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Biomedical subjects

Jose I Suarez

Publications and source records attributed to Jose I Suarez.

27 records · Page 2Linked to original sources
PubMed2003

Timing of neurologic deterioration in massive middle cerebral artery infarction: a multicenter review.

OBJECTIVE: To determine the time interval between symptom onset and neurologic deterioration related to cerebral edema in patients with massive middle cerebral artery infarction. The time period between onset and neurologic deterioration represents the window for surgical intervention. DESIGN: Multicenter retrospective chart review. SETTINGS: Five university-affiliated medical centers. PATIENTS: Fifty-three patients with massive middle cerebral artery infarction who experienced neurologic deterioration defined by a decrease in the Glasgow Coma Scale score of two or more points attributable to mass effect. MEASUREMENTS AND MAIN RESULTS: A total of 53 patients (mean age, 62 +/- 18 yrs; 25 [47%] were men) with neurologic deterioration were identified by using International Classification of Diseases (9th revision) codes and local registries. Medical records and neuroimaging studies were reviewed by a stroke neurologist or neurointensivist to identify the time of neurologic deterioration. Thrombolytics were used at presentation in 19 (35%) patients. A total of 19 (36%) patients had neurologic deterioration within 24 hrs of symptom onset. By 48 hrs, 36 (68%) patients had manifested clinical deterioration. A few patients had later neurologic deterioration on day 3 (n = 10), day 4 (n = 2), day 5 (n = 2), and day 6 or after (n = 3). A total of 25 (47%) of the 53 patients died during hospitalization. The highest frequency of deaths occurred on day 3. CONCLUSIONS: Neurologic deteriorations related to cerebral edema after massive middle cerebral artery infarction occur in most patients within 48 hrs of symptom onset.

Brain Edema↗
PubMed2003

Primary hypertension-induced cerebellar encephalopathy causing obstructive hydrocephalus. Case report.

Hypertension-induced encephalopathy is a recognized pathological process commonly focused in the parietal and occipital lobes of the cerebral hemispheres. The parenchyma of the posterior fossa is infrequently involved. The authors report on two cases of isolated edema of the cerebellar hemispheres, which occurred in the setting of hypertensive crisis and led to complete obstruction of or significant impingement on the fourth ventricle and potentially lethal hydrocephalus. To the best of the authors' knowledge, these are the first reported cases of hypertensive encephalopathy centered in the posterior fossa. Two patients presented with profound decreases in neurological status subsequent to development of malignant hypertension. Imaging studies revealed diffusely edematous cerebellar hemispheres with effacement of the fourth ventricle, causing dilation of the lateral and third ventricles. Following emergency placement of external ventricular drains, control of systemic blood pressure was accomplished, and neurological functioning returned to baseline. Although neurological deterioration resolved swiftly following placement of ventricular catheters and administration of diuretic agents, systemic blood pressure did not fluctuate with the release of cerebrospinal fluid and resolution of increased intracranial pressure. Decrease in systemic blood pressure lagged well behind improvement in neurological status; the patients remained morbidly hypertensive until systemic blood pressure was controlled with multiple parenteral medications. The authors hypothesize that the development of hypertension beyond the limits of cerebral autoregulation led to breakdown of the blood-brain barrier in the cerebellum and development of posterior fossa edema secondary to the focal transudation of protein and fluid. Correction of the elevated blood pressure led to amelioration of cerebellar edema. In the appropriate clinical setting, hypertension as the inciting cause of cerebellar encephalopathy should be considered.

Anti-Inflammatory Agents↗
PubMed2003

Stroke-free survival and its determinants in patients with symptomatic vertebrobasilar stenosis: a multicenter study.

