Enamel Hypomineralization and Structural Defects in Amelotin-deficient Mice.

Amelotin (AMTN) is a relatively recently discovered enamel protein that is predominantly expressed by ameloblasts during the maturation stage of amelogenesis and is present at lower levels in the junctional epithelium of erupted teeth. Previous studies have suggested a function of this protein in enamel mineralization and cell attachment. Genetic mouse models have been instrumental in defining the role of many enamel-related proteins, but a genetic mouse model lacking the Amtn gene has not been reported. Here, we describe the generation of amelotin-deficient mice and the analysis of their enamel phenotype in comparison with that of wild-type animals. Ablation of AMTN expression resulted in mechanically inferior enamel of mandibular incisors that showed chipping and fractures at the incisal edge. Enamel mineralization was delayed, resulting in hypomineralized inner enamel and structural defects in the outer enamel. Erupted enamel close to the gingival margin showed increased surface roughness. The expression levels of the enamel matrix proteins AMEL, AMBN, ENAM, and ODAM and the enamel proteases MMP-20 and KLK-4 were not significantly altered, although the expression of KLK-4 was delayed. The morphology of ameloblasts showing prominent Tomes' processes during the secretory stage was not altered, and there was no indication of disruption of cell structures or activities, but a residual layer, presumably consisting of organic material, remained at the enamel surface close to the gingival margin. The integrity of the dentogingival attachment at the junctional epithelium appeared unaffected by AMTN deficiency. These observations indicate that AMTN plays a subtle yet critical role in enamel biomineralization, particularly during the establishment of the outer and surface enamel layers. This role appears to be largely independent of other enamel proteins.

The dioxin TCDD protects against aflatoxin-induced mutation in female rats, but not in male rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant and a potent carcinogen in laboratory rodents. When combined with other environmental toxins, it has been shown to increase the (geno)toxicity of some compounds. In this study, the effect of TCDD on the mutagenicity of aflatoxin-B1 (AFB1) was examined in the rat liver using a lacI transgenic rodent mutation assay. AFB1 induces GC-->TA transversions. Since TCDD is known to have a differential effect in male and female rodents, both sexes were studied. The data showed that a 6-week pre-exposure to TCDD had no significant effect on the frequency of aflatoxin-induced mutation in the liver of male rats. However, the TCDD treatment completely prevented the aflatoxin-induced transversion mutations in female animals.

Management of traumatic lung injury: a Western Trauma Association Multicenter review.

BACKGROUND: Improved outcomes following lung injury have been reported using "lung sparing" techniques. METHODS: A retrospective multicenter 4-year review of patients who underwent lung resection following injury was performed. Resections were categorized as "minor" (suture, wedge resection, tractotomy) or "major" (lobectomy or pneumonectomy). Injury severity, Abbreviated Injury Scale (AIS) score, and outcome were recorded. RESULTS: One hundred forty-three patients (28 blunt, 115 penetrating) underwent lung resection after sustaining an injury. Minor resections were used in 75% of cases, in patients with less severe thoracic injury (chest AIS scores "minor" 3.8 +/- 0.9 vs. "major" 4.3 +/- 0.7, p = 0.02). Mortality increased with each step of increasing complexity of the surgical technique (RR, 1.8; CI, 1.4-2.2): suture alone, 9% mortality; tractotomy, 13%; wedge resection, 30%; lobectomy, 43%; and pneumonectomy, 50%. Regression analysis demonstrated that blunt mechanism, lower blood pressure at thoracotomy, and increasing amount of the lung resection were each independently associated with mortality. CONCLUSION: Blunt traumatic lung injury has higher mortality primarily due to associated extrathoracic injuries. Major resections are required more commonly than previously reported. While "minor" resections, if feasible, are associated with improved outcome, trauma surgeons should be facile in a wide range of technical procedures for the management of lung injuries.

