What influences medical students' choice of surgical careers.

BACKGROUND: Recent emphasis in medical education has been to encourage students to pursue primary care careers. This could have a negative impact on applications to surgical residencies. METHODS: To determine what factors are most influential for a student to pursue a surgical career in spite of this environment, third- and fourth-year medical students were surveyed with a 40-item questionnaire. RESULTS: The response rate was 37% (76/205). Those students considering a career in surgery were more likely than their counterparts to be motivated by role models (P <.006), career opportunities (P <.006), and academic opportunities (P <.013) in surgery. They were less likely than their counterparts to be discouraged from surgery on the basis of lifestyle (P <.001), time commitment (P <.001), call schedules (P <.001), or residency length (P <.028). No differences regarding financial rewards, research opportunities, or intellectual challenges were seen between the groups. Neither race nor sex had a significant role in the selection of surgery as a career. CONCLUSIONS: The data suggests that students are more likely to be influenced to pursue surgical careers by offering early exposure to positive role models and career and academic opportunities in surgery. Knowledge of these influences on student career choices should help surgical educators attract and maintain student interest in surgical careers.

Systemic consequences of oxidative stress following aortic surgery correlate with the degree of antioxidant defenses.

The purpose of this study was to correlate the preoperative level of antioxidant defenses, measured by the plasma total antioxidant capacity (TAC), to the degree of postoperative systemic inflammatory response, measured by the severity of pulmonary injury following elective aortic surgery. Twenty-four patients had TAC measured preoperatively and 24 hr postoperatively. Chest radiography and arterial blood gases were obtained preoperatively and serially during the first 24 hr after surgery. Using objective radiologic criteria and blood gas analysis, the degree of pulmonary edema and pulmonary dysfunction were quantified. All patients showed evidence of pulmonary dysfunction in the first 24 hr following surgery. Fifteen of the 24 patients showed radiographic evidence of noncardiogenic pulmonary edema in the immediate postoperative period. In this group, the TAC was lower than in those without pulmonary edema immediately following surgery (p = 0.03). Preoperative TAC was associated with the degree of pulmonary edema in the postoperative period (r = -0.372, p = 0.067). These results suggest that preoperative antioxidant supplementation may favorably impact the severity of systemic inflammatory response following ischemia and reperfusion injury.

Awake aortic aneurysm repair in patients with severe pulmonary disease.

BACKGROUND: We report the use of retroperitoneal aortic aneurysm repair utilizing exclusive regional anesthesia (no intubation or inhalation anesthetic) in high pulmonary risk patients. METHODS: Six patients were retrospectively reviewed. Pulmonary disease was diagnosed by clinical history and pulmonary function tests. Patients received intravenous sedation and regional anesthesia. Retroperitoneal aortoiliac aneurysm repair was performed. RESULTS: All patients used inhaled steroids and albuterol. Three required theophylline and home oxygen. FEV1 = 23% +/- 5% predicted, FVC = 34% +/- 5% predicted, and PO2 = 62 +/- 2 mm Hg. Operative time was 247 +/- 25 minutes. Blood loss was 840 +/- 479 mL. Five of six patients (83%) tolerated awake aneurysm repair and had intensive care unit stays of 2.4 +/- 0.6 days, and postoperative hospital stays of 8.2 +/- 1.8 days. One patient was converted to general anesthesia and had a prolonged hospital stay. CONCLUSIONS: With thorough patient communication, awake retroperitoneal aortic aneurysm repair can be safely performed in select patients with severe pulmonary disease.

Fibroblast growth factor-2-toxin induced cytotoxicity: differential sensitivity of co-cultured vascular smooth muscle cells and endothelial cells.

Recombinant FGF-2-SAP is a mitotoxin consisting of the plant-derived ribosome-inactivating toxin saporin (SAP) fused to basic fibroblast growth factor (FGF-2). FGF-2-SAP targets and kills cells bearing upregulated FGF receptors. In vivo, FGF-2-SAP inhibits smooth muscle cell hyperplasia in models of restenosis. The present study examined the potential for a differential effect of FGF-2-SAP on canine vascular endothelial cells (EC) and smooth muscle cells (SMC) separately as well as in a novel co-culture model. Canine vascular SMC and EC cultures were established separately and made quiescent once cells reached 80% confluence. Following the release from growth arrest, both cell types were treated with FGF-2-SAP, or FGF-2, or SAP alone for 48 h. [3H]TdR incorporation was used to determine the growth response of SMC and EC. The co-culture system was created by plating canine vascular SMC and EC on either side of a microporous 13 microm thick polyester membrane insert. Both cell types were grown to 80% confluence and independently made quiescent. Following the release from growth arrest, cells were treated with FGF-2-SAP, or FGF-2, or SAP alone. Negative and positive control groups were untreated wells containing phosphate buffered saline and complete growth media, respectively. After 48 h, both [3H]TdR incorporation and total DNA content, by fluorometric measurement, were quantitated in SMC and EC independently. FGF-2-SAP showed a concentration-dependent cytotoxicity in both canine SMC and EC but cytotoxicity for EC required substantially higher concentrations. In co-cultured SMC, FGF-2-SAP significantly decreased both [3H]TdR uptake and total DNA content at 0.5, 5, 50, and 500 ng/ml (0.01-10 nM) compared to positive controls. In co-cultured EC, FGF-2-SAP decreased [3H]TdR uptake at 50 and 500 ng/ml and total DNA content at 500 ng/ml compared to positive controls. Neither SAP alone nor FGF-2 alone showed a significant effect on [3H]TdR uptake or DNA content of either SMC or EC. In this unique co-culture model, which better replicates the relationship between SMC and EC in vivo, we demonstrated a dose-response range of FGF-2-SAP at which both the proliferation and total cell number of SMC, but not EC, is significantly reduced. These data suggest that FGF-2-SAP may have therapeutic utility in inhibiting myointimal hyperplasia in the absence of a deleterious effect on regenerating endothelium following vascular reconstructions.

