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Biomedical subjects

E E Moore

Publications and source records attributed to E E Moore.

At least 19 recordsLinked to original sources
PubMed1992

Liver injury is a reversible neutrophil-mediated event following gut ischemia.

The purposes of this study were to characterize the temporal relationship of distant organ dysfunction after mesenteric ischemia/reperfusion (I/R), and to ascertain if the neutrophil is critical to this process. Normal and neutrophil-depleted rats (vinblastine sulfate, 0.75 mg/kg intravenously) underwent 45 minutes of superior mesenteric artery occlusion and after 0, 6, and 18 hours of reperfusion, blood was sampled and liver and lungs were harvested. Iodine 125 albumin leak was used as a marker for pulmonary and liver injury, and serum acetoacetate/3-hydroxybutyrate (AcAc/3-OHB) was used as an index of hepatic mitochondrial redox state. Gut I/R at 6 hours increased 125I-albumin lung/blood ratio (gut I/R, 0.077 +/- 0.006; control, 0.045 +/- 0.004) and 125I-albumin liver/blood ratio (gut I/R, 0.120 +/- 0.007; control, 0.077 +/- 0.003), while AcAc/3-OHB decreased significantly (gut I/R, 0.420 +/- 0.040; control, 0.880 +/- 0.120). Neutrophil depletion eliminated these changes at 6 hours (blood AcAc/3-OHB, 0.720 +/- 0.100; 125I liver/blood, 0.068 +/- 0.006; 125I lung/blood, 0.046 +/- 0.007). We conclude the following: (1) intestinal I/R produces simultaneous liver and lung injury; (2) injury was present at 6 hours but is reversed at 18 hours; and (3) the I/R-induced liver and lung injuries were neutrophil mediated.

Animals↗
PubMed1992

Postinjury shock and early bacteremia. A lethal combination.

Gut bacteria translocation has been invoked as a prime cause of early postinjury death. To examine this hypothesis, we obtained emergency department blood cultures in 132 acutely injured patients requiring urgent laparotomy for trauma. In the latter half of these patients, mesenteric lymph node and liver biopsy cultures were also performed. The incidence of early bacteremia was 11% (10/94) in the patients without shock compared with 32% (12/38) in the group with shock. The majority (73%) were gram-positive bacteremias. Most notably, Staphylococcus was isolated in 13% (5/38) of the patients with shock, but these isolates were of no apparent clinical significance. In contrast, 18% (7/38) of the patients with shock had enteric bacteremias, and all of these patients died. Cultures were positive in 11% of the liver samples and 15% of the mesenteric lymph nodes. With the exception of two patients with concurrent enteric bacteremias, these hepatic and mesenteric lymph node bacteria were of no clinical significance. In conclusion, bacterial translocation occurs infrequently, and virtually all enteric bacteria were found in dying patients; the cause or effect remains to be defined.

Adult↗
PubMed1992

Endotoxin after gut ischemia/reperfusion causes irreversible lung injury.

We have recently reported that 45 min of gut ischemia causes moderate 125I-albumin lung leak at 6 hr of reperfusion which was reversed at 18 hr. Our purpose was to determine the effect of a second insult, low dose endotoxin (LPS, 2.5 mg/kg), given 6 hr after gut ischemia/reperfusion (I/R) on this lung injury as assessed by 125I-albumin leak, neutrophil influx (myeloperoxidase assay, MPO), histopathology, and mortality. Rats were randomized to either sham laparotomy (LAP) or 45 min of superior mesenteric artery occlusion and 6 hr later were treated with LPS or saline. At 18 hr reperfusion the lungs were harvested, assayed for 125I-albumin leak and MPO, and microscopically examined by an unbiased observer after routine H&E staining. We observed that LPS increased lung neutrophil levels both with or without gut I/R. However, only the combined insult (I/R + LPS) increased 125I-albumin leak at 18 hr of reperfusion. Lung histology confirmed that the sequential combination of I/R + LPS caused marked interstitial edema and neutrophil sequestration accompanied by alveolar edema, hemorrhage, and fibrinous exudate, while I/R or LAP + LPS did not. The mortality rate of I/R + LPS was 39% which was significantly higher than LAP alone (0%), gut I/R alone (0%), or LAP + LPS (4%). In conclusion, a delayed exposure to low dose endotoxin converts moderate gut I/R-induced lung dysfunction into advanced organ failure.

