a frequent electrolyte abnormality in critically ill patients. Intravenous replacement therapy is empiric and serum Mg concentrations have traditionally been used as guidelines for measuring efficacy. Recent studies have shown that the Mg content of mononuclear blood cells (MBCs) may provide a better index for Mg status than serum concentrations. The purpose of this study was to evaluate the effects of intravenous Mg replacement therapy on MBC Mg content and serum Mg concentrations in critically ill hypomagnesemic patients. Adult patients admitted to the trauma intensive-care unit (ICU) with serum Mg concentration 133 mumol/L), pregnancy, or those who were seropositive for HIV were excluded. Ten patients with moderate (> 0.4-0.6 mmol/L [> 1.0-1.5 mg/dL]) and severe ( 0.7). The doses of MgSO4 (0.5-0.75 mmol/kg) used in this study increased serum Mg concentrations, but did not result in a statistically significant change of MBC Mg content in this group of trauma ICU patients.

The efficacy of prophylactic vena caval filters (VCF) in reducing morbidity and mortality from pulmonary embolism (PE) in high-risk trauma patients has been shown, but minimal follow-up data is currently available. VCFs were prophylactically placed in 110 patients between August 1991 and June 1995. There was an early VCF complication rate of 7%. Twenty-two patients died; the remaining 88 patients formed the basis for the follow-up study. Forty-five patients were located and interviewed by phone, and 30 of these patients (34%) returned for evaluation. The mean follow-up time was 18 months (range, 4-42 months). There was no incidence of caval thrombosis on follow-up. Eleven patients had physical findings, and duplex evidence consistent with postphlebitic syndrome. An additional three patients had evidence of old deep venous thrombosis (DVT) by duplex, but no significant symptomatology. VCF are effective in preventing PE related deaths and have few major complications. The long-term morbidity associated with posttraumatic venous thrombosis is significant. This morbidity is related not to PE or VCF, but to the underlying DVT. Improved strategies against DVT are necessary.

Objective : Recently, transesophageal echocardiography (TEE) has been proposed as the standard for the diagnosis of traumatic disruption of the aorta (TDA), replacing aortography. The purpose of this study was to evaluate the accuracy and practicality of TEE in the diagnosis of TDA. Design : Prospective clinical trial. Materials and Methods : Patients with blunt trauma admitted with a suspected diagnosis of TDA were evaluated with TEE and aortography. Measurements and Main Results : Thirty-four patients were evaluated with TEE and aortography. TEE was unsuccessful in five patients (15%). Of the remaining 29 patients, TEE results were true-positive in four and true-negative in 20. TEE results were false-positive in two patients, and three injuries were missed (two were proximal to the left subclavian artery, and one was a localized aortic disruption). Sensitivity and specificity of TEE were 57% and 91%, respectively, compared with aortography, for which sensitivity was 89% and specificity was 100%. Conclusion : Although the use of TEE in the diagnosis of TDA has several advantages, it is not more accurate than aortography. TEE should not replace aortography as the standard for the diagnosis of TDA.

Debridement, fecal diversion, and rectal washout have been proposed as the primary therapy for complex perineal lacerations, but, in most series, survivors have a pelvic sepsis rate of 40-80%. In a retrospective study, six of 18 patients sustaining severe perineal lacerations died within the first few hours of injury due to exsanguination from pelvic injuries. The remaining 12 patients underwent sigmoidoscopy, diversion of the fecal stream with irrigation of the distal rectal stump, and radical initial debridement of necrotic soft tissue. Enteral access was obtained in two patients. In the patients with mandatory daily debridement and pulsatile irrigation, no pelvic sepsis occurred. In three patients without daily debridement, pelvic sepsis complicated recovery. The ability of patients to resume oral nutrition was significantly delayed, necessitating total parenteral nutrition in three patients. We conclude that sigmoidoscopy, total diversion of the fecal stream with irrigation of the distal rectal stump, enteral access for feeding, radical initial debridement of necrotic soft tissue, and mandatory daily debridement with pulsatile irrigation optimize recovery from this devastating injury.

Over the past 10 years, several clinical and experimental studies report the potential benefit of enteral nutrition as primary therapy after multiple system trauma. In this study, 98 patients sustaining blunt and penetrating trauma were randomised to receive either enteral or parenteral feeding for 15 days. There were significantly fewer infectious complications in patients randomised to receive enteral feeding with particular benefit shown in the most severely injured patients. Serum protein concentrations correlated with the clinical outcome with an increase in constitutive protein and decrease in acute phase protein concentrations occurring in the enteral group through a decrease in septic complications and possible direct hepatic 'reprioritisation'. Enteral feeding serves as a primary therapy affecting the outcome of critically ill patients.

