Comparison of North American Symptomatic Carotid Endarterectomy Trial and population-based outcomes for carotid endarterectomy.

PURPOSE: The North American Symptomatic Carotid Endarterectomy Trial (NASCET) advocated the use of carotid endarterectomy (CEA) for transient ischemic attacks (TIAs), nondisabling strokes, and ipsilateral high-grade stenosis in highly selected patients. Whether similar results are achieved when CEA is applied to an entire geographically defined population is unknown but important if the NASCET recommendations are to be applied broadly to all community patients. METHODS: To determine the survival rate to ipsilateral stroke after CEA for all symptomatic patients in a defined population, we reviewed the medical records of all patients residing in Olmsted County, Minn. (approximately 100,000), who underwent a CEA for TIA or nondisabling stroke between 1970 and 1995. Their outcomes were compared with the NASCET results. RESULTS: In the community of Olmsted County, 297 patients (108 women and 189 men) underwent 322 CEAs during the study period. TIAs or nondisabling stroke was the indication in 254 patients (86%), whereas the remaining 14% had asymptomatic stenosis. After CEA for symptomatic lesions, survival rate free of ipsilateral stroke was 97% at 2 years, 93% at 5 years, and 92% at 10 years. These results are similar to the NASCET survival rates free of ipsilateral stroke at 2 years (91%). However, the 30-day postoperative stroke rate for patients older than 80 years was significantly higher than that for patients younger than 80 years. CONCLUSIONS: When the NASCET results are compared with a population-based experience in which all symptomatic patients undergoing CEA were analyzed, the early outcomes were similar. Our population-based data also document the remarkably durable long-term results of CEA in preventing stroke and present another benchmark for carotid stent angioplasty.

The effects of hyperosmolarity on the viability and function of endothelial cells.

Hypertonic solutions have been demonstrated to be efficacious in the treatment of hypovolemic shock. Their continued use when serum osmolarity is elevated may be harmful because they induce cellular dehydration. Because the hyperosmotic tolerance of cells is largely unknown, we determined the effects of increased media osmolarity on in vitro endothelial cell viability and function following periods of normoxia, anoxia, and anoxia with reoxygenation. Bovine aortic endothelial cells were exposed to hypertonic media of 330-570 mOsm/liter for 6-30 hr. Cell viability and function were ascertained utilizing trypan blue exclusion, lactate dehydrogenase (LDH) enzyme release, and cell replating assays. Endothelial cells exposed to media of 460 mOsm/liter demonstrated no significant decrease in the percentage of viable cells (69.81 +/- 6.03 vs 70.64 +/- 4.62% for controls), LDH activity (334.67 +/- 7.91 vs 228.03 +/- 191.28 Berger-Broida U/ml), and replating efficiency (58.27 +/- 42.07 vs 59.10 +/- 5.79%) after 30 hr of normoxic incubation. Hypertonic media up to 570 mOsm/liter did not adversely affect cell viability following a 6-hr anoxic insult. A 6-hr anoxic insult followed by 24 hr of reoxygenation in media of 530 and 570 mOsm/liter resulted in significantly increased viability and replating efficiency compared to 30 hr of normoxia. Our data demonstrate that in vitro endothelial cells tolerate media osmolarity of up to 460 mOsm/liter without apparent decrement in viability or replating efficiency even in adverse conditions of anoxia and reoxygenation. Our data also suggest that exposure to anoxia may induce tolerance of endothelial cells to hyperosmotic media.

Colloid infusion after brain injury: effect on intracranial pressure, cerebral blood flow, and oxygen delivery.