OBJECTIVE: We sought to determine the long-term stroke-free survival of patients who present with ischemic events related to intracranial vertebrobasilar stenosis. METHODS: A retrospective cohort of patients diagnosed with symptomatic vertebrobasilar stenosis on the basis of magnetic resonance angiography and/or conventional angiography was identified at four academic medical centers. Patients' clinical and follow-up information was obtained through hospitalization records, clinic visits, and telephone interviews. Kaplan-Meier analysis was performed to determine the rate of stroke-free survival for a 5-year period. Cox proportional hazards analysis was performed to determine the effect of demographic and clinical factors on stroke-free survival. RESULTS: A total of 102 patients were included, whose mean age was 64 +/- 12 years. Fifty-five (54%) of the patients were men. The mean follow-up period was 15 +/- 15.9 months (range, 1-60 mo). During the follow-up period, 14 (14%) of the patients experienced recurrent stroke. The overall mortality rate was 21% (n = 21). Stroke-free survival, calculated by using the Kaplan-Meier curve, was 76% at 12 months (95% confidence interval [CI], 66-83%) and 48% at 5 years (95% CI, 27-65%). The risk of recurrent stroke was 10.9 per 100 patient-years, and the rate of recurrent stroke and/or death was 24.2 per 100 patient-years. Cox proportional hazards analysis revealed that increasing age (hazards ratio, 1.05; 95% CI, 1.00-1.09) decreased stroke-free survival. Treatment with either antiplatelet agents or warfarin (hazards ratio, 0.018; 95% CI, 0.003-0.11) had a protective effect on stroke-free survival after adjusting for age, sex, race, hypertension, diabetes mellitus, smoking, hyperlipidemia, and lesion location. CONCLUSION: A low rate of stroke-free survival is observed in patients with symptomatic vertebrobasilar stenosis. Further studies are required to evaluate new medical and endovascular treatment options for this group of patients to improve long-term stroke-free survival.

Aged↗
PubMed2002

Symptomatic vasospasm diagnosis after subarachnoid hemorrhage: evaluation of transcranial Doppler ultrasound and cerebral angiography as related to compromised vascular distribution.

OBJECTIVE: To evaluate the reliability of transcranial Doppler ultrasound in detecting symptomatic vasospasm in patients after aneurysmal subarachnoid hemorrhage and monitoring response after hypertensive and endovascular treatments. DESIGN: Retrospective chart review. SETTING: Neurosciences critical care unit in a tertiary-care university hospital. PATIENTS: All patients admitted to a neurosciences critical care unit with the diagnosis of subarachnoid hemorrhage between January 1990 and June 1997. INTERVENTIONS: None MEASUREMENTS AND MAIN RESULTS: We reviewed transcranial Doppler ultrasound data of 199 patients; 55 had symptomatic vasospasm. Clinical symptoms and corresponding vascular distributions were identified, as was angiographic vasospasm (n = 35). The sensitivity and specificity of transcranial Doppler ultrasound for anterior circulation vessels were calculated by using a mean cerebral blood flow velocity criterion of >120 cm/sec. Clinical diagnosis of symptomatic vasospasm was used as the standard to determine sensitivity and specificity of transcranial Doppler ultrasound and cerebral angiography. The sensitivity of transcranial Doppler ultrasound for anterior circulation in patients with symptomatic vasospasm was 73% with a specificity of 80%. The sensitivity of cerebral angiography was 80%. For individual vessels, the sensitivity and specificity of transcranial Doppler ultrasound were middle cerebral artery, 64% and 78%; anterior cerebral artery, 45% and 84%; and internal carotid artery, 80% and 77%, respectively. The mean times for symptomatic and transcranial Doppler ultrasound signs of vasospasm presentation were 6.4 +/- 2 and 6.1 +/- 3 days, respectively. In patients without symptomatic vasospasm, the mean time for mean cerebral blood flow velocities >120 cm/sec was 7.0 +/- 3 days (p <.05). Symptomatic vasospasm also was associated with thickness of clot on head computed tomography scan and rapidly increasing mean cerebral blood flow velocities. Transcranial Doppler ultrasound signs of vasospasm improved after endovascular treatment in 30 patients. CONCLUSIONS: The reliability of transcranial Doppler ultrasound was better at detecting high mean cerebral blood flow velocities in patients with symptomatic vasospasm related to middle cerebral and internal carotid artery distributions than for anterior cerebral artery distribution. Transcranial Doppler ultrasound was as sensitive as cerebral angiography at detecting symptomatic vasospasm. High mean cerebral blood flow velocities can be apparent before the presence of symptomatic vasospasm. Daily transcranial Doppler ultrasound monitoring could provide early identification of patients with aneurysmal subarachnoid hemorrhage who are at high risk for symptomatic vasospasm and may be helpful at following success of endovascular treatment.

