Failure to rescue the elderly: a superior quality metric for trauma centers.

BACKGROUND: Trauma centers require reliable metrics to better compare the quality of care delivered. We compared mortality after a reported complication, termed failure to rescue (FTR), and FTR in the elderly (age >65 years) (FTRE) to determine which is a superior metric to assess quality of care delivered by trauma centers. METHODS: This was a retrospective review of the National Trauma Databank (NTDB) research data sets 2010 and 2011. Patients ≥16 years admitted to centers reporting ≥80% of AIS and/or ≥ 20% of comorbidities with > 200 subjects in the NTDB were selected. Centers were classified based on the rate of FTR and FTRE (<5 vs. 5-14 vs. ≥15%). The primary outcome was adjusted mortality for each group of trauma centers based on FTR and FTRE classifications. RESULTS: The overall mean ± SD FTR rate was 7.2 ± 5.2% and FTRE was 10.4 ± 7.9%. The adjusted odds ratio (AOR) for mortality was not different when centers with FTR <5% were compared to those with FTR of 5-14 or ≥15%. In contrast, a stepwise increase in FTRE predicted a significantly higher mortality when centers with FTRE 5% were compared to those with 5-14% (AOR: 1.05, p = 0.031) and ≥15% (AOR: 1.13, p < 0.001). Similarly, stepwise increase in FTRE predicted higher adjusted mortality for severely and critically injured patients, whereas FTR did not. CONCLUSIONS AND RELEVANCE: Higher FTRE predicts increased adjusted mortality better than FTR after trauma and should, therefore, be considered an important metric when comparing quality care delivered by trauma centers.

Long-term results justify autogenous infrainguinal bypass grafting in patients with end-stage renal failure.

INTRODUCTION: Infrainguinal bypass grafting for limb-threatening ischemia in patients with end-stage renal disease is generally thought to be associated with increased operative risk and poor long-term outcome. This retrospective study was undertaken to examine the modern-era, long-term results of infrainguinal bypass grafting in dialysis-dependent patients. METHODS: Over the past 5 years in a single institution, 425 lower extremities (368 consecutive patients) were revascularized for the indication of limb salvage. Sixty-four patients (82 limbs) were dialysis-dependent at the time of revascularization, and this group was analyzed separately. They exhibited statistically significant higher incidences of diabetes (83% vs 56%; P <.001), hypertension (91% vs 74%; P <.001), and more distal vascular disease, which required a greater proportion of proximal anastomoses at the popliteal level (24% vs 11%; P <.01) and distal anastomoses at the infrapopliteal level (75% vs 65%; P <.05). RESULTS: Despite the higher prevalence of comorbid conditions and distal disease in patients with renal failure, their perioperative 30-day mortality rate remained low (4.9%) and was not significantly different from that in patients with functioning kidneys (2.9%; P = not significant). After a median follow-up of 11 months (range, 0-60 months), the 3-year autogenous conduit secondary graft patency in patients with renal failure was no different than in patients with functioning kidneys (67% +/- 9% vs 64% +/- 5%; P = not significant). Nonautogenous conduits in dialysis-dependent patients exhibited a significantly poorer outcome with only 27% +/- 12% remaining secondarily patent at 2 years. As expected, both limb salvage and patient survival were significantly less in patients with renal faiture, although both exceeded 50% at 3 years (limb salvage 59% +/- 8% vs 68% +/- 5%; P <.05; patient survival 60% +/- 8% vs 86% +/- 4%; P <.001). The often-quoted phenomenon of limb loss, despite a patent bypass graft, occurred infrequently in this study (n = 3 of 82 limbs). CONCLUSION: Infrainguinal revascularization can be performed in dialysis-dependent patients with acceptable perioperative and long-term results, especially in patients in whom adequate autologous conduit is available.

Patency and limb salvage after infrainguinal bypass with severely compromised ("blind") outflow.