Albumins↗
PubMed1992

Gut and liver coordinated metabolic response following major torso injury.

Major trauma provokes a stress response which is mediated, in part, via glucagon, catecholamines, and cortisol. These stress hormones modulate the choice of energy substrate for various tissues. While glucose and fatty acids are considered the preferred fuels, ketone bodies (26/ATP/mole) may be a viable alternative. In this study, we measured the concentrations of acetoacetate and beta-hydroxybutyrate (3-OHB) in the portal as well as systemic circulations of 10 critically injured patients (revised trauma score = 6.8 +/- 0.5, injury severity score = 27 +/- 3) during the first 5 postoperative days. At 6 hr postinjury, 3-OHB was elevated in the portal system (0.34 +/- 0.01 mM) while depressed systemically (0.09 +/- 0.02 mM), indicating that the gut was capable of ketogenesis. In contrast, at 24 hr, 3-OHB rose systemically (0.39 +/- 0.02 mM) while decreasing in portal blood (0.09 +/- 0.01 mM) implying gut ketone consumption. Moreover, the systemic ketone body ratio became elevated at 24 hr, suggesting an enhanced liver energy status. In summary, we believe ketogenesis is stimulated by major trauma. Initially, the gut supports ketone concentration in the systemic circulation, whereas, by 24 hr, the gut becomes a ketone consumer and the liver maintains circulating levels.

Abdominal Injuries↗
PubMed1992

Gut ischemia/reperfusion-induced liver dysfunction occurs despite sustained oxygen consumption.

We have previously shown that gut ischemia/reperfusion (I/R) causes liver dysfunction in vivo (increased [I125]albumin leak, decreased mitochondrial redox potential). Our purpose was to investigate liver dysfunction due to gut I/R in an ex vivo model where oxygen delivery (DO2) could be controlled. Rats underwent laparotomy (sham) or 45 min of superior mesenteric artery (SMA) occlusion (I/R) and 6 hr later the gut and liver were isolated in situ. Pressures were monitored while recirculating blood was perfused via the hepatic artery (2.5 ml/min) for 90 min and the SMA (7.5 ml/min) for the first 30 min, then the portal vein (7.5 ml/min) for 60 min. Both gut and liver DO2 and VO2 (Fick method) were maintained throughout the study period in the gut I/R as well as sham groups. Despite maintenance of liver VO2, however, gut I/R resulted in a marked and persistent reduction in bile flow. In conclusion, dysfunctional bile production after gut I/R is not due to impaired VO2, but rather gut-liver signaling yet to be defined.

Animals↗
PubMed1992

Efficacy of selective intrabronchial air insufflation in acute lobar collapse.

Flexible fiberoptic bronchoscopy (FFB) to remove mucous plugs followed by selective intrabronchial air insufflation (SII) to expand the atelectatic lung was used in 17 surgical intensive care unit (SICU) patients with pulmonary lobar collapse. Thirteen patients were admitted for acute trauma, and the remainder were elderly postoperative patients. Lobar collapses occurred on SICU days 1 to 18 (mean +/- SEM: 5 +/- 1 days), and duration ranged from 4 to 258 hours (mean: 77 +/- 18 hours). Indications for FFB with SII included critical hypoxemia in 5 patients, worsening collapse in 2, and failure to respond to aggressive respiratory care in 10 (59%). FFB with SII was effective in 14 (82%) patients: 10 achieved full lung re-expansion, and 4 partial lung re-expansion. When lobar collapse was of less than 72 hours' duration, 92% (12 of 13) of patients had lungs re-expanded compared with 50% (2 of 4) whose collapse existed for more than 72 hours. The mean PaO2/FIO2 (fraction inspired oxygen) ratio was 135 +/- 18 prior to FFB with SII and increased to 205 +/- 21 after FFB with SII. Complications were minor and clinically insignificant. In conclusion, SII appears to be a simple, safe, effective adjunct to FFB in the treatment of SICU patients with pulmonary lobar collapse.