Cerebral Angiography↗
PubMed2002

Endovascular administration after intravenous infusion of thrombolytic agents for the treatment of patients with acute ischemic strokes.

OBJECTIVE: To determine the feasibility of combined intravenous and intra-arterial thrombolytic therapy for acute ischemic strokes and to evaluate its associated risks, using magnetic resonance imaging as a triage tool. Intravenous treatment followed by intra-arterial infusion may increase the rate of recanalization and lead to better clinical results, with reduced frequency of intracranial hemorrhage. METHODS: Our Brain Attack Team evaluated patients who presented within 3 hours after symptom onset. Patients who did not demonstrate improvement and exhibited no evidence of intracranial hemorrhage on head computed tomographic scans were treated with intravenously administered recombinant tissue plasminogen activator (0.6 mg/kg) and underwent emergency magnetic resonance imaging of the head. T2-weighted turbo-gradient and spin echo and echo-planar diffusion- and perfusion-weighted imaging scans were obtained. Patients with evidence of imaging abnormalities indicating acute cortical infarction underwent cerebral angiography. After determination of vessel occlusion, intra-arterially administered urokinase (up to 750,000 units) or intra-arterially administered recombinant tissue plasminogen activator (maximal dose, 0.3 mg/kg) was used to achieve recanalization. RESULTS: We treated 45 patients with this protocol. The mean age was 67 +/- 13 years, and 58% of the patients were women. There was a significant improvement in National Institutes of Health Stroke Scale scores after treatment. There was good correlation between abnormal perfusion-weighted imaging findings and cerebral angiographic findings (complete vessel occlusion). The incidence of symptomatic intracranial hemorrhage was 4.4% in this cohort. Seven patients died in the hospital, and the majority of survivors (77%) experienced good outcomes (Barthel index of >or=95) 3 months after treatment. CONCLUSION: Our data demonstrate that this protocol is feasible and that combined intravenous and intra-arterial thrombolysis to treat acute ischemic strokes is sufficiently safe to warrant further evaluation.

Acute Disease↗
PubMed2002

Intracerebral hemorrhages associated with neurointerventional procedures using a combination of antithrombotic agents including abciximab.

BACKGROUND: We report the occurrence of fatal intracerebral hemorrhage associated with using a combination of antithrombotic agents, including abciximab, in patients undergoing neurointerventional procedures. SUMMARY OF REPORT: Seven patients (average age 60, range 46 to 73 years) developed fatal intracerebral hemorrhages associated with neurointerventional procedures and the use of intravenous abciximab. The procedures included angioplasty and stent placement in the cervical internal carotid artery (n=4), angioplasty of the intracranial internal carotid artery (n=1), and angioplasty of the middle cerebral artery (n=2). Clinical deterioration was observed within 1 hour of the procedure in 5 patients and 7 and 8 hours after the procedure, respectively, in the remaining 2 patients. All patients had received heparin and clopidogrel; 6 had also received aspirin. CONCLUSIONS: Intracerebral hemorrhages can occur after neurointerventional procedures in patients with recent cerebral ischemic events, particularly when aggressive antithrombotic treatment is used.

