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Editorials

Chest. 2014;145(4):671-672. doi:10.1378/chest.13-2696

COPD is a progressive, chronic inflammatory disorder caused by exposure to noxious agents. The condition is associated with considerable heterogeneity and progressive disability leading to increased mortality. Measurement of FEV1 is key in establishing the diagnosis of COPD and assessing its severity both as a single measure or in multidimensional tools. Decreasing FEV1 has been associated with increased respiratory and cardiovascular mortality.1,2 The classic definition of COPD describes progressive FEV1 decline over time, but we now know that this measure is variable3,4 and affected by the development of COPD exacerbations.5 Studies have shown that patients with COPD may, indeed, show rapid decline in FEV1, decline similar to the normal population, or even no actual FEV1 decline over time.4

Chest. 2014;145(4):672-674. doi:10.1378/chest.13-2908

The validation and use of staging in interstitial lung disease (ILD) is long overdue. Treatment decisions made by clinicians are dichotomous: essentially, to introduce a treatment or to enroll a patient in a treatment trial. The data on which such decisions tend to be made are continuous (eg, measured FVC values), which immediately poses the question of which severity thresholds should be used to identify patients at higher risk of disease progression. In idiopathic pulmonary fibrosis (IPF), staging systems have been based on a combination of the composite physiologic index and 6-min walk data1 and on the integration of spirometric volumes, gas transfer levels, age, and sex (the GAP model).2 In non-IPF chronic ILD, the evaluation of high-resolution CT (HRCT) scanning has been combined with pulmonary function tests in staging ILD in systemic sclerosis,3 other forms of connective tissue disease,4 and sarcoidosis.5 However, until now, informative severity thresholds have been disease-specific and, by virtue of this fact, are less likely to be applied with confidence in mixed populations of patients with ILD.

Chest. 2014;145(4):674-676. doi:10.1378/chest.13-2590

Orphan diseases are often managed according to evidence from similar, more common conditions. This should be avoided, since differences in pathophysiology, morbidity, and prognosis will likely lead to problems of treatment failure and lack of adherence. The prevalence of primary ciliary dyskinesia (PCD)1 is approximately one-fourth that of cystic fibrosis (CF) (one in 10,000 and one in 2,500, respectively), and it is, therefore, not particularly rare. Despite recent advances in PCD research and clinical infrastructure,2 there have been no randomized controlled trials, and current management guidelines are mostly limited to expert consensus extrapolated from evidence from CF.3

Second Opinion

Chest. 2014;145(4):677. doi:10.1378/chest.145.4.677
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Point/Counterpoint Editorials

Chest. 2014;145(4):678-680. doi:10.1378/chest.13-2404
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In 1990, LiPuma and colleagues1 described person-to-person transmission of Pseudomonas cepacia (now Burkholderia cepacia) between young adults with cystic fibrosis (CF) attending an educational program. One of the newly infected individuals had been previously in good health, but deteriorated rapidly and died within several months. This tragic case highlights the potential for catastrophic consequences from person-to-person transmission of bacterial pathogens in CF. This report and others from around the world that also described person-to-person transmission of B cepacia associated with acceleration of pulmonary disease and death led to the recommendation that people infected with B cepacia not attend Cystic Fibrosis Foundation (CF Foundation)-sponsored events. Reports describing person-to-person transmission of other more prevalent CF pathogens, most notably Pseudomonas aeruginosa, soon followed. In response, the CF Foundation published recommendations for infection prevention and control in 2003.2 Over the last 10 years, accumulating evidence has described further instances of person-to-person transmission of CF pathogens as well as poor clinical outcomes associated with transmission of certain strains of P aeruginosa, methicillin-resistant Staphylococcus aureus (MRSA), and Burkholderia.3 In response, the CF Foundation commissioned an update of the guidelines and invited public comment on a draft version. The period for public comment is now closed.

Chest. 2014;145(4):680-683. doi:10.1378/chest.13-2406
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In 2011, the Cystic Fibrosis Foundation (CF Foundation) assembled an infection prevention and control committee to update the CF Foundation’s 2003 Infection Control Recommendations for Patients with Cystic Fibrosis.1 In March 2013, acting on a recommendation made orally by committee members and included in the written draft guideline circulated later (Infection Prevention and Control Committee, CF Foundation, written communication, May 19, 2013), the CF Foundation announced a new policy2:

Chest. 2014;145(4):683-684. doi:10.1378/chest.13-2405
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Authors on both sides of this debate agree that evidence exists for person-to-person transmission of virulent pathogens between individuals with cystic fibrosis (CF) in non-health-care settings that has resulted in worsened outcomes.1,2 Our disagreement stems from each side’s perspective on the relevance of that evidence to the recommendation that only one individual with CF be allowed to attend Cystic Fibrosis Foundation (CF Foundation)- or CF center-sponsored indoor events.

Chest. 2014;145(4):684-685. doi:10.1378/chest.13-2407
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This debate concerns a policy of the Cystic Fibrosis Foundation (CF Foundation) and the science that supports it—or does not—and we thank Dr Jain and colleagues1 for their willingness to address this issue. First, some clarification. Dr Jain and colleagues1 speak of “recommendations.” Dr Jain and his colleagues all served on the committee that recommended updates (Infection Prevention and Control Committee, CF Foundation, written communication, May 19, 2013) to the CF Foundation’s guidelines.2 But with respect to the recommendation that led to the ban, it was the CF Foundation that made it into policy. Dr Jain and colleagues are responsible for their recommendations; the CF Foundation is responsible for its policy.

Giants in Chest Medicine

Chest. 2014;145(4):686-687. doi:10.1378/chest.13-3080

Marvin I. Schwarz, MD, is the James C. Campbell Professor of Pulmonary Medicine at the University of Colorado. He was born to immigrant parents from Vienna, Austria, a mere 2 weeks after their arrival in this country upon their successful flight due to the Nazi invasion. Although Dr Schwarz (“Marvin” to many of us) had originally dreamed of being a basketball player, he found himself drawn to medicine, as his father was an obstetrics and gynecology practitioner. When asked why he did not follow directly in his father’s footsteps, Dr Schwarz replied, “I never liked women,” in a tongue-in-cheek fashion demonstrative of his whimsical irony. Dr Schwarz graduated from Bard College and was an Alpha Omega Alpha graduate of the Tulane University School of Medicine. He completed his internal medicine training at the Charity Hospital of Louisiana and was most influenced by his earliest mentor, Morton Ziskind, MD, at Tulane. Importantly, he was captivated by the clinical prowess exhibited by Dr Ziskind in the care of patients with pulmonary diseases. Following his pulmonary fellowship, Dr Schwarz completed his military obligations in the US Army. He was then recruited to the University of Colorado by Tom Petty, MD, in 1972, and his career in Colorado has flourished ever since.

