Intravascular cooling for fever control.
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Journal Article↗
Biomedical subjects
Stephan A Mayer
Publications and source records attributed to Stephan A Mayer.
Cerebral vasospasm after subarachnoid hemorrhage.
PURPOSE OF REVIEW: To summarize new pathophysiologic insights and recent advances in the diagnosis and treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage. RECENT FINDINGS: Important, newly recognized mediators of cerebral arterial spasm after subarachnoid hemorrhage include superoxide free radicals, ferrous hemoglobin (which acts as a nitric oxide scavenger), endothelins, protein kinase C, and rho kinase. Microvascular dysfunction and autoregulatory failure also has been an area of increasing research focus in recent years. New diagnostic modalities include measures of cerebral blood flow such as single-photon emission computed tomography and perfusion computed tomography, magnetic resonance imaging, intracranial brain oxygen tension probes, and jugular venous oxygen saturation monitors. Proton magnetic resonance spectroscopy and microdialysis can detect tissue biochemical abnormalities, but these techniques have not found their way into routine clinical practice as of yet. In addition to nimodipine and hypertensive hypervolemic therapy, promising new treatments for vasospasm or its ischemic complications include magnesium sulfate, fasudil hydrochloride, tirilazad mesylate, erythropoietin, and induced hypothermia. Balloon angioplasty has emerged as the primary weapon for treating medically refractory ischemia from vasospasm and in many centers is being used as a first-line treatment or even prophylactically. SUMMARY: The neurointensive care management of vasospasm after subarachnoid hemorrhage has evolved significantly over the past 10 years, with many new diagnostic modalities and promising treatments now available. Clinical trials are needed to evaluate the efficacy of these new techniques and to further define the optimal management of this often devastating complication.
Aneurysm, Ruptured↗
Ultra-early hemostatic therapy for intracerebral hemorrhage.
BACKGROUND: Intracerebral hemorrhage (ICH) causes higher morbidity and mortality than other forms of stroke and has no proven effective treatment. Hematoma volume is a powerful predictor of outcome after ICH. SUMMARY OF REVIEW: Historically, ICH bleeding was considered to be a monophasic event that stopped quickly as a result of clotting and tamponade by surrounding brain tissue. More recently, prospective and retrospective CT-based studies have demonstrated that hematoma growth occurs in up to 38% of patients initially scanned within 3 hours of onset and in 16% scanned between 3 and 6 hours, even in the absence of coagulopathy. Progressive bleeding of this type has been associated with contrast extravasation on CT angiography and poor outcome after early (<4 hours) surgical clot evacuation. On the basis of these observations, it is plausible that ultra-early hemostatic therapy given in the emergency setting might reduce ICH volume in some patients and improve outcome. Among candidate agents for this indication, the most promising is recombinant activated factor VIIa, which promotes local hemostasis at sites of vascular injury in both coagulopathic and normal patients. CONCLUSIONS: Ultra-early hemostatic therapy, given within 3 to 4 hours of onset, may potentially arrest ongoing bleeding and minimize hematoma growth after ICH. Given the current lack of effective therapy for ICH, clinical trials testing this treatment approach are justified.
Cerebral Angiography↗
Refractory status epilepticus: frequency, risk factors, and impact on outcome.
BACKGROUND: Refractory status epilepticus (RSE) is a life-threatening condition in which seizures do not respond to first- and second-line anticonvulsant drug therapy. How often RSE occurs, risk factors that predispose to this condition, and the effect of failure to control seizures on clinical outcome are poorly defined. OBJECTIVE: To determine the frequency, risk factors, and impact on outcome of RSE. DESIGN: Retrospective cohort study. SETTING: Large academic teaching hospital. PATIENTS: Consecutive sample of 83 episodes of status epilepticus in 74 patients (mean age, 63 years). MAIN OUTCOME MEASURES: Refractory status epilepticus was defined as seizures lasting longer than 60 minutes despite treatment with a benzodiazepine and an adequate loading dose of a standard intravenous anticonvulsant drug. Factors associated with RSE were identified using univariate and backward stepwiselogistic regression analyses. RESULTS: In 57 episodes (69%), seizures occurred after treatment with a benzodiazepine, and in 26 (31%), seizures occurred after treatment with a second-line anticonvulsant drug (usually phenytoin), fulfilling our criteria for RSE. Nonconvulsive SE (P=.03) and focal motor seizures at onset (P=.04) were identified as independent risk factors for RSE. Eleven (42%) of 26 patients with RSE had seizures after receiving a third-line agent (usually phenobarbital). Although mortality was not increased (17% overall), RSE was associated with prolonged hospital length of stay (P<.001) and more frequent functional deterioration at discharge (P=.02). CONCLUSIONS: Refractory status epilepticus occurs in approximately 30% of patients with SE and is associated with increased hospital length of stay and functional disability. Nonconvulsive SE and focal motor seizures at onset are risk factors for RSE. Randomized controlled trials are needed to define the optimal treatment of RSE.
