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Biomedical subjects

E E Moore

Publications and source records attributed to E E Moore.

At least 199 records · Page 11Linked to original sources
PubMed1994

Early predictors of postinjury multiple organ failure.

OBJECTIVE: To find a predictive model for postinjury multiple organ failure (MOF). DESIGN: A 3-year cohort study ending December 1992 (first year: retrospective; last 2 years: prospective). SETTING: Denver General Hospital (Colo) is a regional level I trauma center. PATIENTS: Consecutive trauma patients with an Injury Severity Score (ISS) greater than 15, with an age greater than 16 years, and who survived longer than 24 hours. Stepwise logistic regression analysis was performed in all patients (n = 394), in the subgroup of patients with 0 to 12 hours, plus 12 to 24 hours base deficit (BD) results (n = 220), and in a second subgroup of patients with BD plus lactate results at 0 to 12 hours and 12 to 24 hours (n = 106). MAIN OUTCOME: Postinjury MOF. RESULTS: The following variables were identified as independent predictors of MOF in the analysis of all patients: age more than 55 years, ISS greater than or equal to 25, and more than 6 U of red blood cells in the first 12 hours after admission (U RBC/12 hours). In the subgroup with BD results, the same analysis identified age greater than 55 years, greater than 6 U RBC/12 hours, and BD greater than 8 mEq/L (0 to 12 hours), while in the last subgroup analysis including BD and lactate results, greater than 6 U RBC/12 hours, BD greater than 8 mEq/L (0 to 12 hours), and lactate greater than 2.5 mmol/L (12 to 24 hours) were independently associated with MOF. CONCLUSIONS: Age greater than 55 years, ISS greater than or equal to 25, and greater than 6 U RBC/12 hours are early independent predictors of MOF. Subgroup analyses indicate that BD and lactate levels may add substantial predictive value. Moreover, these results emphasize the predominant role of the initial insult in the pathogenesis of postinjury MOF.

Adolescent↗
PubMed1994

Interleukin-6 potentiates neutrophil priming with platelet-activating factor.

BACKGROUND: Polymorphonuclear neutrophil (PMN) priming appears to be an important event in the pathogenesis of hyperinflammatory states, resulting in adult respiratory distress syndrome or multiple organ failure. Interleukin-6 (IL-6) is an integral mediator of the acute stress response to injury and infection, but excessive and prolonged systemic levels have been associated with morbidity and mortality following trauma, burns, and elective surgery. We hypothesized that IL-6 primed PMNs for exaggerated cytotoxicity. However, we have been unable to directly prime PMNs for superoxide release with IL-6. OBJECTIVE: To determine whether IL-6 acted in concert with another inflammatory mediator (platelet-activating factor [PAF]) to prime PMNs. METHODS: Polymorphonuclear neutrophils isolated from healthy human donors were incubated for varying times with IL-6 (0.01 to 100 ng/mL), PAF (0.01 to 100 ng/mL), or a combination of IL-6 and PAF. Superoxide production was then measured with and without the addition of the PMN-activating formylpeptide formyl-methionyleucylphenylalanine. RESULTS: Over the range of times (5 to 90 minutes) and doses tested, IL-6 did not prime PMNs, while PAF primed PMNs in a dose- and time-dependent manner. Interleukin 6 (10 ng/mL) combined with a nonpriming concentration of PAF (0.1 ng/mL) primed PMNs for superoxide production over a range of incubation times. CONCLUSION: The inflammatory mediators IL-6 and PAF act synergistically to prime PMNs in vitro. This observation may begin to elucidate the mechanistic role of IL-6 in pathologic clinical states.

Analysis of Variance↗
PubMed1994

Phospholipase A2 regulates critical inflammatory mediators of multiple organ failure.