Commentary

Chest. 2014;145(4):688-694. doi:10.1378/chest.13-2363

The number of medical emergencies onboard aircraft is increasing as commercial air traffic increases and the general population ages, becomes more mobile, and includes individuals with serious medical conditions. Travelers with respiratory diseases are at particular risk for in-flight events because exposure to lower atmospheric pressure in a pressurized cabin at cruising altitude may result in not only hypoxemia but also pneumothorax due to gas expansion within enclosed pulmonary parenchymal spaces based on Boyle’s law. Risks of pneumothorax during air travel pertain particularly to those patients with cystic lung diseases, recent pneumothorax or thoracic surgery, and chronic pneumothorax. Currently available guidelines are admittedly based on sparse data and include recommendations to delay air travel for 1 to 3 weeks after thoracic surgery or resolution of the pneumothorax. One of these guidelines declares existing pneumothorax to be an absolute contraindication to air travel although there are reports of uneventful air travel for those with chronic stable pneumothorax. In this article, we review the available data regarding pneumothorax and air travel that consist mostly of case reports and retrospective surveys. There is clearly a need for additional data that will inform decisions regarding air travel for patients at risk for pneumothorax, including those with recent thoracic surgery and transthoracic needle biopsy.

Original Research: COPD

Chest. 2014;145(4):695-703. doi:10.1378/chest.13-0799

Objective:  Cigarette smoking is the most important risk factor for COPD in the United States. Host factors that influence the rapid rate of FEV1 decline in smokers and how decline rate influences risk for developing COPD are unknown. The aim of this study was to characterize the rate of FEV1 decline in ever smokers, compare the risk of incident COPD between those with rapid decline and others, and determine the effect of selected drugs on rapid decline.

Methods:  A total of 1,170 eligible ever smokers from the longitudinal Lovelace Smokers Cohort with repeat spirometry tests over a minimum follow-up period of 3 years (mean follow-up, 5.9 years) were examined, including 809 ever smokers without a spirometric abnormality at baseline. Longitudinal absolute decline in postbronchodilator FEV1 from the slope of the spirometric values over all examinations was annualized and classified as rapid (≥ 30 mL/y), normal (0-29.9 mL/y), or no (> 0 mL/y) decline. Logistic regression and Kaplan-Meier survival curves were used for the analysis.

Results:  Approximately 32% of ever smokers exhibited rapid decline. Among ever smokers without a baseline spirometric abnormality, rapid decline was associated with an increased risk for incident COPD (OR, 1.88; P = .003). The use of angiotensin-converting enzyme (ACE) inhibitors at baseline examination was protective against rapid decline, particularly among those with comorbid cardiovascular disease, hypertension, or diabetes (ORs 0.48, 0.48, and 0.12, respectively; P ≤ .02 for all analyses).

Conclusions:  Ever smokers with a rapid decline in FEV1 are at higher risk for COPD. Use of ACE inhibitors by smokers may protect against this rapid decline and the progression to COPD.

Chest. 2014;145(4):704-710. doi:10.1378/chest.13-1308

Background:  Whether Native American ancestry (NAA) is associated with COPD or lung function in a racially admixed Hispanic population is unknown.

Methods:  We recruited 578 Costa Ricans with and without COPD into a hybrid case-control/family-based cohort, including 316 members of families of index case subjects. All participants completed questionnaires and spirometry and gave a blood sample for DNA extraction. Genome-wide genotyping was conducted with the Illumina Human610-Quad and HumanOmniExpress BeadChip kits (Illumina Inc), and individual ancestral proportions were estimated from these genotypic data and reference panels. For unrelated individuals, linear or logistic regression was used for the analysis of NAA and COPD (GOLD [Global Initiative for Chronic Obstructive Lung Disease] stage II or greater) or lung function. For extended families, linear mixed models and generalized estimating equations were used for the analysis. All models were adjusted for age, sex, educational level, and smoking behavior; models for FEV1 were also adjusted for height.

Results:  The average proportion of European, Native American, and African ancestry among participants was 62%, 35%, and 3%, respectively. After adjustment for current smoking and other covariates, NAA was inversely associated with COPD (OR per 10% increment, 0.55; 95% CI, 0.41-0.75) but positively associated with FEV1, FVC, and FEV1/FVC. After additional adjustment for pack-years of smoking, the association between NAA and COPD or lung function measures was slightly attenuated. We found that about 31% of the estimated effect of NAA on COPD is mediated by pack-years of smoking.

Conclusions:  NAA is inversely associated with COPD but positively associated with FEV1 or FVC in Costa Ricans. Ancestral effects on smoking behavior partly explain the findings for COPD but not for FEV1 or FVC.

Chest. 2014;145(4):711-722. doi:10.1378/chest.13-0873

Background:  COPD is characterized by chronic inflammation. CD8+ T cells and CD4+ T cells have both been implicated in the inflammatory response. We investigated whether the lymphocyte and T-cell subpopulations in BAL differ between patients with COPD who are current smokers and those who are ex-smokers.

Methods:  Forty never smokers, 40 smokers with normal lung function, and 38 patients with COPD, GOLD (Global Initiative for Chronic Obstructive Pulmonary Disease) stage I-II (27 smokers and 11 ex-smokers) underwent BAL. Using flow cytometry, cells were analyzed from BAL and blood for T-cell subsets, B cells, natural killer cells, and natural killer T (NKT)-like cells. The differentiation status of CD4+ T cells was also determined.

Results:  Smokers with or without COPD had higher percentages of CD8+ T cells and NKT-like cells in BAL than did never smokers and ex-smokers with COPD. Most of the NKT-like cells were CD8+. In contrast, the percentages of CD4+ T cells were lower in the smoking than in the nonsmoking groups. In blood, the frequency of CD4+ T cells was increased in the two smoking groups. Current smokers also had increased numbers of activated (CD69+) naive and effector CD4+ T cells in BAL compared with nonsmokers, particularly in patients with COPD. In male smokers with COPD, the percentage of CD8+ T cells in BAL positively correlated with the number of cigarettes per day.

Conclusions:  Current smoking status has a greater impact than airway obstruction on the distribution of T-cell subsets in BAL of patients with mild to moderate COPD. This fact must be considered when the role of T cells in COPD is evaluated. Our results stress the importance of subgrouping patients with COPD in terms of smoking.