Adult↗
Intracerebral hemorrhage: natural history and rationale of ultra-early hemostatic therapy.
Stroke is a major health problem worldwide, causing high morbidity and mortality. Intracerebral hemorrhage (ICH) accounts for 15% of stroke cases in the US and Europe and up to 30% in Asian populations. It is less treatable than other forms of stroke and causes higher morbidity and disability. Data suggest that early hematomy growth is the principal cause of early neurological deterioration after ICH. Prospective and retrospective studies indicate that early hematoma growth occurs in 18-38% of patients scanned within 3 h of ICH onset, and that hematoma volume is an important predictor of 30-day mortality. As hematoma growth in acute ICH is a dynamic process, intervention with ultra-early hemostatic therapy could lead to minimization and even prevention of early hematomy growth. Recombinant activated factor VII (rFVIIa, 'NovoSeven'), a powerful initiator of hemostasis, is approved for the treatment of bleeding in patients with hemophilia and inhibitors and may also promote hemostasis in patients with normal coagulation. rFVa acts locally at the bleeding site without activating systemic coagulation and may be a valuable therapy during the hyperacute stage of ICH. A randomized, double-blind, placebo-controlled, dose-ranging trial is currently in progress to investigate the potential of rFVIIa as an ultra-early hemostatic therapy to prevent or minimize hematoma growth in ICH patients without coagulopathy.
Aprotinin↗
Hypothermia for neuroprotection after cardiac arrest.
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Adolescent↗
Continuous electroencephalographic monitoring in neurocritical care.
This article reviews current and future applications of continuous electroencephalography (cEEG) to monitor brain function and physiology in the neurologic intensive care unit. In comatose patients, cEEG may provide otherwise unobtainable information and influence therapeutic management, and also help determine the prognosis of patients with acute brain injury. This technique is best used for the detection of subclinical seizures, which may frequently occur during or after treatment of convulsive status epilepticus and after many types of acute brain injury, particularly trauma. The other main application of cEEG is as a primary monitor of brain function. cEEG can detect focal cerebral ischemia, such as that caused by vasospasm after subarachnoid hemorrhage, as well as global ischemia related to intracranial pressure elevation and insufficient cerebral perfusion pressure. Other potential applications include prognostication in coma and titration of continuous infusion sedative therapy. New technologic developments include continuous digital video EEG, automated seizure-detection software, and user-friendly online quantitative EEG analysis.
Brain Injuries↗
Treatment of refractory status epilepticus with pentobarbital, propofol, or midazolam: a systematic review.