PLA2 is a family of regulatory enzymes that control eicosanoid synthesis and PAF production. PLA2 must be tightly regulated within the cell or cell destruction results. Circulatory release of PLA2 occurs in states of profound illness including sepsis, shock, severe injury, and pancreatitis, all of which are linked to the development of ARDS and MOF. Experimental and clinical evidence suggests that PLA2 may serve a primary regulatory role in the development of these inflammatory disorders. This evidence suggests that inhibitors of PLA2 activation could play an important role in future intensive care management.

Animals↗
PubMed1994

Endotoxin pretreatment inhibits neutrophil proliferation and function.

Gut ischemia/reperfusion (I/R) induces lung injury by a mechanism that involves neutrophils (PMNs). We have previously shown that endotoxin (LPS), when administered after gut I/R, amplifies this lung injury, while treatment with LPS prior to gut I/R prevents lung injury. The purpose of this study was to determine whether LPS pretreatment (Pre Rx) alters the PMN inflammatory component of the gut I/R injury. Specifically, we focused on whether LPS Pre Rx effected (i) PMN stem cell proliferation, (ii) gut I/R-induced PMN priming, and (iii) gut I/R-induced PMN lung sequestration. Bone marrow was harvested from normal and LPS-pretreated (0.5 mg/kg, ip, 3 days prior) rats, and colony forming units--granulocyte/macrophage (CFU-GM) were quantitated using a soft agar culture technique. In another experiment, normal and LPS-pretreated rats were subjected to gut I/R (45 min superior mesenteric artery occlusion/6 hr reperfusion), and blood and lungs were then harvested. The in vivo priming of PMN was assessed by measuring the difference in superoxide production (O2-) with and without the activating stimulus, N-formylmethionyl-leveyl-phenylalanine (fMLP). The quantity of myeloperoxidase (MPO) was used as an index of the number of PMN sequestered in lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Gut ischemia induces bone marrow failure and increases risk of infection.

Hemorrhagic shock leads to bone marrow (BM) failure and renders the host susceptible to infection. We hypothesized that splanchnic hypoperfusion may play a mechanistic role in this process. BM was harvested from normal rats and, on Postprocedure Days 1 and 3, from rats that had undergone laparotomy (LAP) or gut ischemia/reperfusion (I/R; 45 min superior mesentery artery occlusion). Granulocyte-macrophage colony-forming unit (CFU-GM) proliferation, a measure of BM myeloid progenitors, was quantitated using a standard soft agar culture technique. On Postprocedure Days 1 and 3, BM proliferation of CFU-GM was depressed in gut I/R rats, compared to control and LAP animals (P < 0.05). Next, six rats were subjected to I/R, LAP, ANEST (anesthesia control), or no treatment (NL, normal control); 1 day later, 3.5 x 10(7) Staphylococcus aureus, suspended in 0.25 ml of saline, were injected subcutaneously in four sites on the back of each animal. Five days later, the NL rats had developed 23 abscesses, ANEST 23, and LAP 22, while the gut I/R rats had 24. The abscesses were excised, weighed, and measured. The weight and size of abscesses were greater in the gut I/R animals (P < 0.05). In summary, gut I/R depressed BM proliferation and rendered animals susceptible to infection in a manner similar to that observed following hemorrhagic shock. These data suggest that splanchnic hypoperfusion, a common sequela of hemorrhagic shock, may play a mechanistic role in BM failure and infection after hemorrhage.

Abscess↗
PubMed1994

A critical analysis of acutely injured children managed in an adult level I trauma center.

