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Biomedical subjects

H R Winn

Publications and source records attributed to H R Winn.

At least 55 records · Page 3Linked to original sources
PubMed1998

Balloon angioplasty for the treatment of vasospasm: results of first 50 cases.

OBJECTIVE: To report the results of the first 50 consecutive patients with vasospasm secondary to subarachnoid hemorrhage treated with balloon angioplasty after failure of medical management. METHODS: Retrospective uncontrolled study of 50 consecutive patients treated with balloon angioplasty between February 1988 and July 1992. Forty-six had objective clinical deterioration despite maximal medical therapy, whereas four were treated on the basis of rapidly accelerating transcranial Doppler velocities and decreased regional blood perfusion detected by technetium-99m-exametazime brain single photon emission computed tomography. All patients had evidence of marked vasospasm demonstrated by angiography. Thirty-two (64%) and 46 (92%) patients underwent angioplasty within 12 and 18 hours, respectively. RESULTS: Of the patients with clinical evidence of vasospasm-induced ischemia, 28 (61%) showed sustained neurological improvement within 72 hours of angioplasty. Three (6%) patients deteriorated within 72 hours after angioplasty, with two (4%) patients dying immediately after angioplasty as a result of vessel rupture and the other patient's Glasgow Coma Scale score decreasing by 2. Two additional patients in poor condition with Hunt and Hess Grade V at the time of angioplasty subsequently died during hospitalization. Two other patients died as a result of unclipped aneurysms that subsequently bled 4 and 12 days after angioplasty, respectively. The improvement demonstrated clinically, angiographically, and by transcranial Doppler after angioplasty was sustained, with only one patient requiring subsequent angioplasty of a previously dilated segment (total, 170 vessel segments dilated). Two patients developed vasospasm in previously undilated segments. CONCLUSION: Timely balloon angioplasty can reverse delayed ischemic deficit caused by vasospasm in patients for whom medical therapy has failed.

Angioplasty, Balloon↗
PubMed1998

Accuracy of continuous jugular bulb oximetry in the intensive care unit.

OBJECTIVE: To address the accuracy of a bedside jugular bulb oxygen saturation (SjO2) catheter monitor (Baxter-Edwards, Santa Ana, CA) versus in vitro co-oximetry measurements in the intensive care unit (ICU). METHODS: By prospective protocol, we compared blood gas measurements with simultaneously recorded continuous bedside oximetric monitor values for 31 ICU patients with traumatic brain injury undergoing jugular bulb catheter monitoring. For suboptimal fiberoptic light signal quality indices, the catheter was repositioned, flushed, or both before drawing the sample for in vitro measurement. Laboratory and bedside monitor data were examined for association using the chi2 and paired t tests and a linear regression model. RESULTS: We assessed 195 samples (median, 5 per patient; range, 1-14) who were monitored an average of 3.4 (range, 1-6) days. The in vivo monitor (range, 32-94%) and in vitro co-oximetry (range, 38-93%) values had acceptable correlation (y = 0.94x + 4.4, r2 = 0.80). For bedside monitor detection of jugular bulb desaturation (SjO2 < 50% for 10 min), the kappa statistic was 0.35, the sensitivity was 45 to 50%, and the specificity was 98 to 100%. CONCLUSION: Continuous ICU SjO2 monitoring correlates significantly with in vitro values, but less so than previously described during intracranial surgery. Although sensitivity of the bedside monitor to detect confirmed desaturations remains an issue, the high specificity indicates that it is less of a concern that patients may be misdiagnosed as having desaturations resulting in unnecessary interventions. Nonetheless, suspected jugular bulb desaturation should be verified before taking therapeutic actions.

Adolescent↗
PubMed1998

Risks and benefits of diagnostic angiography after aneurysm surgery: a retrospective analysis of 597 studies.