Abciximab↗
PubMed2002

Response to intra-arterial and combined intravenous and intra-arterial thrombolytic therapy in patients with distal internal carotid artery occlusion.

BACKGROUND AND PURPOSE: The objective of this study was to determine the clinical features, angiographic findings, and response to treatment with thrombolytic therapy in patients with ischemic stroke caused by acute occlusion of the distal internal carotid artery. METHODS: This is a retrospective case series from a prospectively collected stroke database for patients with acute internal carotid occlusion presenting within 6 hours of stroke onset to evaluate safety, feasibility, and response to thrombolytic therapy. The University Hospital-based brain attack database was reviewed over a 5-year period. Demographics, clinical features, stroke mechanisms, severity, imaging findings, type of thrombolysis, treatment responses, mortality, and long-term outcome using modified Rankin Scale and Barthel Index were determined. The short-term outcome was assessed using the National Institutes of Health Stroke Scale (NIHSS). Acute thrombolytic therapy was administered using recombinant tissue plasminogen activator or urokinase given intra-arterially or in combination with intravenous (IV) routes. RESULTS: Two hundred seven patients treated with thrombolysis between 1995 and 2000 were reviewed, and of these, 101 were studied with cerebral angiography. Eighteen patients were identified with acute ischemic stroke and ipsilateral occlusion of the distal internal carotid artery. Time to treatment was the most powerful predictor of response to thrombolytic therapy (P<0.001). The response to therapy also correlated well with the severity of the initial clinical deficit as judged by the NIHSS (P<0.001). There was no difference in recanalization rate, symptomatic hemorrhage, and NIHSS for IV/intra-arterial (IA) versus IA alone (P=NS). Complete angiographic recanalization was accomplished in 80% of those who received combined IV/IA thrombolysis and in 62% of those who received IA therapy (P=NS). Those with distal occlusions extending to the middle and anterior cerebral arteries were the least likely to respond to thrombolysis. Symptomatic intracerebral hemorrhage occurred in 20% of the patients receiving IV/IA therapy, and in 15% of the IA only (P=NS). At 24 hours, the NIHSS dropped by 3 points in the IA group and 4 points in the IV/IA group (P=NS). Mild disability with independence was found in 77% of the survivors at 3-month follow-up. The mortality rate was 50% in this group despite thrombolysis. CONCLUSIONS: Thrombolytic therapy using a combination of IV and IA routes and using the IA-only route may be effective in improving outcome for the patients suffering from occlusion of the distal internal carotid artery. Shorter intervals between onset and treatment seem to be correlated with higher rate of recanalization and improved outcome.

Aged↗
PubMedDate not supplied

A prospective multicenter study to evaluate the feasibility and safety of aggressive antihypertensive treatment in patients with acute intracerebral hemorrhage.

The authors performed a multicenter prospective observational study to evaluate the feasibility and safety of intravenous antihypertensive protocol for acute hypertension in patients with intracerebral hemorrhage (ICH). Twenty-seven patients with ICH and acute hypertension (mean age 61.37 +/- 14.27; 10 were men) were treated to maintain the systolic blood pressure (BP) below 160 mm Hg and diastolic BP below 90 mm Hg within 24 hours of symptom onset. Neurological deterioration (defined as a decrease in initial Glasgow Coma Scale score > or = 2) was observed in 2 (7.4%) of 27 patients during treatment. Among patients who underwent follow-up computed tomography, hematoma expansion (more than 33% increase in hematoma size at 24 hours) was observed in 2 (9.1%) of 22 patients. Patients treated within 6 hours of symptom onset were more likely to be functionally independent (modified Rankin scale < or = 2) at 1 month compared with patients who were treated between 6 and 24 hours (8 of 18 versus 0 of 9,P = .03). Aggressive pharmacological treatment of acute hypertension in patients with ICH can be initiated early with a low rate of neurological deterioration and hematoma expansion.

Acute Disease↗