The triage of all injured children to regional pediatric trauma centers may be impractical and unnecessarily exclude adult level I trauma centers from the care of the acutely injured child. The purpose of this study was to critically evaluate the outcome of injured children treated in an adult level I trauma center by adult trauma surgeons. The records of 410 consecutively treated children (age < or = 15 years) and 188 young adults (age 16 to 18 years) admitted to the trauma service during a 2-year period (ending December 1991) were studied. The probability of survival was calculated using TRISS methodology. Results were analyzed using the Z statistic, permitting objective comparison with national norms (Major Trauma Outcome Study). Severity of injury (RTS and ISS) was equivalent (P > .05) in children and young adults. The observed survival (98.0%) in children compared favorably with the predicted survival (TRISS) of 97.7%. Calculation of the Z statistic showed no difference in outcomes of acutely injured children (+0.47) relative to young adults (+0.45) or national norms (MTOS). The triage of injured children to an adult level I trauma center does not adversely affect outcome. Subset analysis of injured children showed no differences in observed outcome relative to predicted outcome (national control) or outcome in young adults (institutional control). These data support the continued triage of acutely injured children to regional trauma centers regardless of pediatric or adult designation.

Acute Disease↗
PubMed1994

Cardiac enzymes are irrelevant in the patient with suspected myocardial contusion.

BACKGROUND: Myocardial contusion is commonly diagnosed following blunt chest trauma, and has potentially lethal complications. Cost-effective case management in patients with suspected myocardial contusion is confounded by the low incidence of complications and the lack of a reliable test to predict them. The clinical usefulness of elevated cardiac enzyme levels is controversial. METHODS: We analyzed a 4-year experience of 359 patients with high-risk blunt chest trauma who were assessed using an established practice guideline. Our multivariate statistical model evaluated all of the early risk factors included in the guideline, specifically focusing on cardiac enzyme levels. RESULTS: Myocardial contusion was diagnosed in 30% of patients, and complications (dysrhythmias and cardiogenic shock) occurred in 5%. In no case was cardiac enzyme elevation the sole predictor of a complication. The cost of routine cardiac enzyme assay was substantial. CONCLUSION: Cardiac enzyme determinations have no useful role in the evaluation of patients with suspected myocardial contusion. They should be eliminated from current practice guidelines.

Adolescent↗
PubMed1994

Gut ischemia/reperfusion produces lung injury independent of endotoxin.

OBJECTIVE: Bacterial translocation from the gut has been invoked as a common inciting event for postinjury multiple organ failure. We previously showed that gut ischemia/reperfusion induces remote organ injury. The purpose of this study was to ascertain if endotoxin has a pivotal mechanistic role in this process. DESIGN: Prospective, randomized study. SETTING: Animal laboratory. SUBJECTS: Sprague-Dawley rats weighing 300 to 350 g. INTERVENTIONS: Anesthetized animals underwent 45 mins of superior mesenteric artery occlusion and 2 hrs of reperfusion; sham laparotomy served as controls. Endotoxin was eliminated with the murine immunoglobulin (Ig) M antibody E5, 3 mg/kg i.v. before the study. MEASUREMENTS AND MAIN RESULTS: Plasma endotoxin was measured by the limulus amebocyte lysate assay. At 2 hrs of reperfusion, circulating neutrophil priming was determined by the difference in superoxide generation with and without the activating stimulus, N-formyl-Met-Leu-Phe. Neutrophil sequestration in the lung was quantitated by myeloperoxidase activity, and by lung endothelial permeability by 125I albumin lung/blood ratio. Endotoxin concentrations were not significantly (significance determined as p < .05) different between the gut ischemia/reperfusion and laparotomy groups (n = > or = 5) during ischemia or reperfusion. Circulating neutrophil priming, neutrophil accumulation in the lung, and lung injury were provoked by gut ischemia/reperfusion, but not altered by endotoxin elimination. CONCLUSION: Gut ischemia/reperfusion primes circulating neutrophils and produces lung injury by a mechanism independent of endotoxin.

Animals↗
PubMed1994

Transesophageal echocardiography in the evaluation of a transmediastinal gunshot wound: case report.

Transesophageal echocardiography is a safe, minimally invasive imaging modality that may be useful in the evaluation of transmediastinal gunshot wounds. In this report, we describe a hemodynamically stable patient who sustained a gunshot wound to the ascending aorta. Routine diagnostic evaluation, including aortography, failed to confirm the suspected diagnosis. Transesophageal echocardiography definitively detailed the injury to the aorta enabling definitive surgical repair.

