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Biomedical subjects

E E Moore

Publications and source records attributed to E E Moore.

At least 73 records · Page 4Linked to original sources
PubMed1999

Male gender is a risk factor for major infections after surgery.

BACKGROUND: Accumulating clinical and epidemiological evidence suggests significant gender differences in the incidence of and outcome following major infection. In a rodent model of hemorrhagic shock, investigators have shown that males manifest depressed cell-mediated immunity that is reversed by castration or pharmacologic testosterone receptor blockade. Female rats, in contrast, show enhanced immune function that is reduced to male levels by testosterone administration. This sexual dimorphism is believed responsible for the improved outcome in female mice following septic challenge. HYPOTHESIS: Male gender is a risk factor for major infections following severe injury. DESIGN: Five-year prospective cohort study ending October 1998. SETTING: Urban level I regional trauma center. PATIENTS AND METHODS: A total of 545 trauma patients older than 15 years with an Injury Severity Score greater than 15 and survival more than 48 hours were prospectively identified and studied. Collected data included age, injury mechanism, and Injury Severity Score. Major infections, defined as pneumonia, abdominal and pelvic abscess, wound infection requiring operative debridement, and meningitis, were tabulated. The occurrence of major infections in males and females was compared using multiple logistic regression analysis. MAIN OUTCOME MEASURE: Postinjury major infectious complications. RESULTS: Of the 545 patients, 135 (24.8%) were female and 410 (75.2%) were male. Major infections occurred in 219 (40.2%) patients. Logistic regression confirmed that male gender is an independent risk factor for major infections (P=.04) after controlling for age and Injury Severity Score. Males had a 58% greater risk of developing a major infection (odds ratio, 1.58; 95% confidence interval, 1.01-2.48). CONCLUSIONS: Male gender is associated with a dramatically increased risk of major infections following trauma. This effect is most significant following injuries of moderate severity (Injury Severity Score 16-25) and persists in all age groups.

Adolescent↗
PubMed1999

Disparities in the respiratory burst between human and rat neutrophils.

The importance of reactive oxygen species (ROS) in neutrophil (PMN)-mediated injury to host tissues has been strongly implicated in a number of animal models. Peculiarities of the laboratory rat PMN, including an apparent paucity of superoxide release, prompted us to examine disparities in the respiratory burst between human and rat PMNs. Using isolated PMNs, we examined oxygen consumption, superoxide release, nitrate/nitrite release, and dihydrorhodamine (DHR) oxidation in response to an array of soluble stimuli. Our findings confirm that intact rat PMNs release little superoxide in comparison to human PMNs when primed and activated by soluble stimuli. For example, PMA-activated human PMNs released superoxide at 10.1 +/- 2.7 times the rate of rat PMNs (P < 0.01). However, measurements of oxygen consumption, cell-associated oxidant production (by DHR oxidation) and release of superoxide from electroporated cells suggests that rat PMNs generate oxidants at rates equivalent to human PMNs but preferentially release them in an intracellular compartment. Implications for the study of PMN-mediated oxidant injury in animal models are discussed.

Animals↗
PubMed1999

Cardiopulmonary bypass renders patients at risk for multiple organ failure via early neutrophil priming and late neutrophil disability.

BACKGROUND: Cardiopulmonary bypass (CPB) is associated with a systemic inflammatory response syndrome (SIRS) and these patients are recognized to be at increased risk for delayed infectious complications. We have documented that circulating neutrophils (PMNs) from patients manifesting SIRS have evidence of early postinjury priming for cytotoxicity. Consequently, we hypothesized that CPB would result in early postoperative PMN hyperresponsiveness (priming). MATERIALS AND METHODS: Six patients (mean age 50 +/- 2.9 years) who underwent CPB for CABG had sequential blood samples obtained perioperatively. PMNs were isolated and superoxide anion (O(-)(2)) generation (nmol O(-)(2)/3.75 x 10(5) PMNs/min) was measured by reduction of cytochrome c after exposure to fMLP, C5a, or PMA; elastase release (% total PMN elastase content) was measured by cleavage of AAPV-pNA after exposure to fMLP or C5a. RESULTS: PMNs were activated for increased elastase release 6 h after initiation of CPB. Significant PMN priming for O(-)(2) production was discovered at 3, 6, and 12 h following CPB and for elastase release at 3 and 6 h after CPB. At 2 to 3 days after CPB, O(-)(2) generation was significantly less than that of the preoperative control. Neutrophil primability with PAF was detected at 6 h after CPB. A similar defect in PAF-primable O(-)(2) production was seen 2 and 3 days post-CPB. Direct PMN interrogation with the receptor-independent activator PMA revealed loss of integrity of the NADPH oxidase at 2 and 3 days following CPB. CONCLUSIONS: A vulnerable window exists between 3 and 12 h after CPB when PMNs are primed for enhanced cytotoxicity via O(-)(2) production and elastase release. Paradoxically, PMN oxidase integrity becomes deficient 48 h post-CPB, while protease degranulation remains intact. These events render the bypass patient at risk for multiple organ failure via both early PMN-mediated tissue injury and delayed infectious complications.

