Background: Assessment of medical students in the clinical learning environment is fraught with challenges. Seemingly small variations in clinical clerkship evaluation can significantly impact a student's future. As such, the integrity of the grade selection process must be heavily scrutinized.
View Article and Find Full Text PDFCurrent advanced cardiac life support (ACLS) guidelines for the management of ventricular fibrillation (VF) and pulseless ventricular tachycardia is defibrillation. However, refractory VF, which is defined as VF that persists despite three defibrillation attempts, is challenging for all ACLS providers; the best resuscitation strategy for patients that persist in refractory VF remains unclear. We report on a 51-year-old man who presented to the emergency department with chest pain and subsequently went into witnessed VF cardiac arrest.
View Article and Find Full Text PDFObjectives: The History, Electrocardiography, Age, Risk factors, Troponin (HEART) score enables rapid risk stratification of emergency department patients presenting with chest pain. However, the subjectivity in scoring introduced by the history component has been criticized by some clinicians. We examined the association of 3 objective scoring models with the results of noninvasive cardiac testing.
View Article and Find Full Text PDFThe authors have investigated the incidence of acute kidney injury (AKI) and short-term mortality following an activated STEMI and stroke alert at a tertiary referral and academic center. A single center, retrospective chart review of STEMI and stroke activation patients from January 2010 to March 2012. Data was collected and reviewed from an institutional database following IRB-approval.
View Article and Find Full Text PDFWilms tumor is found in 1 in 10,000 children and most commonly presents in asymptomatic toddlers whose care givers notice a nontender abdominal mass in the right upper quadrant. This case of Wilms tumor presented as a critically ill eleven-year old with significant tachypnea, dyspnea, vague abdominal pain, intermittent emesis, new onset seizure, metabolic acidosis, and hypoxemia. This is the first case in the literature of Wilms Tumor with cavoatrial involvement and seizure and pulmonary embolism resulting in aggressive resuscitation and treatment.
View Article and Find Full Text PDFObjectives: The administration of empiric systemic anticoagulation (ESA) before confirmatory radiographic testing in patients with suspected pulmonary embolism (PE) may improve outcomes, but no data have been published regarding current practice. We describe the use of ESA in a large prospective cohort of emergency department (ED) patients and report the outcomes of those treated with ESA compared with patients not receiving ESA.
Methods: 12-center, noninterventional study of ED patients who presented with symptoms concerning for PE.
Right ventricular (RV) dysfunction contributes to poor clinical prognosis after pulmonary embolism (PE). The present studies evaluate the effects of angiotensin (1-7) (ANG (1-7)) upon RV function during experimental PE in rats. Circulating ANG II increased 8-fold 6 hr after PE (47±13 PE vs.
View Article and Find Full Text PDFPulmonary embolism (PE) causes pulmonary hypertension by mechanical obstruction and constriction of non-obstructed vasculature. We tested if experimental PE impairs pulmonary vascular endothelium-dependent dilation via activation of arginase II. Experimental PE was induced in male Sprague-Dawley rats by infusing 25 μm microspheres in the right jugular vein, producing moderate pulmonary hypertension.
View Article and Find Full Text PDFBackground: The right ventricle normally operates as a low pressure, high-flow pump connected to a high-capacitance pulmonary vascular circuit. Morbidity and mortality in humans with pulmonary hypertension (PH) from any cause is increased in the presence of right ventricular (RV) dysfunction, but the differences in pathology of RV dysfunction in chronic versus acute occlusive PH are not widely recognized.
Methods And Results: Chronic PH that develops over weeks to months leads to RV concentric hypertrophy without inflammation that may progress slowly to RV failure.
Background: Patients identified with sepsis in the emergency department often are treated on the basis of the presumption of infection; however, various noninfectious conditions that require specific treatments have clinical presentations very similar to that of sepsis. Our aim was to describe the etiology of illness in patients identified and treated for severe sepsis in the emergency department.
Methods: We conducted a prospective observational study of patients treated with goal-directed resuscitation for severe sepsis in the emergency department.