Mutations induced by 2-amino-1-methyl-6-phenylimidazo [4,5-b]pyridine (PhIP) in cecum and proximal and distal colon of lacI transgenic rats.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a food-borne mutagen and carcinogen that induces tumors of the colon and the prostate gland in male rats and of the mammary gland in female rats. In this study we describe the frequency and specificity of PhIP-induced mutations in the cecum, proximal colon and distal colon of male and female lacI transgenic rats. This is the first report of mutational data from discrete regions of the colon. After 61 days of treatment with 200 p.p.m. PhIP mixed into the diet, PhIP-induced mutant frequencies were elevated 7-fold in the cecum and 14- to 21-fold in the colon of male and female rats compared with untreated controls. PhIP-induced mutant frequencies increased significantly (overall trend, P < 10(-4)) along the length of the colon of both males and females, with cecum < proximal colon < distal colon. A total of 754 PhIP mutants (363 male, 391 female) were sequenced to provide the mutational spectra for each of the three tissue sections from males and females. These mutational spectra consisted predominantly of G:C-->T:A and G:C-->C:G transversions and deletions of G:C base pairs. There were no significant differences between the mutational spectra with respect to sex or position in the colon. Therefore, we surmise that following induction of mutations by PhIP in male and female colons, non-mutagenic factors, possibly hormonal, preferentially influence the formation of tumors in the colon of male rats.

Timing of urgent thoracotomy for hemorrhage after trauma: a multicenter study.

HYPOTHESIS: It is possible to quantify an amount of thoracic hemorrhage, after blunt and penetrating injury, at which delay of thoracotomy is associated with increased mortality. DESIGN: A retrospective case series. SETTING: Five urban trauma centers. STUDY SELECTION: Patients undergoing urgent thoracotomy (within 48 hours of injury) for hemorrhage (excluding emergency department thoracotomy). DATA EXTRACTION: Respective registries identified patients who underwent urgent thoracotomy. Injury characteristics, initial and subsequent chest tube outputs, time before thoracotomy, and outcomes were evaluated. MAIN OUTCOME MEASURE: Death. RESULTS: One hundred fifty-seven patients (36 with blunt and 121 with penetrating injuries) underwent urgent thoracotomy for hemorrhage between January 1, 1995, and December 31, 1998. Mortality correlated with mean (+/- SD) Injury Severity Score (38 +/- 19 vs 22 +/- 12.6 for survivors; P<.01) and mechanism (24 [67%] for blunt vs 21 [17%] for penetrating injuries; P<.01). Mortality increased as total chest blood loss increased, with the risk for death at blood loss of 1500 mL being 3 times greater than at 500 mL. Blunt-injured patients waited a significantly longer time to thoracotomy than penetrating-injured patients (4.4 +/- 9.0 h vs 1.6 +/- 3.0 h; P =.02) and also had a greater total chest tube output before thoracotomy (2220 +/- 1235 mL vs 1438 +/- 747 mL; P =.001). CONCLUSIONS: The risk for death increases linearly with total chest hemorrhage after thoracic injury. Thoracotomy is indicated when total chest tube output exceeds 1500 mL within 24 hours, regardless of injury mechanism.

Tris(2,3-dibromopropyl)phosphate causes a gradient of mutations in the cortex and outer and inner medullas of the kidney of lacI transgenic rats.

Tris(2,3-dibromopropyl)phosphate (TDBP) is a kidney carcinogen in rats in which exposure results in tumors specifically in the outer medulla. We have previously shown that TDBP induces mutation in the rat kidney. Here we demonstrate that TDBP induces mutation in the kidney of the F344 Big Blue lacI transgenic rat in a gradient with the highest induction (6.4-fold) in the cortex and lowest induction (2.2-fold) in the inner medulla, when given at 2000 ppm in the feed for 45 days. Similar results were obtained at 100 ppm, although the gradient effect was less pronounced. Because exposure to TDBP results in increased cell proliferation in the outer medulla, our results suggest that tissue-specific targeting of TDBP-induced kidney tumors reflects the combination of cell proliferation and mutation induction. This is also the first known case when transgenic animals have been used to study mutation at the suborgan level.

