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Biomedical subjects

Edward C Jauch

Publications and source records attributed to Edward C Jauch.

At least 19 recordsLinked to original sources

Association of serial biochemical markers with acute ischemic stroke: the National Institute of Neurological Disorders and Stroke recombinant tissue plasminogen activator Stroke Study.

BACKGROUND AND PURPOSE: Biochemical markers of acute neuronal injury may aid in the diagnosis and management of acute ischemic stroke. Serum samples from the National Institute for Neurological Disorders and Stroke (NINDS) recombinant tissue plasminogen activator Stroke Study were analyzed for the presence of 4 biochemical markers of neuronal, glial, and endothelial cell injury. These biochemical markers, myelin basic protein (MBP), neuron-specific enolase (NSE), S100beta, and soluble thrombomodulin, were studied for an association with initial stroke severity, infarct volume, and functional outcome. METHODS: In the original NINDS study, serum samples were drawn from all patients on presentation to the Emergency Department and at approximately 2 and 24 hours after initiation of study therapy. In this analysis, stored serum samples were available for 359 patients; 107 patients had samples for all 3 time points. Serum marker concentrations were measured by ELISA techniques. We examined the relation between serum concentrations of each marker and the degree of baseline neurological deficit, functional outcome, and infarct size on computed tomography at 24 hours and the effect of fibrinolytic therapy. RESULTS: Higher 24-hour peak concentrations of MBP, NSE, and S100beta were associated with higher National Institutes of Health Stroke Scale baseline scores (r=0.186, P<0.0001; r=0.117, P=0.032; and r=0.263, P<0.0001, respectively). Higher peak concentrations of MBP and S100beta (r=0.209, P<0.0001; r=0.239, P<0.0001) were associated with larger computed tomography lesion volumes. Patients with favorable outcomes had smaller changes in MBP and S100beta (P<0.05) concentrations in the first 24 hours. Soluble thrombomodulin was not associated with any severity or outcome measure. CONCLUSIONS: This study corroborates previous work demonstrating correlations of MBP, NSE, and S100beta with clinical and radiographic features in acute stroke. Despite significantly better outcomes in the tissue plasminogen activator-treated group, we found no difference in the early release of the 4 biomarkers between treatment groups. Further study will define the role of biomarkers in acute stroke management and prognostication.

Acute Disease↗

Lack of evidence for an association between hemodynamic variables and hematoma growth in spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Early hematoma expansion in spontaneous intracerebral hemorrhage (ICH) is associated with worse clinical outcome. We hypothesized that hemodynamic parameters are associated with the increase in hematoma volume owing to their relationship to blood vessel wall stresses. METHODS: We performed a post hoc analysis of clinical and computed tomography (CT) data from patients enrolled in a prospective observational study of ICH patients presenting within 3 hours from symptom onset. Hematoma volumes were measured at hospital arrival and at 1 and 20 hours from presentation. Blood pressure and heart rate, recorded at 19 time points between presentation and 20 hours, were used to derive hemodynamic variables. Multivariable logistic-regression models were constructed to assess the relation between hemodynamic parameters and hematoma growth, adjusted for clinical covariates. RESULTS: From the original study, 98 patients underwent baseline and 1-hour CT scans; of these, 65 had 20-hour CT scans. Substantial hematoma growth was observed in 28% within the first hour. Of the 65 patients not undergoing surgery within 20 hours, 37% experienced hematoma growth by 20 hours. Neither baseline or peak hemodynamic parameters nor changes in hemodynamic parameters were significantly associated with hematoma growth at either 1 or 20 hours. CONCLUSIONS: We found no blood pressure or heart rate parameters, individually or in combination, that were associated with hematoma growth. Our data suggest the influence of hemodynamic parameters on vessel wall stress to be an unlikely target for intervention in reducing the risk of early hematoma growth in ICH.

Cerebral Hemorrhage↗

Gene expression in blood changes rapidly in neutrophils and monocytes after ischemic stroke in humans: a microarray study.