BACKGROUND: New continuous infusion antiepileptic drugs (cIV-AEDs) offer alternatives to pentobarbital for the treatment of refractory status epilepticus (RSE). However, no prospective randomized studies have evaluated the treatment of RSE. This systematic review compares the efficacy of midazolam (MDL), propofol (PRO), and pentobarbital (PTB) for terminating seizures and improving outcome in RSE patients. METHODS: We performed a literature search of studies describing the use of MDL, PRO, or PTB for the treatment of RSE published between January 1970 and September 2001, by using MEDLINE, OVID, and manually searched bibliographies. We included peer-reviewed studies of adult patients with SE refractory to at least two standard AEDs. Main outcome measures were the frequency of immediate treatment failure (clinical or electrographic seizures occurring 1 to 6 h after starting cIV-AED therapy) and mortality according to choice of agent and titration goal (cIV-AED titration to "seizure suppression" versus "EEG background suppression"). RESULTS: Twenty-eight studies describing a total of 193 patients fulfilled our selection criteria: MDL (n = 54), PRO (n = 33), and PTB (n = 106). Forty-eight percent of patients died, and mortality was not significantly associated with the choice of agent or titration goal. PTB was usually titrated to EEG background suppression by using intermittent EEG monitoring, whereas MDL and PRO were more often titrated to seizure suppression with continuous EEG monitoring. Compared with treatment with MDL or PRO, PTB treatment was associated with a lower frequency of short-term treatment failure (8 vs. 23%; p < 0.01), breakthrough seizures (12 vs. 42%; p < 0.001), and changes to a different cIV-AED (3 vs. 21%; p < 0.001), and a higher frequency of hypotension (systolic blood pressure <100 mm Hg; 77 vs. 34%; p < 0.001). Compared with seizure suppression (n = 59), titration of treatment to EEG background suppression (n = 87) was associated with a lower frequency of breakthrough seizures (4 vs. 53%; p < 0.001) and a higher frequency of hypotension (76 vs. 29%; p < 0.001). CONCLUSIONS: Despite the inherent limitations of a systematic review, our results suggest that treatment with PTB, or any cIV-AED infusion to attain EEG background suppression, may be more effective than other strategies for treating RSE. However, these interventions also were associated with an increased frequency of hypotension, and no effect on mortality was seen. A prospective randomized trial comparing different agents and titration goals for RSE with obligatory continuous EEG monitoring is needed.
Anticonvulsants↗
Respiratory complications of rapidly progressive neuromuscular syndromes: Guillain-Barré syndrome and myasthenia gravis.
Neuromuscular respiratory failure is a common complication of both the Guillain-Barré syndrome and myasthenia gravis. Several key pathophysiological mechanisms contribute to the spiral of respiratory insufficiency in these diseases, including inspiratory, expiratory, and bulbar muscle weakness. It is important to identify patients with impending respiratory failure early to avoid emergency intubations. Several clinical features and bedside pulmonary function tests (PFTs) are useful in guiding decisions about intubation. Weaning is initiated when respiratory muscles have recovered sufficiently, and again, PFT criteria are helpful. Intravenous immunoglobulin and plasmapheresis are the cornerstones of specific therapy for both illnesses when complicated by respiratory failure. Mortality and morbidity are dramatically increased by respiratory failure and are mainly due to associated medical complications. Optimal outcomes depend on avoidance of these and prompt implementation of immunomodulatory therapy.
Journal Article↗
Nonconvulsive status epilepticus after subarachnoid hemorrhage.
OBJECTIVE: Although in-hospital seizures have been reported for 3 to 24% of patients with aneurysmal subarachnoid hemorrhage (SAH), nonconvulsive status epilepticus (NCSE) has not been previously described. We sought to determine the frequency and clinical features of NCSE among comatose patients with SAH. METHODS: Between November 1997 and February 2000, we performed continuous electroencephalographic (cEEG) monitoring for at least 24 hours for all patients with aneurysmal SAH who were treated in our neurological intensive care unit and exhibited unexplained coma or neurological deterioration. NCSE was diagnosed when cEEG monitoring demonstrated continuous or repetitive electrographic seizures exceeding 1 hour in duration. Refractory NCSE was treated aggressively with intravenous anticonvulsant administration and continuous-infusion midazolam therapy. RESULTS: Of 233 patients with SAH who survived the first 48 hours of hospitalization, 101 were stuporous or comatose at some point during their hospitalization. Twenty-six of those patients underwent cEEG monitoring, and eight were diagnosed as having NCSE, an average of 18 days (range, 5-38 d) after SAH. All eight patients were receiving prophylactic anticonvulsant therapy. Four patients were persistently comatose and four demonstrated deterioration to stupor or coma; only one exhibited overt tonicoclonic activity. A worst Hunt and Hess grade of IV or V, older age, ventricular drainage, and cerebral edema on computed tomographic scans were identified as risk factors for NCSE (all P < 0.01). NCSE was successfully terminated for five patients (63%), but only one experienced clinical improvement, which was transient; all eight patients eventually died after a period of prolonged coma. CONCLUSION: cEEG monitoring detected NCSE for 8% of patients with SAH and otherwise unexplained coma or neurological deterioration. The seizures were highly refractory to therapy, and the prognosis for these patients was extremely poor. Routine postoperative cEEG monitoring of patients with SAH who are at high risk for NCSE, allowing earlier diagnosis and treatment, offers the best chance of improving the outcomes for patients with this disorder.