Prostate mutations in rats induced by the suspected human carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine.

Male lacl transgenic rats were fed a diet containing 200 ppm of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a heterocyclic amine present in cooked meats. PhIP was found to be a powerful prostate mutagen. After 61 days of treatment, the lacl mutant frequency was 71 x 10(-5), >20-fold higher than the spontaneous mutant frequency of 3.2 x 10(-5). The predominant PhIP-induced mutations were G:C->T:A transversions and deletions of G:C bp. The results directly link PhIP-induced mutations with the earlier observation of PhIP-induced prostate cancer in rats and suggest that exposure to dietary PhIP could be a risk factor in the incidence of human prostate cancer.

Prediction of outcome in intensive care unit trauma patients: a multicenter study of Acute Physiology and Chronic Health Evaluation (APACHE), Trauma and Injury Severity Score (TRISS), and a 24-hour intensive care unit (ICU) point system.

OBJECTIVE: To conduct a multicenter study to validate the accuracy of the Acute Physiology and Chronic Health Evaluation (APACHE) II system, APACHE III system, Trauma and Injury Severity Score (TRISS) methodology, and a 24-hour intensive care unit (ICU) point system for prediction of mortality in ICU trauma patient admissions. METHODS: The study population consisted of retrospectively identified, consecutive ICU trauma admissions (n = 2,414) from six Level I trauma centers. Probabilities of death were calculated by using logistic regression analysis. The predictive power of each system was evaluated by using decision matrix analysis to compare observed and predicted outcomes with a decision criterion of 0.50 for risk of hospital death. The Youden Index (YI) was used to compare the proportion of patients correctly classified by each system. Measures of model calibration were based on goodness-of-fit testing (Hosmer-Lemeshow statistic less than 15.5) and model discrimination were based on the area under the receiver operating characteristic curve (AUC). RESULTS: Overall, APACHE II (sensitivity, 38%; specificity, 99%; YI, 37%; H-L statistic, 92.6; AUC, 0.87) and TRISS (sensitivity, 52%; specificity, 94%; YI, 46%; H-L statistic, 228.1; AUC, 0.82) were poor predictors of aggregate mortality, because they did not meet the acceptable thresholds for both model calibration and discrimination. APACHE III (sensitivity, 60%; specificity, 98%; YI, 58%; H-L statistic, 7.0; AUC, 0.89) was comparable to the 24-hour ICU point system (sensitivity, 51%; specificity, 98%; YI, 50%; H-L statistic, 14.7; AUC, 0.89) with both systems showing strong agreement between the observed and predicted outcomes based on acceptable thresholds for both model calibration and discrimination. The APACHE III system significantly improved upon APACHE II for estimating risk of death in ICU trauma patients (p < 0.001). Compared with the overall performance, for the subset of patients with nonoperative head trauma, the percentage correctly classified was decreased to 46% for APACHE II; increased to 71% for APACHE III (p < 0.001 vs. APACHE II); increased to 59% for TRISS; and increased to 62% for 24-hour ICU points. For operative head trauma, the percentage correctly classified was increased to 60% for APACHE II; increased to 61% for APACHE III; decreased to 43% for TRISS (p < 0.004 vs. APACHE III); and increased to 54% for 24-hour ICU points. For patients without head injuries, all of the systems were unreliable and considerably underestimated the risk of death. The percentage of nonoperative and operative patients without head trauma who were correctly classified was decreased, respectively, to 26% and 30% for APACHE II; 33% and 29% for APACHE III; 33% and 19% for TRISS; 20% and 23% for 24-hour ICU points. CONCLUSION: For the overall estimation of aggregate ICU mortality, the APACHE III system was the most reliable; however, performance was most accurate for subsets of patients with head trauma. The 24-hour ICU point system also demonstrated acceptable overall performance with improved performance for patients with head trauma. Overall, APACHE II and TRISS did not meet acceptable thresholds of performance. When estimating ICU mortality for subsets of patients without head trauma, none of these systems had an acceptable level of performance. Further multicenter studies aimed at developing better outcome prediction models for patients without head injuries are warranted, which would allow trauma care providers to set uniform standards for judging institutional performance.