HYPOTHESIS: Infrainguinal graft patency and limb salvage are adversely affected by severely compromised outflow. DESIGN: Retrospective review of all infrainguinal bypass procedures performed at a single institution during a 5-year period. SETTING: University teaching hospital. PATIENTS: Two hundred seventy-four patients underwent infrainguinal bypass for limb salvage (351 grafts in 307 limbs). INTERVENTIONS: All infrainguinal bypasses originated from a femoral artery. The distal anastomosis in 279 grafts was located in an artery with at least 1 patent outflow vessel with anatomically normal end-artery runoff (Society for Vascular Surgery/International Society for Cardiovascular Surgery ad hoc committee runoff score, 1-9). The distal anastomosis of 72 grafts was located in an artery with only collateral outflow ("blind bypass"; runoff score, 10). MAIN OUTCOME MEASURES: Perioperative morbidity and mortality, primary-assisted and secondary graft patency, limb salvage, and survival. RESULTS: All data are presented as mean +/- SEM. Patients undergoing blind bypass were older (age, 70 +/- 2 vs. 66 +/- 1 years; P <.05) and had a higher incidence of hypertension (90% vs 70%; P <.05) and end-stage renal disease (24% vs. 13%; P <.05). Comparing patients undergoing blind bypass to bypass with at least 1 patent outflow vessel, there were no differences in the use of nonautogenous conduits (50% vs 59%; P =.21) or postoperative warfarin (30% vs 32%; P =.69), or in perioperative mortality rates (2.7% vs 3.2%; P =.79). After a median follow-up of 13 months (range, 0-60 months), 2-year secondary graft patency for the entire group was 63% +/- 4%. The secondary patency rate of blind bypass grafts was no different from that of grafts with at least 1 patent outflow vessel (67% +/- 7% vs. 64% +/- 4%; P was not significant). However, the 2-year limb salvage rate in limbs with blind outflow was significantly worse than in limbs with at least 1 patent outflow vessel (67% +/- 7% vs. 76% +/- 3%; P =.04). CONCLUSION: Acceptable long-term patency rates can be achieved in infrainguinal bypass grafts with blind outflow, although blind outflow remains a marker for subsequent limb loss in the chronically ischemic leg.

Angioplasty does not affect subsequent operative renal artery revascularization.

BACKGROUND: Although increased application of percutaneous renal artery angioplasty and stenting has facilitated nonoperative renal revascularization, patient outcomes after failed angioplasty are not established. METHODS: Renal artery revascularization was performed in 31 patients (38 arteries) from 1993 to 1999. Twenty patients underwent primary surgical repair, and 11 patients underwent secondary reconstruction after angioplasty (n = 7) or angioplasty and stenting (n = 4). Before operation, all patients had severe hypertension (blood pressure 166+/-5.2/92 +/- 2.7 mm Hg) that required an average of 3.0 +/- 0.2 medications for control. In addition, 12 patients (primary 45% vs secondary 27%; P = NS) had evidence of renal insufficiency (creatinine > or =1.7 mg/dL). RESULTS: There was no difference between primary and secondary procedures in the length of hospital stay (12+/- 1.4 vs. 12+/-3.2 days; P = NS), major morbidity (10% vs. 18%; P = NS) or perioperative mortality (overall mortality 2 of 31; primary 5% vs secondary 9%; P = NS). The majority of patients demonstrated improvement or cure of hypertension (primary 94% vs secondary 90%; P = NS) and stable or decreased creatinine (primary 74% vs secondary 82%; P = not significant). Overall survival (mean follow-up 22+/-3.5 months) was 89%+/-5.7%. CONCLUSIONS: Although this surgical series does not address the true outcomes of renal artery angioplasty, the results suggest that renal artery angioplasty does not prejudice subsequent surgical outcomes in patients who are carefully followed after angioplasty.

Estimating the contemporary in-hospital costs of carotid endarterectomy.