Ischemic brain and peripheral white blood cells release cytokines, chemokines and other molecules that activate the peripheral white blood cells after stroke. To assess gene expression in these peripheral white blood cells, whole blood was examined using oligonucleotide microarrays in 15 patients at 2.4+/-0.5, 5 and 24 h after onset of ischemic stroke and compared with control blood samples. The 2.4-h blood samples were drawn before patients were treated either with tissue-type plasminogen activator (tPA) alone or with tPA plus Eptifibatide (the Combination approach to Lysis utilizing Eptifibatide And Recombinant tPA trial). Most genes induced in whole blood at 2 to 3 h were also induced at 5 and 24 h. Separate studies showed that the genes induced at 2 to 24 h after stroke were expressed mainly by polymorphonuclear leukocytes and to a lesser degree by monocytes. These genes included: matrix metalloproteinase 9; S100 calcium-binding proteins P, A12 and A9; coagulation factor V; arginase I; carbonic anhydrase IV; lymphocyte antigen 96 (cluster of differentiation (CD)96); monocarboxylic acid transporter (6); ets-2 (erythroblastosis virus E26 oncogene homolog 2); homeobox gene Hox 1.11; cytoskeleton-associated protein 4; N-formylpeptide receptor; ribonuclease-2; N-acetylneuraminate pyruvate lyase; BCL6; glycogen phosphorylase. The fold change of these genes varied from 1.6 to 6.8 and these 18 genes correctly classified 10/15 patients at 2.4 h, 13/15 patients at 5 h and 15/15 patients at 24 h after stroke. These data provide insights into the inflammatory responses after stroke in humans, and should be helpful in diagnosis, understanding etiology and pathogenesis, and guiding acute treatment and development of new treatments for stroke.

Adult↗

Management of arterial hypertension in patients with acute stroke.

Management of arterial hypertension in the hyperacute period immediately after stroke ictus remains controversial. Extremes of blood pressure (BP) are associated with poor outcomes in all stroke subtypes. Severely hypertensive patients likely benefit from modest BP reductions, but aggressive BP reduction may worsen outcome. Although little evidence is currently available to definitively establish guideline recommendations for optimal BP goals at stroke presentation, recently published research is shedding some light on how to approach management of BP after stroke. Antihypertensive treatment should probably be deferred in ischemic stroke patients except in cases of severe hypertension or when thrombolytic therapy is warranted and the patient's BP is above acceptable levels. Hypertensive hemorrhagic stroke patients may benefit from modest BP reductions. Relative hypotension causing regional hypoperfusion is an increasingly understood concept immediately following ischemic or hemorrhagic stroke, emphasizing the need for careful titration of appropriate medications to minimize fluctuations in BP for treated patients. Ongoing trials will improve our current knowledge regarding BP management after ischemic and hemorrhagic stroke.

Journal Article↗

Neurologic education in emergency medicine training programs.

OBJECTIVES: Neurologic complaints are a frequent cause of emergency department visits. The morbidity and mortality of neurologic complaints such as headache and stroke can be extensive. Thus, emergency medicine residency programs should ensure adequate training in such neurologic emergencies. The authors sought to determine what methods are being used to educate residents on neurologic emergencies. METHODS: A two-page survey was mailed to directors of all 126 accredited emergency medicine residency programs in the United States. The number and types of lectures to residents, required rotations, and electives offered were assessed. Means, standard deviations (SDs), and proportions are used to describe the data. Ninety-five percent confidence intervals of proportions (95% CIs) were calculated. RESULTS: The response rate was 78% (98 of 126). Programs had a mean (+/- SD) of 5.4 (+/- 1.0) hours of didactic lectures per week, with a mean of 12.0 (+/- 5.9) lecture hours devoted to neurologic emergencies annually. A neurology rotation was required for 16 of the 92 programs providing these data (17.4%; 95% CI = 10.6% to 27.0%), and a neurosurgery rotation was required for 14 of these 92 programs (15.2%; 95% CI = 8.9% to 24.6%). One program (1.1%; 95% CI = 0.1% to 6.8%) required both a neurology and a neurosurgery rotation, and one program (1.1%; 95% CI = 0.1% to 6.8%) required either a neurology or a neurosurgery rotation. On 15 of the 32 required neurologic rotations (46.9%; 95% CI = 29.5% to 65.0%), time was spent only in the intensive care unit. The remaining 17 rotations used outpatient clinic and general floor neurology settings. Electives in neurology, neurosurgery, or neuroradiology were available for 32 programs (32.7%; 95% CI = 24.2% to 42.4%) but were seldom used. CONCLUSIONS: Currently, the primary method of educating residents to treat neurologic emergencies is through didactic lectures, as opposed to clinical rotations in neurology or neurosurgery. Improving resident education in neurologic emergencies within the current educational format must focus on improving didactic lectures in neurologic topics. Expanding clinical rotations or electives to enhance education in neurologic emergencies also warrants future attention.

