Biomedical subjects
Katja E Wartenberg
Publications and source records attributed to Katja E Wartenberg.
Impact of medical complications on outcome after subarachnoid hemorrhage.
OBJECTIVE: Medical complications occur frequently after subarachnoid hemorrhage (SAH). Their impact on outcome remains poorly defined. DESIGN: Inception cohort study. PATIENTS: Five-hundred eighty patients enrolled in the Columbia University SAH Outcomes Project between July 1996 and May 2002. SETTING: Neurologic intensive care unit. INTERVENTIONS: Patients were treated according to standard management protocols. MEASUREMENTS AND MAIN RESULTS: Poor outcome was defined as death or severe disability (modified Rankin score, 4-6) at 3 months. We calculated the frequency of medical complications according to prespecified criteria and evaluated their impact on outcome, using forward stepwise multiple logistic regression after adjusting for known predictors of poor outcome. Thirty-eight% had a poor outcome; mortality was 21%. The most frequent complications were temperature>38.3 degreesC (54%), followed by anemia treated with transfusion (36%), hyperglycemia>11.1 mmol/L (30%), treated hypertension (>160 mm Hg systolic; 27%), hypernatremia>150 mmol/L (22%), pneumonia (20%), hypotension (<90 mm Hg systolic) treated with vasopressors (18%), pulmonary edema (14%), and hyponatremia<130 mmol/L (14%). Fever (odds ratio [OR], 2.0; 95% confidence interval [CI], 1.1-3.4; p=.02), anemia (OR, 1.8; 95% CI, 1.1-2.9; p=.02), and hyperglycemia (OR, 1.8; 95% CI, 1.1-3.0; p=.02) significantly predicted poor outcome after adjustment for age, Hunt-Hess grade, aneurysm size, rebleeding, and cerebral infarction due to vasospasm. CONCLUSIONS: Fever, anemia, and hyperglycemia affect 30% to 54% of patients with SAH and are significantly associated with mortality and poor functional outcome. Critical care strategies directed at maintaining normothermia, normoglycemia, and prevention of anemia may improve outcome after SAH.
Medical complications after subarachnoid hemorrhage: new strategies for prevention and management.
PURPOSE OF REVIEW: To summarize new concepts regarding the occurrence, prevention, and management of medical complications following subarachnoid hemorrhage. RECENT FINDINGS: Data regarding the impact of common medical complications after subarachnoid hemorrhage on delayed cerebral ischemia and neurological outcome after subarachnoid hemorrhage are available from recent outcomes studies. Fever, anemia requiring transfusion, hyperglycemia, electrolyte abnormalities, pneumonia, hypertension, and neurogenic stunned myocardium and pulmonary edema occur frequently after subarachnoid hemorrhage. Fever, anemia, hyperglycemia, and acute hypoxia and hypotension related to neurogenic stunned myocardium have the greatest impact on mortality and functional outcome after subarachnoid hemorrhage. Potential treatment interventions for these complications include the development of acute resuscitation strategies to optimize cerebral perfusion in poor-grade patients, maintaining normothermia with systemic cooling devices, administration of erythropoietin to prevent severe anemia, preserving normoglycemia with continuous insulin infusions, and goal-directed hemodynamic support guided by brain tissue oxygenation. SUMMARY: Clinical trials to investigate interventions targeted at preventing or treating common medical complications after subarachnoid hemorrhage are needed.
CT and CT-perfusion findings of reversible leukoencephalopathy during triple-H therapy for symptomatic subarachnoid hemorrhage-related vasospasm.