Acute Disease↗
PubMed1992

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.

Adult↗
PubMed1992

A.T.L.S. on the ski slopes--a steamboat experience.

The Steamboat Mountain Ski Patrol incorporates local emergency physicians and a visiting trauma surgeon as a second-tier response to life-threatening mountain events. The case of a 48-year-old man surviving a potentially lethal postinjury tension pneumothorax and a review of the 1989-1990 major trauma experience on this ski mountain underscores the value of this concept.

Adolescent↗
PubMed1992

Simultaneous liver and lung injury following gut ischemia is mediated by xanthine oxidase.

We have previously shown that gut ischemia/reperfusion (I/R) causes simultaneous liver and lung dysfunction and that neutrophils play a critical role in this process. The purpose of this study was to ascertain whether xanthine oxidase (XO) was likewise operational. Normal and XO-inactivated rats (given a tungsten-enriched, molybdenum-depleted diet for 3 weeks) underwent 45 minutes of occlusion of the superior mesenteric artery, and control rats were subjected to a sham laparotomy. After zero and six hours of reperfusion, blood was sampled and livers and lungs harvested. Iodine-125-labeled albumin leak was used as a marker for pulmonary and liver capillary permeability barrier function, and serum acetoacetate/3-hydroxybutyrate (AcAc/3-OHB) levels as an index of hepatic mitochondrial redox state. Gut ischemia/six hours of reperfusion (I/R) increased the 125I albumin lung/blood ratio and the 125I albumin liver/blood ratio; AcAc/3-OHB levels decreased significantly. Xanthine oxidase activation eliminated the observed lung and liver capillary leak as well as the hepatic metabolic derangement induced by gut I/R. In conclusion, the simultaneous lung and liver dysfunction produced by gut I/R is mediated by XO.

Animals↗
PubMed1992

Incommensurate oxygen consumption in response to maximal oxygen availability predicts postinjury multiple organ failure.

Untreated flow-dependent oxygen consumption (VO2) has recently been implicated as an unrecognized risk factor for multiple organ failure (MOF). We therefore prospectively studied 39 severely injured patients with known risk factors for multiple organ failure who were subjected to an established resuscitation protocol aimed at maximizing oxygen delivery (DO2 greater than 600 mL/min.m2) to attain a VO2 goal of greater than 150 mL/min.m2. Fifteen (38%) of these high risk patients did not meet this VO2 goal by 12 hours. These nonresponding patients had significantly elevated lactate levels, suggesting defective aerobic metabolism. Of note, this blunted VO2 response despite maximal efforts to enhance peripheral oxygen availability predicted MOF. These data serve to re-emphasize the importance of the initial shock insult in causing or priming the host for the development of late MOF.

Adult↗
PubMed1992

Percutaneous tracheostomy/gastrostomy in brain-injured patients--a minimally invasive alternative.