Intensive care after carotid endarterectomy: a prospective evaluation.

BACKGROUND: Through prior investigation we established that only a small minority of patients who undergo carotid endarterectomy (CEA) have a complicated postoperative course requiring an intensive care unit (ICU) stay. An appropriate policy for patient management was established. This study prospectively analyzes the safety and efficacy of this policy. STUDY DESIGN: Patients were transferred directly to a nonmonitored surgical ward, regardless of preoperative comorbidity, if they remained stable from a neurologic and a hemodynamic standpoint during a short (less than three hour) stay in the recovery room. Patients whose status was questionable remained in recovery longer or were transferred to an ICU. RESULTS: One hundred forty-six (79 percent) of 185 patients were transferred safely to a ward. Average length of stay in recovery was one hour 59 minutes. No complications occurred that required a return to the operating suite or a move to an ICU. Most of these patients (88 percent) were discharged within 24 hours of surgery. Thirty-nine (21 percent) patients, each identified in recovery, required intervention or monitoring in an intensive care setting. Fourteen required prolonged, aggressive intravenous treatment of hypertension; 14 had sustained hypotension; three were observed to rule out myocardial infarction, and three had neurologic deficits. Two patients had ventricular arrhythmias, two had wound hematomas, and one patient required reintubation. This group (n = 39) remained in the recovery room two hours 40 minutes on average, spent 20 hours in the ICU, and remained in the hospital 32 hours after CEA. CONCLUSIONS: Most patients who undergo CEA follow a predictably benign postoperative course. Patients are easily identified by a recovery room protocol and approximately 80 percent can avoid ICU costs.

The changing face of carotid endarterectomy.

PURPOSE: The economic milieu and improvements in care have altered the diagnostic and therapeutic algorithm of the patient with carotid stenosis. This study analyzes the efficacy and safety of these changes. METHODS: The records of patients who underwent 320 consecutive carotid endarterectomies performed by three surgeons at our institution from 1990 to 1994 were reviewed retrospectively. Use of diagnostic angiography, use of carotid duplex ultrasound, length of hospital stay, postanesthesia recovery observation, intensive care unit (ICU) observation, complications, and hospital charges were analyzed. RESULTS: The average length of hospital stay decreased from 6.18 days to 2.00 days (p < or = 0.001). The day of discharge decreased from 3.10 days to 1.24 days after surgery (p < or = 0.01). By 1993, 68% were discharged by the first day after surgery, increasing to 73% by 1994. From 1990 to 1992, average postoperative ICU observation time fluctuated between 18 and 25 hours; this time decreased to 12.2 hours by 1994. In 1993, only 12.5% of patients were admitted to the ICU, down from 94.8% in 1990; by 1994, only 7.3% were admitted to the ICU (p < or = 0.001). Postanesthesia recovery observation time decreased from 3.77 hours to 1.63 hours during this time (p < or = 0.04). With regard to preoperative diagnosis, angiography was performed in 93.1% of patients in 1990; by 1994, only 32.8% underwent this procedure (p < or = 0.0001). Average hospital charges decreased significantly (1990, $14,378; 1994, $10,436) with these modifications in patient care (p < or = 0.001). The complication rate reflected no significant changes over the course of the study. There were six incidences of cerebrovascular accident (6/320, 1.9%), including one death. There were four incidences of transient ischemic attack (4/320, 1.3%), with no significant differences noted from year to year. CONCLUSIONS: This study confirms the changing nature of carotid endarterectomy and documents that these changes have not adversely affected the safety of the operation.

In vivo tissue distribution of fibroblast growth factor-1 after intraarterial delivery.