Redefining cardiovascular performance during resuscitation: ventricular stroke work, power, and the pressure-volume diagram.

OBJECTIVES: (1) To compare left ventricular stroke work index (SW) and left ventricular power output (LVP), hemodynamic variables that encompass blood pressure as well as blood flow, with the purely flow-derived hemodynamic and oxygen transport variables as markers of perfusion and outcome in critically injured patients during resuscitation. (2) To use the ventricular pressure-volume diagram to define characteristic hemodynamic patterns in the determinants of SW and LVP that are associated with survival. METHODS: This was a cohort study at a university Level I trauma center during the course of 1 year. A consecutive series of patients was monitored with a volumetric pulmonary artery catheter during the initial 48 hours of resuscitation. Heart rate, SW, LVP, cardiac index, and oxygen delivery and consumption during resuscitation were compared using multivariate logistic regression analysis with regard to the ability to clear lactate in less than 24 hours and survival. Receiver operating characteristic curves were constructed to determine threshold values for SW and LVP. Ventricular pressure-volume diagrams were used to describe characteristic patterns in the determinants of SW and LVP in survivors and nonsurvivors. Preload was expressed as left ventricular end-diastolic volume index, afterload as aortic input impedance (Ea), and contractility as ventricular end-systolic elastance (Ees). The ratio of Ea/Ees (RATIO) was used as a measure of ventricular-arterial coupling, which describes the efficacy of energy transfer from the heart to the vascular system. RESULTS: One hundred eleven patients (87 survivors, 24 nonsurvivors) met study criteria. Survivors had a significantly higher SW (4,510 +/- 1,070 vs. 3,440 +/- 980 mm Hg x mL x m(-2); p < 0.0001) and LVP (370 +/- 94 vs. 270 +/- 81 mm Hg x L x min(-2) x m(-2); p < 0.0001) than nonsurvivors. Heart rate, SW, and LVP were the only studied variables that were significantly related to lactate clearance and survival by logistic regression. Threshold values determined by the receiver operating characteristic curves were 4,000 mm Hg x mL x m(-2) for SW and 320 mm Hg x L x min(-1) x m(-2) for LVP. Survivors had better ventricular-arterial coupling than nonsurvivors, indicated by a lower RATIO (0.32 +/- 0.22 vs. 0.54 +/- 0.38; p = 0.003). This lower RATIO was attributable to lower levels of Ea (2.7 +/- 0.7 vs. 3.4 +/- 0.8 mm Hg x mL(-1) x m(-2); p = 0.0003) and a trend toward higher levels of Ees (13 +/- 11 vs. 9.9 +/- 7.3 mm Hg x mL(-1) x m(-2); p = 0.12). CONCLUSION: Thermodynamic perfusion variables that encompass both pressure and flow, such as SW and LVP, are more closely related to perfusion and outcome than the purely flow-derived variables. The higher SW and LVP in survivors is related to better ventricular-arterial coupling, and therefore more efficient cardiac function. Cutoff values for LVP of 320 mm Hg x L x min(-1) x m(-2) and for SW of 4,000 mm Hg x mL x m(-2) may be useful thresholds for evaluating hemodynamic performance during resuscitation.

A prospective, randomized trial limiting perioperative red blood cell transfusions in vascular patients.