Original Research: Diffuse Lung Disease

Chest. 2014;145(4):723-728. doi:10.1378/chest.13-1474

Background:  Risk prediction is challenging in chronic interstitial lung disease (ILD) because of heterogeneity in disease-specific and patient-specific variables. Our objective was to determine whether mortality is accurately predicted in patients with chronic ILD using the GAP model, a clinical prediction model based on sex, age, and lung physiology, that was previously validated in patients with idiopathic pulmonary fibrosis.

Methods:  Patients with idiopathic pulmonary fibrosis (n = 307), chronic hypersensitivity pneumonitis (n = 206), connective tissue disease-associated ILD (n = 281), idiopathic nonspecific interstitial pneumonia (n = 45), or unclassifiable ILD (n = 173) were selected from an ongoing database (N = 1,012). Performance of the previously validated GAP model was compared with novel prediction models in each ILD subtype and the combined cohort. Patients with follow-up pulmonary function data were used for longitudinal model validation.

Results:  The GAP model had good performance in all ILD subtypes (c-index, 74.6 in the combined cohort), which was maintained at all stages of disease severity and during follow-up evaluation. The GAP model had similar performance compared with alternative prediction models. A modified ILD-GAP Index was developed for application across all ILD subtypes to provide disease-specific survival estimates using a single risk prediction model. This was done by adding a disease subtype variable that accounted for better adjusted survival in connective tissue disease-associated ILD, chronic hypersensitivity pneumonitis, and idiopathic nonspecific interstitial pneumonia.

Conclusion:  The GAP model accurately predicts risk of death in chronic ILD. The ILD-GAP model accurately predicts mortality in major chronic ILD subtypes and at all stages of disease.

Chest. 2014;145(4):729-737. doi:10.1378/chest.13-0603

Background:  Treatment of autoimmune pulmonary alveolar proteinosis (aPAP) by subcutaneous injection or inhaled therapy of granulocyte-macrophage colony-stimulating factor (GM-CSF) has been demonstrated to be safe and efficacious in several reports. However, some reports of subcutaneous injection described transient benefit in most instances. The durability of response to inhaled GM-CSF therapy is not well characterized.

Methods:  To elucidate the risk factors for recurrence of aPAP after GM-CSF inhalation, 35 patients were followed up, monitoring for the use of any additional PAP therapies and disease severity score every 6 months. Physiologic, serologic, and radiologic features of the patients were analyzed for the findings of 30-month observation after the end of inhalation therapy.

Results:  During the observation, 23 patients remained free from additional treatments, and twelve patients required additional treatments. There were no significant differences in age, sex, symptoms, oxygenation indexes, or anti-GM-CSF antibody levels at the beginning of treatment between the two groups. Baseline vital capacity (% predicted, %VC) were higher among those who required additional treatment (P < .01). Those patients not requiring additional treatment maintained the improved disease severity score initially achieved. A significant difference in the time to additional treatment between the high %VC group (%VC ≥ 80.5) and the low %VC group was seen by a Kaplan-Meier analysis and a log-rank test (P < .0005).

Conclusions:  These results demonstrate that inhaled GM-CSF therapy sustained remission of aPAP in more than one-half of cases, and baseline %VC might be a prognostic factor for disease recurrence.

Trial registry:  ISRCTN Register and JMACCT Clinical Trial Registry; No.: ISRCTN18931678 and JMAIIA00013; URL: http://www.isrctn.org and http://www.jmacct.med.or.jp

Original Research: Genetic and Developmental Disorders

Chest. 2014;145(4):738-744. doi:10.1378/chest.13-1162

Background:  Impaired mucociliary clearance causes pulmonary disease in primary ciliary dyskinesia (PCD) and contributes to cystic fibrosis (CF) lung disease. Although the sinopulmonary disease is similar, morbidity and mortality are different. Both patients with PCD and patients with CF with pancreatic sufficiency (CF-PS) show no nutrient malabsorption and are diagnosed at a later age compared with patients with CF with pancreatic insufficiency (CF-PI).

Methods:  Clinical status, microbiology, FEV1, and high-resolution CT (HRCT) scans presented as total Brody score (CT-TBS) were compared for patients with PCD, CF-PI, and CF-PS, all treated at the same medical center, by the same team, and by a similar routine follow-up.

Results:  One hundred sixty-four patients, 34 with PCD, 88 with CF-PI, and 42 with CF-PS were enrolled. PCD was diagnosed at a similar age as CF-PS but significantly later than CF-PI. Mean FEV1 % predicted was similar for the three groups. The rate of FEV1 change with age in PCD was similar to CF-PS but significantly lower than in CF-PI. Severity of structural lung disease (CT-TBS) was similar for PCD and CF-PS and significantly higher in CF-PI. No correlation between TBS or Pseudomonas aeruginosa infection and FEV1 in PCD was seen, whereas a negative correlation with FEV1 was observed for both CF groups.

Conclusions:  Although in our study PCD was similar to CF-PS, the lack of correlation between FEV1 and age, CT-TBS, and P aeruginosa infection in PCD suggests that impaired mucociliary clearance is not the only cause for inducing pulmonary damage in these diseases. Furthermore, a comparison of disease characteristics for PCD and CF should distinguish between CF-PI and CF-PS as different entities.

Original Research: Critical Care

Chest. 2014;145(4):745-752. doi:10.1378/chest.13-1722

Background:  Observational studies have found an increased risk of adverse effects such as hemorrhage, stroke, and increased mortality in patients taking selective serotonin reuptake inhibitors (SSRIs). The impact of prior use of these medications on outcomes in critically ill patients has not been previously examined. We performed a retrospective study to determine if preadmission use of SSRIs or serotonin norepinephrine reuptake inhibitors (SNRIs) is associated with mortality differences in patients admitted to the ICU.

Methods:  The retrospective study used a modifiable data mining technique applied to the publicly available Multiparameter Intelligent Monitoring in Intensive Care (MIMIC) 2.6 database. A total of 14,709 patient records, consisting of 2,471 in the SSRI/SNRI group and 12,238 control subjects, were analyzed. The study outcome was in-hospital mortality.

Results:  After adjustment for age, Simplified Acute Physiology Score, vasopressor use, ventilator use, and combined Elixhauser score, SSRI/SNRI use was associated with significantly increased in-hospital mortality (OR, 1.19; 95% CI, 1.02-1.40; P = .026). Among patient subgroups, risk was highest in patients with acute coronary syndrome (OR, 1.95; 95% CI, 1.21-3.13; P = .006) and patients admitted to the cardiac surgery recovery unit (OR, 1.51; 95% CI, 1.11-2.04; P = .008). Mortality appeared to vary by specific SSRI, with higher mortalities associated with higher levels of serotonin inhibition.

