Benchmarking a Center of Excellence in Vascular Surgery: Using Acute Physiology and Chronic Health Evaluation II to Validate Outcomes in a Tertiary Care Institute.

OBJECTIVE: The Society of Vascular Surgery (SVS) has made it a top priority to implement verification of vascular "centers of excellence". Our institutional aortic network was established in 2008 in order to standardize care of patients with suspected acute aortic pathology. The implementation and success of this program has been previously reported. We sought to use our experience as a benchmark for which to develop prognostic modeling to quantify clinical status upon admission and help predict outcomes. Our objective was to validate the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system using a cohort of aortic emergencies transferred by an organized transfer network. METHOD: This was a retrospective, single institution review of patients transferred through an institutional aortic network for acute aortic pathology from 2017-2018. Demographics, comorbidities, aortic diagnosis, APACHE II score, as well as 30-day mortality were recorded. Associations with 30-day mortality were evaluated using two-sample t-tests, ANOVA models, Pearson chi-square tests and Fisher exact tests. Receiver operating characteristic (ROC) curves were fit overall and by pathology to predict 30-day mortality by Apache II total score. RESULTS: There were 395 consecutive transfers were identified. The mean age was 64.7 years. Diagnoses included Type A Dissection (n = 134), Type B (n = 81), Aortic Aneurysm (n = 122), and PAU/IMH (n = 27). Mean APACHE II score on arrival was 12. Overall there were 53 deaths (13.4%) in the cohort. Patients that died had significantly higher Apache II total scores (11.3 vs 16.5, P < .001). The area under the receiver operator characteristic (ROC) curve (AUC) was .66 for the full cohort, indicating a poor clinical prediction test. CONCLUSION: APACHE II score is a poor predictor of 30-day mortality in a large transfer network accepting all aortic emergencies. The authors believe further refining a prognostic model for diverse population will not only help in predicting outcomes but to objectively quantify illness severity in order to have a basis for comparison among institutions and verification of "centers of excellence".

External beam irradiation for inhibition of intimal hyperplasia following prosthetic bypass: preliminary results.

To determine whether external beam irradiation delivered immediately after graft implantation can inhibit anastomotic intimal hyperplasia (IH) 1 month following polytetrafluoroethylene (PTFE) bypass in a sheep carotid artery model, 23 sheep underwent bilateral bypass of the ligated common carotid artery with 8-mm PTFE immediately followed by a single dose of irradiation (15, 21, or 30 Gy) to one side. The 15 animals with bilaterally patent grafts were euthanized at 1 month and graft-arterial anastomoses harvested. Using computer-aided image analysis, IH areas and thicknesses were measured. Graft patency in this model was 83% at 1 month and did not differ according to treatment administered. In the control animals, IH was greatest at mid-anastomosis, but minimal within the native vessel. All three radiation doses markedly inhibited mid-anastomotic IH area and thickness. At the proximal anastomosis, 30 Gy reduced the IH area 20-fold, from 2.06 to 0.14 mm2 (p < 0.0001 by ANOVA), and IH thickness 70-fold, from 29.0 to 0.4 micron (p < 0.0002); similar effects were seen at the distal anastomosis. No adverse effects of radiation treatment were observed. External beam irradiation in doses of 15 to 30 Gy delivered in a single fraction immediately after operation markedly inhibits development of intimal hyperplasia 1 month following end-to-side anastomosis with PTFE in sheep.

Clinical implications of internal iliac artery embolization in endovascular repair of aortoiliac aneurysms.

To overcome constraints imposed by iliac artery anatomy, the anatomic inclusion criteria for endovascular aortic aneurysm repair can be extended by means of intentional coil occlusion of one or both internal iliac arteries and extension of the distal limb of the graft into an external iliac artery. We reviewed our experience with this intervention to determine the safety and efficacy of this approach to aneurysm repair. Over a 30-month period, 84 patients underwent endovascular abdominal aortic aneurysm repair; 23 underwent intentional unilateral (22) or bilateral (1) internal iliac artery occlusion. Morbidity, mortality, and long-term clinical outcomes were evaluated in these 23 patients. Patients were specifically questioned about exercise-induced buttock and extremity symptoms. Our results showed that intentional internal iliac artery embolization to allow endovascular repair of abdominal aortic aneurysms is accompanied by significant morbidity and should be approached with caution.

Alcohol withdrawal after open aortic surgery.