BACKGROUND: Reversible leukoencephalopathy syndrome (RLS) is an acute neurological syndrome associated with altered mental status and visual disturbances described in patients with sudden elevations in systemic blood pressure and other medical conditions. In this process, neuroimaging studies usually demonstrate diffuse edema involving the subcortical structures of the posterior regions of the brain. Triple H (HHH) therapy is an established treatment for symptomatic vasospasm following subarachnoid hemorrhage (SAH). RLS has not been reported in the scientific literature as a complication of HHH therapy with perfusion computed tomography (CTP) imaging documentation. CASE: A 73-year-old woman developed iatrogenic RLS during HHH therapy for SAH-related vasospasm. The computed tomography (CT) revealed bilateral parieto-occipital hypodensities. The CTP study showed increased cerebral blood volume and blood flow as well as decreased mean transit time in both parietal-occipital regions, which is compatible with vasogenic edema. CONCLUSION: The induction of hypertension as part of HHH therapy for SAH-related cerebral vasospasm may result in RLS. Therefore, it should be considered as a potentially reversible cause in the differential diagnosis of neurological deterioration in SAH patients while on HHH therapy. CTP study can offer an alternative for the assessment of this cerebrovascular syndrome.
Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified fisher scale.
OBJECTIVE: We developed a modification of the Fisher computed tomographic rating scale and compared it with the original Fisher scale to determine which scale best predicts symptomatic vasospasm after subarachnoid hemorrhage. METHODS: We analyzed data from 1355 subarachnoid hemorrhage patients in the placebo arm of four randomized, double-blind, placebo-controlled studies of tirilazad. Modified Fisher computed tomographic grades were calculated on the basis of the presence of cisternal blood and intraventricular hemorrhage. Crude odds ratios (OR) reflecting the risk of developing symptomatic vasospasm were calculated for each scale level, and adjusted ORs expressing the incremental risk were calculated after controlling for known predictors of vasospasm. RESULTS: Of 1355 patients, 451 (33%) developed symptomatic vasospasm. For the modified Fisher scale, compared with Grade 0 to 1 patients, the crude OR for vasospasm was 1.6 (95% confidence interval [CI], 1.0-2.5) for Grade 2, 1.6 (95% CI, 1.1-2.2) for Grade 3, and 2.2 (95% CI, 1.6-3.1) for Grade 4. For the original Fisher scale, referenced to Grade 1, the OR for vasospasm was 1.3 (95% CI, 0.7-2.2) for Grade 2, 2.2 (95% CI, 1.4-3.5) for Grade 3, and 1.7 (95% CI, 1.0-3.0) for Grade 4. Early angiographic vasospasm, history of hypertension, neurological grade, and elevated admission mean arterial pressure were identified as risk factors for symptomatic vasospasm. After adjusting for these variables, the modified Fisher scale remained a significant predictor of vasospasm (adjusted OR, 1.28; 95% CI, 1.06-1.54), whereas the original Fisher scale was not. CONCLUSION: The modified Fisher scale, which accounts for thick cisternal and ventricular blood, predicts symptomatic vasospasm after subarachnoid hemorrhage more accurately than original Fisher scale.
The STICH trial: the end of surgical intervention for supratentorial intracerebral hemorrhage?
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Reversal of locked-in syndrome with anticoagulation, induced hypertension, and intravenous t-PA.
INTRODUCTION: Widespread use of intravenous tissue plasminogen activator (t-PA) for acute ischemic stroke is limited by multiple contraindications to its use. CASE REPORT: This article describes a patient with stuttering symptoms of pontine ischemia caused by vertebrobasilar dissection who suddenly deteriorated into a locked-in state 32 hours after symptom onset. The quadriparesis was successfully reversed within 3 hours of onset with the combination of pharmacologically induced hypertension, anticoagulation, and intravenous t-PA. DISCUSSION: Even in the face of numerous contraindications (including hypertension, anticoagulation, and treatment beyond 3 hours of symptom onset), intravenous t-PA can be used successfully in carefully selected cases.
Is magnetic resonance spectroscopy superior to conventional diagnostic tools in hypoxic-ischemic encephalopathy?
Anoxic brain injury carries a poor prognosis. Therefore, a diagnostic tool sensitive enough to predict its outcome is needed. The authors describe the case of a 51-year-old woman who suffered cardiorespiratory arrest. Electroencephalography, somatosensory evoked potentials, and magnetic resonance imaging did not prove to be useful in establishing a definitive prognosis. Magnetic resonance spectroscopy demonstrated the presence of significant neuronal loss in the cortex and cerebellum and was the only diagnostic procedure closely associated with this patient's prognosis.