Thinking outside the box: re-evaluating the approach to penetrating cardiac injuries.

INTRODUCTION: Penetrating cardiac injuries are infrequent but highly lethal. To address these injuries, cardiopulmonary bypass and cardiothoracic surgery availability are required for Level I trauma center verification. However, acute care surgeons are more readily available for this time-sensitive injury. The purpose of this study was to review an acute care surgery-based experience with penetrating cardiac trauma at an urban Level 1 trauma center. Our hypothesis was that care provided solely by acute care surgeons was both safe and effective for this patient population. METHODS: All patients with injuries to the 'cardiac box' following penetrating thoracic trauma were identified from 2005-2010. Demographic and injury related data were obtained. The types and location of cardiac injury, as well as patient outcomes, were determined from operative reports. RESULTS: 1701 patients with penetrating chest trauma were admitted during the study period. 260 patients were identified as having high-risk injuries and were included in the review. 37 patients underwent resuscitative thoracotomy, with a survival rate of 8 %. 76 patients (29 %) suffered a cardiac injury. 72 % of these patients had a preoperative FAST exam, which had a sensitivity and specificity of 56.5 and 82.5 % respectively. 82 % underwent a pericardial window, which had a positive predictive value of 81.4 %. 61 % (n = 46) of the patients with a cardiac injury survived, while the overall death rate in this cohort was 21 %. No patients in the cohort required cardiopulmonary bypass for emergent repair of cardiac injury and acute care surgeons performed all cases. CONCLUSION: Penetrating injury to the heart is highly lethal and time-sensitive. Increasingly, FAST and subxyphoid pericardial window are relied upon to make the diagnosis in patients arriving in varying stages of shock to the resuscitation room. Acute care surgeons are the most appropriate surgeons to care for these injuries and provide safe and effective care.

Stress ulceration requiring definitive surgery after severe trauma.

Despite antiulcer prophylaxis 19 severely injured patients at our institution developed stress ulceration (SU) between 1989 and 1999 requiring surgery for perforation (n = 4) or bleeding (n = 15). A herald bleed (HB) 10.7 +/- 1.2 days after admission, 7.2 +/- 1.2 days before definitive operative therapy, and requiring 7.1 +/- 0.9 units of blood occurred in 93 per cent of patients operated on for bleeding. Bleeding preceded perforation in one patient. Central nervous system damage was part of the injury pattern in 68 per cent of the patients including spinal cord (42%), severe head injury (16%), or both (10%). Forty-two per cent had acalculous cholecystitis found at surgery. Eight patients had vagotomy and antrectomy (VA), and 11 patients had vagotomy and pyloroplasty (VP). VA required more time than VP (255 +/- 41 vs 158 +/- 13 minutes; P = 0.02). One patient (12.5%) rebled after VA versus two (18%) after VP; one patient in each group required reoperation. There was no difference in mortality, length of stay, or intensive care unit stay. A herald bleed preceded recurrent hemorrhage of SU by one week. Spinal cord or head injury increase the risk of SU. More than 40 per cent of patients with SU had acalculous cholecystitis found at operation. VA provides no benefit on rebleeding or reoperation over VP, so anatomical considerations and not rebleed rates should determine the surgical procedure.

The mucosa-associated lymphoid tissue structure, function, and derangements.

Nearly 50% of the immune cells in the body lie just beneath the moist mucosal surfaces at intestinal and extra-intestinal sites. The study of this mucosal immune system in response to shock and to route and type of nutrition provides a cogent explanation for the reduced incidence of pneumonia with enteral feeding. Changes in immune cell mass and function are associated with deterioration of previously established immunity at mucosal surfaces, especially the respiratory tract. By understanding the mechanisms involved in this breakdown, therapeutic strategies can be developed to reduce septic complications in critical illness.

TPN decreases IL-4 and IL-10 mRNA expression in lipopolysaccharide stimulated intestinal lamina propria cells but glutamine supplementation preserves the expression.

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.

Enteral nutrition prevents remote organ injury and death after a gut ischemic insult.