This study was designed to test the hypothesis that unexpected alcohol withdrawal-like syndrome (AWLS) is more common following aortic, but not other, vascular or nonvascular procedures. All patients undergoing open aortic surgery at our institution in 1997 who survived at least 48 hr were identified, as were those undergoing carotid endarterectomy, infrainguinal bypass, and total colectomy. AWLS was defined as prolonged confusion or agitation and response to conventional treatment for withdrawal, providing that all other sources had been ruled out or a significant history was present. Our results show that, for unknown reasons, AWLS is more common after aortic surgery than after other vascular and high-stress, nonaortic intraabdominal procedures at our institution, and is associated with increased length of stay and morbidity. Because prophylaxis may improve outcome, better efforts to identify patients at risk are required.

Blunt renal artery injury: incidence, diagnosis, and management.

Renal artery injury is a rare complication of blunt abdominal trauma. Increasing use of CT scans to evaluate blunt abdominal trauma identifies more blunt renal artery injuries (BRAIs) that may have otherwise been missed. We identified patients with BRAI to examine the incidence and to evaluate the current diagnosis and management strategies. Patients admitted from 1986 to 2000 at a regional Level I trauma center sustaining BRAI were evaluated. Patients undergoing revascularization or nonoperative management were followed for renovascular hypertension. Twenty-eight patients with BRAI were identified out of 36,938 blunt trauma admissions between 1986 and 2000 (incidence 0.08%). Most renal artery injuries were diagnosed by CT scans (93%) with seven confirmatory angiograms. Nine patients had nephrectomy (one bilateral), and three patients with unilateral injuries were revascularized. Sixteen were managed nonoperatively including one patient who had endovascular stent placement. Three patients died from shock and sepsis. Follow-up for all patients ranged from one month to 8 years. Two patients developed hypertension: one who was revascularized (33%) and one was managed nonoperatively (6%). The frequency of diagnosis of BRAI is increasing because of the increased use of CT. Nonoperative management of unilateral injuries can be successful with a 6 per cent risk for developing renovascular hypertension. The role of endovascular stenting is promising, and further study is necessary.

Reperfusion and compartment syndromes: strategies for prevention and treatment.

Reperfusion syndrome refers to the damage done by restoration of blood flow to ischemic tissues and is distinct from the original ischemic insult itself, whereas compartment syndrome refers to the damage resulting from increased pressure within an enclosed fascial compartment that occurs after blood flow has been restored. Despite extensive experimental work directed toward the treatment of established reperfusion injury and prevention of compartment syndrome, clinical outcome over the past decade has not appreciably changed. Although the systemic insult, thought to be an inevitable result of reperfusion injury, may be less injurious than "conventional wisdom" would suggest, no better strategy for treating compartment syndrome other than early recognition and decompression has yet been developed.

Impact of stomach and colon injuries on intra-abdominal abscess and the synergistic effect of hemorrhage and associated injury.

BACKGROUND: Colon wounds are recognized to be highly associated with intra-abdominal abscess (IAA) after penetrating trauma, whereas gastric wounds are thought to contribute minimally to abscess because of the bactericidal effect of low pH. This study evaluated the impact of stomach or colon wounds, the contribution of other risk factors, and associated abdominal injuries on IAA. METHODS: Patients with penetrating colon or stomach wounds during a 10-year period were reviewed and stratified by age, Injury Severity Score, transfusions, and associated abdominal injuries. Early deaths (<48 hours) from hemorrhage were excluded. Outcomes analyzed were IAA and death. RESULTS: A total of 812 patients were identified. There were 32 late deaths (4%), of which 28% were attributable to IAA and multiple organ failure. IAA rates for isolated stomach or colon wounds were 0 and 4.2%, respectively. The presence of associated injuries increased IAA rates to 7.5 and 8.8%, respectively. Independent predictors of IAA determined by multivariate analysis included age, transfusions, gunshot wounds, and associated injuries to the liver, pancreas, and kidney. CONCLUSION: Gastric injuries are equivalent to colon wounds in their contribution to IAA. Contamination from either organ without associated injury is minimally associated with IAA, but injury to both appears synergistic. The immunosuppressive effects of age and hemorrhage, in addition to significant associated injury, enhance the development of IAA.

Transient inhibition of CD18-dependent leukocyte functions after hemorrhage and polymicrobial sepsis.