Adult↗
PubMed1994

Trauma surgeons can render definitive surgical care for major thoracic injuries.

Restrictions on the operative domain of general surgeons threaten the viability of trauma surgery as a career choice. Our study hypothesis is that an experienced trauma surgeon can provide definitive care for life-threatening thoracic trauma. This analysis is based on clinical outcomes at an ACS-verified level I center in which there are more than 3000 trauma admissions managed annually under the direction of four academic trauma surgeons. We selected penetrating cardiac wounds and blunt tears of the thoracic aorta because these injuries are managed exclusively by the trauma service and the endpoints are distinct. During the past 4 years, 40 patients with cardiac wounds were delivered to the ED; 23 patients arrived dead. In the remaining 17, injury mechanisms were 15 stab wounds (SW), one gunshot wound (GSW), and one shotgun (SGW). Four of these patients required ED thoracotomy, and the remaining 13 underwent some form of prethoracotomy pericardial decompression. Survival rate without neurologic deficit was 94% (16 of 17). During this same period, 19 patients with a torn thoracic aorta from blunt injuries arrived with signs of life. In this group the injury mechanisms were automobile crash in 15, and the mean ISS was 39.7 +/- 2.3. One patient was transferred for total cardiopulmonary bypass; 17 of the remaining patients underwent aortic repair employing partial left heart bypass. Sixteen of our 18 patients lived and none developed paraplegia. In summary, excluding patients who arrived dead, survival for penetrating cardiac wounds was 94% and for blunt thoracic aortic tears 89%. In conclusion, these data support our contention that trauma surgeons can render definitive care for thoracic injuries with survival rates comparable to those reported by cardiothoracic surgeons.

Adolescent↗
PubMed1994

Lipopolysaccharide-induced CD11B-mediated neutrophil-endothelial adhesion is not required for polymorphonuclear cell priming.

Previous work has implicated both neutrophil-endothelial cell (PMN-EC) adhesion and PMN priming (enhanced superoxide production following activation) in the development of postinjury adult respiratory distress syndrome (ARDS) and multiple organ failure (MOF). CD11B, a member of the integrin family of PMN surface receptors, has been alleged to have a prominent role in these inflammatory PMN-EC processes. The purpose of the present study was to test the hypothesis that CD11B-mediated PMN-EC adhesion is necessary for endotoxin (LPS)-induced PMN priming. Human neutrophils, isolated by Percoll gradient centrifugation, were exposed to LPS (100 ng/mL). At fixed times over 120 minutes (a) superoxide following fMLP activation (i.e., priming), (b) PMN-EC adhesion, and (c) expression of CD11B were assayed. Superoxide production was measured by cytochrome c reduction, PMN-EC adhesion with indium-labelled PMN adherence to human umbilical vein endothelial cell (HUVEC) monolayer cultures, and CD11B expression with fluorescent labelled anti-CD11B (60.1) antibodies. The PMN-EC adhesion was biphasic, with an early maximum at 15 minutes followed by a nadir at 60 minutes and secondary rise through 120 minutes of LPS exposure. CD11B expression changed dramatically in temporal association with early PMN-EC adhesion, but the secondary increase in adhesion was associated with only a mild rise in CD11B expression. PMN priming increased after a latency of 15 minutes to a maximum of 800 nmol/10(6) cells/min after 60 minutes of LPS exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion↗
PubMed1994

Cardiopulmonary effects of permissive hypercapnia in the management of adult respiratory distress syndrome.

