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Surgical training programs use various objective and subjective means to evaluate housestaff performance. However it is less clear how to assess the quality of the educational experience the program itself provides. This study examines the use of a resident-directed survey as a means of identifying and rectifying weakness in a surgical training curriculum. Multiple choice questionnaires covering each of 14 senior rotations were prepared by chief residents and distributed to all senior surgical residents in April 1989 (year I). The survey covered factors considered vital to resident education, including operative experience, input into preoperative and postoperative decisions, autonomy, and time demands, and an overall rating (OR) of the educational quality of the rotations. Responses were numerically graded: 1, appropriate; 0, fair; -1, inadequate (or "excessive" for the variable "time demands"). The results, which were presented and discussed at a departmental retreat that spring, prompted specific curriculum changes for the 1989-1990 academic year. An identical survey was conducted the next spring (year II). Major reorganizational changes were made in three of the four negatively rated rotations from year I. The OR for each of the rotations improved dramatically in year II (average increase of 0.64/rotation; p less than 0.05). None of the eight favorably rated rotations in year I suffered a reduction in OR as a result of the changes. Case load, intraoperative involvement, and input in both preoperative and postoperative decisions correlated most frequently with favorable ORs in both years. This study shows that a resident survey is an effective tool for critically assessing the education curriculum of a surgical training program.

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Oxygen free radicals (OFRs) generated during reperfusion are putative mediators of postischemic renal dysfunction. To address this issue, the renal response to ischemia and reperfusion was compared to the response to OFR generation without ischemia. Isolated rat kidneys were perfused at 37 degrees C and 90-100 mm Hg with an asanguinous modified Krebs' buffer. Kidneys were subjected to 30 min of ischemia followed by reperfusion or to OFRs generated by combining 25 mumole hypoxanthine with 1 unit xanthine oxidase. Both insults caused a 50% increase in vascular resistance. This was accompanied by a 30% reduction in perfusate flow rate and an 80% reduction in glomerular filtration and urine flow rates. The OFR scavengers, superoxide dismutase (SOD, 250 units/ml) and catalase (CAT, 500 units/ml), prevented these alterations after OFR generation but not after 30 min of ischemia and reperfusion. SOD and CAT also afforded no protection against the less severe dysfunction observed after 10 or 20 min of ischemia and reperfusion. OFRs do not appear to be prominent mediators of postischemic renal dysfunction; other factors, probably associated with ischemia must be primarily responsible.

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There is no consensus regarding the most appropriate management of pediatric blunt liver injury. This study addresses this issue by reviewing our experience with blunt liver trauma in relationship to the grade of injury. Forty-one pediatric patients with blunt abdominal trauma and documented liver injury were managed from 1979 to 1989. Fifteen (37%) underwent celiotomy. Three children had extensive parenchymal injuries (grade IV or V) requiring resection and three others died intraoperatively, secondary to exsanguinating hemorrhage of associated injuries (grade V) to the hepatic veins and inferior vena cava. The need for celiotomy was obvious in these patients. In 9 of the 15 children who underwent exploration (60%), bleeding from the liver injury (grade II or III) had ceased by the time of celiotomy. These children did not appear to benefit from the operation. Twenty-six of the 41 patients (63%) were selected for nonoperative management because they were hemodynamically stable after initial resuscitation and did not show signs of associated intraabdominal injuries requiring surgical intervention. These children underwent evaluation by abdominal computed axial tomography scan (grade I, II, III, and IV injuries). Blood transfusions were given to keep the hematocrit above 30%. Seventeen of the 26 children managed nonoperatively (65%) did not require blood replacement. The mean (+/- SEM) transfusion volume for the remaining nine children was 14.8 +/- 2.5 mL/kg. Blunt liver injury represents a spectrum from a minimal parenchymal hematoma to massive liver disruption. We conclude that celiotomy is necessary for hepatic injury hemodynamically stable injured children with transfusion requirements less than 40 mL/kg can be managed nonoperatively in an appropriate setting.