Adolescent↗
PubMed1999

Age of transfused blood is an independent risk factor for postinjury multiple organ failure.

BACKGROUND: Blood transfusion has repeatedly been demonstrated to be an independent risk factor for postinjury multiple organ failure (MOF). Previously believed to represent a surrogate for shock, packed red blood cell (PRBC) transfusion has recently been shown to result in neutrophil priming and pulmonary endothelial cell activation. We have previously observed that the generation of inflammatory mediators is related to the length of PRBC unit storage. The purpose of this study was to determine if age of transfused PRBC is a risk factor for the development of postinjury MOF. METHODS: Using our prospective database of trauma patients at risk for developing MOF, we identified patients who developed MOF (MOF+) and received 6 to 20 units of PRBCs in the first 12 hours following injury. A similar cohort of patients, matched for ISS and transfusion requirement, who did not develop MOF (MOF-) were also identified. The age of each unit of PRBC transfused in the first 6 hours was determined. Multiple logistic regression was performed to determine if age of transfused blood is an independent risk factor. RESULTS: Sixty-three patients were identified, 23 of whom were MOF+. There was no difference in ISS and transfusion requirement between MOF+ and MOF- groups. MOF+ patients, however, were significantly older (46+/-4.7 years versus 33+/-2.3 years). Moreover, mean age of transfused blood was greater in the MOF+ patients (30.5+/-1.6 days versus 24+/-0.5 days). Similarly, the mean number of units older than 14 and 21 days old were greater in the MOF+ patients. Multivariate analysis identified mean age of blood, number of units older than 14 days, and number of units older than 21 days as independent risk factors for MOF. CONCLUSION: The age of transfused PRBCs transfused in the first 6 hours is an independent risk factor for postinjury MOF. This suggests that current blood bank processing and storage technique should be reexamined. Moreover, fresh blood may be more appropriate for the initial resuscitation of trauma patients requiring transfusion.

Adult↗
PubMed1999

Release of anti-inflammatory mediators after major torso trauma correlates with the development of postinjury multiple organ failure.

BACKGROUND: Soluble tumor necrosis factor receptor (sTNFr) and interleukin-1 receptor antagonist (IL-1ra) have been identified as endogenous inhibitors of TNF-alpha and IL-1beta. While TNF-alpha and IL-1beta levels are not systematically elevated in postinjury patients who developed multiorgan failure (MOF), their involvement at the tissue level has been suggested. Our study hypothesis was that levels of sTNFr-I and IL-1ra would discriminate patients at risk for postinjury MOF. METHODS: Serial plasma levels of sTNFr and IL-1ra were measured in 29 trauma patients at high risk for postinjury MOF. RESULTS: sTNFr-I levels were higher in MOF compared with non-MOF patients at 12, 84, and 132 hours postinjury. MOF patients also had higher IL-1ra values 36, 60, 84, and 132 hours postinjury. CONCLUSIONS: Anti-inflammatory mechanisms are activated after trauma. Since increased levels of sTNFr and IL-1ra correlate with postinjury MOF, they may contribute to our understanding of the pathogenesis as well as prediction of outcome. High levels of antagonists to TNF-alpha and IL-1beta suggest tissue level involvement of these cytokines in postinjury hyperinflammation.

Adult↗
PubMed1999

Autologous blood transfusion does not reduce postoperative infection rates in elective surgery.

BACKGROUND: The influence of blood transfusions in the risk of postoperative infection remains controversial. We examined the association between autologous (AB) and homologous (HB) blood transfusions with postoperative infection in elective surgery. METHODS: The medical records of 991 Medicare patients aged > or =65 years submitted to hysterectomy and hip and knee replacement were reviewed. Logistic regression analysis was used to control for age, comorbidity, year, and type of procedure. RESULTS: Overall, 451 (46%) patients required transfusions. AB was given to 324 (72%), HB to 94 (21%); 33 (7%) patients received both. Forty-two patients (4%) developed postoperative infections. The infection rate was not different among patients receiving HB (7%), AB (5%), AB+HB (0), and nontransfused patients (4%); P = 0.18). After adjustment for confounders, HB and AB remained not associated with infections. CONCLUSION: In elective surgery with small volume transfusion, neither AB nor HB transfusions were associated with an increased risk of postoperative infections.

Aged↗
PubMed1999

Optimizing screening for blunt cerebrovascular injuries.

