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Search Results: 1 - 10 of 465739 matches for " Stephan A Mayer "
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Clinical review: Critical care management of spontaneous intracerebral hemorrhage
Fred Rincon, Stephan A Mayer
Critical Care , 2008, DOI: 10.1186/cc7092
Abstract: Intracerebral hemorrhage (ICH) is defined as the spontaneous extravasation of blood into the brain parenchyma. Non-traumatic forms of ICH account for 10% to 30% of all stroke hospital admissions [1], leading to catastrophic disability, morbidity, and a mortality of 30% to 50% at 30 days [1]. Death at 1 year varies by different location: 51% for deep, 57% for lobar, 42% for cerebellar and 65% for brain stem hemorrhages [2]. In a recent population-based study, the overall incidence of ICH was estimated to be 12 to 15 cases per 100,000 population [3]. The cost of ICH alone is estimated to be USD $125,000 per person per year, with a total cost of USD $6 billion per year in the United States alone [4,5] related to both acute and chronic medical care costs, as well as the loss of productivity.Depending on the underlying cause of hemorrhage, ICH may be classified as primary when it originates from the spontaneous rupture of small arterioles damaged by chronic hypertension or cerebral amyloid angiopathy, representing at least 85% of all cases; or secondary when associated with vascular malformations, bleeding related to an ischemic stroke, tumors, abnormal coagulation [6,7], trauma [8], or vasculitis. In approximately 40% of the cases, blood may also extend into the ventricles – intra-ventricular hemorrhage (IVH) – potentially leading to neurological death related to acute obstructive hydrocephalus resulting in a substantial worsening of the prognosis.Despite ongoing attempts to find effective interventions based on the physiopathological understanding of this disease, options are limited, and outcomes remain poor. Evidence-based medical therapies for ICH are limited to guidelines or options regarding blood pressure (BP) reduction, intracranial pressure (ICP) monitoring, osmotherapy with adequate fluid resuscitation, fever and glycemic control, seizure prophylaxis, and care in a specialized stroke or neurological intensive care unit (ICU) [9]. Recently published guidelines
Can a simple blood test quantify brain injury?
Stephan A Mayer, Guillermo Linares
Critical Care , 2009, DOI: 10.1186/cc7929
Abstract: The first decade of the 21st century has witnessed explosive growth in therapies for the critically ill neurological patient. Some of these treatments, such as the use of recombinant tissue plasminogen activator for the treatment of acute cerebral infarction, target very specific pathogenic pathways. Others, such as hypothermia for the treatment of brain injury after cardiac arrest, have multiple additive and synergistic mechanisms of action that culminate in the protection of nervous tissue. To guide these treatments, technological advances in imaging and neuromonitoring can now provide a window into the metabolic and physiologic status of the injured brain, allowing us to evaluate the effect of our therapeutic interventions in real time.Despite these promising advances, it remains difficult to precisely measure the extent of neurological injury in patients affected by stroke, trauma, or cardiac arrest. In the intensive care unit, where neurological deterioration is often obscured by encephalopathy or sedative medications, determination of the extent of primary and secondary injury often eludes clinicians, making prognostication imprecise and difficult.For decades, researchers have sought clinically useful biomarkers of nervous system injury, and these efforts have intensified in the past few years. Early candidates for brain injury biomarkers included lactate dehydrogenase and creatinine kinase enzyme subtypes in the serum and cerebrospinal fluid. These proved to be of little use given their lack of specificity for nervous tissue injury. The ideal biomarker would be highly sensitive and specific for neurological injury, rapidly available from the serum or other easily obtained body fluid other than cerebrospinal fluid, and released in proportion to the severity of the injury, with little variability across different diagnostic and demographic groups.Although the ideal biomarker remains elusive, several different molecules have shown promise. Of these, neuron speci
Brain injury clinical trials: new agents or new statistics?