Hypermetabolic, critically ill patients rapidly mobilize lean tissue, releasing large quantities of amino acids into the circulating amino acid pool for distribution to the liver, intestine, bone marrow, and injured or healing tissues. Within these sites, gluconeogenesis, immune cell proliferation, and fibroblast proliferation support the body’s attempts to seal and heal its injuries while maintaining defenses against bacterial challenges. Glutamine and alanine synthesis up-regulated through the metabolism of branched-chain amino acids by skeletal muscle provide specific fuels for enterocytes and rapidly proliferating immunocytes as well as sources of carbon skeletons for gluconeogenesis [1]. In addition, amino acids from the general amino acid pool are synthesized by the liver into acute-phase production to upregulate effectiveness of the reticuloendothelial system in clearing foreign material from the bloodstream [2]. While current opinion suggests that well-nourished patients can maintain a vigorous metabolic response for a week or perhaps longer, certain mechanisms of mucosal defenses may be influenced by nutrition support even in well-nourished patients.

In health, a symbiotic relationship exists between the human body and the bacteria which colonize its surfaces. Under normal circumstances, products of bacterial metabolism, such as short-chain fatty acids or vitamins, are critical for human well being. A single cell layer of mucosal epithelium with a complex underlying immunologic system and various innate nonspecific mechanisms allow absorption of nutrients while maintaining an effective barrier against the 1-1.5 kg of bacteria and other toxic factors. In times of illness, this balance is upset. Changes in gut permeability, inability to ingest nutrients, antibiotic pressure and many other factors alter the normal checks and balances between coexistence and absorption of toxic intraluminal products and sepsis. While two decades of research have focused on epithelial changes in permeability to toxins and bacteria, recent investigations of intestinal immunity and responses of bacteria to altered body defensives are modifying concepts of host defenses during critical illness. These new concepts in immunology and bacterial responses are the focus of this review.

The incidence of pneumonia and intra-abdominal abscess decreases when critically injured patients are fed enterally as opposed to intravenously or not at all [1, 2]. Our work has focused on mechanisms underlying these clinical findings. In attempting to determine how nutrient, hormonal, or pharmacologic manipulation improves immune dysfunction occurring in fasted or intravenously fed patients, the key question has been: Why does the route of nutrition impair respiratory tract defenses in critically ill patients? To pursue this issue one must understand the normal mechanisms of defense at mucosal surfaces. Our work has demonstrated a key link between the gastrointestinal tract and respiratory immunity with important observations that route of nutrition influences the structure and function of the gut-associated lymphoid tissue (GALT) [3]. GALT cellular changes influence the cytokine environment, IgA production, endothelial cell activation and recruitment.

Several randomized, prospective studies of critically injured trauma patients demonstrate a significant reduction in pneumonia or intra-abdominal abscess in patients receiving enteral nutrition compared with intravenous (IV) nutrition or no post-operative feeding [1–4]. Since these benefits do not occur in well-nourished patients undergoing elective gastrointestinal surgery or less severely injured trauma victims, the results suggest an immunologic or host defense defect induced by severity of injury or by chronic nutritional depletion. With the majority of nutrition-related infectious complications occurring in the respiratory tract, mechanisms protecting moist mucosal surfaces offer an unexplored area of research potential.

Background: Colon wounds are recognized to be highly associated with intra-abdominal abscess (IAA) after penetrating trauma, whereas gastric wounds are thought to contribute minimally to abscess because of the bactericidal effect of low pH. This study evaluated the impact of stomach or colon wounds, the contribution of other risk factors, and associated abdominal injuries on IAA. Methods: Patients with penetrating colon or stomach wounds during a 10-year period were reviewed and stratified by age, Injury Severity Score, transfusions, and associated abdominal injuries. Early deaths (