Carotid endarterectomy (CEA) is the treatment of choice for symptomatic carotid stenosis and selective asymptomatic lesions. Alternative approaches have recently been championed under the guise of increased efficacy and decreased cost. The purpose of this study was to determine the results and in-hospital costs of CEA in a university hospital in the modern era. A retrospective chart review was undertaken for all patients undergoing CEA between January 1995 and December 1997. This corresponded to the implementation of a clinical path and extended efforts toward cost reduction. Patients undergoing combined CEA and cardiopulmonary bypass were excluded (n = 3). Cost was analyzed by the hospital Office of Program Planning using TSI (Transition Systems, Inc.) software. Direct costs are related to the utilization of clinical resources and are therefore manageable by clinicians (bed, room, supplies, nursing staff, OR staff, radiology, pharmacy, etc.). Total costs additionally include administration and overhead costs not directly chargeable to patient accounts. The results of this study showed that CEA can be safely performed with brief hospital stays and reasonable hospital costs. Results of alternative interventions for the treatment of carotid stenosis should be compared to these contemporary data.

Effective hemodynamic diameter: an intrinsic property of vein grafts with predictive value for patency.

INTRODUCTION: Conduit size and quality are major determinants of the long-term success of infrainguinal autologous vein grafting. However, accurate measurement of the internal diameter of vein grafts is difficult given their variable wall thickness and taper. The purpose of this study was to define the "effective" internal diameter of a vein graft according to its hemodynamic properties and to determine its significance for graft patency. METHODS: Sixty infrainguinal bypass grafts performed on 57 patients were evaluated intraoperatively. Proximal and distal graft pressure and blood flow (Q(meas)) were measured with fluid-filled catheter transduction and ultrasonic transit-time flowimetry, respectively, after unclamping. Waveforms were recorded digitally at 200 Hz under baseline conditions and after stimulation with 60 mg of papaverine. According to Fourier transformation of the measured pressure gradient (DeltaP), the Womersley solution for fluid flow in a straight rigid tube was used to calculate theoretical flow waveforms (Q(calc)) for a range of graft diameters. The theoretical waveforms were then compared with the measured flow waveforms and the best-fit diameter chosen as the "effective hemodynamic diameter" (EHD). Only grafts in which the correlation coefficient of Q(calc) versus Q(meas) was more than 0.90 were accepted (n = 47) to assure validity of the hemodynamic model. After a mean follow-up of 12.5 months (range, 0.1-43.9 months), patency was determined by the life table method. Hemodynamic and clinical variables were tabulated, and their effect on patency determined the use of univariate and multivariate Cox regression. RESULTS: Mean EHD was 4.1 +/- 0.1 mm with a range of 2.5 to 5.7 mm. Administration of papaverine caused profound changes in DeltaP (+78% +/- 17%) and Q(meas) (+71% +/- 12%) as expected, but had no effect on EHD (+0.05% +/- 0.1%). Univariate regression identified five variables associated with decreased secondary patency (P <.10): low EHD, conduit source other than the greater saphenous vein, high baseline DeltaP(mean), female sex, and redo operation. Of these, only low EHD was significant after multivariate analysis (P =.03). Patency of small diameter grafts (EHD < 3.6 mm; n = 11) was compared with patency of larger grafts (EHD > 3.6 mm; n = 36) to test a frequently espoused clinical guideline. Grafts with an EHD less than 3.6 mm exhibited significantly lower secondary patency compared with larger grafts (P =.0001). The positive and negative predictive values for an EHD less than 3.6 mm for secondary graft failure for grafts with at least 1 year follow-up were 86% and 88%, respectively. CONCLUSION: An EHD is a unique parameter that quantifies conduit size and has a significant impact on vein graft patency. An EHD less than 3.6 mm portends graft failure.

Measuring faculty effort and contributions in medical education.