OBJECTIVES: We sought to determine the effects of colloid osmotic pressure on cerebral edema formation after brain injury. We hypothesized that an increase in plasma oncotic pressure accompanying a colloid infusion would be associated with a decrease in intracranial pressure and increases in cerebral blood flow and oxygen delivery when compared with isotonic crystalloid. DESIGN: Prospective, laboratory study. SETTING: University surgical research laboratory. SUBJECTS: Adult swine, both genders. INTERVENTIONS: Cryogenic brain injury with intravenous fluid infusion of either lactated Ringer's solution or 6% dextran-70 in normal saline. The effect of this intervention was monitored for 24 hrs. MEASUREMENTS: Mean arterial pressure, central venous pressure, intracranial pressure, hemoglobin concentration, plasma oncotic pressure, serum osmolality, cerebral blood flow, and specific gravity of cortical biopsies. RESULTS: Cryogenic injury significantly increased the cortical water content and the intracranial pressure and significantly decreased the cerebral blood flow and oxygen delivery (p < .05). Dextran infusion significantly increased the colloid oncotic pressure. There were no differences between the lactated Ringer's solution and dextran groups in intracranial pressure, cerebral oxygen delivery, or cortical water content after 24 hrs. CONCLUSIONS: Colloid infusion after a focal cryogenic injury does not increase cerebral oxygen delivery or reduce either cerebral edema formation or intracranial pressure when compared with lactated Ringer's solution. Colloid is not superior to isotonic crystalloid in the management of isolated brain injury.

Regional anesthesia in pediatric surgery: complications and postoperative comfort level in 174 children.

Postoperative pain control (PPC) in children is a difficult management problem. Systemic narcotics often result in respiratory depression, while nonnarcotic analgesics are associated with inconsistent PPC. This report reviews a 29-month (January 1989 through July 1991) experience with 174 children (aged < 18 years) who received regional PPC through indwelling catheters. There were 105 males and 69 females. Patient age ranged from 1 day to 17 years 10 months (mean age, 97 months). All catheters were placed using introduction needles ranging from 24 to 16 gauge. Agents were delivered as either continuous infusion (151 patients, 87%) or bolus injections (23 patients, 13%). Analgesics were age- and weight-determined dosages of bupivacaine with or without narcotic supplementation. All patients had surgical procedures except two who had catheters placed for pain control after trauma and one who had a catheter for intractable abdominal pain of unknown etiology. Twenty-five (15%) children had thoracic incisions, 76 (43%) abdominal, 16 (9%) flank, and 54 (31%) extremity. Catheter placement included 40 thoracic epidurals (23%), 100 lumbar (57%), 27 caudal (16%), and 7 pleural (4%). Catheters were utilized for a duration of 0.5 to 8 days (mean, 2.1 +/- 1.2 days). One hundred forty-four children required no additional pain medications (83%). Thirty (17%) patients required supplemental medications. Acetaminophen was used in 6 (3%), acetaminophen with codeine in 4(2%), morphine in 18 (10%), and Percocet in 1(1%). Minor complications occurred 21 times in 16 children (9%).(ABSTRACT TRUNCATED AT 250 WORDS)

Blunt colonic injury--a multicenter review.

During the past decade there has been a shift in the management of injuries of the colon to primary repair without a protective diverting colostomy. Unfortunately, reports concerning this practice contain relatively few patients with blunt trauma and it is unclear whether the principles established for penetrating injury should be applied in the setting of blunt colon injury. A retrospective review of 54,361 major blunt trauma patients admitted to nine regional trauma centers from January 1, 1986, through December 31, 1990, was conducted. Statistical analysis of the data collected regarding 286 (0.5%) of these patients who suffered colonic injury revealed: (1) injury to the colon is found in more than 10% of patients undergoing laparotomy following blunt trauma; (2) available diagnostic modalities are unreliable in detecting isolated colonic pathology; (3) primary repair of full-thickness injuries or resection and anastomosis may be safely performed without diversion; (4) gross fecal contamination is the strongest contraindication to primary repair. Further, delay of surgery, shock, and the timing of antibiotic administration were not associated with significantly increased morbidity.

The deleterious effects of intraoperative hypotension on outcome in patients with severe head injuries.