Curriculum↗

Hypercholesterolemia, HMG-CoA reductase inhibitors, and risk of intracerebral hemorrhage: a case-control study.

BACKGROUND AND PURPOSE: Several studies have demonstrated an association between hypocholesterolemia and intracerebral hemorrhage (ICH). We tested the hypothesis that hypercholesterolemia or use of HMG-CoA reductase inhibitors (statin) agents, or both, are associated with ICH. METHODS: This study was part of the preplanned midway analysis of an ongoing, population-based, case-control study of the genetic and environmental risk factors of hemorrhagic stroke. Conditional stepwise logistic regression modeling was used to determine if self-reported hypercholesterolemia or statin use, or both, were independent risk factors for ICH. RESULTS: Between December 1, 1997, and June 30, 2000, 188 cases of ICH and 366 age-, race-, and gender-matched controls were enrolled. Hypercholesterolemia and statin use were less common among cases than controls: 25% versus 38% (P=0.003) and 9% versus 17% (P=0.03), respectively. Hypercholesterolemia with statin use was associated with less risk of ICH (OR=0.30; P=0.0008) in multivariable analysis after controlling for alcohol use, hypertension, previous stroke, first-degree relative with ICH, education level, and apolipoprotein E alleles. CONCLUSIONS: Hypercholesterolemia was associated with a lower risk of ICH. We have not found an increased risk of ICH with the widespread use of statins in our population. Given the lack of cholesterol levels in the current study, further studies are needed to determine if lower cholesterol levels secondary to statin use bear the same risk as low cholesterol levels for ICH.

Aged↗

Effect of education and guidelines for treatment of uncomplicated dental pain on patient and provider behavior.

STUDY OBJECTIVE: Patients with uncomplicated odontalgia use a significant proportion of emergency department (ED) resources. Some odontalgia patients are unaware that routine dental care is unavailable in most EDs. Using extensive input from regional dentists and oral surgeons, and after reviewing the dental literature, guidelines for the ED management of uncomplicated odontalgia were written for physician and patient use. The guidelines, which emphasize appropriate community dental clinic referrals and the use of nonsteroidal anti-inflammatory drugs, were developed to reflect community standard of care. We hypothesize that patient education and treatment guidelines will decrease the number of ED visits, return visits, and narcotic prescriptions written for odontalgia. METHODS: This retrospective, observational study used primary International Classification of Diseases, Ninth Revision codes to identify visits for odontalgia during the year before and the year after guideline implementation in a tertiary care teaching hospital with 161,181 ED visits during the 2-year period of our study. RESULTS: There were 5,930 visits for odontalgia during the study. The proportion (95% confidence interval [CI]) of visits with odontalgia decreased after guideline implementation from 4.3% (95% CI 4.2% to 4.5%) to 3.1% (95% CI 3.0% to 3.2%). The proportion of patients with return visits decreased from 19.8% (95% CI 18.1% to 21.6%) to 9.2% (95% CI 7.9% to 10.8%). The proportion of patients filling narcotic prescriptions for odontalgia decreased from 29.6% (95% CI 28.1% to 31.2%) to 9.5% (95% CI 8.5% to 10.8%). CONCLUSION: Implementing odontalgia guidelines and providing patients with written information about alternative treatments and a list of dental clinics can reduce the burden of uncomplicated odontalgia on EDs that do not provide routine dental care.

Adult↗

Bilirubin as a cerebrospinal fluid marker of sentinel subarachnoid hemorrhage: a preliminary report in pigs.