A national panel on medical education was appointed as a component of the AAMC's Mission-based Management Program and charged with developing a metrics system for measuring medical school faculty effort and contributions to a school's education mission. The panel first defined important variables to be considered in creating such a system: the education programs in which medical school faculty participate; the categories of education work that may be performed in each program (teaching, development of education products, administration and service, and scholarship in education); and the array of specific education activities that faculty could perform in each of these work areas. The panel based the system on a relative value scale, since this approach does not equate faculty performance solely to the time expended by a faculty member in pursuit of a specific activity. Also, a four-step process to create relative value units (RVUs) for education activities was developed. This process incorporates quantitative and qualitative measures of faculty activity and also can measure and value the distribution of faculty effort relative to a school's education mission. When adapted to the education mission and culture of an individual school, the proposed metrics system can provide critical information that will assist the school's leadership in evaluating and rewarding faculty performance in education and will support a mission-based management strategy in the school.

Endothelial permeability and IL-6 production during hypoxia: role of ROS in signal transduction.

Prolonged hypoxia produces reversible changes in endothelial permeability, but the mechanisms involved are not fully known. Previous studies have implicated reactive oxygen species (ROS) and cytokines in the regulation of permeability. We tested whether prolonged hypoxia alters permeability to increasing ROS generation, which amplifies cytokine production. Human umbilical vein endothelial cell (HUVEC) monolayers were exposed to hypoxia while secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1alpha, IL-6, and IL-8 was measured. IL-6 and IL-8 secretion increased fourfold over 24 h in a pattern corresponding to changes in HUVEC permeability measured by transendothelial electrical resistance (TEER). Addition of exogenous IL-6 to normoxic HUVEC monolayers caused time-dependent changes in TEER that mimicked the hypoxic response. An antibody to IL-6 significantly attenuated the hypoxia-induced changes in TEER (86 +/- 4 vs. 63 +/- 3% with hypoxia alone at 18 h), whereas treatment with anti-IL-8 had no effect. To determine the role of hypoxia-induced ROS on this response, HUVEC monolayers were incubated with the antioxidants ebselen (50 microM) and N-acetyl-L-cysteine (NAC, 1 mM) before hypoxia. Antioxidants attenuated hypoxia-induced IL-6 secretion (13 +/- 2 pg/ml with ebselen and 19 +/- 3 pg/ml with NAC vs. 140 +/- 15 pg/ml with hypoxia). Ebselen and NAC prevented changes in TEER during hypoxia (94 +/- 2% with ebselen and 90 +/- 6% with NAC vs. 63 +/- 3% with hypoxia at 18 h). N-nitro-L-arginine (500 microM) did not decrease hypoxia-induced changes in dichlorofluorescin fluorescence, IL-6 secretion, or TEER. Thus ROS generated during hypoxia act as signaling elements, regulating secretion of the proinflammatory cytokines that lead to alterations of endothelial permeability.

Decrease in mucosal alkaline phosphatase: a potential marker of intestinal reperfusion injury.

Intestinal ischemia necessitates rapid re-establishment of blood flow to prevent irreversible anoxic tissue damage. However, reperfusion results in additional injury as a consequence of the generation of oxygen free radicals. To date, no clear-cut marker to differentiate between ischemia versus reperfusion injury is available. In this regard, previous studies from our laboratory utilizing a rat in vitro lipid peroxidation model demonstrated that the generation of free radicals resulted in the inactivation of only the intestinal brush border alkaline phosphatase enzyme, with no effect on other membrane-bound digestive enzymes. Current studies were designed to assess the possibility of alkaline phosphatase being a specific marker of the reperfusion injury in canine and human ex vivo ischemia/reperfusion models. Small bowels harvested from canines and organ donors were subjected to ischemia followed by reperfusion. Brush border membrane enzymes, alkaline phosphatase, sucrase, maltase, and gamma-glutamyl transpeptidase were assayed in mucosal extracts from intestines with ischemia versus reperfusion. In both experimental models, there was no change in any enzyme activity with warm ischemia alone. In contrast, alkaline phosphatase activity was significantly decreased in both the canine and human reperfusion models, with no change in specific activities of sucrase, maltase, and gamma-glutamyl transpeptidase. Our data indicate that the alkaline phosphatase enzyme activity may represent a potential marker of intestinal reperfusion injury and may permit quantitative assessments of therapeutic interventions in human intestinal reperfusion injury.