INTRODUCTION: Cerebral angiography performed after aneurysm surgery can identify causes of morbidity and mortality that may be corrected. The risks and benefits of angiography that is performed after aneurysm surgery, however, have not been clearly defined. We therefore reviewed our experience with postoperative angiography to determine its dangers and benefits. METHODS: During 10 years, 543 consecutive patients received treatment for cerebral aneurysms. A retrospective analysis of 597 diagnostic angiograms obtained after aneurysm surgery for 494 of these patients was performed. RESULTS: Catheter-induced vessel spasm and dissection, occurring most frequently in the internal carotid artery, were observed in seven (1.2%) and six (1%) studies, respectively. No angiography-associated strokes were identified. No association between age, smoking, hypertension, blood pressure, atherosclerosis, or severe vasospasm and angiographic complications was observed. Aneurysm remnants were identified in 36 (5.7%) of the 637 aneurysms that were surgically treated. Atherosclerosis (P < 0.01) or multiple clip applications (P < 0.01) were significantly associated with aneurysm remnants. Angiographic vessel occlusion was observed in 28 (5.7%) patients and resulted in stroke in 14 of these patients. Vessel occlusion was significantly associated with increasing aneurysm size (P < 0.001), atherosclerosis (P < 0.001), temporary clips (P < 0.001), multiple clips (P=0.03), multiple clip applications (P=0.001), and a new postoperative neurological deficit (P=0.002). Severe vasospasm and newly identified aneurysms were observed in 51 and 16 patients, respectively. CONCLUSION: Angiography after aneurysm surgery is safe and can be routinely performed. Angiography after aneurysm surgery should be particularly considered for patients with large aneurysms or cerebrovascular atherosclerosis and for those who develop new postoperative neurological deficits.

Adolescent↗
PubMed1998

An illuminating retractor for intracranial microneurosurgery.

During certain microneurosurgical procedures, the illumination provided by current coaxial microscope light sources is suboptimal. One potential solution is the surgical light blade (SLB), a malleable retractor incorporating a flat fiberoptic bundle along its surface. The SLB provides intense illumination within the surgical field without decreasing the amount of limited operating space. A prototype of the SLB was tested in six patients. Results suggest that with further development the SLB could become useful for intracranial microneurosurgery.

Brain Diseases↗
PubMed1998

Relationship between intracranial pressure and the development of vasospasm after aneurysmal subarachnoid hemorrhage.

The relationship between intracranial pressure (ICP) and the development of vasospasm after subarachnoid hemorrhage caused by the rupture of an intracranial aneurysm was investigated. Eleven patients were divided into high (6 cases) and low (5 cases) ICP groups based on ICP data obtained during the perioperative period by continuous ICP monitoring. Transcranial Doppler ultrasonography was performed every 24 hours for 7 days and the severity, distribution, and duration of vasospasm were assessed. The high ICP group tended to have severe, prolonged, and diffuse vasospasm compared with the low ICP group. However, only duration of vasospasm was statistically different. The relationship between cerebral perfusion pressure (CPP) and the development of vasospasm was also examined. CPP had a less significant effect than ICP although similar tendencies for high ICP and low CPP were observed. High ICP worsens vasospasm and treatment for decreasing ICP with perioperative ICP monitoring has potential for avoiding the development of vasospasm.

Adult↗
PubMed1998

Comparison of balloon angioplasty and papaverine infusion for the treatment of vasospasm following aneurysmal subarachnoid hemorrhage.