The clinical applicability of fibroblast growth factor-1 (FGF-1) plus heparin delivery in optimizing the healing of both autogenous vein and synthetic vascular grafts has been suggested. The authors have reported enhanced endothelial cell proliferation, concurrent increased capillarization, and minimal intimal hyperplasia using suspensions of FGF-1 and heparin impregnated onto expanded polytetrafluoroethylene grafts. The current study characterizes the tissue distribution of 125I-FGF-1 delivered by continuous intraarterial infusion. 125I-FGF-1 delivered by continuous intraarterial infusion. 125I-FGF-1 (1.1 ng) and heparin (28 U) were continuously infused into the thoracic aorta via the proximal end of the ligated left carotid artery for 24 hr in four New Zealand white rabbits using an Alzet (Alza Corp., Palo Alto, CA) osmotically activated pumping device. Rabbits were sacrificed after 24 hr, exsanguinated, and biopsies taken from the liver, kidneys, spleen, lungs, heart, thyroid gland, muscle, and fat. These samples were assayed for radioactivity and results expressed as cpm 125I/gram of both wet and dry weight of tissue. 125I-FGF-1 uptake (cpm/g dry wt.) was greatest in the thyroid (551.1 +/- 131.4). This was 2.5-5.5 x greater (p < or = 0.01) than those organs with intermediate uptake (lungs, liver, kidneys, spleen, and heart). Lowest uptake was noted in the blood, muscle, and fat. A similar distribution pattern was found in wet weight comparisons. Total organ 125I-FGF-1 content was greatest in the liver at 818.1 +/- 176.3 cpm (p < or = 0.002) and intermediate in the lungs (204.7 +/- 38.5 cpm) and kidneys (191.2 +/- 11.9 cpm). Although no FGF-1-induced toxicity has yet been reported, these results will allow for future tissue-specific toxicology studies before clinical trials.

Pharmacologic modulation of intimal hyperplasia in canine vein interposition grafts.

PURPOSE: The purpose of this study was to evaluate the efficacy of three drugs (cilazapril, cyclosporine, and aspirin) in modulating the progression of intimal hyperplasia during short postoperative times in short-segment, autogenous vein bypass grafts in a canine model. The relative effects of the drugs on the progression of intimal hyperplasia were compared with the Gilman parameter, a measure used extensively as a wound healing descriptor. To our knowledge this is the first use of the Gilman parameter in assessing vascular disease. METHODS: Seventy-two conditioned mongrel dogs were randomly and equally divided according to a three-factor analysis of variance. The factors included (1) drug treatments (cilazapril [10 mg/kg/day], cyclosporine [4 mg/kg/day], aspirin [325 mg/day], and control [nonmedicated]), (2) implantation sites (femoral and carotid arteries), and (3) postoperative times of graft harvest (1, 3, and 6 weeks). Each dog had 2 cm segments of autogenous jugular vein interpositioned bilaterally into each of the paired carotid and femoral arteries. Quantitative data on luminal narrowing over time from intimal hyperplasia were compared from calculated Gilman parameters after image analysis of retrieved, histologically processed graft sections. RESULTS: The observed variability in the data was attributed to drug treatments and time. At 1 week after operation the mean Gilman parameters did not differ significantly among the treatment groups in either midgraft or distal graft segments. At 3 weeks the mean Gilman parameters of midgraft and distal graft sections of cyclosporine-treated dogs differed significantly (p < 0.05) from those of the control group and the cilazapril and aspirin-treated groups, which did not differ from each other. At 6 weeks after operation, mean Gilman parameters from aspirin- and cyclosporine-treated dogs differed statistically from control and cilazapril-medicated dogs and from each other (p < 0.001). CONCLUSIONS: These data support the efficacy of aspirin and cyclosporine in reducing intimal hyperplasia in short-segment arterialized vein grafts during short postoperative periods. Additional studies are required to ascertain whether the beneficial effects of aspirin and cyclosporine persist long-term.

Endothelial cell seeding improves 4 mm PTFE vascular graft performance in antiplatelet medicated dogs.

The ideal prosthetic vascular graft for the replacement or bypass of small vessels has not yet been developed. Many studies have documented the success of endothelial cell seeding in small-diameter Dacron grafts, but few have reported the application of this protocol to small-diameter PTFE grafts, and none have reported seeding small-diameter PTFE grafts in antiplatelet medicated dogs. The present study was undertaken to assess the efficacy of endothelial cell seeding of small-diameter (4 mm ID) PTFE (Gore-Tex) carotid artery interposition grafts in the antiplatelet medicated dog. Twenty-five male mongrel dogs were included in this study. In each dog one carotid artery was replaced with an endothelial cell seeded PTFE graft; the contralateral artery was replaced with a nonseeded graft. The in vivo progress of graft performance was evaluated from 1 to 4 weeks postoperatively. The endothelial cell seeded grafts achieved significantly higher patencies and mean thrombus-free surfaces than nonseeded grafts. Midgraft endothelium was identified only on the seeded grafts at 3 and 4 weeks, with a maximal luminal coverage of 10-12%. The measurements of prostacyclin (PGI2) production indicated that the antiplatelet agent therapy did inhibit endothelial cell cyclooxygenase. The presence of outer capsule vasa vasora, anastomotic pannus ingrowth, transinterstitial cellular ingrowth, and thin inner capsules characterized the endothelial cell seeded grafts in contrast to the nonseeded grafts. We conclude that enhancement of graft performance is achieved by combining both an antiplatelet regimen and endothelial cell seeding in small-diameter PTFE vascular grafts.