Prolonged hypoxia alters endothelial barrier function.

BACKGROUND: It is well recognized that hypoxia/reoxygenation and exposure to inflammatory mediators such as cytokines and neutrophils alter the barrier function of the vascular endothelium. The experiments we conducted tested whether hypoxia alone could produce changes in permeability and whether a prolonged period of hypoxia alters the surface expression of cell adhesion molecules. METHODS: Endothelial cells were cultured from human umbilical vein endothelial cells (HUVECs). Hypoxia was created by isolating the cells in a chamber through which 1% 02, 5% CO2, and 94% N2 were insufflated (30 min at 1/min). Oxygen tension was measured through oxygen-quenching phosphorescence. Hypoxia was maintained for 24 hours. Changes in endothelial permeability were measured by transendothelial electrical resistance (TEER). Endothelial leukocyte adhesion molecule 1 (ELAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression were assessed by flow cytometry (mean +/ standard error of the mean [SEM]. RESULTS: Exposure of endothelial cells to hypoxia resulted in increased permeability between 6 and 24 hours, with the greatest decrease in TEER at 18 hours (63% +/ 3%; P < .05). Prolonged hypoxia produced no change in the surface expression of ELAM-1 or ICAM-1. CONCLUSIONS: Hypoxia alone produced a significant reversible alteration in endothelial permeability. However, this change was observed only under severe hypoxic conditions (eg, below 20 mm Hg); higher oxygen tensions (25 and 35 mm Hg) had no significant effect. Unlike observations made after cytokine exposure, hypoxic breakdown of endothelial barrier function was unassociated with up-regulation of either ELAM-1 or ICAM-1.

Improving perioperative management of carotid endarterectomy.

Multiple components of the perioperative course of patients who undergo carotid endarterectomy must be tightly controlled in order to maintain an acceptably low complication rate. These factors include appropriate patient selection, routine assessment of cardiac risk factors, precise control of blood pressure intraoperatively and postoperatively, meticulous surgical technique and reliable monitoring for intraoperative cerebral ischemia. This discussion focuses on the vascular practice patterns at the University of Chicago and emphasizes intraoperative management and the safe utilization of intraluminal shunts.

Assessing outcomes, costs, and benefits of emerging technology for minimally invasive saphenous vein in situ distal arterial bypasses.

BACKGROUND: Instrumentation for a minimally invasive angioscopic in situ peripheral arterial bypass (MIAB) with catheter-directed side-branch occlusion has recently been approved for use. Despite the attractiveness of this approach (2 short incisions), benefits such as lower morbidity and shorter hospitalizations remain undocumented. To justify wide acceptance, minimally invasive surgical techniques must match conventional procedures in durability and cost while enhancing patient comfort. Often such comparisons are difficult during the implementation phase of a new procedure. OBJECTIVE: To compare the outcomes of the MIAB procedures with a concurrent group of patients undergoing conventional in situ bypass procedures. DESIGN: Retrospective review. SETTING: University medical center. PATIENT: The first 20 consecutive MIAB procedures in 19 patients performed between August 1, 1995, and July 31, 1997, were compared with 19 contemporaneous consecutive conventional in situ bypass procedures performed at the same institution. MAIN OUTCOME MEASURES: Operative time, postoperative length of stay, hospital costs, complications, primary assisted and secondary patency, limb salvage, and survival. RESULTS: The patient groups were comparable with respect to age, sex, incidence of smoking, coronary artery disease, hypertension, diabetes, renal failure, cerebrovascular disease, indication, and distal anastomosis level. The median operative time was significantly greater for the MIAB group (6.6 hours vs 5.7 hours; P=.009), and intraoperative completion arteriography more frequently showed retained arteriovenous fistulas in the MIAB group (55% vs 21%; P=.05). The median postoperative length of stay and total cost were 6.5 days and $18,000 for the MIAB group and 8 days and $27,800 for the conventional group (P > or = .05). There were no significant differences in major complications (10% in the MIAB group vs 11% in the conventional group), wound complications (10% vs 11%, respectively), primary assisted patency at 1 year (68%+/-11% vs 78%+/-10%, respectively), secondary patency at 1 year (79%+/-10% vs 88%+/-8%, respectively), limb salvage at 1 year (85%+/-10% vs 94%+/-6%, respectively), or patient survival at 1 year (89%+/-8% vs 61%+/-13%, respectively). CONCLUSION: Patients undergoing the MIAB procedure avoided lengthy vein exposure incisions without sacrificing short-term results. There was a trend toward decreased hospital stay and cost, which may be further realized as the clinical experience broadens. Although longer follow-up and larger cohorts will always be required to define durability, immediate access to outcomes and costs on small numbers of patients facilitates the early assessment of emerging technology.