OBJECT: A model of subarachnoid hemorrhage (SAH) in pigs was developed to investigate bilirubin concentration in cerebrospinal fluid (CSF) as a potential marker of sentinel SAH. METHODS: Seven male Yorkshire pigs received a 250-microl injection of either whole autologous arterial blood (four animals) or isotonic saline (three animals) into the cisternae magna in an effort to produce volumetrically a model of sentinel SAH and a control injection model, respectively. Cerebrospinal fluid volumes of 100 microl were then collected from both the lumbar cistern and cisternae magna at 1 to 2-hour intervals for a total of 24 hours postinjection. The CSF was then tested for bilirubin. Mean concentrations of bilirubin (+/- standard deviation [SD]) obtained from the lumbar cistern 24 hours following the injection of blood or saline were 4.38 +/- 1.04 microM in the SAH animals and 1.02 +/- 0.05 microM in the controls. At 24 hours postinjection, mean concentrations (+/- SD) of cisternae magna bilirubin were 7.29 +/- 1.33 microM and 1.33 +/- 0.14 microM in the SAH animals and controls, respectively. In the SAH group, both the lumbar cistern and cisternae magna bilirubin concentrations differed significantly from baseline values 12 hours following SAH. CONCLUSIONS: Elevated concentrations of CSF bilirubin can be detected following a low-volume SAH, and the production of bilirubin occurred over a predictable time course. Twelve hours after hemorrhage, an elevated CSF bilirubin concentration was an indicator of hemolysis occurring in the subarachnoid spaces. The presence of bilirubin in CSF is a potential marker for differentiating SAHs from traumatic lumbar punctures in humans.

Animals↗

A case of Lemierre's syndrome.

Lemierre's syndrome is a rare but potentially life-threatening entity that follows an oropharyngeal infection. The syndrome is characterized by an antecedent acute oropharyngeal infection, with secondary suppurative thrombophlebitis of the internal jugular vein and septic emboli. In the pre-antibiotic era, it had a 90% mortality rate. Now, with the advent of antibiotics, the prognosis is favorable, but delays in diagnosis may result in increased morbidity and mortality. Its incidence appears to be increasing. We present a case of Lemierre's syndrome, most notable for the patient's essentially benign physical examination and lack of clinical improvement with penicillin.

Adolescent↗

C-tau biomarker of neuronal damage in severe brain injured patients: association with elevated intracranial pressure and clinical outcome.

Following traumatic brain injury, the neuronally-localized intracellular protein MAP-tau is proteolytically cleaved (C-tau) and gains access to cerebrospinal fluid (CSF) and serum. The present study compared initial CSF C-tau levels, initial Glasgow Coma Scale (GCS) scores and elevated intracranial pressure (ICP) as predictors of clinical outcome. In this preliminary, prospective study of consecutive severe traumatic brain injured patients (TBI) clinical outcome was quantified with the Glasgow Outcome Scale (GOS) at discharge (n=28). Sensitivity and specificity of initial C-tau levels and initial GCS scores as predictors of clinical outcome is reported. To assess disease specificity C-tau levels were compared between TBI patients and neurologic (n=87) and non-neurologic control patients (n=67). Initial CSF C-tau levels were elevated 40,000 fold in TBI patients compared to either neurologic or non-neurologic control patients (P<0.001). Initial C-tau levels were correlated with clinical outcome (P=0.006) and were a significant predictor of dichotomized clinical outcome (P=0.011) demonstrating a sensitivity of prediction of 92% and a specificity of 94%. Initial C-tau levels were also a significant predictor of subsequent ICP with higher initial C-tau levels associated with elevated ICP (P=0.014). Initial GCS score were correlated with clinical outcome (P=0.026) and demonstrated a sensitivity of 50% and a specificity of 100% for predicting dichotomized clinical outcome. Statistical analysis indicated that initial C-tau levels and initial GCS scores were independent predictors of clinical outcome. The present preliminary study demonstrates that initial CSF C-tau levels are a significant predictor of ICP and clinical outcome with particular sensitivity for identifying severe TBI patients with good clinical outcome. Future studies employing a larger sample size and clinical outcome assessment at longer periods after hospitalization will be needed to determine the utility of initial C-tau levels as a clinical biomarker in TBI.

Adolescent↗

Isoforms of apolipoprotein E can modulate tPA-induced clot lysis in vitro.