Joshua Z Willey, Stephan A Mayer
Critical Care , 2011, DOI: 10.1186/cc10350
Abstract: The results of clinical trials for brain injury, be it stroke or trauma, have tended to follow the same pattern: animal model, preclinical, and phase II studies all show great promise only to be followed by the disappointment of a negative phase III trial. Dozens of negative clinical trials for stroke and traumatic brain injury (TBI) have been published, and we are left with few, if any, pharmaco-logical treatment options, particularly for neuroprotection.Several hypotheses have been proposed to explain why the majority of neuroprotective agents have failed to show benefit in clinical trials. These include lack of a meaningful biological treatment effect, unrealistically prolonged windows of time, lack of sufficient statistical power, or the choice of an inadequate or inappropriate outcome or statistical analysis plan. Roozenbeek and colleagues [1], in a previous issue of Critical Care, addressed the last of these concerns. The authors examined data from the Corticosteroid Randomization After Significant Head Injury (CRASH) trial [2,3] to illustrate how alternative methodological and statistical analyses increase statistical power, reduce sample size requirements, and allow efficacy to be detected.Like those who have conducted analyses for other agents for TBI [4] and stroke [5], the authors evaluated two different statistical methods: proportional odds logistic regression (a type of polytomous logistic regression) and the sliding-dichotomy approach. Both methods have been used in epidemiological studies [6] and increasingly in clinical trials [7-9]. They have common strengths, including accounting for floor and ceiling effects in a chosen outcome, improved statistical power, and accounting for variation in the quality and range of recovery after brain injury. A lot of clinically relevant information is lost when clinical efficacy is evaluated as a simple yes/no outcome.In proportional odds logistic regression, outcomes are not treated as binary but as distributions
The effect of window rooms on critically ill patients with subarachnoid hemorrhage admitted to intensive care
Hannah Wunsch, Hayley Gershengorn, Stephan A Mayer, Jan Claassen
Critical Care , 2011, DOI: 10.1186/cc10075
Abstract: This was a secondary analysis of a prospective cohort study. Seven ICU rooms had windows, and five ICU rooms did not. Admission to a room was based solely on availability.We analyzed data from 789 patients with subarachnoid hemorrhage (SAH) admitted to the neurological ICU at our hospital from August 1997 to April 2006. Patient information was recorded prospectively at the time of admission, and patients were followed up to 1 year to assess mortality and functional status, stratified by whether care was received in an ICU room with a window.Of 789 SAH patients, 455 (57.7%) received care in a window room and 334 (42.3%) received care in a nonwindow room. The two groups were balanced with regard to all patient and clinical characteristics. There was no statistical difference in modified Rankin Scale (mRS) score at hospital discharge, 3 months or 1 year (44.8% with mRS scores of 0 to 3 with window rooms at hospital discharge versus 47.2% with the same scores in nonwindow rooms at hospital discharge; adjusted odds ratio (aOR) 1.01, 95% confidence interval (95% CI) 0.67 to 1.50, P = 0.98; 62.7% versus 63.8% at 3 months, aOR 0.85, 95% CI 0.58 to 1.26, P = 0.42; 73.6% versus 72.5% at 1 year, aOR 0.78, 95% CI 0.51 to 1.19, P = 0.25). There were also no differences in any secondary outcomes, including length of mechanical ventilation, time until the patient was able to follow commands in the ICU, need for percutaneous gastrostomy tube or tracheotomy, ICU and hospital length of stay, and hospital, 3-month and 1-year mortality.The presence of a window in an ICU room did not improve outcomes for critically ill patients with SAH admitted to the ICU. Further studies are needed to determine whether other groups of critically ill patients, particularly those without acute brain injury, derive benefit from natural light.Natural light can be helpful for treating jet lag and insomnia [1,2], seasonal affective disorder and nonseasonal depression [3,4,3]. Light may also improve outcomes