Conclusions:  We found significant increases in hospital stay mortality among those patients in the ICU taking SSRI/SNRIs prior to admission as compared with control subjects. Mortality was higher in patients receiving SSRI/SNRI agents that produce greater degrees of serotonin reuptake inhibition. The study serves to demonstrate the potential for the future application of advanced data examination techniques upon detailed (and growing) clinical databases being made available by the digitization of medicine.

Chest. 2014;145(4):753-761. doi:10.1378/chest.13-1962

Background:  ABO glycosyltransferases catalyze antigen modifications on various glycans and glycoproteins and determine the ABO blood types. Blood type A has been associated with increased risk of vascular diseases and differential circulating levels of proteins related to inflammation and endothelial function. The objective of this study was to determine the association of ABO blood types with ARDS risk in patients with major trauma and severe sepsis.

Methods:  We conducted prospective cohort studies in two populations at an urban tertiary referral, level I trauma center. Critically ill patients (n = 732) presenting after major trauma were followed for 5 days for ARDS development. Additionally, 976 medical patients with severe sepsis were followed for 5 days for ARDS. Multivariable logistic regression was used to adjust for confounders.

Results:  ARDS developed in 197 of the 732 trauma patients (27%). Blood type A was associated with increased ARDS risk among whites (37% vs 24%; adjusted OR, 1.88; 95% CI, 1.14-3.12; P = .014), but not blacks (adjusted OR, 0.61; 95% CI, 0.33-1.13; P = .114). ARDS developed in 222 of the 976 patients with severe sepsis (23%). Blood type A was also associated with an increased ARDS risk among whites (31% vs 21%; adjusted OR, 1.67; 95% CI, 1.08-2.59; P = .021) but, again, not among blacks (adjusted OR, 1.17; 95% CI, 0.59-2.33; P = .652).

Conclusions:  Blood type A is associated with an increased risk of ARDS in white patients with major trauma and severe sepsis. These results suggest a role for ABO glycans and glycosyltransferases in ARDS susceptibility.

Original Research: Sleep Disorders

Chest. 2014;145(4):762-771. doi:10.1378/chest.13-1115

Background:  CPAP is considered the therapy of choice for OSA, but the extent to which it can reduce BP is still under debate. We undertook a systematic review and meta-analysis of randomized controlled trials (RCTs) to quantify the effect size of the reduction of BP by CPAP therapy compared with other passive (sham CPAP, tablets of placebo drug, conservative measures) or active (oral appliance, antihypertensive drugs) treatments.

Methods:  We searched four different databases (MEDLINE, EMBASE, Web of Science, and the Cochrane Library) with specific search terms and selection criteria.

Results:  From 1,599 articles, we included 31 RCTs that compared CPAP with either passive or active treatment. In a random-effects meta-analysis vs passive treatment (29 RCTs, 1,820 subjects), we observed a mean ± SEM net difference in systolic BP of 2.6 ± 0.6 mm Hg and in diastolic BP of 2.0 ± 0.4 mm Hg, favoring treatment with CPAP (P < .001). Among studies using 24-h ambulatory BP monitoring that presented data on daytime and nighttime periods, the mean difference in systolic and diastolic BP was, respectively, 2.2 ± 0.7 and 1.9 ± 0.6 mm Hg during daytime and 3.8 ± 0.8 and 1.8 ± 0.6 mm Hg during nighttime. In meta-regression analysis, a higher baseline apnea/hypopnea index was associated with a greater mean net decrease in systolic BP (β ± SE, 0.08 ± 0.04). There was no evidence of publication bias, and heterogeneity was mild (I2, 34%-36%).

Conclusions:  Therapy with CPAP significantly reduces BP in patients with OSA but with a low effect size. Patients with frequent apneic episodes may benefit the most from CPAP.

Original Research: Asthma

Chest. 2014;145(4):772-778. doi:10.1378/chest.13-2298

Background:  Inhaled corticosteroids, known to be effective as a maintenance medication in chronic asthma, have also been suggested as a therapy for acute asthma when given at high doses.

Methods:  A double-blind, randomized, placebo-controlled trial was conducted in children aged 2 to 12 years with moderate or severe acute asthma, as determined based on a clinical score of 5 to 15 points, where 15 is the most severe. We compared the addition of budesonide 1,500 μg vs placebo to standard acute asthma treatment, which included salbutamol, ipratropium bromide, and a single dose of prednisolone 2 mg/kg given at the beginning of therapy. The primary outcome was hospital admission rate within 4 h.

Results:  A total of 906 ED visits by children with moderate or severe acute asthma were evaluated. Seventy-five cases out of 458 (16.4%) in the budesonide group vs 82 of 448 (18.3%) in the placebo group were admitted (OR, 0.84; 95% CI, 0.58-1.23; P = .38). However, among cases with high baseline clinical score (≥ 13), significantly fewer children were admitted in the budesonide group (27 of 76 [35.5%]) than in the placebo group (39 of 73 [53.4%]; OR, 0.42; 95% CI, 0.19-0.94; P = .03).

Conclusions:  The addition of budesonide nebulization did not decrease the admission rate of children with acute asthma overall. However, it may decrease the admission rate of children with severe acute asthma.

Trial registry:  ClinicalTrials.gov; No.: NCT01524198; URL: www.clinicaltrials.gov

Chest. 2014;145(4):779-786. doi:10.1378/chest.13-1235

Background:  β-Blockers are avoided in asthma over concerns regarding acute bronchoconstriction. Risk is greatest following acute exposure, including the potential for antagonism of β2-agonist rescue therapy.

Methods:  A systematic review of databases was performed to identify all randomized, blinded, placebo-controlled clinical trials evaluating acute β-blocker exposure in asthma. Effect estimates for changes in respiratory function, symptoms, and β2-agonist response were pooled using random effects meta-analysis with heterogeneity investigated.

Results:  Acute selective β-blockers in the doses given caused a mean change in FEV1 of −6.9% (95% CI, −8.5 to −5.2), a fall in FEV1 of ≥ 20% in one in eight patients (P = .03), symptoms affecting one in 33 patients (P = .18), and attenuation of concomitant β2-agonist response of −10.2% (95% CI, −14.0 to −6.4). Corresponding values for acute nonselective β-blockers in the doses given were −10.2% (95% CI, −14.7 to −5.6), one in nine patients (P = .02), one in 13 patients (P = .14), and −20.0% (95% CI, −29.4 to −10.7). Following investigation of heterogeneity, clear differences were found for celiprolol and labetalol. A dose-response relationship was demonstrated for selective β-blockers.