Prehospital or admission hypotension doubles the mortality for patients with severe head injury (SHI = Glasgow Coma Scale score less than or equal to 8). To our knowledge no study to date has determined the effects of intraoperative hypotension [IH: systolic blood pressure (SBP) less than 90 mm Hg] on outcome in patients with SHI. This study examined 53 patients who had SHI and required early surgical intervention (surgery within 72 hours of injury). All patients were initially normotensive on arrival. There were 17 patients (32%) who developed IH and 36 (68%) who remained normotensive throughout surgery. The mortality rate was 82% in the IH group and 25% in the normotensive group (p less than 0.001). The duration of IH was inversely correlated with Glasgow Outcome Scale using linear regression (R = -0.30; p = 0.02). Despite vigorous fluid resuscitation in the IH group, additional pharmacologic support was used in only 32%. These data suggest that IH is not uncommon after SHI (32%) and that it does have a significant effect on patient outcome.

An analysis of the relationship between fluid and sodium administration and intracranial pressure after head injury.

Severe head injury is the leading cause of traumatic death. When a severe head injury is combined with hypotension the mortality doubles. The use of asanguineous salt solutions to maintain blood pressure, however, may contribute to cerebral swelling and intracranial hypertension. For this reason, restrictions of fluids (FLD) and sodium (Na) have been advocated. To our knowledge, however, there are no clinical data to support this recommendation. We hypothesized that in adult patients sustaining severe head injuries (Glasgow Coma Scale score less than or equal to 8) with or without associated injuries: (1) FLD balance and total Na administered during the initial 72 hours of hospital admission are positively and significantly correlated with each other, and (2) total FLD, FLD balance, and total Na administration during the initial 72 hours are significantly and positively correlated with changes in ICP and adverse outcome. We retrospectively studied 40 adult trauma patients with severe head injuries. We found a significant correlation between total Na and FLD balance (R2 = 0.54; p less than 0.05). However, we found no significant correlation between total FLD and maximum ICP (R2 = 0.081), ICP score (R2 = 0.01), or outcome (R2 = 0.066), no significant correlation between FLD balance and maximum ICP (R2 = 0.000), ICP score (R2 = 0.000), or outcome (R2 = 0.01), and no significant correlation between total Na and maximum ICP (R2 = 0.000), ICP score (R2 = 0.001), or outcome (R2 = 0.02). We conclude that Na and FLD administration are not independent determinants of ICP during the initial 72 hours after brain injury.

Focal brain injury results in severe cerebral ischemia despite maintenance of cerebral perfusion pressure.

Severe head injury often causes an increase in intracranial pressure (ICP) and decreases in cerebral blood flow (CBF) and cerebral oxygen delivery (CO2del). To determine if this reduction in CBF and CO2del would produce cerebral ischemia and if this reduction would be abrogated by maintaining global cerebral perfusion pressure (CPP), we studied CPP, ICP, CBF, CO2del, cerebral oxygen extraction ratio (CO2ER), and cortical water content (CWC) in a porcine model of focal cryogenic brain injury. Fifteen mature swine were randomized to two groups. The experimental group (n = 7) had a brain lesion and was studied for 24 hours. The control group (n = 8) was instrumented only. Cryogenic injury significantly increased ICP and decreased CBF and CO2del compared with controls. There were no significant differences in CPP between the groups for the entire experiment, and the CPP was well above the ischemic threshold. The CO2ER significantly increased in the first three hours after brain injury. However, CO2ER in experimental animals tended to decrease 12 hours after brain injury and was not significantly different from that in controls. Cryogenic injury significantly increased the CWC in the lesioned hemisphere. These data indicate that focal brain injury results in persistent ischemia despite the normalization of CPP, suggesting that a significant increase in cerebral vascular resistance (CVR) occurs after brain injury. We conclude that in addition to maintenance of CPP, intervention to reduce CVR may be important in the management of brain injury.