Amyloid β-Related Angiitis Causing Coma Responsive to Immunosuppression
Shennan A. Weiss,David Pisapia,Stephan A. Mayer,Joshua Z. Willey,Kiwon Lee
Case Reports in Pathology , 2012, DOI: 10.1155/2012/678746
Abstract: Introduction. Amyloid-beta-related angiitis (ABRA) is a form of CNS vasculitis in which perivascular beta-amyloid in the intracerebral vessels is thought to act as a trigger for inflammation mediated by CD68
Amyloid β-Related Angiitis Causing Coma Responsive to Immunosuppression
Shennan A. Weiss,David Pisapia,Stephan A. Mayer,Joshua Z. Willey,Kiwon Lee
Case Reports in Pathology , 2012, DOI: 10.1155/2012/678746
Abstract: Introduction. Amyloid-beta-related angiitis (ABRA) is a form of CNS vasculitis in which perivascular beta-amyloid in the intracerebral vessels is thought to act as a trigger for inflammation mediated by CD68+ macrophages and CD3+ T lymphocytes. Patients with severe ABRA may develop coma responsive to immunosuppressive treatment. Case Presentation. A 57-year-old man presented to the neurological intensive care unit febrile, obtunded, and with a left hemiparesis. He had suffered from intermittent left arm weakness and numbness for several months prior. Serum and cerebrospinal fluid studies showed a lymphocytic leukocytosis in the cerebrospinal fluid (CSF), but no other evidence of infection, and the patient underwent a brain biopsy. Histopathological examination demonstrated amyloid angiopathy, with an extensive perivascular lymphocytic infiltrate, indicative of ABRA. The patient was started on cyclophosphamide and steroids. Following a week of treatment he awakened and over several weeks made a significant neurological recovery. Conclusions. ABRA can have a variety of clinical presentations, including impairments in consciousness and coma. Accurate pathological diagnosis, followed by aggressive immunosuppression, can lead to impressive neurological improvements. This diagnosis should be considered in patients with paroxysmal recurrent neurological symptoms and an accelerated progression. 1. Introduction Deposition of beta-amyloid in the cerebral vasculature affects 30% of the healthy elderly and 90% of those with Alzheimer’s disease [1]. This process has been termed amyloid angiopathy and is a recognized cause of cerebral microhemorrhages and cerebral lobar hemorrhages. Amyloid-beta-related angiitis (ABRA) is a rare complications of amyloid angiopathy and is considered a form of CNS angiitis in which perivascular of beta-amyloid is thought to act as a trigger for inflammation [2]. Primary CNS vasculitis, encompassing all subtypes including ABRA, is rare occurring in 2.4 cases per 1,000,000 patient years [3]. We describe a patient with ABRA who was comatosed and responded to aggressive immunosuppression. 2. Case Presentation A 57-year-old man with a past history of hypertension, diabetes mellitus type 2, hyperlipidemia, and crack cocaine use was admitted to a community hospital for flu like symptoms of one-week duration and ongoing paroxysmal episodes of left hand numbness and weakness occurring over several months. In the emergency department patient was febrile to 38.9°C. He had a slight peripheral white count and CSF demonstrated a lymphocytic
Ethics roundtable: 'Open-ended ICU care: Can we afford it?'