Serum proteins facilitate neutrophil induction of endothelial leukocyte adhesion molecule 1.

BACKGROUND: Although the individual actions of neutrophils and serum proteins such as complement in acute inflammation are well characterized, less is known about their effects in combination. We investigated the combined effects of neutrophil contact and active serum proteins on the expression of endothelial leukocyte adhesion molecule 1 (ELAM-1). METHODS: Confluent monolayers of human umbilical vein endothelial cells were incubated with neutrophils in the presence and absence of fresh human serum. Flow cytometry was used to assess expression of endothelial intercellular adhesion molecule 1 (ICAM-1) and ELAM-1. In addition, neutrophils were retained in a semipermeable insert, which allowed their secretions to contact the endothelium but restricted neutrophil-endothelial contact. RESULTS: ELAM-1 expression was significantly increased on the cells coincubated with neutrophils and fresh human serum (25.8%; p < 0.001). There was no significant change in ELAM-1 expression on endothelial cells incubated with fresh human serum alone (3.9%; p > 0.01) or in those incubated with neutrophils and heat-inactivated serum (9.3%; p > 0.01). In the absence of neutrophil contact, ELAM-1 expression was increased only in the presence of fresh human serum (9.6%; p < 0.05). CONCLUSIONS: These findings suggest that serum proteins may potentiate the volume or potency of neutrophil-derived diffusable mediators of ELAM-1 expression. These effects are eliminated with the heat inactivation of serum proteins, implicating a heat sensitive mediator such as the complement cascade.

Juxtalumenal location of plaque necrosis and neoformation in symptomatic carotid stenosis.