BACKGROUND: Patients undergoing major arterial reconstruction have traditionally been transfused with red blood cells to keep hemoglobin concentrations above 10 g/dL in order to prevent anemia-induced myocardial ischemia. There are no data to support this practice. The hypothesis that vascular patients will tolerate a hemoglobin concentration of 9 g/dL was examined. METHODS: Ninety-nine patients undergoing elective aortic and infrainguinal arterial reconstructions were prospectively randomized preoperatively to receive transfusions to maintain a hemoglobin level of either 10 g/dL or 9 g/dL. RESULTS: Despite significantly different postoperative hemoglobin levels of 11.0 +/- 1.2 versus 9.8 +/- 1.3 g/dL (P <0.0001), there were no differences in mortality or cardiac morbidity rates or length of hospital stay. There were no differences in hemodynamic parameters. Oxygen delivery was lower in the group with lower hemoglobin levels, but there was no difference in O2 consumption between the groups. CONCLUSIONS: A lower hemoglobin concentration was tolerated without adverse clinical outcome. Patients did not compensate for anemia by increased myocardial work, but by increasing O2 extraction in the peripheral tissues.

Clinical application of ventricular end-systolic elastance and the ventricular pressure-volume diagram.

The ability to clinically assess myocardial contractility in a load-independent fashion facilitates the selection of appropriate inotropes, when needed, during shock resuscitation. Within the framework of the ventricular pressure-volume diagram, the slope of the ventricular end-systolic pressure-volume relationship (expressed as ventricular end-systolic elastance, Ees), has been shown to accurately reflect ventricular inotropic state, and to be insensitive to loading conditions. It has not, however, been widely used at the bedside. Our goal was to evaluate the clinical utility of Ees and the ventricular pressure-volume diagram as bedside methods of hemodynamic assessment. We performed a prospective study of 123 hemodynamic interventions in 100 trauma patients during shock resuscitation in which contractility (Ees), preload (left ventricular end-diastolic volume index), and afterload (effective arterial elastance) were calculated before and after addition of inotropes, fluid bolus, and afterload reduction. Mean values of each variable were compared before and after each type intervention using the paired t test. The ventricular pressure-volume diagram was used to predict changes in the studied variables, and the experimental results were compared with predicted changes. Ees (mmHg/mL/m2) increased significantly with inotropes (4.7 +/- 3.2 to 10 +/- 8.7, p < .0001), but was not affected by clinically significant fluid administration (7.0 +/- 4.7 to 8.3 +/- 8.0, p = .10) or afterload reduction (9.6 +/- 5.2 to 9.2 +/- 4.7, p = .72). Left ventricular end-diastolic volume index (mL/m2) improved with fluid administration (54 +/- 8.9 to 62 +/- 9.8, p < .0001) and effective arterial elastance (mmHg/mL/m2) decreased with afterload reduction (3.3 +/- .9 to 2.6 +/- .7, p < .0001). We conclude that Ees is a load-independent measure of contractility, which is measurable at the bedside. The pressure-volume diagram is a useful method of monitoring hemodynamic changes associated with interventions during shock resuscitation.

Individual patient cohort analysis of the efficacy of hypertonic saline/dextran in patients with traumatic brain injury and hypotension.

BACKGROUND: Resuscitation with hypertonic saline/dextran (HSD) has been suggested to be efficacious in patients who have traumatic brain injury and are hypotensive. We undertook a cohort analysis of individual patient data from previous prospective randomized double-blinded trials to evaluate improvements in survival at 24 hours and discharge after initial treatment with HSD in patients who had traumatic brain injury (head region Abbreviated Injury Score > or = 4) and hypotension (systolic blood pressure < or = 90 mm Hg). METHODS: All variables and end points were defined before initiation of data handling. Investigators were blind as to the treatment. Case report forms were received from six studies. Of these, 223 patients met the inclusion for traumatic brain injury. Comparisons between HSD and standard of care were made using stratified analysis and logistic regression to assess efficacy, confounding, and interaction. Potential confounding variables of pre-fluid treatment, Glasgow Coma Scale score (3-8 vs. 9-15), injury type, and systolic blood pressure can be considered a priori factors that were known before randomization. Effects of the various trials was also considered. RESULTS: Treatment with HSD resulted in a survival until discharge of 37.9% (39 of 103) compared with 26.9% (32 of 119) with standard of care (p = 0.080). Using logistic regression, adjusting for trial and potential confounding variables, the treatment effect can be summarized by the odds ratio of 2.12 (p = 0.048) for survival until discharge. CONCLUSIONS: Patients who have traumatic brain injuries in the presence of hypotension and receive HSD are about twice as likely to survive as those who receive standard of care.