David Crippen, Dick Burrows, Nino Stocchetti, Stephan A Mayer, Peter Andrews, Tom Bleck, Leslie Whetstine
Critical Care , 2010, DOI: 10.1186/cc8962
Abstract: A fundamental tenet of legal justice is that it is better to let ten guilty men go free than convict one innocent man. The reciprocal in medicine is that it is better to artificially maintain life in ten death spirals than miss one expected survivor. Physicians are famous for ignoring impediments to the care of their individual patients. No long-shot treatment is shelved and no expense is spared no matter how dim the potential outcome. A righteous contempt is shown toward administrative pleas to consider cost.In the past, this strategy worked only as well as the ability of the resource allocation system providing for it: an open-ended credit card with an unclear path to replete funds. Now we are seeing strong evidence of a new health care allocation system that will create a closed system whereby excising some portions of the pie directly affects the size of the other portions. The bigger some portions get, the fewer are available.The amount of money spent on end-of-life care, specifically dying at the end of life, dwarfs other expenditures. And the unique situation of critical care will create a double dip for each patient maintained on artificial life support. If we are willing to maintain 100 moribund patients in ICUs for a prolonged period to yield one long-shot survivor, we do not pay for just the survivor. We pay also to warehouse the other 99 failures not quite dead or alive but with stable vital signs.Since it is difficult to know on admission which patients will benefit from life-supporting organ failure reversal, we admit all comers for a trial. Now comes a logical extension of that policy. At any time in the course of treatment, it is equally difficult to predict outcome, so we should maintain most if not all moribund patients indefinitely to avoid killing the occasional unexpectedly survivor.In the case presented here, we have a long-term ICU patient with a small but potentially survivable prognosis on a seemingly endless course of life support. Ten year
Nutritional support and brain tissue glucose metabolism in poor-grade SAH: a retrospective observational study
J Michael Schmidt, Jan Claassen, Sang-Bae Ko, Hector Lantigua, Mary Presciutti, Kiwon Lee, E Sander Connolly, Stephan A Mayer, David S Seres, Neeraj Badjatia
Critical Care , 2012, DOI: 10.1186/cc11160
Abstract: We used a retrospective observational cohort study of 50 mechanically ventilated poor-grade (Hunt-Hess 4 or 5) aneurysmal SAH patients who underwent brain microdialysis monitoring for an average of 109 hours. Enteral nutrition was started within 72 hours of admission whenever feasible. Intensive insulin therapy was used to maintain serum glucose levels between 5.5 and 7.8 mmol/l. Serum glucose, insulin and caloric intake from enteral tube feeds, dextrose and propofol were recorded hourly. Cerebral metabolic distress was defined as a lactate to pyruvate ratio (LPR) > 40. Time-series data were analyzed using a general linear model extended by generalized estimation equations (GEE).Daily mean caloric intake received was 13.8 ± 6.9 cal/kg and mean serum glucose was 7.9 ± 1 mmol/l. A total of 32% of hourly recordings indicated a state of metabolic distress and < 1% indicated a state of critical brain hypoglycemia (< 0.2 mmol/l). Calories received from enteral tube feeds were associated with higher serum glucose concentrations (Wald = 6.07, P = 0.048), more insulin administered (Wald = 108, P < 0.001), higher body mass index (Wald = 213.47, P < 0.001), and lower body temperature (Wald = 4.1, P = 0.043). Enteral feeding (Wald = 1.743, P = 0.418) was not related to brain glucose concentrations after accounting for serum glucose concentrations (Wald = 67.41, P < 0.001). In the presence of metabolic distress, increased insulin administration was associated with a relative reduction of interstitial brain glucose concentrations (Wald = 8.26, P = 0.017), independent of serum glucose levels.In the presence of metabolic distress, insulin administration is associated with reductions in brain glucose concentration that are independent of serum glucose levels. Further study is needed to understand how nutritional support and insulin administration can be optimized to minimize secondary injury after subarachnoid hemorrhage.Hyperglycemia, defined as serum glucose > 11 mmol/l after suba
Effects of the neurological wake-up test on clinical examination, intracranial pressure, brain metabolism and brain tissue oxygenation in severely brain-injured patients