BACKGROUND: The goals were (1) to characterize physiologic changes after a combined insult of hemorrhage plus sepsis in a large animal model and (2) to determine whether transient inhibition of the neutrophil CD18 adherence receptor during fluid resuscitation impairs host defense during recovery from this injury. METHODS: Two series of experiments were performed in anesthetized swine. In the first series (n = 22), the cecum was ligated and incised immediately before 35% hemorrhage. After 1 hour, shed blood plus supplemental fluid was administered to restore and stabilize hemodynamics. On the basis of these results, a second series examined effects of anti-CD18 (2 mg/kg R15.7; n = 9) or its saline placebo (n = 10) administered during fluid resuscitation. RESULTS: In the first series the mortality rate was 41% (9 of 22). Early deaths occurred 3.0 +/- 0.8 days after injury and were distinguished by significantly lower neutrophil counts on resuscitation. Those alive a 7 days had intraabdominal abscesses and bacteremia. Alveoli and peribronchial spaces were congested, with edema and fibrin deposition in capillaries and alveoli. Livers were congested with biliary stasis. Despite these pathologic findings, hemodynamic, electrolyte, and serum enzyme changes were minimal. In the second series the mortality rate at 4 days was 30% with placebo (3 of 10) versus 33% with anti-CD18 (3 of 9). Lung changes (i.e., pneumonia, pleuritis, thrombosis, and edema) were similar in both groups, but liver congestion and hemorrhage were attenuated by anti-CD18. Some aspects of host defense were altered by anti-CD18. At 24 and 48 hours the oxidative burst potential for circulating granulocytes was 208% +/- 57% and 383% +/- 73% with placebo versus 1273% +/- 351% and 762% +/- 226% in anti-CD18. At 72 hours the granularity of circulating neutrophils was unchanged from baseline with placebo but was reduced to 82% +/- 5% by anti-CD18. At 48 hours lipopolysaccharide-evoked tumor necrosis factor production in vitro was reduced to 62% +/- 22% with placebo but was increased to 148% +/- 16% with anti-CD18. CONCLUSIONS: Anti-CD18 during fluid resuscitation did not increase vulnerability to endogenous pathogens because the transient inhibition of neutrophil demargination was balanced by enhanced oxidative burst, degranulation, and production of tumor necrosis factor in circulating cells later during recovery. Thus a single administration of antiadhesion therapy does not worsen posttrauma outcome even if given during ongoing sepsis.

Granulocyte colony-stimulating factor improves host defense to resuscitated shock and polymicrobial sepsis without provoking generalized neutrophil-mediated damage.

BACKGROUND: Granulocyte colony-stimulating factor (G-CSF) increases production and release of neutrophil precursors and activates multiple functions of circulating polymorphonuclear neutrophils (PMNs). G-CSF has therapeutic effects in many experimental models of sepsis; its actions with superimposed reperfusion insults are unknown. In traumatic conditions, G-CSF could exacerbate unregulated, PMN-dependent injury to otherwise normal host tissue or, it could partially reverse trauma-induced immune suppression, which may improve long-term outcome. This study tested whether stimulating PMN proliferation and function with G-CSF during recovery from trauma+sepsis potentiated reperfusion injury or whether it improved host defense. METHODS: Anesthetized swine were subjected to cecal ligation and incision, 35% hemorrhage, and 1 hr of hypotension. Resuscitation consisted of intravenous G-CSF (5 microg/kg) or placebo followed by shed blood and 40 mL/kg of lactated Ringer's solution. The control group received laparotomy only. G-CSF or placebo was given daily. Animals were killed at 4 days. Observers, blind to the protocol, graded autopsy samples for localization of infection and quality of abscess wall formation. Data included complete blood count, granulocyte oxidative burst after phorbol myristate acetate stimulation in vitro (GO2B), bronchoalveolar lavage (BAL) cell count, BAL noncellular protein, lipopolysaccharide-stimulated tumor necrosis factor production in whole blood in vitro (lipopolysaccharide-tumor necrosis factor), and lung tissue myeloperoxidase (MPO). RESULTS: Neutrophilia and localization of infection, were significantly improved by G-CSF. Variables altered by G-CSF, though not significantly, showed GO2B potential increased by 50%, lipopolysaccharide-tumor necrosis factor decreased by 50%, and improved survival versus placebo (100% vs. 70%). G-CSF did not increase lung MPO, BAL cell count, or BAL protein. Both arterial and venous O2 saturations were unaltered. CONCLUSIONS: Our data show that G-CSF initiated at the time of resuscitation reduced the sequelae of posttrauma sepsis by increasing PMN proliferation and function without potentiating PMN-mediated lung reperfusion injury.

Effect of transfusion on physiologic changes after resuscitated trauma.