OBJECT: The purpose of this study was to test the hypothesis that balloon angioplasty is superior to papaverine infusion for the treatment of proximal anterior circulation arterial vasospasm following subarachnoid hemorrhage (SAH). Between 1989 and 1995, 125 vasospastic distal internal carotid artery or proximal middle cerebral artery vessel segments were treated in 52 patients. METHODS: Blood flow velocities of the involved vessels were assessed by using transcranial Doppler (TCD) monitoring in relation to the day of treatment with balloon angioplasty or papaverine infusion. Balloon angioplasty and papaverine infusion cohorts were compared based on mean pre- and posttreatment velocity at 24 and 48 hours using the one-tailed, paired-samples t-test. Balloon angioplasty alone was performed in 101 vessel segments (81%) in 39 patients (75%), whereas papaverine infusion alone was used in 24 vessel segments (19%) in 13 patients (25%). Although repeated treatment after balloon angioplasty was needed in only one vessel segment, repeated treatment following papaverine infusion was required in 10 vessel segments (42%) in six patients because of recurrent vasospasm (p < 0.001). Seven vessel segments (29%) with recurrent spasm following papaverine infusion were treated with balloon angioplasty. Although vessel segments treated with papaverine demonstrated a 20% mean decrease in blood flow velocity (p < 0.009) on posttreatment Day 1, velocities were not significantly lower than pretreatment levels by posttreatment Day 2 (p = 0.133). Balloon angioplasty resulted in a 45% mean decrease in velocity to a normal level following treatment (p < 0.001), a decrease that was sustained. CONCLUSIONS: Balloon angioplasty is superior to papaverine infusion for the permanent treatment of proximal anterior circulation vasospasm following aneurysmal SAH.

Adult↗
PubMed1998

Methylprednisolone or tirilazad mesylate administration after acute spinal cord injury: 1-year follow up. Results of the third National Acute Spinal Cord Injury randomized controlled trial.

OBJECT: A randomized double-blind clinical trial was conducted to compare neurological and functional recovery and morbidity and mortality rates 1 year after acute spinal cord injury in patients who had received a standard 24-hour methylprednisolone regimen (24MP) with those in whom an identical MP regimen had been delivered for 48 hours (48MP) or those who had received a 48-hour tirilazad mesylate (48TM) regimen. METHODS: Patients for whom treatment was initiated within 3 hours of injury showed equal neurological and functional recovery in all three treatment groups. Patients for whom treatment was delayed more than 3 hours experienced diminished motor function recovery in the 24MP group, but those in the 48MP group showed greater 1-year motor recovery (recovery scores of 13.7 and 19, respectively, p=0.053). A greater percentage of patients improving three or more neurological grades was also observed in the 48MP group (p=0.073). In general, patients treated with 48TM recovered equally when compared with those who received 24MP treatments. A corresponding recovery in self care and sphincter control was seen but was not statistically significant. Mortality and morbidity rates at 1 year were similar in all groups. CONCLUSIONS: For patients in whom MP therapy is initiated within 3 hours of injury, 24-hour maintenance is appropriate. Patients starting therapy 3 to 8 hours after injury should be maintained on the regimen for 48 hours unless there are complicating medical factors.

Activities of Daily Living↗
PubMed1998

Management of cerebral aneurysms. How can current management be improved?

In the present article, we have reviewed potential avenues for improvement in the care of and present management of patients with cerebral aneurysms. Opportunities exist in areas of prevention, systems approach and organization of centers, physician and patient education, screening, and advances in surgical and endovascular therapy. All such advances, however, depend on rigorous academic evaluation. This issue represents a review of the current management of cerebral aneurysms, hopefully providing a basis for future improvements in the treatment of these lesions.

Case Management↗
PubMed1998

Management of the ruptured aneurysm.

Rupture of cerebral aneurysms is a complex and devastating pathophysiologic event. The successful management of aneurysm rupture requires a dedicated multidisciplinary team. This article reviews pathophysiology; clinical grading that can be used to predict outcome and guide therapy; factors that may affect outcome such as rebleeding, poor clinical grade, intracerebral hemorrhage, intraventricular hemorrhage, and acute hydrocephalus; preoperative care and assessment; pharmacological therapy; anesthetic, surgical, and endovascular considerations; and postoperative care following aneurysm rupture.

Aneurysm, Ruptured↗
PubMed1998

Surgical approaches to basilar bifurcation aneurysms.