Raimund Helbok, Pedro Kurtz, Michael J Schmidt, Morgan R Stuart, Luis Fernandez, Sander E Connolly, Kiwon Lee, Erich Schmutzhard, Stephan A Mayer, Jan Claassen, Neeraj Badjatia
Critical Care , 2012, DOI: 10.1186/cc11880
Abstract: This prospective observational study was performed in a neuroscience intensive care unit in a tertiary-care academic center. Twenty consecutive severely brain-injured patients with multimodal neuromonitoring were analyzed for levels of brain lactate, pyruvate and glucose, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and brain tissue oxygen tension (PbtO2) during IS trials.Of the 82 trial days, 54 IS-trials were performed as interruption of sedation and analgesics were not considered safe on 28 days (34%). An increase in the FOUR Score (Full Outline of UnResponsiveness score) was observed in 50% of IS-trials by a median of three (two to four) points. Detection of a new neurologic deficit occurred in one trial (2%), and in one-third of IS-trials the trial had to be stopped due to an ICP-crisis (> 20 mmHg), agitation or systemic desaturation. In IS-trials that had to be aborted, a significant increase in ICP and decrease in PbtO2 (P < 0.05), including 67% with critical values of PbtO2 < 20 mmHg, a tendency to brain metabolic distress (P < 0.07) was observed.Interruption of sedation revealed new relevant clinical information in only one trial and a large number of trials could not be performed or had to be stopped due to safety issues. Weighing pros and cons of IS-trials in patients with acute brain injury seems important as related side effects may overcome the clinical benefit.Titrating sedatives and analgesics to achieve the right balance between deep sedation and wakefulness and to ameliorate patients' comfort in the intensive care unit (ICU) is an integral part of critical care [1]. Over-sedation can lead to prolonged duration of mechanical ventilation and ICU stay and increase the incidence of secondary complications, including nosocomial infections and delirium.Daily interruption of sedation trials (IS-trials) have been implemented in many surgical and medical ICUs after randomized controlled trials demonstrated that IS decreased the duration of
Tonic-Clonic Activity at Subarachnoid Hemorrhage Onset: Impact on Complications and Outcome
Gian Marco De Marchis, Deborah Pugin, Hector Lantigua, Christopher Zammit, Prasanna Tadi, J. Michael Schmidt, M. Cristina Falo, Sachin Agarwal, Stephan A. Mayer, Jan Claassen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071405
Abstract: Objective Tonic-clonic activity (TCA) at onset complicates 3% to 21% of cases of subarachnoid hemorrhage (SAH). The impact of onset TCA on in-hospital complications, including seizures, remains unclear. One study associated onset TCA with poor clinical outcome at 6 weeks after SAH, but to our knowledge no other studies have confirmed this relationship. This study aims to assess the impact of onset TCA on in-hospital complications, poor functional outcome, mortality, and epilepsy at 3 months. Methods Analysis of a prospective study cohort of 1479 SAH patients admitted to Columbia University Medical Center between 1996 and 2012. TCA within 6 hours of hemorrhage onset was identified based on accounts of emergency care providers or family witnesses. Results TCA at onset was described in 170 patients (11%). Patients with onset TCA were younger (P = 0.002), presented more often with poor clinical grade (55% vs. 26%, P<0.001) and had larger amounts of cisternal, intraventricular, and intracerebral blood than those without onset TCA (all, P<0.001). After adjusting for known confounders, onset TCA was significantly associated with in-hospital seizures (OR 3.80, 95%-CI: 2.43–5.96, P<0.001), in-hospital pneumonia (OR 1.56, 95%-CI: 1.06–2.31, p = 0.02), and delayed cerebral ischemia (OR 1.77, 95%-CI: 1.21–2.58, P = 0.003). At 3 months, however, onset TCA was not associated with poor functional outcome, mortality, and epilepsy after adjusting for age, admission clinical grade, and cisternal blood volume. Conclusions Onset TCA is not a rare event as it complicates 11% of cases of SAH. New and clinically relevant findings are the association of onset TCA with in-hospital seizures, pneumonia and delayed cerebral ischemia. Despite the increased risk of in-hospital complications, onset TCA is not associated with disability, mortality, and epilepsy at 3 months.
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