Spectrum of spontaneous mutations in liver tissue of lacI transgenic mice.

The advent of transgenic technology has greatly facilitated the study of mutation in animals in vivo. The Big Blue mouse system, transgenic for the lacI gene, permits not only the quantification of mutations in different tissues but also provides for the generation of in vivo-derived mutational spectra. This report details the sequence alterations of 348 spontaneous mutations recovered from the liver of 6-8-week-old male Big Blue mice. The spectra recovered from two strains of mice, C57BI/6 and B6C3F1, were compared and found to be very similar. The predominant mutations are G:C-->A:T transitions, with 75% of these occurring at 5'-CpG-3' sequences. This mutational bias is consistent with deamination-directed mutation at methylated cytosine bases. The second most common class of mutations is G:C-->T:A transversions. A significant clonal expansion of mutants was found in several animals, and this was used to make an approximate correction of the mutant frequency such that the most conservative estimate of mutation frequency is presented. The establishment of this substantial database of spontaneous mutations in the liver of Big Blue mice is intended to serve as a reference against which mutations recovered after treatment can be compared.

Spontaneous mutants recovered from liver and germ cell tissue of low copy number lacI transgenic rats.

The finding of a large discordance between animal species in their response to a carcinogenic challenge, has led to the realization that the useful extrapolation of animal test data to humans requires a better understanding of animal interspecies differences. With the development of transgenic shuttle vector based animal systems we are now able to study mutation of the same genetic target in both mice and rats. We have begun to analyze mutants recovered from rat lines carrying low copy numbers of the same lambda/lacI constructs carried by the Big Blue mouse. A large database on mutations in lacI transgenic mice is already available for comparison. The data indicate that the differences between the mutations recovered from rat liver and germ cell tissues are similar to those recovered from transgenic mice, but when compared with a large database of mutations available for mice, some site-to-site differences may exist. This study represents the first interspecies look into the molecular nature of mutations in the lacI transgenic rodents.

An efficient laboratory protocol for the sequencing of large numbers of lacI mutants recovered from Big Blue transgenic animals.

Mutational spectra provide a powerful approach to investigate both the mutagenic potential and the mechanism of action of suspected mutagens and carcinogens. Recently, transgenic techniques have made it possible to generate mutational spectra in animals. Such a spectrum may consist of 50 to 200 mutants depending on the nature of the mutations, and many spectra can be generated depending on the design of the experiment. This report describes a practical approach for the processing and sequencing of large numbers of lacI mutants recovered from Big Blue animals.

Improved predictions from a severity characterization of trauma (ASCOT) over Trauma and Injury Severity Score (TRISS): results of an independent evaluation.