Objectives: By using abdominal computed tomographic scans in the evaluation of blunt splenic trauma, we previously identified the presence of vascular blush as a predictor of failure, with a failure of nonoperative management of 13% in that series. This finding led to an alteration in our management scheme, which now includes the aggressive identification and embolization of splenic artery pseudoaneurysms. Methods: The medical records of 524 consecutive patients with blunt splenic injury managed over a 4.5-year period were reviewed for the following information: age, Injury Severity Score (ISS), American Association for the Surgery of Trauma splenic injury grade (SIG), method and outcome of management. Results: Of the patients, 66% were male with a mean age of 32± 16, and mean ISS of 25 ± 13. A total of 180 patients (34%) were managed with urgent operation on admission (81% splenectomy (SIG 4.0), 19% splenorrhaphy (SIG 2.6)). The remaining 344 patients (66%) were hemodynamically stable and underwent computed tomographic scan and planned nonoperative management. Of these patients, 322 patients (94%) were successfully managed nonoperatively (61% of total splenic injuries). In 26 patients (8%), a contrast blush identified on computed tomographic scan was confirmed as a parenchymal pseudoaneurysm on arteriography. Twenty patients (SIG, 2.8) were successfully embolized. In six patients, technical failure precluded embolization; all required splenectomy (SIG, 4.0). A total of 22 patients (6%) failed nonoperative management, including the six with unsuccessful embolization attempts. Sixteen patients (SIG, 3.0) who had no evidence of pseudoaneurysm were explored for a falling hematocrit, hemodynamic instability, or a worsening follow-up computed tomography: 13 patients had splenectomy, and three patients had splenorrhaphy. Conclusions: Aggressive surveillance for and embolization of posttraumatic splenic artery pseudoaneurysms improved the rate of successful nonoperative management of blunt splenic trauma to 61%, with a nonoperative failure rate of only 6%. In comparison with our previous work, this reduction in failure of nonoperative management is a significant improvement (p < 0.03).

Introduction: Recent literature supports a conservative trend in the management of pancreatic injuries. Contrary to this trend, some recommend defining ductal integrity by pancreatography, implying that the results alter management. This study examines our recent 5-year experience with a simplified approach to all pancreatic injuries. Methods: Retrospective analysis of patients sustaining pancreatic injuries was performed. Results: One hundred thirty-four patients were identified. Overall mortality was 13%, and pancreatic-related mortality was 2%. Analyses were based on 124 pancreatic injuries among patients who survived >12 hours. Thirty-seven proximal injuries were treated with drainage alone, with a pancreatic morbidity of 11%. Eighty-seven distal pancreatic injuries occurred, 54 with indeterminate ductal status. Twenty-four had high probability for duct injury and were treated by distal resection; 30 with a low probability of ductal injury were drained. Pancreatic morbidity was not different between these groups. Conclusions: Pancreatic injuries including those with indeterminate ductal status can be successfully managed with low morbidity and mortality using this simplified management protocol.

The early catabolic phase of severe injury is associated with acute growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin-like growth factor binding protein-3 (IGFBP-3) deficiency. The metabolic half-life of circulating IGF-1 is prolonged by its binding to IGFBP-3. The role of this binding protein in nutritionally repleted multiple-injury patients has not been previously evaluated. We have measured plasma levels of these polypeptides and nitrogen (N) balance in 18 adult (15 males/3 females ; mean age, 45 years), severely injured, hypermetabolic, and highly catabolic trauma patients within 48 to 60 hours after injury, when they were receiving maintenance fluids without calories or N and during 6 days of total parenteral nutrition (TPN). Before instituting TPN, the patients were randomized to receive (group H, n = 9) or not to receive (group C, n = 9) daily recombinant human growth hormone (rhGH), 0.15 mg/kg IM. Adjuvant rhGH significantly increases plasma levels of GH, IGF-1, IGFBP-3, and insulin. In addition, it shows better improvement in N balance. The bioavailability of IGF-1 is increased, as indicated by the decrease in IGFBP-3 :IGF-1 ratio. A significant correlation between IGF-1 and IGFBP-3 levels is present in the trauma patients who received TPN and rhGH. A GH/IGF-1/IGFBP-3 axis that closely regulates the metabolic status of the patient is established in trauma.

Hepatic failure is frequently seen following severe hemorrhagic shock, sepsis, and trauma. Clearance of various drugs has been used to evaluate hepatocellular dysfunction, including indocyanine green (ICG), an organic anionic dye that is transported similarly to bilirubin, and antipyrine (AP), a marker of oxidative phosphorylation. Previous investigators have noted a decrease in ICG excretion following systemic hemorrhage. The effect of isolated hepatic ischemia on the clearances of ICG and AP was studied in 16 pigs after 90 minutes of vascular occlusion to the liver. Antipyrine clearance decreased almost 50% from baseline values at 24 and 72 hours after the ischemia procedure, indicating a significant depression in the cytochrome P-450 system. On the other hand, ICG clearance did not change significantly. In conclusion, ICG clearance is not depressed after isolated hepatic ischemia in pigs. Changes in organic anion clearance after systemic hemorrhage may be because of release of toxic products from ischemic peripheral tissue.