Basilar bifurcation aneurysms are technically challenging and their treatment is often associated with greater morbidity than aneurysms located in the anterior circulation. These lesions can be treated using surgical, endovascular, or a combination of techniques. Several surgical approaches have evolved to treat basilar bifurcation aneurysms; none, however, is suitable for all aneurysms in this location. This article reviews the natural history, clinical presentation, evaluation, and selection of treatment approach and details various surgical techniques. The use of endovascular techniques is reviewed briefly.

Basilar Artery↗
PubMed1997

Neurotoxicity in organotypic hippocampal slices mediated by adenosine analogues and nitric oxide.

Adenosine (ADO) and nitric oxide (NO) have been implicated in a variety of neurophysiological actions, including induction of long-term potentiation, regulation of cerebral blood flow, and neurotoxicity/neuroprotection. ADO has been shown to promote NO release from astrocytes by a direct effect on A1 and A2 receptors, thus providing a link between actions of NO and adenosine in the brain. However, while adenosine acts as an endogenous neuroprotectant, NO is believed to be the effector of glutamate neurotoxicity. To resolve this apparent paradox, we have further investigated the effects of adenosine and NO on neuronal viability in cultured organotypic hippocampal slices exposed to sub-lethal (20') in vitro ischemia. Up to a concentration of 500 microM ADO did not cause toxicity while exposures to 100 microM of the stable ADO analogue chloroadenosine (CADO) caused widespread neuronal damage when paired to anoxia/hypoglycemia. CADO effects were significantly prevented by the ADO receptor antagonist theophylline and blockade of NO production by L-NA (100 microM). Moreover, CADO effects were mimicked by the NO donor SIN-1 (100 microM). Application of 100 microM ADO following blockade of adenosine deaminase (with 10 microM EHNA) replicated the effects of CADO. CADO, ADO + EHNA but not ADO alone caused a prolonged and sustained release of nitric oxide as measured by direct amperometric detection. We conclude that at high concentrations and/or following blockade of its enzymatic catabolism, ADO may cause neurotoxicity by triggering NO release from astrocytes. These results demonstrate for the first time that activation of pathways other than those involving neuronal glutamate receptors can trigger NO-mediated neuronal cell death in the hippocampus.

2-Chloroadenosine↗
PubMed1997

Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study.

OBJECTIVE: To compare the efficacy of methylprednisolone administered for 24 hours with methyprednisolone administered for 48 hours or tirilazad mesylate administered for 48 hours in patients with acute spinal cord injury. DESIGN: Double-blind, randomized clinical trial. SETTING: Sixteen acute spinal cord injury centers in North America. PATIENTS: A total of 499 patients with acute spinal cord injury diagnosed in National Acute Spinal Cord Injury Study (NASCIS) centers within 8 hours of injury. INTERVENTION: All patients received an intravenous bolus of methylprednisolone (30 mg/kg) before randomization. Patients in the 24-hour regimen group (n=166) received a methylprednisolone infusion of 5.4 mg/kg per hour for 24 hours, those in the 48-hour regimen group (n=167) received a methylprednisolone infusion of 5.4 mg/kg per hour for 48 hours, and those in the tirilazad group (n=166) received a 2.5 mg/kg bolus infusion of tirilazad mesylate every 6 hours for 48 hours. MAIN OUTCOME MEASURES: Motor function change between initial presentation and at 6 weeks and 6 months after injury, and change in Functional Independence Measure (FIM) assessed at 6 weeks and 6 months. RESULTS: Compared with patients treated with methylprednisolone for 24 hours, those treated with methylprednisolone for 48 hours showed improved motor recovery at 6 weeks (P=.09) and 6 months (P=.07) after injury. The effect of the 48-hour methylprednisolone regimen was significant at 6 weeks (P=.04) and 6 months (P=.01) among patients whose therapy was initiated 3 to 8 hours after injury. Patients who received the 48-hour regimen and who started treatment at 3 to 8 hours were more likely to improve 1 full neurologic grade (P=.03) at 6 months, to show more improvement in 6-month FIM (P=.08), and to have more severe sepsis and severe pneumonia than patients in the 24-hour methylprednisolone group and the tirilazad group, but other complications and mortality (P=.97) were similar. Patients treated with tirilazad for 48 hours showed motor recovery rates equivalent to patients who received methylprednisolone for 24 hours. CONCLUSIONS: Patients with acute spinal cord injury who receive methylprednisolone within 3 hours of injury should be maintained on the treatment regimen for 24 hours. When methylprednisolone is initiated 3 to 8 hours after injury, patients should be maintained on steroid therapy for 48 hours.

