J Collen
Walter Reed National Military Medical Center
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Featured researches published by J Collen.
Chest | 2012
J Collen; Nicholas Orr; Christopher J. Lettieri; Kevin Carter; Aaron B. Holley
BACKGROUNDnSleep complaints are common among patients with traumatic brain injury. Evaluation of this population is confounded by polypharmacy and comorbid disease, with few studies addressing combat-related injuries. The aim of this study was to assess the prevalence of sleep disorders among soldiers who sustained combat-related traumatic brain injury.nnnMETHODSnThe study design was a retrospective review of soldiers returning from combat with mild to moderate traumatic brain injury. All underwent comprehensive sleep evaluations. We determined the prevalence of sleep complaints and disorders in this population and assessed demographics, mechanism of injury, medication use, comorbid psychiatric disease, and polysomnographic findings to identify variables that correlated with the development of specific sleep disorders.nnnRESULTSnOf 116 consecutive patients, 96.6% were men (mean age, 31.1 ± 9.8 years; mean BMI, 27.8 ± 4.1 kg/m²), and 29.5% and 70.5% sustained blunt and blast injuries, respectively. Nearly all (97.4%) reported sleep complaints. Hypersomnia and sleep fragmentation were reported in 85.2% and 54.3%, respectively. Obstructive sleep apnea syndrome (OSAS) was found in 34.5%, and 55.2% had insomnia. Patients with blast injuries developed more anxiety (50.6% vs 20.0%, P = .002) and insomnia (63% vs 40%, P = .02), whereas patients with blunt trauma had significantly more OSAS (54.3% vs 25.9%, P = .003). In multivariate analysis, blunt trauma was a significant predictor of OSAS (OR, 3.09; 95% CI, 1.02-9.38; P = .047).nnnCONCLUSIONSnSleep disruption is common following traumatic brain injury, and the majority of patients develop a chronic sleep disorder. It appears that sleep disturbances may be influenced by the mechanism of injury in those with combat-related traumatic brain injury, with blunt injury potentially predicting the development of OSAS.
Chest | 2013
Aaron B. Holley; Sarah Petteys; Joshua Mitchell; Paul R. Holley; J Collen
OBJECTIVESnUS soldiers suffer catastrophic injuries during combat. We sought to define risk factors and rates for VTE in this population.nnnMETHODSnWe gathered data each hospital day on all patients injured in Afghanistan or Iraq who were admitted to the Walter Reed Army Medical Center (WRAMC). We analyzed prophylaxis rates and efficacy and identified risk factors for VTE.nnnRESULTSnWe recorded data on 506 combat casualties directly admitted to WRAMC after medical air evacuation. The average injury severity score for the group was 18.4 ± 11.7, and the most common reason for air evacuation was injury by improvised explosive device (65%). As part of the initial resuscitation, patients received 4.7 ± 9.0 and 4.00 ± 7.8 units of packed RBCs and fresh frozen plasma, respectively, and 42 patients received factor VIIa. Forty-six patients (9.1%) were given a diagnosis of VTE prior to discharge, 18 (3.6%) during air evacuation, and 28 (5.5%) during the hospital stay. In Cox regression analysis, administration of 1 unit of packed RBCs was associated with a hazard ratio (HR) of 1.04 (95% CI, 1.02-1.07; P = .002), and enoxaparin, 30 mg bid, administered subcutaneously for the majority of hospital days was associated with a HR of 0.31 (95% CI, 0.11-0.86; P = .02) for VTE during the hospitalization.nnnCONCLUSIONSnPatients who suffer traumatic injuries in combat overseas are at high risk for VTE duringxa0evacuation and recovery. Those with large resuscitations are at particularly high risk, and low-molecular-weight heparin is associated with a decrease in VTE.
Current Respiratory Care Reports | 2012
John Sherner; J Collen; Christopher S. King; Steven D. Nathan
A significant proportion of patients with idiopathic pulmonary fibrosis have concurrent pulmonary hypertension. In most, elevations in pulmonary pressures are modest, but approximately 10xa0% have disproportionately elevated pulmonary pressures. Pulmonary hypertension is associated with decreased functional status and increased mortality. The etiology remains incompletely understood, but likely involves a complex interplay of abnormal angiogenesis, vascular ablation, remodeling, and vasoconstriction. Transthoracic echocardiogram, six-minute walk testing, pulmonary function testing and biomarkers may suggest pulmonary hypertension, but none are sensitive or specific enough to rule in or exclude the diagnosis. Right heart catheterization remains the diagnostic gold standard. Supplemental oxygen should be provided if required and sleep-disordered breathing should be addressed. Small trials suggest that vasodilator therapy may improve exercise tolerance, but no mortality benefit has been demonstrated. Patients with disproportionate pulmonary hypertension should be encouraged to enroll in clinical trials of vasodilator therapy so that the role of these agents can be better defined. Ultimately, genetic profiling technology may serve to individualize therapy in such patients.