BACKGROUND: The recognition that early diagnosis and intervention, prior to ischemic neurologic injury, has the potential to improve outcome following blunt cerebrovascular injuries (BCVI), led to a policy of aggressive screening for these injuries. The resultant epidemic of BCVI has created a dilemma, as widespread screening is impractical. We sought to identify independent predictors of BCVI, to focus resources. METHODS: Cerebral arteriography was performed based on signs or symptoms of BCVI, or in asymptomatic patients with high-risk mechanisms (hyperextension, hyperflexion, direct blow) or injury patterns. Logistic regression analysis identified independent predictors. RESULTS: A total of 249 patients underwent arteriography; 85 (34%) had injuries. Independent predictors of carotid arterial injury were Glasgow coma score < or =6, petrous bone fracture, diffuse axonal brain injury, and LeFort II or III fracture. Having one of these factors in the setting of a high-risk mechanism was associated with 41% risk of injury. Of patients with cervical spine fracture, 39% had vertebral arterial injury. CONCLUSIONS: Patients sustaining high-risk injury mechanisms or patterns should be screened for BCVI. In the face of limited resources, screening efforts should be focused on those with high-risk predictors.

Adult↗
PubMed1999

Blunt cerebrovascular injuries.

On the basis of our experience and the available literature, we submit that aggressive screening for BCI based on injury patterns is warranted. However, several important clinical issues remain unresolved. The precise injury patterns and relative cerebrovascular risks remain to be defined. Furthermore, the optimal diagnostic screening test remains to be identified, with consideration of the relative risk-benefit profile. Finally, we must determine the best methods for the treatment of BCI. Although the definitive study has yet to be completed, the use of heparin was associated with a trend toward improved outcomes in symptomatic patients. In addition, no asymptomatic patient experienced the development of new neurologic deficits during heparin therapy. Therefore we believe that the early institution of heparin therapy is indicated. The role of endovascular stenting, however, remains unclear.

Brain Injuries↗
PubMed1999

Nonoperative management of solid organ injuries in children results in decreased blood utilization.

BACKGROUND: The administration of blood products to injured children has been recognized as a potential risk of nonoperative management. The purpose of this study was to evaluate blood utilization in the management of solid organ injuries in pediatric blunt abdominal trauma victims. METHODS: One hundred sixty-one children (< or =16 years old) with solid organ injuries over an 8-year study period (1990 through 1997) were identified from the trauma registries at 2 urban regional trauma centers. RESULTS: Mean age of the study patients was 7.9+/-0.4 years, 95 (59%) were boys, and their mean injury severity score (ISS) was 17.8+/-1.2. Patients were divided into 4-year study cohorts (1990 through 1993 and 1994 through 1997) to examine changes in operative management and blood utilization. For each time period examined, those treated nonoperatively received fewer blood transfusions (46% v 9% and 44% v 13%, P<.05 by Fisher's Exact test), and the hospital length of stay was shorter (12.3+/-2.1 v 5.0+/-0.7 and 7.8+/-1.9 v 4.2+/-0.4 days, P<.0001 by analysis of variance/Scheffe's) compared with the laparotomy cohort. CONCLUSIONS: The appropriate nonoperative management of injured children actually reduces the risks of receiving blood transfusion and decreases the length of hospital stay compared with aggressive operative intervention. Blood transfusion should be reserved only for those injured children with solid organ injuries who are hemodynamically unstable.

Adolescent↗
PubMed1999

Stanniocalcin 2: characterization of the protein and its localization to human pancreatic alpha cells.

Stanniocalcin (STC) is a hormone that was originally identified in fish, where it inhibits calcium uptake by the gills and gut and stimulates phosphate adsorption by the kidney. Recently, two mammalian homologues of stanniocalcin were identified. The first (STC1) shows 61% identity to the fish stanniocalcins and appears to have a function similar to that of the fish stanniocalcins. The second homologue (STC2) is 30-38% identical to the fish stanniocalcins, and is characterized by unique cysteine and histidine motifs that are not found in the other stanniocalcins. We purified both the native hamster and recombinant human STC2 proteins and obtained a partial amino acid sequence of the hamster protein. Both proteins behave as a disulfide bonded homodimer, which undergoes post-translational modification(s). The STC2 gene was localized to human chromosome 5q35. Northern blot analysis revealed that the primary site of human STC2 production is the pancreas, and immunostaining localized the STC2 protein to a subpopulation of cells in the islet. Double immunostaining for STC2 and either insulin or glucagon revealed that STC2 protein is found in the alpha cells, but not the beta cells. We speculate that STC2 may play a role in glucose homeostasis.

Amino Acid Sequence↗
PubMed1999

Circulating postinjury neutrophils are primed for the release of proinflammatory cytokines.