Background: Acute pulmonary embolism (PE) causes pulmonary hypertension (PH) via several mechanisms including pulmonary vasospasm. We hypothesize that PE with associated PH leads to alterations in plasma protein concentrations indicative of disease severity and prognosis.
Objective: To identify plasma proteins altered in abundance by PE in rats.
Introduction: Early structured resuscitation of severe sepsis has been suggested to improve short term mortality; however, no previous study has examined the long-term effect of this therapy. We sought to determine one year outcomes associated with implementation of early goal directed therapy (EGDT) in the emergency department (ED) care of sepsis.
Methods: We performed a longitudinal analysis of a prospective before and after study conducted at a large urban ED.
Study Objective: Acute pulmonary embolism can produce abnormalities on ECG that reflect severity of pulmonary hypertension. Early recognition of these findings may alter the estimated pretest probability of pulmonary embolism and prompt more aggressive treatment before hemodynamic instability ensues, but it is first important to test whether these findings are specific to patients with pulmonary embolism. We hypothesize that ECG findings consistent with pulmonary hypertension would be observed more frequently in patients with pulmonary embolism.
View Article and Find Full Text PDFBackground: No published data have systematically documented pulmonary artery pressure over an intermediate time period after submassive pulmonary embolism (PE). The aim of this work was to document the rate of pulmonary hypertension, as assessed noninvasively by estimated right ventricular systolic pressure (RVSP) of >or= 40 mm Hg 6 months after the diagnosis of submassive PE.
Methods: We enrolled 200 normotensive patients with CT angiography-proven PE and a baseline echocardiogram to estimate RVSP.
Objective: Few studies have documented the incidence and significance of non-sustained hypotension in emergency department (ED) patients with sepsis. We hypothesized that ED non-sustained hypotension increases risk of in-hospital mortality in patients with sepsis.
Methods: Secondary analysis of a prospective cohort study.
Background: Elevated blood concentrations of troponin proteins or brain natriuretic peptide (BNP) worsen the prognosis of patients with pulmonary embolism (PE). Novel biomarkers that reflect mechanisms of right ventricle (RV) damage from PE may provide additional prognostic value. We compare the prognostic use of BNP, troponin I, D-dimer, monocyte chemoattractant protein-1, matrix metalloproteinase, myeloperoxidase, C-reactive protein, and caspase 3 as biomarkers of RV damage and adverse outcomes in submassive PE.
View Article and Find Full Text PDFChem Res Toxicol
December 2001
Despite the utility of cyclooxygenase (COX) inhibition as an antiinflammatory strategy, prostaglandin (PG) products of COX-1 and -2 provide important regulatory functions in some pathophysiological states. Scattered reports suggest that COX inhibition may also promote adverse drug events. Here we demonstrate a protective role for endogenous COX-derived products in a murine model of acetaminophen (APAP)-induced acute liver injury.
View Article and Find Full Text PDFChem Res Toxicol
February 1999
Cytochrome P450 2C11 in rats was recently found to metabolize diclofenac into a highly reactive product that covalently bound to this enzyme before it could diffuse away and react with other proteins. To determine whether cytochromes P450 in human liver could catalyze a similar reaction, we have studied the covalent binding of diclofenac in vitro to liver microsomes of 16 individuals. Only three of 16 samples were found by immunoblot analysis to activate diclofenac appreciably to form protein adducts in a NADPH-dependent pathway.
View Article and Find Full Text PDFBackground: Compound A, a degradation product of sevoflurane, causes renal corticomedullary necrosis in rats. Although the toxicity of this compound was originally hypothesized to result from the biotransformation of its cysteine conjugates into toxic thionoacyl halide metabolites by renal cysteine conjugate beta-lyase, recent evidence suggests that alternative mechanisms may be responsible for compound A nephrotoxicity. The aim of this study was to evaluate these issues by determining whether mercapturates and glutathione conjugates of compound A could produce renal corticomedullary necrosis in rats, similar to compound A, and whether renal covalent adducts of the thionacyl halide metabolite of compound A could be detected immunochemically.
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