OBJECTIVE: To determine whether parenteral feeding (IV-TPN) influences the local and systemic response to an intestinal insult. SUMMARY BACKGROUND DATA: Parenteral feeding increases ICAM-1 expression and attracts neutrophils (PMNs) to the intestine compared with enterally fed animals. Because the gut is a priming bed for PMNs, the authors hypothesized that IV-TPN may affect organ injury after gut ischemia-reperfusion (I/R). METHODS: Mice were randomized to chow, IV-TPN, intragastric TPN, or complex enteral diet for 5 days' feeding. In experiment 1, 162 mice underwent 15 or 30 minutes of gut I/R, and death was recorded at 72 hours. In experiment 2, 43 mice underwent 15 minutes of gut ischemia and permeability was measured by 125I-labeled albumin at 3 hours after reperfusion. Lung PMN accumulation was measured by myeloperoxidase assay. In experiment 3, albumin leak was tested in the complex enteral diet group (n = 5) and the intragastric TPN group (n = 5) after 30 minutes of gut ischemia and 1 hour of reperfusion. RESULTS: In experiment 1, enteral feeding significantly reduced the death rate compared with IV-TPN after 15 minutes of I/R. After 30 minutes of gut ischemia, the IV-TPN and intragastric TPN groups showed a higher death rate than the chow and enteral diet groups. In experiment 2, IV-TPN significantly increased pulmonary and hepatic 125I albumin leak compared with enteral feeding without increasing pulmonary myeloperoxidase levels. In experiment 3, there were no differences in 125I albumin leak between the complex enteral diet and intragastric TPN groups. CONCLUSION: Enteral feeding reduced the death rate and organ permeability after 15 minutes of ischemia. However, prolonged ischemia (30 minutes) eliminated any benefits of intragastric TPN on survival.

Lack of enteral feeding increases expression of E-selectin after LPS challenge.

BACKGROUND: Total parenteral nutrition (IV-TPN) increases neutrophil accumulation in the small intestine, expression of intestinal ICAM-1 and P-selectin, and upregulates E-selectin expression in the lung. Endothelial activation induced by lack of enteral nutrition may change the response to injury or infection. This study investigated whether nutrition influenced the expression of the adhesion molecule, E-selectin and ICAM-1, following endotoxin challenge. MATERIALS AND METHODS: Forty-three mice were injected with saline, 2, 20, 200, 2000, or 10000 microg/kg lipopolysaccharide (LPS) intraperitoneally. E-selectin expression in the lung, small intestine, and heart was quantified at 3 h after challenge, while ICAM-1 was measured at 5 h, using the dual-radiolabeled monoclonal antibody technique. Next, 80 mice were fed chow, intragastric (IG)-TPN, or IV-TPN for 5 days, and then received intraperitoneal 2 or 200 microg/kg LPS. E-selectin and ICAM-1 expression in organs was measured at 3 and 5 h after endotoxin, respectively. RESULTS: E-selectin expression in organs increased LPS dose dependently. ICAM-1 levels reached early peaks in the lung and in the intestine. Also, IV-TPN significantly increased E-selectin expression in the small intestine and tended to increase pulmonary E-selectin, when compared to chow or IG-TPN animals. There were no significant differences in E-selectin expression among three diet groups after 200 microg/kg LPS challenge. No differences in ICAM-1 expression were observed in any organ among the three groups after 2 or 200 microg/kg LPS injection. CONCLUSIONS: E-selectin rather than ICAM-1, because of the expression pattern after various dosages of LPS challenge, may be a determining factor for the degree of LPS-induced inflammation at the early phase. Lack of enteral nutrition may increase inflammatory response through enhanced gut E-selectin levels after a small dose of LPS.

Modulation of organ ICAM-1 expression during IV-TPN with glutamine and bombesin.

The gut primes neutrophils (PMNs) during injury, which can then induce distant organ damage after a second insult. ICAM-1 is an important adhesion molecule in PMN attachment to the vascular endothelium. Parenteral nutrition (TPN) decreases gut levels of interleukin (IL)-4 and IL-10, two cytokines that are normal inhibitors of ICAM-1 expression. TPN also increases gut ICAM-1 expression and PMN accumulation. Since glutamine (GLN) and bombesin (BBS) prevent TPN-associated impairment of mucosal immunity, we hypothesized that GLN and BBS would modulate organ ICAM-1 expression in association with normalization of IL-4 and IL-10 levels. Forty-four mice were fed chow, TPN, or GLN-TPN (isonitrogenous 2% GLN-enriched TPN). After 5 days of diets, ICAM-1 expression was quantified in organs using the dual radiolabeled monoclonal antibody technique. In the next experiment, 29 mice were fed chow, TPN, or BBS-TPN (BBS 15 microg/kg TID) for 5 days to measure organ ICAM-1 expression. Total IL-4 and IL-10 levels were measured with ELISA from intestinal homogenates of another set of 52 mice fed chow, TPN, GLN-TPN, or BBS-TPN. TPN significantly increased ICAM-1 expression in the lung, kidney, and intestine compared with chow mice. GLN-TPN decreased intestinal, but not lung, ICAM-1 expression, while BBS-TPN reduced pulmonary, but not gut, ICAM-1 levels. GLN- and BBS-TPN returned gut IL-4 levels to normal, but failed to increase IL-10 levels. GLN and BBS had different effects on organ ICAM-1 expression induced by lack of enteral nutrition. Mechanisms other than recovery of IL-4 alone may be responsible for gut ICAM-1 expression.