Conclusions:  Selective β-blockers are better tolerated but not completely risk-free. Risk from acute exposure may be mitigated using the smallest dose possible and β-blockers with greater β1-selectivity. β-Blocker-induced bronchospasm responded partially to β2-agonists in the doses given with response blunted more by nonselective β-blockers than selective β-blockers. Use of β-blockers in asthma could possibly be based upon a risk assessment on an individual patient basis.

Topics: asthma , agonists
Chest. 2014;145(4):787-793. doi:10.1378/chest.13-1619

Background:  Productivity loss is an overlooked aspect of the burden of chronic health conditions. While modern guidelines emphasize achieving clinical control in asthma management, few studies have reported on the relationship between asthma control and productivity loss. We calculated the productivity loss that can be avoided by achieving and maintaining clinical control in employed adults with asthma.

Methods:  We prospectively recruited a population-based random sample of adults with asthma in British Columbia, Canada. We measured productivity loss due to absenteeism and presenteeism using validated instruments, and ascertained asthma control according to the GINA (Global Initiative for Asthma) classification. We estimated the average gain in productivity for each individual if the individual’s asthma was controlled in the past week, by fitting two-part regression models associating asthma control and productivity loss, controlling for potential confounding variables.

Results:  The final sample included 300 employed adults (mean age, 47.9 years [SD 12.0]; 67.3% women). Of these, 49 (16.3%) reported absenteeism, and 137 (45.7%) reported presenteeism. Productivity loss due to presenteeism, but not absenteeism, was associated with asthma control. A person with uncontrolled asthma would avoid $184.80 (Canadian dollars [CAD]) in productivity loss by achieving clinical control during a week, CAD$167.50 (90.6%) of which would be due to presenteeism. The corresponding value was CAD$34.20 for partially controlled asthma and was not statistically significant.

Conclusions:  Our results indicate that substantial gain in productivity can be obtained by achieving asthma control. Presenteeism is more responsive than absenteeism to asthma control, and, thus, is a more important source of preventable burden.

Chest. 2014;145(4):794-802. doi:10.1378/chest.13-1413

Objective:  Self-reported respiratory symptoms are poor predictors of exercise-induced bronchoconstriction (EIB) in athletes. The objective of this study was to determine whether athletes have an inadequate perception of bronchoconstriction.

Methods:  One hundred thirty athletes and 32 nonathletes completed a standardized questionnaire and underwent eucapnic voluntary hyperpnea (EVH) and methacholine inhalation test. Perception scores were quoted on a modified Borg scale before each spirometry measurement for cough, breathlessness, chest tightness, and wheezing. Perception slope values were also obtained by plotting the variation of perception scores before and after the challenges against the fall in FEV1 expressed as a percentage of the initial value [(perception scores after − before)/FEV1].

Results:  Up to 76% of athletes and 68% of nonathletes had a perception score of ≤ 0.5 at 20% fall in FEV1 following methacholine. Athletes with EIB/airway hyperresponsiveness (AHR) had lower perception slopes to methacholine than nonathletes with asthma for breathlessness only (P = .02). Among athletes, those with EIB/AHR had a greater perception slope to EVH for breathlessness and wheezing (P = .02). Female athletes had a higher perception slope for breathlessness after EVH and cough after methacholine compared with men (P < .05). The age of athletes correlated significantly with the perception slope to EVH for each symptom (P < .05).

Conclusions:  Minimal differences in perception of bronchoconstriction-related symptoms between athletes and nonathletes were observed. Among athletes, the presence of EIB/AHR, older age, and female sex were associated with slightly higher perception scores.

Original Research: Tobacco Cessation and Prevention

Chest. 2014;145(4):803-809. doi:10.1378/chest.13-0960

Background:  Indoor group water-pipe tobacco smoking, commonly referred to as water-pipe smoking (WPS), especially in coffee shops, has gained worldwide popularity. We performed a comprehensive laboratory and clinical evaluation of the acute effects of active and passive indoor group WPS.

Methods:  This comparative study evaluated pre- and post-30-min active and passive indoor group WPS. The outcome parameters were carboxyhemoglobin (COHb), nicotine, and cotinine levels; CBC count; and cardiorespiratory parameters. Exhaled breath condensate (EBC) cytokines and endothelial function (using the EndoPat device [Itamar Medical Ltd]) were measured only in active smokers. Statistical methods used were Student t test, Wilcoxon signed rank test, Fisher exact test, analysis of variance, and Newman-Keuls post hoc test where relevant.

Results:  Sixty-two volunteers aged 24.9 ± 6.2 years were included; 47 were active smokers, and 15 were passive smokers. COHb level increased postactive WPS (active smokers, 2.0% ± 2.9% vs 17.6% ± 8.8%; P < .00001); six subjects (12.7%) had a > 25% increase, and two subjects (4.2%) had a > 40% increase. Plasma nicotine level increased postactive WPS (active smokers, 1.2 ± 4.3 ng/mL vs 18.8 ± 13.9 ng/mL; P < .0001); plasma cotinine and urinary nicotine and cotinine levels also increased significantly. EBC IL-4, IL-5, IL-10, IL-17, and γ-interferon decreased significantly with postactive smoking; endothelial function did not change. WPS was associated with adverse cardiorespiratory changes. In passive smokers, COHb level increased (0.8% ± 0.25% vs 1.2% ± 0.8%, respectively, P = .003) as did respiratory rate.

Conclusions:  One session of active indoor group WPS resulted in significant increases in COHb and serum nicotine levels (eightfold and 18-fold, respectively) and was associated with adverse cardiorespiratory health effects. The minor effects found in passive smokers suggest that they too may be affected adversely by exposure to WPS. The results call for action to limit the continuing global spread of WPS in coffee shops.

Trial registry:  ClinicalTrials.gov; No.: NCT1237548; URL: www.clinicaltrials.gov

Original Research: Pulmonary Vascular Disease

Chest. 2014;145(4):810-817. doi:10.1378/chest.13-1766

Background:  Sarcoidosis-associated pulmonary hypertension (SAPH) is a common problem in patients with persistent dyspneic sarcoidosis. The objective of this study was to determine the effect of bosentan therapy on pulmonary arterial hemodynamics in patients with SAPH.