PURPOSE: The structural features that underlie carotid plaque disruption and symptoms are largely unknown. We have previously shown that the chemical composition and structural complexity of critical carotid stenoses are related to plaque size regardless of symptoms. To further determine whether the spatial distribution of individual plaque components in relation to the lumen corresponds to symptomatic outcome, we evaluated 99 carotid endarterectomy plaques. METHODS: Indications for operation were symptomatic disease in 59 instances (including hemispheric transient ischemic attack in 29, stroke in 19, and amaurosis fugax in 11) and angiographic asymptomatic stenosis > 75% in 40. Plaques removed after remote symptoms beyond 6 months were excluded. Histologic sections from the most stenotic region of the plaque were examined using computer-assisted morphometric analysis. The percent area of plaque cross-section occupied by necrotic lipid core with or without associated plaque hematoma, by calcification, as well as the distance from the lumen or fibrous cap of each of these features, were determined. The presence of foam cells, macrophages, and inflammatory cell collections within, on, or just beneath the fibrous cap was taken as an additional indication of plaque neoformation. RESULTS: The mean percent angiographic stenosis was 82% +/- 11% and 79% +/- 13% for the asymptomatic and symptomatic groups, respectively (p > 0.05). The necrotic core was twice as close to the lumen in symptomatic plaques when compared with asymptomatic plaques (0.27 +/- 0.3 mm vs 0.5 +/- 0.5 mm; p < 0.01). The percent area of necrotic core or calcification was similar for both groups (22% vs 26% and 7% vs 6%, respectively). There was no significant relationship to symptom production of either the distance of calcification from the lumen or of the percent area occupied by the lipid necrotic core or calcification. The number of macrophages infiltrating the region of the fibrous cap was three times greater in the symptomatic plaques compared with the asymptomatic plaques (1114 +/- 1104 vs 385 +/- 622, respectively, p < 0.009). Regions of fibrous cap disruption or ulceration were more commonly observed in the symptomatic plaques than in the asymptomatic plaques (32% vs 20%). None of the demographic or clinical atherosclerosis risk factors distinguished between symptomatic and asymptomatic plaques. CONCLUSIONS: These findings indicate that proximity of plaque necrotic core to the lumen and cellular indicators of plaque neoformation or inflammatory reaction about the fibrous cap are associated with clinical ischemic events. The morphologic complexity of carotid stenoses does not appear to determine symptomatic outcome but rather the topography of individual plaque components in relation to the fibrous cap and the lumen. Imaging techniques that precisely resolve the position of the necrotic core and evidence of inflammatory reactions within carotid plaques should help identify high-risk stenoses before disruption and symptomatic carotid disease.

Loss of endothelial barrier function requires neutrophil adhesion.

BACKGROUND: The inflammatory response is characterized by cytokine-induced up-regulation of endothelial adhesion molecules followed by polymorphonuclear neutrophil (PMN) adhesion and breakdown of tight junctions between cells. The purpose of this investigation was to determine whether PMN adhesion is an essential element in the alteration of endothelial permeability or whether cytokines alone can produce this change. METHODS: Human umbilical vein endothelial cells (HUVECs) were exposed to formylated met-leu-phe-activated PMNs. In a second series of experiments, PMNs were contained in a microporous membrane that allowed passage of secreted cytokines but not cells. Permeability was quantified by using transendothelial electrical resistance (TEER, ohm.cm2,) whereas expressions of two cell adhesion molecules (endothelial leukocyte adhesion molecule-1 [ELAM-1] and intercellular adhesion molecule-1 [ICAM-1]) were measured by flow cytometry (% shift). Cytokine production was monitored with enzyme-linked immunosorbant assays (picograms per milliliter). RESULTS: Stimulated PMNs secreted comparable amounts of cytokines whether allowed access to HUVECs or trapped in a microporous membrane (interleukin-1 alpha, 5.88 +/- 2.38 versus 3.65 +/- 1.84 pg/ml; tumor necrosis factor-alpha, 10.27 +/- 3.21 versus 6.61 +/- 1.82 pg/ml). Up-regulation of ELAM-1 and ICAM-1 was observed whether PMNs were free or restricted (52.97% +/- 2.14% versus 75.32% +/- 4.19% and 71.66% +/- 7.37% versus 73.66% +/- 4.32%, respectively). TEER was unchanged in controls and when PMNs were membrane restricted. In contrast, TEER decreased precipitously (51% +/- 5.9% of control, p < 0.05) if PMNs were allowed access to HUVECs. CONCLUSIONS: Cytokine secretion by PMNs is independent of endothelial contact and is sufficient to upregulate adhesion molecules. However, PMN adhesion is essential for the loss of endothelial barrier function, which leads to diapedesis of activated PMNs and eventual tissue injury.

Tapping the power of information: an orientation for academic medical centers.