Individual neuropeptides regulate gut-associated lymphoid tissue integrity, intestinal immunoglobulin A levels, and respiratory antibacterial immunity.

BACKGROUND: Total parenteral nutrition (TPN) leads to atrophy of the gut-associated lymphoid tissue (GALT) and a significant decrease in intestinal immunoglobulin A (IgA) levels, a major constituent of mucosal immunity. Bombesin (BBS) prevents TPN-induced GALT atrophy and maintains intestinal IgA levels. BBS, a neuropeptide analogous to gastrin-releasing peptide in humans, stimulates the release of other gut neuropeptides including cholecystokinin (CCK), gastrin, and neurotensin (NT). This study investigates the ability of CCK, gastrin, or NT to individually prevent TPN-induced GALT atrophy and preserve respiratory immunity. METHODS: Experiment 1: Male mice were randomly assigned to receive chow, TPN, TPN plus CCK, TPN plus gastrin, or TPN plus NT. After 5 days of feeding, Peyer's patches (PP) from the proximal and distal small bowel were harvested and analyzed for cell yields. PP cells were also analyzed for GALT cell type. Small bowel IgA levels were measured by enzyme-linked immunosorbent assay (ELISA). Experiment 2: Mice were randomly assigned to receive either liposomes containing Pseudomonas antigen or liposomes without antigen. After 10 days, mice were randomly assigned to the same five treatment groups, fed for 5 days, and then given intratracheal Pseudomonas. Mortality was assessed after 48 hours. RESULTS: Experiment 1: GALT cell reductions due to IV-TPN were greater in the distal than proximal small bowel. All three neuropeptides prevented most TPN-induced GALT atrophy due mainly to the maintenance of the B-cell and T-cell populations in the PP of the distal bowel. Intestinal IgA levels were significantly higher in the animals treated with neuropeptides than animals treated with TPN only; however, these IgA levels were not maintained at levels observed in chow-fed animals. Experiment 2: Immunization resulted in significantly lower mortality in animals fed chow, TPN plus CCK, and TPN plus gastrin. TPN alone and TPN plus NT resulted in loss of immunity and mortality rate at comparable levels to unimmunized animals. CONCLUSIONS: Supplementation of IV-TPN with CCK, gastrin, and NT prevents GALT atrophy, primarily in the distal bowel. Intestinal IgA levels improve but not to normal levels. CCK and gastrin reversed IV-TPN-induced effects on antibacterial pneumonia in immunized animals while NT did not.

Glutamine-enriched total parenteral nutrition maintains intestinal interleukin-4 and mucosal immunoglobulin A levels.

BACKGROUND: Total parenteral nutrition (TPN) prevents progressive malnutrition but fails to maintain intestinal gut-associated lymphoid tissue (GALT) or established respiratory antiviral or antibacterial mucosal immunity. Our previous work demonstrated that decreases in intestinal immunoglobulin A (IgA) were associated with decreases in Th2-type IgA-stimulating cytokines, interleukin (IL)-4 and IL-10. Because glutamine supplementation of TPN partially preserves respiratory defenses and normalizes GALT, we investigated the ability of parenteral glutamine to normalize respiratory and intestinal IgA levels and measured Th2 cytokines in intestinal homogenates. METHODS: Animals were cannulated and randomly assigned to receive chow (n = 17), TPN (n = 18), or an isonitrogenous, isocaloric TPN solution formulated by removing the appropriate amount of amino acids and replacing them with 2% glutamine (n = 18) for 5 days. Respiratory tract and intestinal washings were obtained for IgA and the intestine homogenized and analyzed for IL-4 and IL-10. RESULTS: TPN decreased intestinal and respiratory IgA in association with decreases in intestinal IL-4 and IL-10 compared with chow-fed animals. Glutamine significantly improved respiratory and intestinal IgA levels, significantly improved IL-4 compared with TPN animals, and maintained IL-10 levels midway between chow-fed and TPN animals. CONCLUSIONS: Glutamine-enriched TPN preserved both extraintestinal and intestinal IgA levels and had a normalizing effect on Th2-type IgA-stimulating cytokines.