Methods:  This 16-week study was a double-blind, placebo-controlled trial of either bosentan or placebo in patients with SAPH confirmed by right-sided heart catheterization. Patients were enrolled from multiple academic centers specializing in sarcoidosis care. They were stable on sarcoidosis therapy and were receiving no therapy for pulmonary hypertension. The cohort was randomized two to one to receive bosentan at a maximal dose of 125 mg or placebo bid for 16 weeks. Pulmonary function studies, 6-min walk test, and right-sided heart hemodynamics, including pulmonary artery mean pressure and pulmonary vascular resistance (PVR), were performed before and after 16 weeks of therapy.

Results:  Thirty-five patients completed 16 weeks of therapy (23 treated with bosentan, 12 with placebo). For those treated with bosentan, repeat hemodynamic studies at 16 weeks demonstrated a significant mean ± SD fall in PA mean pressure (−4 ± 6.6 mm Hg, P = .0105) and PVR (−1.7 ± 2.75 Wood units, P = .0104). For the patients treated with placebo, there was no significant change in either PA mean pressure (1 ± 3.7 mm Hg, P > .05) or PVR (0.1 ± 1.42 Wood units, P > .05). There was no significant change in 6-min walk distance for either group. Two patients treated with bosentan required an increase of supplemental oxygen by > 2 L after 16 weeks of therapy.

Conclusions:  This study demonstrated that bosentan significantly improved pulmonary hemodynamics in patients with SAPH.

Trial registry:  ClinicalTrials.gov; No: NCT00581607; URL: www.clinicaltrials.gov

Chest. 2014;145(4):818-823. doi:10.1378/chest.13-0797

Background:  CT pulmonary angiography (CTPA) is considered the gold standard for the diagnosis of pulmonary embolism (PE) and is frequently performed in patients with cardiopulmonary complaints. However, indiscriminate use of CTPA results in significant exposure to ionizing radiation and contrast. We studied the accuracy of a bedside ultrasound protocol to predict the need for CTPA.

Methods:  This was an observational study performed by pulmonary/critical care physicians trained in critical care ultrasonography. Screening ultrasonography was performed when a CTPA was ordered to rule out PE. The ultrasound examination consisted of a limited ECG, thoracic ultrasonography, and lower extremity deep venous compression study. We predicted that CTPA would not be needed if either DVT was found or clear evidence of an alternative diagnosis was established. CTPA parenchymal and pleural findings, and, when available, formal DVT and ECG results, were compared with our screening ultrasound findings.

Results:  Of 96 subjects who underwent CTPA, 12 subjects (12.5%) were positive for PE. All 96 subjects had an ultrasound study; two subjects (2.1%) were positive for lower extremity DVT, and 54 subjects (56.2%) had an alternative diagnosis suggested by ultrasonography, such as alveolar consolidation consistent with pneumonia or pulmonary edema, which correlated with CTPA findings. In no patient did the CTPA add an additional diagnosis over the screening ultrasound study.

Conclusions:  We conclude that ultrasound examination indicated that CTPA was not needed in 56 of 96 patients (58.3%). A screening, point-of-care ultrasonography protocol may predict the need for CTPA. Furthermore, an alternative diagnosis can be established that correlates with CTPA. This study needs further verification, but it offers a possible approach to reduce the cost and radiation exposure that is associated with CTPA.

Chest. 2014;145(4):824-832. doi:10.1378/chest.13-1422

Background:  COPD is associated with significant morbidity primarily driven by acute exacerbations. Relative pulmonary artery (PA) enlargement, defined as a PA to ascending aorta (A) diameter ratio greater than one (PA:A > 1) identifies patients at increased risk for exacerbations. However, little is known about the correlation between PA:A, echocardiography, and invasive hemodynamics in COPD.

Methods:  A retrospective observational study of patients with severe COPD being evaluated for lung transplantation at a single center between 2007 and 2011 was conducted. Clinical characteristics, CT scans, echocardiograms, and right-sided heart catheterizations were reviewed. The PA diameter at the bifurcation and A diameter from the same CT image were measured. Linear and logistic regression were used to examine the relationships between PA:A ratio by CT scan and PA systolic pressure (PASP) by echocardiogram with invasive hemodynamics. Receiver operating characteristic analysis assessed the usefulness of the PA:A ratio and PASP in predicting resting pulmonary hypertension (PH) (mean pulmonary artery pressure [mPAP] > 25 mm Hg).

Results:  Sixty patients with a mean predicted FEV1 of 27% ± 12% were evaluated. CT scan-measured PA:A correlated linearly with mPAP after adjustment for multiple covariates (r = 0.30, P = .03), a finding not observed with PASP. In a multivariate logistic model, mPAP was independently associated with PA:A > 1 (OR, 1.44; 95% CI, 1.02-2.04; P = .04). PA:A > 1 was 73% sensitive and 84% specific for identifying patients with resting PH (area under the curve, 0.83; 95% CI, 0.72-0.93; P < .001), whereas PASP was not useful.

Conclusions:  A PA:A ratio > 1 on CT scan outperforms echocardiography for diagnosing resting PH in patients with severe COPD.

Original Research: Pulmonary Procedures

Chest. 2014;145(4):833-838. doi:10.1378/chest.13-1971

Background:  The current approaches for tissue diagnosis of a solitary pulmonary nodule are transthoracic needle aspiration, guided bronchoscopy, or surgical resection. The choice of procedure is driven by patient and radiographic factors, risks, and benefits. We describe a new approach to the diagnosis of a solitary pulmonary nodule, namely bronchoscopic transparenchymal nodule access (BTPNA).

Methods:  In anesthetized dogs, fiducial markers were placed and thoracic CT images acquired. From the CT scan, the BTPNA software provided automatic point-of-entry prescribing of a bronchoscopic path (tunnel) through parenchymal tissue directly to the lesion. The preplanned procedure was uploaded to a virtual bronchoscopic navigation system. Bronchoscopic access was performed through the tunnels created. Proximity of the distal end of the tunnel sheath to the target was measured, and safety was recorded.

Results:  In four canines, 13 tunnels were created. The average length of the tunnels was 32.3 mm (range, 24.7-46.7 mm). The average proximity measure was 5.7 mm (range, 0.1-12.9 mm). The distance from the pleura to the nearest point within the target was 7.4 mm (range, 0.1-15 mm). Estimated blood loss was < 2 mL per case. There were no pneumothoraces.