BACKGROUND: The purpose of this experimental study was to test whether transfusion potentiated physiologic changes associated with fluid resuscitated trauma in controlled conditions. METHODS: Anesthetized and ventilated mongrel pigs were subjected to soft-tissue injury plus 35% hemorrhage and 1 hour shock and then were resuscitated with either autologous (shed) or heterologous (cross-transfused) fresh whole blood. Leukocyte differential counts, T-lymphocyte subsets, neutrophil adherence molecule (CD18) expression, granulocyte oxidative burst, plasma cortisol, and serum chemistries were monitored in awake animals with indwelling catheters on 3 consecutive days. Changes were referenced to preinjury baseline values and to a control group that received heterologous transfusion but no shock. To determine whether these changes might have influenced host defense, a low-dose challenge with Escherichia coli endotoxin (lipopolysaccharide [LPS]; 1 to 2 micrograms/kg for 30 minutes) was administered on day 4. RESULTS: During recovery, neutrophil counts, neutrophil CD18 expression, and granulocyte oxidative burst were generally increased, but the changes were not potentiated by transfusion. Lymphocyte subpopulations remained relatively constant. Serum enzyme markers were elevated with trauma plus shed blood or trauma plus cross-transfusion, but they remained essentially unchanged after heterologous transfusion only. Plasma cortisol, a nonspecific index of stress, peaked at 3 to 6 times higher than baseline. The increases tended to be higher and later with heterologous transfusion only, relative to trauma plus shed blood or trauma plus cross-transfusion. The delayed LPS challenge evoked profound but transient pulmonary hypertension and leukopenia, followed by subsequent hypoxemia; the time courses and magnitude of these changes were similar in all groups. CONCLUSIONS: If these measured variables before and after LPS challenge are a valid index of host defense in this species, then a 35% transfusion does not potentiate the risk for posttrauma immune dysfunction when the magnitude of injury is constant. Thus the predisposition to infection after human trauma might be due to cold storage of blood; separation of blood into components, or other transfusion-related practices rather than to transfusion per se.

Pancreatic trauma: a simplified management guideline.

INTRODUCTION: Recent literature supports a conservative trend in the management of pancreatic injuries. Contrary to this trend, some recommend defining ductal integrity by pancreatography, implying that the results alter management. This study examines our recent 5-year experience with a simplified approach to all pancreatic injuries. METHODS: Retrospective analysis of patients sustaining pancreatic injuries was performed. RESULTS: One hundred thirty-four patients were identified. Overall mortality was 13%, and pancreatic-related mortality was 2%. Analyses were based on 124 pancreatic injuries among patients who survived >12 hours. Thirty-seven proximal injuries were treated with drainage alone, with a pancreatic morbidity of 11%. Eighty-seven distal pancreatic injuries occurred, 54 with indeterminate ductal status. Twenty-four had high probability for duct injury and were treated by distal resection; 30 with a low probability of ductal injury were drained. Pancreatic morbidity was not different between these groups. CONCLUSIONS: Pancreatic injuries including those with indeterminate ductal status can be successfully managed with low morbidity and mortality using this simplified management protocol.

Radiation inhibition of mdx mouse muscle regeneration: dose and age factors.

A single hind limb was irradiated with 12, 18, 24, or 30 Gy in mdx and C57 mice aged 12, 21, or 42 days to determine regeneration inhibition dose-response curves in different aged dystrophic mice and to characterize radiation side-effects in normal mice. The anterior tibial muscle mass (8 weeks postirradiation) and percent central nucleated (i.e., regenerated) muscle fibers were measures of regeneration inhibition. Twenty-one-day-old mdx mice irradiated with 18 Gy had complete inhibition of muscle regeneration, but 30 Gy only partially blocked regeneration in mdx mice irradiated at 12 and 42 days in age. In working to produce a clinically relevant model for Duchenne dystrophy, it is crucial to regard mouse age as a major factor in determining radiation effects on mdx muscle regeneration.

Twitch and tetanus in mdx mouse muscle.

We compared mdx and C57BL10 anterior tibial muscle force in situ (single pulse, multiple pulse, staircase, posttetanic potentiation, and fatiguing stimulation patterns) to define muscle strength, physiology, and fatigue resistance. The relatively hypertrophied mdx muscle showed: reduced strength (N/cm2), an increased twitch-tetanus ratio, and resistance to post-fatigue twitch slowing. These differences implicate altered mdx calcium regulation, and emphasize the importance of measuring both muscle function and morphology in mdx treatment trials.