In September 1994 the Association of American Medical Colleges' (AAMC's) Advisory Panel on the Mission and Organization of Medical Schools (APMOMS) established a working group to address both the long-term and the immediate implications of the expanding capacity of and need for information technology (IT) within academic medical centers (i.e., medical schools and teaching hospitals). Over a two-year period, group members assessed the utilization of IT through surveys of current practices and interactions with acknowledge leaders in the field. They also had discussions with deans and other institutional leaders. The group developed the consensus that proper use of currently available IT is crucial to virtually every aspect of academic medicine's clinical, educational, and research missions. Moreover, current IT technology will be further enhanced by the powerful new applications that are nearing deployment. All group members agreed that IT must become a core competency of academic and medical centers (AMCs), the profession, and individual physicians and scientists to ensure the survival of AMCs in the current highly competitive environments. The authors outline their arguments for the development of strong information systems within AMCs and present basic characteristics of systems that show promise for successful implementation. The y review some of the major institutional obstacles that have hindered the planing and implementation of IT. They conclude with a list of practical institution strategies for success in planning and implementing IT systems, and suggestions for how the AAMC can help members achieve success in these activities.

Current results of surgical therapy for chronic mesenteric ischemia.

BACKGROUND: Although recognition of chronic mesenteric ischemia has increased in recent years, this disorder has continued to present diagnostic and therapeutic challenges. OBJECTIVE: To examine the modern results of surgical revascularization for chronic mesenteric ischemia. DESIGN: Retrospective review. SETTING: University medical center. PATIENTS: The management of 24 consecutive patients (mean +/- SEM age, 58 +/- 3 years; 5 men, 19 women) who were undergoing surgical treatment of chronic mesenteric ischemia between 1986 and 1996 was reviewed. INTERVENTION: Surgical mesenteric revascularization. MAIN OUTCOME MEASURES: Postoperative course, long-term graft patency rate, and long-term symptom-free survival rate. RESULTS: The most frequent presenting symptoms were postprandial abdominal pain (18 patients [75%]) and weight loss (14 patients [58%]). Less specific complaints included nausea and vomiting (8 patients [33%]), diarrhea (7 patients [29%]), and constipation (4 patients [17%]). Atherosclerotic risk factors were common, including tobacco use (20 patients [83%]), coronary artery disease (10 patients [42%]), and hypertension (10 patients [42%]). The cause was identified as atherosclerosis in 21 patients, median arcuate ligament compression in 2 patients who were monozygotic twins, and Takayasu arteritis in 1 patient. Lesions were localized to all 3 major visceral vessels (celiac artery, superior mesenteric artery [SMA], and inferior mesenteric artery) in 8 patients, celiac artery and SMA in 13, SMA alone in 2, and SMA and inferior mesenteric artery in 1. Seventeen patients underwent antegrade reconstructions from the supraceliac aorta to the SMA and/or celiac artery; 7 patients underwent revascularization by use of a retrograde bypass that originated from the infrarenal aorta or a prosthetic graft. There were no perioperative deaths although 1 patient died in the hospital 6 weeks after early graft failure and sepsis (overall in-hospital mortality, 4%). Follow-up ranged from 3 months to 10 years (median, 2.4 years). The mean +/- SEM 5-year primary graft patency rate, as objectively documented by use of contrast angiography or duplex scanning in 19 of 24 patients, was 78% +/- 11%. Primary failure was documented in 3 patients (at 3 weeks, 5 months, and 7 months). Two patients required a thrombectomy; 1 of these patients subsequently died of an intestinal infarction. The mean +/- SEM 5-year survival rate by use of life-table analysis was 71% +/- 11%. No patient with a patent graft experienced a symptomatic recurrence. CONCLUSIONS: Chronic mesenteric ischemia is usually a manifestation of advanced systemic atherosclerosis. Symptoms almost always reflect midgut ischemia in the distribution of the SMA. An antegrade bypass from the supraceliac aorta can be performed with acceptable operative morbidity and is currently the preferred reconstructive technique. Surgical revascularization affords long-term symptom-free survival in a majority of patients with chronic mesenteric ischemia.