Tracheostomy and gastrostomy are frequent adjunctive procedures required in the management of patients with severe brain injuries to facilitate neurorehabilitation. We therefore evaluated the use of two minimally invasive surgical procedures, percutaneous tracheostomy (PT) and percutaneous endoscopic gastrostomy (PEG), in 27 patients with severe brain injuries. The mean age was 41 +/- 4 years, and 23 (85%) were men. All patients were intubated, and 19 (70%) required mechanical ventilator support on the day of PT/PEG. The endotracheal tubes had been in place for 1 to 21 days (mean, 8.7 +/- 0.8). All patients were stable from their acute brain injury; 13 had intracranial pressure (ICP) monitors in place. The Seldinger technique, as described by Ciaglia, was employed for PT. Following PT, a PEG was inserted by a modification of the Sachs-Vine "push" technique. We were uniformly successful in placing these access tubes. Complications were minor and not clinically significant. Three of 13 patients (23%) with ICP monitors had a transient rise in ICP related to PT and one of these patients developed local subcutaneous emphysema. Another patient experienced a mild cellulitis at the tracheostomy site. Of note, there were no PEG-related complications. In conclusion, PT and PEG are readily learned, minimally invasive procedures. In our experience with patients with severe brain injuries combined PT/PEG is a uniformly safe alternative to gain long-term access to the airway and gut.

Adolescent↗
PubMed1992

Invalidation of the APACHE II scoring system for patients with acute trauma.

The APACHE II scoring system has been promulgated as a useful tool in the assessment of the severity of injury and prognosis for acutely ill patients. The physiologic basis for stratification is weighted toward older patients with chronic medical conditions. Recently, the APACHE II system has been proposed as a method for determining diagnosis related group (DRG) reimbursement for individual trauma patients. The present study applied the APACHE II scoring system to 280 patients with blunt or penetrating trauma who had documented systolic blood pressure < 90 mm Hg. Fifty-seven (20%) died of their injuries within the first 24 hours. APACHE II scores were recorded both in the emergency room (ED) and at 24 hours following admission. Injury Severity Scores (ISS), Revised Trauma Scores (RTS), and TRISSCAN were calculated. The APACHE II (n = 223) recorded at 24 hours (2.5 +/- 0.2) was significantly less than that recorded in the ED (6.6 +/- 0.3, p < 0.05, Mann-Whitney analysis). Using regression analysis, there was no correlation between APACHE II and ISS if recorded in the ED (r2 = 0.06) or 24 hours following admission (r2 = 0.08). APACHE II also demonstrated a poor correlation with the length of hospital stay (r2 = 0.03 [ED], = 0.19 [24 hours]). Whereas APACHE II may be helpful in defining severity of disease among patients with acute-on-chronic medical conditions, the classification lacks an anatomic component, which is essential to assess the magnitude of acute injury in patients who are typically otherwise healthy.

Acute Disease↗
PubMed1992

Balloon tamponade for bilobar transfixing hepatic gunshot wounds.

The nonresectional approach to major liver trauma is clearly preferred. Unfortunately, trachotomy with vessel ligation, selective hepatic arterial ligation, perihepatic pack, and fibrin glue are not viable options with high-energy bilobar liver injuries. We have fashioned a balloon tamponade device that has proved very effective for these transfixing hepatic gunshot wounds.

Adolescent↗
PubMed1992

Studies on the role of tumor necrosis factor in adult respiratory distress syndrome.

Tumor necrosis factor (TNF), rapidly becoming recognized as a mediator of inflammation, may be important in the pathogenesis of acute lung injury. Its role in the development of the adult respiratory distress syndrome (ARDS) in humans, however, has been difficult to clarify. To determine if TNF could be important early in the development of acute lung injury from multiple causes, we enrolled 103 patients within 8 h of meeting the criteria for an at-risk illness (sepsis, aspiration of gastric contents, severe pancreatitis, hypertransfusion, abdominal trauma, chest trauma, multiple fractures) and obtained multiple frequent blood samples for TNF measurements. Using five methods of TNF analysis, we were unable to find an association between TNF and the development of ARDS. However, we found significant differences in TNF measurements depending on the methods of analysis used, which could, at least in part, account for the inconsistencies in the published literature regarding the relationship between TNF and disease processes.

Adult↗
PubMed1992

Increased serum catalase activity in septic patients with the adult respiratory distress syndrome.