BACKGROUND: Despite numerous advances, the mortality from adult respiratory distress syndrome (ARDS) remains high. Traditional ventilator management in ARDS has been to maintain normal PaCO2 by positive pressure ventilation (PPV). However, high levels of PPV may worsen the lung injury by alveolar overdistension. Permissive hypercapnia (PHC) has been proposed as an alternative method of ventilation, but hypercapnia may affect the hemodynamics of a hyperdynamic, critically ill patient. The purpose of this study was to determine the effect of PHC on ventilator requirement, arterial oxygenation, and hemodynamic performance in patients with severe ARDS. METHODS: Ten men and 5 women with established ARDS (mean Murray lung injury score 3.42 +/- 0.1) were prospectively studied using an established protocol when the static pulmonary plateau pressure (Pplat) exceeded 40 cm H2O. The initial tidal volume (V(t)) was decreased to achieve a Pplat < 40 cm H2O or to a lower limit of 5 cc/kg. Arterial blood gas and hemodynamic data were obtained serially. RESULTS: The V(t) was reduced from 9.9 +/- 0.5 mL/kg to 7.7 +/- 0.5 mL/kg at 24 hours, p < 0.05. This reduction of V(t) produced a decrease in minute ventilation (Ve: 18.0 +/- 1.6 to 11.9 +/- 0.7 L/min, p < 0.05), peak airway pressure (PAP: 55 +/- 2 vs 45 +/- 3 cm H2O, p < 0.05), and Pplat (Pplat 45.4 +/- 1.5 vs. 36.7 +/- 1.9) at 24 hours. The PaCO2 rose from 37.9 +/- 1.3 to 56.7 +/- 3.0 mm Hg (p < 0.05), and the pH decreased from 7.41 +/- 0 to 7.31 +/- 0 (p < 0.05) at 24 hours. There were no significant changes in mean airway pressure, static compliance, arterial oxygenation, pulmonary vascular resistance, systemic vascular resistance, cardiac index, or systemic oxygen delivery and consumption. CONCLUSIONS: Permissive hypercapnia by V(t) reduction: (1) decreased Ve, PAP, and Pplat without a change in mean airway pressure, static compliance or arterial oxygenation; (2) caused a mild partially compensated acidosis; and (3) does not adversely affect pulmonary vascular resistance, systemic vascular resistance, cardiac index, or systemic oxygen delivery and consumption.

Adolescent↗
PubMed1994

The spectrum of blunt injury to the carotid artery: a multicenter perspective.

The relative infrequency of blunt carotid artery trauma prompted a multicenter review to determine the spectrum of injuries, treatment strategies, and neurologic outcome. During a six-year period, 60 carotid artery injuries from blunt mechanisms in 49 patients were treated at 11 institutions. There were 11 bilateral injuries. Injury mechanisms were diverse but involved motor vehicles in 35 (72%) patients. In 14 (29%) patients, significant neurologic deficits developed more than 12 hours after a normal admission neurologic examination. The diagnosis was confirmed by angiography in 42 (86%). Duplex ultrasound accurately demonstrated the arterial injury in 12 (86%) of 14 patients. Documented injuries included arterial thrombosis in 20 arteries, arterial dissection alone in 19, dissection with pseudoaneurysm in six, pseudoaneurysm alone in five, frank arterial disruption in seven, and carotid-cavernous fistula in three. Arterial dissection was managed nonsurgically in 15 (79%) of 19 cases, the majority with systemic anticoagulation. Arterial thrombosis was managed with supportive therapy alone for 16 (80%) of 20 arteries; most associated with fixed neurologic deficits. Pseudoaneurysm repair was performed for six (55%) injuries. Carotid-cavernous fistulas were treated in all three instances with balloon occlusion. Overall mortality was 16 of 49 patients (43%). Good neurologic outcome was achieved in 22 (45%) patients. We conclude that: (1) Neurologic symptoms may develop in a delayed fashion; prior clinical suspicion and diagnostic testing are essential; (2) arterial dissection without complete occlusion may effectively be managed by anticoagulation; (3) pseudoaneurysms in accessible anatomic locations can be repaired with good results; and (4) injuries with complete arterial thrombosis are associated with high mortality and poor neurologic outcome in proportion to the initial degree of neurologic impairment.