OBJECTIVE: In 1986, data from 25,000 major trauma outcome study patients were used to relate Trauma and Injury Severity Score (TRISS) values to survival probability. The resulting norms have been widely used. Motivated by TRISS limitations, A Severity Characterization of Trauma (ASCOT) was introduced in 1990. The objective of this study was to evaluate and compare TRISS and ASCOT probability predictions using carefully collected and independently reviewed data not used in the development of those norms. DESIGN: This was a prospective data collection for consecutive admissions to four level I trauma centers participating in a major trauma outcome study. MATERIALS AND METHODS: Data from 14,296 patients admitted to the four study sites between October 1987 through 1989 were used. The indices were evaluated using measures of discrimination (disparity, sensitivity, specificity, misclassification rate, and area under the receiver-operating characteristic curve) and calibration [Hosmer-Lemeshow goodness-of-fit statistic (H-L)]. MEASUREMENTS AND MAIN RESULTS: For blunt-injured adults, ASCOT has higher sensitivity than TRISS (69.3 vs. 64.3) and meets the criterion for model calibration (H-L statistic < 15.5) needed for accurate z and W scores. The TRISS does not meet the calibration criterion (H-L = 30.7). For adults with penetrating injury, ASCOT has a substantially lower H-L value than TRISS (20.3 vs. 138.4), but neither meets the criterion. Areas under TRISS and ASCOT ROC curves are not significantly different and exceed 0.91 for blunt-injured adults and 0.95 for adults with penetrating injury. For pediatric patients, TRISS and ASCOT sensitivities (near 77%) and areas under receiver-operating characteristic curves (both exceed 0.96) are comparable, and both models satisfy the H-L criterion. CONCLUSIONS: In this age of health care decisions influenced by outcome evaluations, ASCOT's more precise description of anatomic injury and its improved calibration with actual outcomes argue for its adoption as the standard method for outcome prediction.

Physician recognition of hypercholesterolemia in patients undergoing peripheral and carotid artery revascularization.

Numerous studies have shown that patients with peripheral and carotid atherosclerosis have a high prevalence of hyperlipidemia, and clinical trials using either angiography or ultrasonography have now demonstrated regression of both femoral and carotid arterial plaque during lipid-lowering therapy. However, whether patients with peripheral and carotid atherosclerosis receive adequate attention to lipid risk factors has not been studied. To evaluate physician recognition and management of hypercholesterolemia in these two patient populations, we reviewed the charts of 80 consecutive patients undergoing revascularization for symptomatic peripheral and carotid occlusive disease at a university medical center between 1990 and 1993. Physician practices were assessed for each patient by noting whether hypercholesterolemia was (1) screened for during the hospitalization and, if present, (2) documented as a problem, (3) managed in-hospital, or (4) given appropriate intervention at discharge. While 73% of patients received some type of lipid case-finding perioperatively, less than one quarter of these were assessed for hyperlipidemia by the physician during the initial history. Moreover, of the 66% of screened patients found to be hypercholesterolemic, only 16% had documentation of the problem, only 24% received in-hospital management, and only 13% received intervention at discharge. These findings suggest that patients with documented peripheral and carotid atherosclerotic vascular disease probably receive inadequate attention to lipid risk factors and indicate the need for greater awareness and management of lipid disorders in these two patient populations by all involved physicians.

Ligation and extraanatomic arterial reconstruction for the treatment of aneurysms of the abdominal aorta.

PURPOSE: Since Blaisdell et al. first described axillobifemoral bypass and aortic exclusion to treat patients at high risk with abdominal aortic aneurysms in 1965, this approach has been controversial. To help define the appropriate application of this procedure, the recent experience of the authors was reviewed. METHODS: Twenty-six patients underwent operation between March 1980 and August 1992. Mean age was 71 +/- 7 years. Average aneurysm diameter was 7.0 +/- 1.5 cm. Sixty-nine percent of the aneurysms were symptomatic; 21% were suprarenal. All patients had serious comorbid factors. All underwent axillobifemoral bypass with iliac artery ligation; the infrarenal aorta was also ligated in 62%. RESULTS: There were two postoperative deaths (7.7%). One- and two-year survival rates were 59% and 38%, respectively. Three patients died of aneurysm rupture (11.5%); the aorta had not been ligated in two of these patients. The remaining late deaths were due to comorbid conditions. Extraanatomic bypass grafts thrombosed in five patients; no limbs were lost. CONCLUSIONS: Axillobifemoral bypass without aortic ligation does not effectively reduce the risk of aneurysm rupture. However, axillobifemoral bypass with aortic ligation is an acceptable treatment for patients with severe medical problems and symptomatic, anatomically complicated, or large abdominal aortic aneurysms. Because the risk of aneurysm rupture is not completely eliminated, this procedure should be reserved for patients with high-risk aneurysms who would not tolerate direct aortic replacement.