Excessive hydrogen peroxide (H2O2) generation appears to contribute to the development of the adult respiratory distress syndrome (ARDS), but H2O2-combatting antioxidant defenses have not been evaluated. We found that serum from septic patients with ARDS scavenged more (p less than 0.05) H2O2 in vitro (82.7 +/- 3.8%) than did serum from septic patients without ARDS (56.9 +/- 3.1%) or control subjects (20.2 +/- 2.4%). Serum from septic patients with ARDS also had more (p less than 0.05) catalase activity (54.9 +/- 10.9 U/ml) than did serum from septic patients without ARDS (28.6 +/- 3.4 U/ml) or control subjects (7.3 +/- 0.8 U/ml). In contrast, serum from septic patients with or without ARDS and control subjects had the same glutathione peroxidase (GPX) activity. Serum H2O2 scavenging activity correlated with serum catalase (r = 0.77) but not GPX (r = 0.33) activity and was inhibitable (greater than 90%) by sodium azide, a catalase inhibitor. Increases in serum catalase activity did not appear to be derived from erythrocytes (RBC) because septic patients with or without ARDS and control subjects had similar RBC hemolysis in response to osmotic stress in vitro and serum haptoglobin concentrations. Serum from septic patients with ARDS also protected endothelial cells against H2O2-mediated damage (34.5 +/- 2.2% 51Cr release) better (p less than 0.05) than serum from septic patients without ARDS (47.3 +/- 7.4%) or control subjects (82.1 +/- 10.2%), but killing of bacteria by neutrophils in vitro was the same in serum from patients and control subjects. Our findings indicate that patients with sepsis and/or ARDS have increased serum catalase activity, which may alter H2O2-dependent processes.

Bacterial Infections↗
PubMed1992

Enteral feeding in the critically injured patient.

Metabolic support is an integral component in the care of the critically injured patient. When hypermetabolism occurs, there are increases in energy demands along with changes in substrate utilization. This article reviews the prospective randomized clinical trials that were undertaken at Denver General Hospital over the past decade that address both the timing of nutritional support and the route of administration in this critically injured population. Also discussed is a review of a meta-analysis that attests to the feasibility of early postoperative enteral feeding with the possibility of decreased septic morbidity in high-risk surgical patients. With the clinical knowledge gained from these trials, an algorithm for nutritional intervention was developed that represents our current standard of practice.

Clinical Protocols↗
PubMed1992

Phospholipase A2 inhibition decouples lung injury from gut ischemia-reperfusion.

BACKGROUND: Phospholipase A2 (PLA2) has recently been implicated as a key enzyme of local inflammation after gut ischemia-reperfusion (I/R). The hypothesis of this study is that PLA2 inhibition decouples remote organ injury from gut I/R. METHODS: Sprague-Dawley rats were pretreated with a PLA2 inhibitor, quinacrine (10 mg/kg, intravenously), before the induction of gut ischemia (45 minutes of superior mesenteric artery occlusion) followed by 6 hours of reperfusion. 125I-labeled albumin leak was employed as a marker of pulmonary endothelial permeability and myeloperoxidase as a monitor of neutrophil (PMN) traffic in the gut and lung. To further characterize the impact of PLA2 inhibition, PMNs were harvested at 6 hours of reperfusion and superoxide production was measured in the presence or absence of an activating stimulus, N-formyl-methionyl-leucyl-phenylalanine. RESULTS: Gut I/R increased gut PLA2 activity, elicited gut PMN influx, and produced lung leak; these events were prevented by PLA2 blockade. Gut I/R also markedly enhanced PMN superoxide production with N-formyl-methionyl-leucyl-phenylalanine, and this priming was ablated by PLA2 inhibition. CONCLUSION: These data suggest that PLA2 activation is a proximal step in the pathogenesis of distant organ injury after splanchnic hypoperfusion, a process that appears to involve PMN priming in the gut bed.

Animals↗