Aged↗
Global cerebral edema after subarachnoid hemorrhage: frequency, predictors, and impact on outcome.
BACKGROUND AND PURPOSE: Cerebral edema visualized by CT is often seen after subarachnoid hemorrhage (SAH). Inflammatory or circulatory mechanisms have been postulated to explain this radiographic observation after SAH. We sought to determine the frequency, causes, and impact on outcome of early and delayed global cerebral edema after SAH. METHODS: We evaluated the presence of global edema on admission and follow-up CT scans in 374 SAH patients admitted within 5 days of onset to our Neurological Intensive Care Unit between July 1996 and February 2001. Using multivariate analysis, we identified predictors of global cerebral edema and evaluated the impact of global edema on outcome 3 months after onset with the modified Rankin Scale. RESULTS: Global edema was present on admission CT scans in 8% (n=29) and developed secondarily in 12% (n=44) of the patients. Global edema on admission was predicted by loss of consciousness at ictus and increasing Hunt-Hess grade. Delayed global edema was predicted by aneurysm size >10 mm, loss of consciousness at ictus, use of vasopressors, and increased SAH sum scores. Thirty-seven percent (n=137) of the patients were dead or severely disabled (modified Rankin Scale 4 to 6) at 3 months. Death or severe disability was predicted by any global edema, aneurysm size >10 mm, loss of consciousness at ictus, increased National Institutes of Health Stroke Scale scores, and older age. CONCLUSIONS: Global edema is an independent risk factor for mortality and poor outcome after SAH. Loss of consciousness, which may reflect ictal cerebral circulatory arrest, is a risk factor for admission global edema, and vasopressor-induced hypertension is associated with the development of delayed global edema. Critical care management strategies that minimize edema formation after SAH may improve outcome.
Adolescent↗
Predictors of cognitive dysfunction after subarachnoid hemorrhage.
BACKGROUND: Cognitive dysfunction is a common and disabling sequela of subarachnoid hemorrhage (SAH). Although several clinical and radiographic findings have been implicated in the pathogenesis of cognitive dysfunction after SAH, few prospective studies have comprehensively and simultaneously evaluated these risk factors. METHODS: Between July 1996 and March 2000, we prospectively evaluated 113 of 248 consecutively admitted nontraumatic SAH patients alive at 3 months with a comprehensive neuropsychological evaluation. Summary scores for 8 cognitive domains were calculated to express test performance relative to the entire study population. Clinical and radiographic variables associated with domain-specific cognitive dysfunction were identified with forward stepwise multiple regression, with control for the influence of demographic factors. RESULTS: The study participants were younger (P=0.005), less often white (P=0.006), and had better 3-month modified Rankin scores (P=0.001) than those who did not undergo neuropsychological testing. The proportion of subjects who scored in the impaired range (>2 SD below the normative mean) on each neuropsychological test ranged from 10% to 50%. Predictors of cognitive dysfunction in 2 or more domains in the multivariate analysis included global cerebral edema (4 domains), left-sided infarction (3 domains), and lack of a posterior circulation aneurysm (2 domains). Other variables consistently associated with cognitive dysfunction in the univariate analysis included admission Hunt-Hess grade >2 and thick SAH in the anterior interhemispheric and sylvian fissures. CONCLUSIONS: Global cerebral edema and left-sided infarction are important risk factors for cognitive dysfunction after SAH. Treatment strategies aimed at reducing neurological injury related to generalized brain swelling, infarction, and clot-related hemotoxicity hold the best promise for improving cognitive outcomes after SAH.
Acute Disease↗
Outcome prediction with serum intercellular adhesion molecule-1 levels after aneurysmal subarachnoid hemorrhage.