Adolescent↗
PubMed1994

Clinical benefits of an immune-enhancing diet for early postinjury enteral feeding.

In this multicenter prospective controlled trial, 98 evaluable patients sustaining major torso trauma were randomized to receive early enteral nutrition with a new "immune-enhancing" diet (study: n = 51) or a standard stress enteral formula (control: n = 47). At baseline, both groups had comparable demographics and Injury Severity Scores. After 7 days of feeding, the groups had equivalent increases in serum total protein, albumin, and transferrin concentrations. Patients receiving the "immune-enhancing" diet, however, experienced significantly greater increases in total lymphocyte (p = 0.014), T lymphocyte (p = 0.04), and T-helper (p = 0.004) cell numbers. Additionally, these patients had significantly fewer intraabdominal abscesses (study, 0% vs. control, 11%; p = 0.023) and significantly less multiple organ failure (study, 0% vs. control, 11%; p = 0.023). In conclusion, this multicenter trial suggests this "immune-enhancing" enteral diet offers clinical benefits in stressed surgical patients.

Abdominal Injuries↗
PubMed1994

Early definitive abdominal evaluation in the triage of unconscious normotensive blunt trauma patients.

The need for simultaneous diagnosis and treatment of life-threatening intracranial mass lesions and intra-abdominal injury results in controversy over the appropriate triage of unconscious blunt trauma patients with stable vital signs. To aid in early decisions for these patients, a retrospective analysis of 290 patients with Glasgow Coma Scale (GCS) scores < or = 8 and systolic blood pressures (SBP) > 90 mm Hg was undertaken. The hypothesis of this study was that life-threatening abdominal injury frequently occurs in these patients and injuries cannot be consistently identified from vital signs alone. Data were analyzed for injury mechanism, SBP, heart rate (HR), Injury Severity Score (ISS), Revised Trauma Score (RTS), Abbreviated Injury Scale score for the abdomen and brain (A-AIS, CNS-AIS), and the need for emergent laparotomy. Patients with concurrent injuries were more likely to come from motor vehicle crashes than falls (p < 0.001). Although severe abdominal injuries (A-AIS > or = 3) were frequently identified based on SBP and HR, the use of clinical signs alone resulted in more missed injuries than did using the results diagnostic peritoneal lavage (DPL). This study suggests that all unconscious normotensive blunt trauma patients undergo immediate DPL to prevent missing life-threatening injuries.

Abdominal Injuries↗
PubMed1994

The postischemic gut serves as a priming bed for circulating neutrophils that provoke multiple organ failure.

Our trauma research center program entitled, "Trauma Primes Cells" is based on the fundamental hypothesis that prior exposure to multiple, sequential, sublethal cellular insults primes constructive or destructive pathways of cellular responses of subsequent injury. A major objective is to design therapy that will reduce the incidence of multiple organ failure. Although a number of inflammatory cascades have been incriminated in the pathogenesis of multiple organ failure (MOF), diffuse PMN-mediated tissue injury remains an attractive unifying concept. We have developed a sequential insult rodent model in which the priming event consisted of superior mesenteric arterial (SMA) clamping for 45 minutes followed by 6 hours of reperfusion. Following this priming event, activation was induced with a low dose of endotoxin (2.5 mg/kg). We believe that these studies support our hypothesis: mesenteric ischemic/reperfusion primes circulating PMNs. When these have been activated they can then be provoked by endotoxin to provoke distant organ injury. Primed PMNs are released from the postischemic mesenteric bed and enter the systemic circulation. They subsequently sequester in the pulmonary vascular bed where they are relatively harmless until they are activated by low dose endotoxin. These activated PMNs then migrate across the endothelium cell and release reactive oxygen metabolites.

Animals↗