Apo E, and its respective isoforms, have been linked to outcome and survival in cerebral vascular and cardiovascular diseases. The effectiveness of intravenous tPA in patients with acute ischemic stroke appears to be enhanced in patients who have an Apo E2 phenotype. The ability of Apo E isoproteins (endogenous Apo E isoproteins or exogenous Apo E isoproteins) to modulate tPA-induced clot lysis in vitro was assessed using an in vitro clot assay system. Blood samples were obtained from 18-volunteers with three Apo E genotypes: E2, E3 and E4. tPA-induced clot lysis (0-4 microgram/ml tPA), was assessed in the presence or absence of supplemental Apo E2, E3 or E4 (9.8 microgram/ml). tPA-induced clot lysis was significantly (P equal or less than 0.0001) enhanced by supplementation with Apo E2 (EC50 0.20 0.06 microgram/ml) as compared to tPA alone (0.72 0.19). Apo E4 supplementation caused a significant (P < or = 0.05) inhibition of clot lysis (0.98 0.23), but there was no significant change caused by Apo E3. The genotype of the volunteer did not significantly affect the ability of the supplemental Apo E from modulating tPA-induced clot lysis. We conclude that the administration of Apo E isoproteins can modulate clot lysis in vitro. Our results suggest that the Apo E isoprotein may have an impact on clot dissolution and the effectiveness of thrombolytic therapy.

Apolipoprotein E2↗

Supplemental oxygen use in ischemic stroke patients: does utilization correspond to need for oxygen therapy?

BACKGROUND: In 1994, the American Heart Association Stroke Council concluded that there were no data to support the routine use of supplemental oxygen in patients who had a stroke. More recently, supplemental oxygen has been suggested to be potentially detrimental. The purpose of this study was to determine the extent of oxygen use in ischemic stroke patients and whether patients receiving oxygen had indications for its use. METHODS: A literature search was performed to generate a comprehensive list of explicit criteria for supplemental oxygen use. When the literature disagreed, the criteria were included in the list to overestimate rather than underestimate the justification for oxygen use. A retrospective chart review of consecutive, nonintubated, ischemic stroke patients admitted to a university hospital was performed. Statistical tests and logistic regression models were constructed to identify the presence of unjustified oxygen use within the sample. Hospital charges were used to quantify opportunities for resource conservation. RESULTS: A total of 167 patient charts were reviewed yielding a total of 600 inpatient days abstracted. One hundred two patients (61.1%) received oxygen during some portion of their hospitalization. Of the 322 days that patients received oxygen, 147 (45.6%) met at least 1 criterion for oxygen use. Of the 278 days that patients did not receive oxygen, 69 (24.8%) met at least 1 of the criteria for oxygen use. There were 384 days for which no criteria were met. Of these, a patient still received oxygen 45.6% of the time (175 days). Factors associated with oxygen use included the presence of at least 1 justifying criteria as well as increasing age and male sex. Withholding oxygen from those not medically justified by the criteria could produce resource savings of roughly 45%. CONCLUSIONS: Using a literature-based list of criteria for supplemental oxygen use, only 45.6% of days of oxygen use were justified in our ischemic stroke population. This study demonstrates that oxygen therapy is commonly given to ischemic stroke patients without clear indication, and opportunities exist for substantial resource conservation.

Age Factors↗

Emergency stroke management: a new era.

This article discusses the recent advances and the current state of treatment of acute stroke. It outlines key components to ensure stroke victims receive emergent treatment in a coordinated and comprehensive healthcare delivery system.

Algorithms↗

Acute ischemic stroke: emergent evaluation and management.

This article discusses stroke, the third leading cause of death and number one cause of adult disability in the United States, inflicting a devastating physical, emotional, and financial toll on its victims and their families. The last decade has seen the emergence of new treatments for acute stroke, energizing stroke care providers and spreading a sense of optimism among them. Because effective stroke treatment is extremely time-dependent, it is paramount that emergency physicians understand and excel in their critical role at the forefront of stroke management. This article outlines the emergent evaluation and management of acute ischemic stroke, emphasizing the importance of the emergency physician in acute stroke treatment.

Anticoagulants↗