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Postischemic renal dysfunction (PIRD) is characterized by a reduction in glomerular filtration and tubular reabsorption of solute. The relative contribution of oxygen free radicals (OFRs) generated during reperfusion remains unclear. This study characterized the renal response to OFRs--independent of an ischemic insult. Isolated rat kidneys were perfused at 37 degrees C and 90-100 mm Hg with a modified Krebs' buffer. Hypoxanthine (25 mumole) and xanthine oxidase (1 unit) were combined and infused proximal to the kidney. There was a 50% increase in vascular resistance. This was accompanied by a 30% reduction in perfusate flow rate and a 70% reduction in glomerular filtration rate. There was also a significant reduction in urine flow rate and oxygen consumption. The percentage reabsorption of filtered water and sodium by the renal tubules was not diminished, however. This pattern was not observed when the xanthine oxidase was inactivated or when the perfusate was pretreated with superoxide dismutase (250 units/ml) and catalase (500 units/ml). The generation of OFRs, independent of an ischemic insult, causes a decrease in glomerular filtration out of proportion to the decrease in renal flow similar to that observed with PIRD. OFRs may contribute to the hemodynamic and glomerular alterations seen with PIRD. Factors other than OFRs, probably associated with ischemia, must be responsible for the tubular dysfunction.

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Renal ischemia is a multifactorial insult consisting of both hypoxia and stagnation of blood flow. This study compared the renal response with hypoxia alone versus ischemia (hypoxia and stagnation of flow). Isolated rat kidneys were perfused at 90 to 110 mm Hg and 37 degrees C with an asanguinous modified Krebs' buffer. Perfusate flow rate, vascular resistance, urine flow rate, glomerular filtration rate (GFR), percent sodium reabsorption, and oxygen consumption were measured. Five groups were examined: 10-minute hypoxia (HYP10), 30-minute hypoxia (HYP30), 10-minute ischemia (ISC10), 30-minute ischemia (ISC30), and time-matched controls. HYP10 resulted in isolated tubular dysfunction, as evidenced by an increase in urine flow rate and a decrease in percent sodium reabsorption. ISC10 caused decreased GFR, oliguria, and more severe tubular dysfunction. The pattern of glomerular and tubular dysfunction after HYP30 was similar to that after ISC30. Glomerular dysfunction was associated with a decrease in perfusate flow rate and an increase in vascular resistance only after ISC30. This suggests that the decrease in GFR seen with postischemic renal dysfunction is not a primary result of decreased flow. Furthermore, hypoxia does not account for the entire reduction in renal function after ischemia of similar duration. The more severe dysfunction after ischemia may be a consequence of the stagnation of renal flow (anaerobic waste product accumulation and inadequate nutrient supply).

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The isolated perfused rat kidney was used to characterize the renal response to hypoxia while flow was maintained. Hypoxia resulted in an 85% reduction in glomerular filtration rate (GFR) without any change in total renal vascular resistance. There was an initial 85% increase in urine flow rate (UV) and a 45% decrease in percent sodium reabsorption due to hypoxic metabolic inhibition of solute reabsorption. As GFR decreased, UV declined to 50% of control. GFR did not increase on reoxygenation. These results suggest that an intrinsic protective tubuloglomerular feedback mechanism is activated during hypoxia that redistributes intrarenal flow to reduce the filtered load and to reduce oxygen demand for solute reabsorption. Delivery of oxygen to the hypoxia-sensitive medulla would also be improved. Decreases in GFR observed with ischemic models of acute renal failure may reflect this protective mechanism in addition to the effects of ischemic injury.

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Models of ischemic acute renal failure (ARF) must consider the combination of tissue hypoxia, insufficient nutrient flow, and anaerobic waste product accumulation. This study utilized isolated perfused rat kidneys to characterize the renal response to a graded hypoxic insult while maintaining flow. Kidneys were perfused at 37 degrees C with an asanguineous Krebs-buffered saline. After a 40-min baseline period, 10 or 30 min of hypoxia was rapidly achieved by reducing perfusate oxygen tension from approximately 550 to 50 mm Hg. Ten minutes of hypoxia resulted in tubular dysfunction evidenced by a 50% increase in urine flow (UV) and a 10% decrease in percent sodium reabsorption (%Na). Glomerular filtration rate (GFR) decreased by 40% during 10 min of hypoxia and returned to control levels after reoxygenation. Thirty minutes of hypoxia caused an irreversible 85% decrease in GFR accompanied by a 50% decrease in UV. This insult also caused more severe tubular dysfunction evidenced by a 20% decrease in %Na and a 35% decrease in oxygen consumption. These results demonstrate a spectrum of renal dysfunction that corresponds to the clinical spectrum from nonoliguric to oliguric ARF. This model of hypoxic ARF allows more specific investigation into the hypoxic component of postischemic renal dysfunction.

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