Adolescent↗
PubMed1997

Delayed ischemia due to cerebral vasospasm occult to transcranial Doppler. An important role for cerebral perfusion SPECT.

Cerebral vasospasm after subarachnoid hemorrhage is very common, but it is not universally detectable by transcranial Doppler. SPECT imaging of regional cerebral blood flow with Tc-99m exametazime serves as a complementary test to transcranial Doppler in the evaluation of patients at high risk for vasospasm. The significance of vasospasm, which may be underestimated by TCD, is readily identified with SPECT cerebral perfusion imaging.

Brain↗
PubMed1997

Gunshot wounds of the internal carotid artery at the skull base: management with vein bypass grafts and a review of the literature.

BACKGROUND: Penetrating trauma to the skull base and distal cervical internal carotid artery (ICA) can result in occlusion or pseudoaneurysm formation. The appropriate management strategy for these rare lesions is controversial and includes observation, anticoagulation, carotid ligation, balloon occlusion, or revascularization. METHODS: We present the management and outcomes of four consecutive patients, two with pseudoaneurysms and two with acute occlusions, after injury to the distal cervical/petrous ICA from gunshot wounds. Preoperative assessment determined intracranial collateral flow patterns and the patency of the distal portion of the petrous ICA. RESULTS: Two patients underwent cervical-to-petrous ICA vein bypass grafts without neurologic complications. Both grafts remain patent without evidence of emboli at 2 years and 3 months, respectively. Both of the conservatively managed patients died, one from a massive cerebral infarction and the other from intracerebral hemorrhage. CONCLUSIONS: These cases underscore the need for an aggressive approach to the assessment and management of patients with penetrating vascular skull-base injuries. Although the optimal treatment of remains controversial, when the goal is exclusion of the injured portion of the carotid artery and revascularization, the cervical to petrous ICA vein bypass graft is a valuable management option that can reduce the potential morbidity and mortality from acute ischemic or delayed embolic or hemorrhagic complications, provide immediate restoration of high flow, and allow good surgical access with minimal risk to intracranial structures.

Adolescent↗
PubMed1997

Thrombotic, infectious, and procedural complications of the jugular bulb catheter in the intensive care unit.

OBJECTIVE: An assessment of the thrombotic, infectious, and technical complications of continuous jugular bulb catheter monitoring in the intensive care unit (ICU) was made. METHODS: Over a 1-year period, 44 patients suffering from traumatic brain injury, subarachnoid hemorrhage, or stroke received jugular bulb catheter monitoring in the ICU. They were followed for catheter insertion complications and the development of bacteremia. In 20 patients chosen randomly, an ultrasonographic evaluation was performed after removal of the catheter for an assessment of internal jugular vein thrombosis. RESULTS: Of the 44 patients, 1 became bacteremic; the source was identified as a thoracostomy site. Among the complications related to the 44 catheter insertions, there were 2 instances of carotid artery puncture (4.5%), 1 misplaced catheter (thoracic placement), and 1 clinically insignificant hematoma. Of the 20 patients investigated with ultrasonography, 8 (40%) had nonobstructive, subclinical internal jugular vein thrombi after jugular bulb catheter monitoring (95% confidence interval, 19-61%). The median monitoring duration was 3 days (range, 1-6 d). No clinical factor was identified to be associated with thrombus formation. CONCLUSION: We conclude the following: 1) the risk of bacteremia related to the jugular bulb catheter was negligible; 2) complications related to catheter insertion were rare and clinically insignificant; and 3) the incidence of subclinical internal jugular vein thrombosis after jugular bulb catheter monitoring is considerable. Although it is worthy to note this complication, no patient with a thrombus became symptomatic in the present series. The risk-benefit assessment of this monitoring technique must include consideration of subclinical thrombosis.