Sleep Medicine Clinics | 2017
Christopher J. Lettieri; Scott G. Williams; J Collen; Emerson M. Wickwire
Obstructive sleep apnea is a common and treatable condition, but therapeutic adherence is limited by numerous factors. Despite advances in positive airway pressure (PAP) technology and a multitude of effective pharmacologic and behavioral therapeutic interventions to overcome the most common barriers to PAP, adherence has not increased significantly over the past 30xa0years. This review aims to identify the most important factors that impact adherence, common barriers to treatment, and evidence-based treatment strategies to maximize the effectiveness of PAP treatment. Complications of PAP treatment and mitigation techniques are also discussed.
Sleep and Breathing | 2018
Ian Grasso; Mark C. Haigney; David Mortara; J Collen; Jordanna M Hostler; Aimee Moores; Karen Sheikh; William Kelly
PurposeObstructive sleep apnea (OSA) syndrome is a common condition that can impact clinical outcomes among patients with cardiovascular disease. Screening all subjects with heart disease via polysomnography (PSG) is costly and resource-limited. We sought to compare a Holter monitor-based algorithm to detect OSA to in-laboratory polysomnography (PSG).MethodsProspective cohort study of patients undergoing in-laboratory attended PSG for the evaluation of OSA. A standard 12-lead Holter monitor was attached to patients at the initiation of PSG. Holter-derived respiratory disturbance index (HDRDI) was extracted from the respiratory myogram, based on detecting skeletal muscle “noise” detected on the baseline. Apneic and hypopneic episodes were identified by comparing sudden changes in the myogram to abrupt increases in heart rate. The HDRDI was compared with the PSG-derived apnea-hypopnea index (PDAHI).ResultsThirty patients underwent simultaneous Holter monitoring and overnight diagnostic PSG. An ROC curve for peak HDRDI was 0.79 (95% CI 0.61, 0.97) for OSA, with sensitivity of 94.4% and specificity of 54.5%. A cutoff value of HDRDIu2009<u200910 appeared to identify those individuals without clinically significant sleep-disordered breathing.ConclusionHolter-derived respiration detected OSA comparable to PSG. Further study is warranted to determine its utility for screening and diagnosing OSA in appropriately selected patients.
Military Medicine | 2018
Aaron B. Holley; Wesley D. Boose; Michael Perkins; Karen L. Sheikh; Nancy Pearl Solomon; Angela M. Dietsch; Jafar Vossoughi; Arthur T. Johnson; J Collen
IntroductionnFollowing reports of respiratory symptoms among service members returning from deployment to South West Asia (SWA), an expert panel recommended pre-deployment spirometry be used to assess disease burden. Unfortunately, testing with spirometry is high cost and time-consuming. The airflow perturbation device (APD) is a handheld monitor that rapidly measures respiratory resistance (APD-Rr) and has promising but limited clinical data. Its speed and portability make it ideally suited for large volume pre-deployment screening. We conducted a pilot study to assess APD performance characteristics and develop normative values.nnnMaterials and MethodsnWe prospectively enrolled subjects and derived reference equations for the APD from those without respiratory symptoms, pulmonary disease, or tobacco exposure. APD testing was conducted by medical technicians who received a 10-min in-service on its use. A subset of subjects performed spirometry and impulse oscillometry (iOS), administered by trained respiratory therapists. APD measures were compared with spirometry and iOS.nnnResultsnThe total study population included 199 subjects (55.8% males, body mass index 27.7 ± 6.0 kg/m2, age 49.9 ± 18.7 yr). Across the three APD trials, mean inspiratory (APD-Ri), expiratory (APD-Re), and average (APD-Ravg) resistances were 3.30 ± 1.0, 3.69 ± 1.2, and 3.50 ± 1.1 cm H2O/L/s. Reference equations were derived from 142 clinically normal volunteers. Height, weight, and body mass index were independently associated with APD-Ri, APD-Re, and APD-Ravg and were combined with age and gender in linear regression models. APD-Ri, APD-Re, and APD-Ravg were significantly inversely correlated with FEV1 (r = -0.39 to -0.42), FVC (r = -0.37 to -0.40), and FEF25-75 (r = -0.31 to -0.35) and positively correlated with R5 (r = 0.61-0.62), R20 (r = 0.50-0.52), X5 (r = -0.57 to -0.59), and FRES (r = 0.42-0.43). Bland-Altman plots showed that the APD-Rr closely approximates iOS when resistance is normal.nnnConclusionnRapid testing was achieved with minimal training required, and reference equations were constructed. APD-Rr correlated moderately with iOS and weakly with spirometry. More testing is required to determine whether the APD has value for pre- and post-deployment respiratory assessment.
Chest | 2018
Lisa K. Moores; Aaron B. Holley; J Collen
Sleep | 2018
Christopher K Pham; C York; J Collen; Michael Polmear; S Terry
Sleep | 2018
Christopher K Pham; Michael Polmear; Aaron B. Holley; J Collen
Sleep | 2018
Aaron B. Holley; S Terry; D Shaha; B Robertson; T Andrada; J Collen