BACKGROUND: Postinjury neutrophil (PMN) priming identifies the injured patient at risk for the subsequent development of multiple organ failure (MOF). PMN priming has previously been shown to cause enhanced release of proteases and superoxide. PMNs, however, are a rich source of proinflammatory cytokines, such as interleukin (IL)-8 and tumor necrosis factor (TNF), which have been implicated in the development of MOF. PMNs also make IL-1ra, which is an anti-inflammatory cytokine that inhibits IL-1. It is our hypothesis that postinjury PMNs are primed for increased stimulated release of the proinflammatory cytokines IL-8 and TNF but not the anti-inflammatory cytokine IL-1ra. METHODS: Twelve trauma patients with a mean Injury Severity Score of 24 (+/-4.6) and 10 elective surgical patients were studied. Postinjury PMNs were isolated from blood obtained at presentation (within 2 hours after injury) and 24 hours after trauma. PMNs from elective surgical patients were obtained preoperatively, immediately postoperatively, and at 24 hours. The PMNs were stimulated with platelet-activating factor (200 nM)/N-formyl-methionyl-leucyl-phenylalanine (1 micromol/L) or lipopolysaccharide (100 ng/mL) incubated for 24 hours in RPMI-1640, and release of IL-8, TNF, and IL-1ra were measured. RESULTS: Postinjury PMNs were primed for both platelet-activating factor/N-formyl-methionyl-leucyl-phenylalanine-stimulated and lipopolysaccharide-stimulated IL-8 and TNF release at 2 hours after injury (fourfold increase of IL-8 release and fivefold increase of TNF release), whereas elective surgical patients demonstrated no priming. In contrast, postinjury patients were not primed for increased release of the counterinflammatory cytokine IL-1ra, suggesting a specific postinjury up-regulation of IL-8 and TNF. CONCLUSION: After injury, PMNs are primed for proinflammatory cytokine release in addition to superoxide and elastase. This augmented release of IL-8 and TNF may be involved in the subsequent development of organ dysfunction and ultimately MOF.

Adult↗
PubMed1999

Adult versus pediatric prehospital trauma care: is there a difference?

BACKGROUND: Management of the injured child in the prehospital setting continues to be debated. Issues raised in the literature include time spent on scene, skill maintenance and performance, and reported poorer outcomes compared with adults. METHODS: Retrospective 2-year review of all pediatric (n = 232) and adult (n = 3,375) patients treated by a single emergency medical services agency and transported and admitted to a Level I trauma center. Patients were divided into two groups, pediatric (age 0 to 12 years) and adult (age >12 years) and further stratified into three Injury Severity Score subgroups; 1 to 15, 16 to 25, and more than 25. RESULTS: There were no significant differences in scene time for any of the groups. The percentage of patients with intravenous access or endotracheal intubation in the field and the mean Injury Severity Score were not different for the moderate or severely injured groups, although in the minor trauma group fewer pediatric patients had intravenous access or intubation performed. There were no differences in outcome for any of the groups. CONCLUSION: Paramedics are able to provide pediatric trauma patients a level of care comparable to that provided adult patients with similar outcome.

Adolescent↗
PubMed1999

Blunt carotid arterial injuries: implications of a new grading scale.

BACKGROUND: Blunt carotid arterial injuries (BCI) have the potential for devastating outcomes. A paucity of literature and the absence of a formal BCI grading scale have been major impediments to the formulation of sound practice guidelines. We reviewed our experience with 109 BCI and developed a grading scale with prognostic and therapeutic implications. METHODS: Patients admitted to a Level I trauma center were evaluated with cerebral arteriography if they exhibited signs or symptoms of BCI or met criteria for screening. Patients with BCI were treated with heparin unless they had contraindications, and follow-up arteriography was performed at 7 to 10 days. Endovascular stents were deployed selectively. A prospective database was used to track the patients. RESULTS: A total of 76 patients were diagnosed with 109 BCI. Two-thirds of mild intimal injuries (grade I) healed, regardless of therapy. Dissections or hematomas with luminal stenosis (grade II) progressed, despite heparin therapy in 70% of cases. Only 8% of pseudoaneurysms (grade III) healed with heparin, but 89% resolved after endovascular stent placement. Occlusions (grade IV) did not recanalize in the early postinjury period. Grade V injuries (transections) were lethal and refractory to intervention. Stroke risk increased with injury grade. Severe head injuries (Glasgow Coma Scale score < or =6) were found in 46% of patients and confounded evaluation of neurologic outcomes. CONCLUSION: This BCI grading scale has prognostic and therapeutic implications. Nonoperative treatment options for grade I BCI should be evaluated in prospective, randomized trials. Accessible grade II, III, IV, and V lesions should be surgically repaired. Inaccessible grade II, III, and IV injuries should be treated with systemic anticoagulation. Endovascular techniques may be the only recourse in high grade V injuries and warrant controlled evaluation in the treatment of grade III BCI.

Adolescent↗