Adolescent↗
PubMed1997

Endothelium-dependent regulation of cerebrovascular tone by extracellular and intracellular ATP.

ATP receptors and ATP-sensitive potassium channels (KATP) are expressed in vascular smooth muscle (VSM) and endothelial cells (EC). In isolated penetrating vessels, ATP caused a dilatation when applied intraluminally but not extraluminally. The actions of ATP were blocked by the nitric oxide (NO) synthesis inhibitor N omega-nitro-L-arginine (0.1 mM) but were only reduced by N-monomethyl-L-arginine (0.1 mM); responses to intraluminal ATP were also prevented by thapsigargin. The KATP opener (KCO) nicorandil (1 microM) caused an NO-independent vasodilatation when applied extraluminally and an NO-dependent response when applied intraluminally. Both responses were blocked by glibenclamide. EC-mediated responses to nicroandil were prevented by blockade of guanylate cyclase by LY-83583 (10 microM). The effects of nicorandil were mimicked by pinacidil (1-10 microM). Exposure of the endothelium to 500 microM cyanide and 0 mM glucose ("in vitro ischemia") caused a vasodilatation that was reduced by exposure to glibenclamide (5 microM). Blockade of NO synthase produced similar effects, suggesting that the ischemic dilation is mediated by KATP and NO. Our results suggest that both VSM and EC mediate the vascular responses induced by KCOs, whereas the dilatation induced by intraluminal ATP is mediated by the endothelium. The endothelium-dependent component of the in vitro ischemic vasodilatation is mediated by opening of endothelial KATP and subsequent release of NO.

Adenosine Triphosphate↗
PubMed1997

Revised Winter-Tozer equation for normalized phenytoin concentrations in trauma and elderly patients with hypoalbuminemia.

OBJECTIVE: To develop a revised equation reflecting the current practice of measuring unbound phenytoin at room temperature, and to evaluate the revised Winter-Tozer method of predicting normalized total phenytoin concentrations in two groups of patients with hypoalbuminemia-elderly nursing home patients and critically ill head trauma patients. DESIGN: Albumin, unbound phenytoin, and total phenytoin concentrations were obtained from two sources: prospectively from a group of elderly nursing home patients and by a retrospective chart review of trauma patients enrolled in a previous double-blind, placebo-controlled study. SETTING: Community nursing homes; a university-affiliated urban teaching hospital. PARTICIPANTS: Elderly nursing home patients (n = 46) taking chronic phenytoin therapy and patients enrolled in a double-blind, placebo-controlled study (n = 58) evaluating the use of phenytoin to prevent posttraumatic seizures. MAIN OUTCOME MEASURES: Prediction error analysis was performed by using the methods proposed by Sheiner and Beal. Bias and precision were evaluated by calculating the mean prediction error (MPE) and root mean squared error (RMSE), respectively. RESULTS: The Winter-Tozer equation consistently overpredicted the normalized phenytoin concentration in the elderly nursing home population (MPE = 3.2, RMSE = 5.9) and the trauma patients (MPE = 3.3, RMSE = 4.8). The equation was revised to reflect the increased protein binding of phenytoin with decreased temperature and resulted in significantly decreased bias in both groups of patients. CONCLUSIONS: The revised equation is useful in predicting normalized phenytoin concentrations in both elderly nursing home patients and critically ill trauma patients.

Adolescent↗