Conclusions:  We describe a new approach to accessing lesions in the lung parenchyma. BTPNA allows bronchoscopic creation of a direct path with a sheath placed in proximity to the target, creating the potential to deliver biopsy tools within a lesion to acquire tissue. The technology appears safe. Further experiments are needed to assess the diagnostic yield of this procedure in animals and, if promising, to assess this technology in humans.

Original Research: Lung Cancer

Chest. 2014;145(4):839-847. doi:10.1378/chest.13-1073

Background:  PET scanning has been shown in randomized trials to reduce the frequency of surgery without cure among patients with potentially resectable non-small cell lung cancer (NSCLC). We examined whether more frequent use of PET scanning at the facility level improves survival among patients with NSCLC in real-world practice.

Methods:  In this prospective cohort study of 622 US veterans with newly diagnosed NSCLC, we compared groups defined by the frequency of PET scan use measured at the facility level and categorized as low (< 25%), medium (25%-60%), or high (> 60%).

Results:  The median age of the sample was 69 years. Ninety-eight percent were men, 36% were Hispanic or nonwhite, and 54% had moderate or severe comorbidities. At low-, medium-, and high-use facilities, PET scan was performed in 13%, 40%, and 72% of patients, respectively (P < .0001). Baseline characteristics were similar across groups, including clinical stage based on CT scanning. More frequent use of PET scanning was associated with more frequent invasive staging (P < .001) and nonsignificant improvements in downstaging (P = .13) and surgery without cure (P = .12). After a median of 352 days of follow-up, 22% of the sample was still alive, including 22% at low- and medium-use facilities and 20% at high-use facilities. After adjustment and compared with patients at low-use facilities, the hazard of death was greater for patients at high-use facilities (adjusted hazard ratio [HR], 1.35; 95% CI, 1.05-1.74) but not different for patients at medium-use facilities (adjusted HR, 1.14; 95% CI, 0.88-1.46).

Conclusions:  In this study of veterans with NSCLC, markedly greater use of PET scanning at the facility level was associated with more frequent use of invasive staging and possible improvements in downstaging and surgery without cure, but greater use of PET scanning was not associated with better survival.

Original Research: Disorders of the Pleura

Chest. 2014;145(4):848-855. doi:10.1378/chest.13-1558

Background:  Pleural infection is associated with a high morbidity and mortality. Development of a validated clinical risk score at presentation to identify those at high risk of dying would enable patient triage and may help formulate early management strategies.

Methods:  A clinical risk score was derived based on data from patients entering the multicenter UK pleural infection trial (first Multicenter Intrapleural Sepsis Trial [MIST1], n = 411). From 22 baseline clinical characteristics, model selection was undertaken to find variables predictive of poor clinical outcome. Outcomes were mortality at 3 months (primary), need for surgical intervention at 3 months, and time from randomization to discharge. The derived scoring system RAPID (renal, age, purulence, infection source, and dietary factors) was validated using patients enrolled in the subsequent MIST2 trial (n = 191).

Results:  Age, urea, albumin, hospital-acquired infection, and nonpurulence predicted poor outcome. Patients were stratified into low-risk (0-2), medium-risk (3-4), and high-risk (5-7) groups. Using the low-risk group as a reference, a RAPID score of 3 to 4 and > 4 was associated with an OR of 24.4 (95% CI, 3.1-186.7; P = .002) and 192.4 (95% CI, 25.0-1480.4; P < .001), respectively, for death at 3 months. In the validation cohort (MIST2), a medium-risk RAPID score was nonsignificantly associated with mortality (OR, 3.2; 95% CI, 0.8-13.2; P = .11), and a high-risk score was associated with increased mortality (OR, 14.1; 95% CI, 3.5-56.8; P < .001). Hospitalization duration was associated with increasing RAPID score (score 0-2: median duration = 7, interquartile range 6-13; score > 5: median duration = 15, interquartile range 9-28, P = .08).

Conclusions:  The RAPID score may permit risk stratification of patients with pleural infection at presentation.

Selected Reports

Chest. 2014;145(4):856-858. doi:10.1378/chest.13-1734

Bakers are exposed daily to flour and may be susceptible to immunologic occupational diseases. A 30-year-old, nonsmoking, female baker was referred for progressive dyspnea on exertion, basal crackles on auscultation, restrictive lung function, decreased diffusing capacity of the lung for carbon monoxide, ground glass hyperdensities with a mosaic pattern on high-resolution CT scan, 25% lymphocytosis by BAL, and cellular chronic bronchiolitis with peribronchiolar interstitial inflammation by lung biopsy specimen. Cultures from flours isolated nine species, including Aspergillus fumigatus. Twenty-six antigens were tested. Serum-specific precipitins were found against A fumigatus, the flour mite Acarus siro, and total extracts from maize and oat. Outcome was favorable with cessation of occupational exposure to flours and transient therapy with prednisone and immunosuppressive agents. To our knowledge, this report is the first of a well-documented case of hypersensitivity pneumonitis due to sensitization to fungi- and mite-contaminated flours. Hypersensitivity pneumonitis—and not only asthma and allergic rhinitis—should be suspected in bakers with respiratory symptoms.

Chest. 2014;145(4):858-860. doi:10.1378/chest.13-1952

We describe the first case, to our knowledge, of Mycobacterium brisbanense species nova with the type strain W6743T (= ATCC 49938T = DSM 44680T) isolated from the lungs of a man with a 6-month history of productive cough and intermittent fever presenting with acute hypoglycemia. A CT scan of the thorax revealed multiple small nodules and consolidation over both lungs with cavitation. Sputum culture repeatedly grew M brisbanense species nova, a novel species never before isolated in Malaysia. The case met the American Thoracic Society criteria for the diagnosis of nontuberculous mycobacterial infection. There was dramatic clinical and radiologic response to treatment with an empirical combination of rifampicin, ethambutol, and levofloxacin and subsequently clarithromycin and levofloxacin once sensitivity was known. This report is the first, to our knowledge, of the pathogen isolated in a patient with chronic cavitary lung infection since it was first identified from an antral sinus in Brisbane, Queensland, Australia, and the first time it is isolated from a human subject in Malaysia.