OBJECT: Although upregulated adhesion molecule expression has been demonstrated in experimental models of subarachnoid hemorrhage (SAH) and in the cerebrospinal fluid of patients with aneurysmal SAH, the clinical significance of these proinflammatory findings remains unclear. The authors hypothesize that 1) serum levels of soluble intercellular adhesion molecule-l (ICAM-1) are increased in all patients with aneurysmal SAH shortly after the hemorrhagic event, and 2) elevated soluble ICAM-1 values are associated with poor patient outcome, even when controlling for the severity of the initial hemorrhagic insult. METHODS: One hundred one patients were prospectively enrolled and stratified according to their admission Hunt and Hess grade and functional status at discharge (modified Rankin Scale [mRS] score). Soluble ICAM-1 levels were determined every other day for 12 days post-SAH by using the enzyme-linked immunosorbent assay. Early soluble ICAM-1 levels (post-SAH Days 2-4) were increased compared with levels in control patients without SAH (p < 0.05). Patients with aneurysmal SAH who had a poor outcome (mRS Grades 4-6) had significantly higher soluble ICAM-1 levels over the first 2 weeks post-SAH compared with patients who had a good outcome (mRS Grades 0-3, p < 0.01). This association with outcome was predicted by late increases (Day 6, p = 0.07; Days 8-12, p < 0.05) rather than early increases (p = not significant) and was best seen in patients with Hunt and Hess Grades I and II. in whom only those with poor outcomes demonstrated delayed ICAM-1 elevations (p < 0.05). CONCLUSIONS: These data demonstrate a correlation between soluble ICAM-1 levels and functional outcome following aneurysmal SAH that appears to be, at least in part, independent of the initial hemorrhage.
Adolescent↗
Rise in serum soluble intercellular adhesion molecule-1 levels with vasospasm following aneurysmal subarachnoid hemorrhage.
OBJECT: Proinflammatory adhesion molecule expression has been demonstrated to be elevated in patients with aneurysmal subarachnoid hemorrhage (SAH). Recent studies have shown that elevations in soluble intercellular adhesion molecule-1 (ICAM-1) may be predictive of poor outcome in patients with good grade (Hunt and Hess Grades 1-2) aneurysmal SAH at delayed time points that correspond with the risk period for cerebral vasospasm. In addition, ICAM-1 is upregulated in experimental models of vasospasm. Unfortunately, the relationship of adhesion molecule expression to human vasospasm remains unclear. The authors hypothesized that the delayed elevation of soluble ICAM-1 in patients with aneurysmal SAH is associated with the development of cerebral vasospasm. METHODS: Eighty-nine patients with aneurysmal SAH were prospectively enrolled in a study and stratified according to the presence or absence of vasospasm, as evidenced by daily monitoring of transcranial Doppler (TCD) velocities (presence, > 200 cm/second; absence, < 120 cm/second). Levels of soluble ICAM-1 were determined using enzyme-linked immunosorbent assay every other day for 12 days post-SAH. An analysis of covariance model was used to evaluate trends in soluble ICAM-1 levels from 2 days prior to 6 days after the occurrence of documented vasospasm. Two groups of patients, matched for admission admission Hunt and Hess grade, were compared: nine patients with TCD velocities greater than 200 cm/second and nine patients with TCD velocities less than 120 cm/second. From among the patients with TCD velocities greater than 200 cm/second six patients with angiographically documented vasospasm were selected. Patients with TCD velocities less than 120 cm/second and matched admission Hunt and Hess grades but without angiographically documented vasospasm were selected. Patients with TCD-demonstrated vasospasm showed a significant mean rate of rise (p < 0.01) in soluble ICAM-1 levels during the perivasospasm period, but admission Hunt and Hess grade-matched control patients did not (p = not significant [NS]). There was a significant difference between these groups' rates of soluble ICAM increase (p < 0.01). Patients with both TCD- and angiographically demonstrated vasospasm likewise showed a highly significant mean rate of increase in soluble ICAM-1 levels during the perivasospasm period (p < 0.01), whereas admission Hunt and Hess grade-matched controls did not (p = NS). The difference beween these groups' rates of increase was highly significant (p < 0.001). CONCLUSIONS: These data suggest a role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae. As this relationship is further elucidated, adhesion molecules such as ICAM-1 may provide novel therapeutic targets in the prevention of vasospasm or its ischemic consequences.
Adult↗
Critical care management of neurologic catastrophes.
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Acute Disease↗