Recent Advances in Chest Medicine

Chest. 2014;145(4):861-875. doi:10.1378/chest.13-1809

In patients with COPD, cardiovascular diseases are the most common concomitant chronic diseases, a leading cause of hospitalization, and one of the main causes of death. A close connection exists between COPD and cardiovascular diseases. Cardiovascular risk scores aim to predict the effect of cardiovascular comorbidities on COPD mortality, but there is a need to better characterize occult and suboccult cardiovascular disease, even in patients with mild to moderate COPD. Among various surrogate markers of cardiovascular risk, arterial stiffness plays a central role and is a strong independent predictor of cardiovascular events beyond classic cardiovascular risk factors. Its measurement is highly suitable, validated, and relatively easy to perform in routine COPD clinical practice. The growing awareness of the increased cardiovascular risk associated with COPD has led to a call for respiratory physicians to measure arterial pulse wave velocity in routine practice. Cross-sectional data establish elevated arterial stiffness as being independently linked to COPD. Candidate mechanisms have been proposed, but surprisingly, only limited data are available regarding the impact of the different COPD treatment modalities on arterial stiffness, although initial studies have suggested a significant positive impact. In this review, we present the various surrogate markers of cardiovascular morbidity in COPD and the central role of arterial stiffness and the underlying mechanisms explaining vascular remodeling in COPD. We also consider the therapeutic impact of COPD medications and exercise training on arterial stiffness and the assessments that should be implemented in COPD care and follow-up.

Medical Ethics

Chest. 2014;145(4):876-882. doi:10.1378/chest.13-1138
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Extracorporeal membrane oxygenation (ECMO) can serve as a bridge to recovery in cases of acute reversible illness, a bridge to transplantation in circumstances of irreversible cardiac or respiratory failure, a bridge to ventricular assist device therapy in select cases of cardiac failure, or a bridge to decision when the prognosis remains uncertain. Recent advances in ECMO technology that allow for prolonged support with decreased complications, the development of mobile ECMO teams, the rapidity of initiation, and the growing body of evidence, much of which remains controversial, have led to a significant increase in the use of ECMO worldwide. This increasing use of a technology that is not a destination device in itself introduces many ethical dilemmas specific to this technology. In this article, we explore some of the ethical issues inherent in the decisions surrounding the initiation and withdrawal of ECMO by raising key questions and providing a framework for clinicians. We will address extracorporeal cardiopulmonary resuscitation, the inability to bridge a patient to transplant or recovery—the so-called “bridge to nowhere”—and the significance of resuscitation preferences in the setting of continual extracorporeal circulatory support.

Special Features

Chest. 2014;145(4):883-895. doi:10.1378/chest.13-2072

Parasitic infestations affect millions of the world’s population. Global immigration and climate change have led to changes in the natural distribution of parasitic diseases far removed from endemic areas. A broad spectrum of helminthic and protozoal parasitic diseases frequently affects the respiratory system. The wide varieties of clinical and radiographic presentations of parasitic diseases make the diagnosis of this entity challenging. Pulmonologists need to become familiar with the epidemiology, clinical presentation, pathophysiologic characteristics, and bronchoscopic findings to provide proper management in a timely fashion. This review provides a comprehensive view of both helminthic and protozoal parasitic diseases that affect the respiratory system, especially the airways.

Topics in Practice Management

Chest. 2014;145(4):896-902. doi:10.1378/chest.13-0251

The Internet has fundamentally transformed the way patients and health-care providers communicate and interact. The use of digital tools and social media platforms, such as blogs, Facebook, Instagram, and Twitter, have empowered patients to expand their health-care knowledge and have provided practitioners with new ways to gain knowledge, lead discussions, promote causes, and build relationships with patients and other providers. In this article, we discuss the difference between digital communication, static one-way digital presence, and two-way social media connections. We also describe ways to establish and foster your digital profile, review the benefits and risks of engaging professionally in social media, and describe ways in which digital and social media tools may prove useful in both reimbursement and practice management.

Postgraduate Education Corner: Contemporary Reviews in Critical Care Medicine

Chest. 2014;145(4):903-912. doi:10.1378/chest.13-0005

This third and final installment of this series on innovative designs for the smart ICU addresses the steps involved in conceptualizing, actualizing, using, and maintaining the advanced ICU informatics infrastructure and systems. The smart ICU comprehensively and electronically integrates the patient in the ICU with all aspects of care, displays data in a variety of formats, converts data to actionable information, uses data proactively to enhance patient safety, and monitors the ICU environment to facilitate patient care and ICU management. The keys to success in this complex informatics design process include an understanding of advanced informatics concepts, sophisticated planning, installation of a robust infrastructure capable of both connectivity and interoperability, and implementation of middleware solutions that provide value. Although new technologies commonly appear compelling, they are also complicated and challenging to incorporate within existing or evolving hospital informatics systems. Therefore, careful analysis, deliberate testing, and a phased approach to the implementation of innovative technologies are necessary to achieve the multilevel solutions of the smart ICU.

Postgraduate Education Corner: Chest Imaging and Pathology for Clinicians

Chest. 2014;145(4):913-918. doi:10.1378/chest.13-1662

A 76-year-old man presented with left-sided hip pain radiating to the leg and foot for 4 weeks. He was a former smoker. The patient’s medical history included coronary artery disease, benign prostatic hypertrophy, and mild chronic renal impairment (serum creatinine, 1.5 mg/dL). Other previous blood chemistry tests and chest radiographs obtained 6 months earlier were unremarkable. The plain radiographs of the lumbosacral spine revealed only mild degenerative changes.

Postgraduate Education Corner: Pulmonary, Critical Care, and Sleep Pearls

Chest. 2014;145(4):919-922. doi:10.1378/chest.13-1965

A 63-year-old man with an extensive smoking history presented with a complaint of persistent dry cough for 3 months. His past medical history was significant for severe COPD with an FEV1 at 40% predicted (stage III by GOLD [Global Initiative for Obstructive Lung Disease] criteria). The patient was retired and a current cigarette smoker, and he had no pets. There was no history of prior malignancy or recent travels. He had no fever, night sweats, or weight loss. He was not receiving any angiotensin-converting enzyme inhibitors. There were no symptoms suggestive of upper airway cough syndrome or gastroesophageal reflux disease.

Postgraduate Education Corner: Ultrasound Corner

Chest. 2014;145(4):e10-e13. doi:10.1378/chest.13-2260

A male teenager presented to the ED complaining of fevers and a sore throat for 1 week. He had previously visited his primary care physician and received a 3-day course of azithromycin without improvement. The initial ED visit showed a normal chest radiograph and unremarkable physical examination; blood was drawn, and he was sent home with a prescription for acetaminophen. The next day his blood cultures grew gram-negative rods, and he was called to return to the ED for follow-up care. He now complained of a worsening sore throat and odynophagia. He had a mild nonproductive cough with no dysphonia, trismus, or neck pain. Review of other systems was normal. Of note, he had no recent dental procedures.

Pectoriloquy

Chest. 2014;145(4):923. doi:10.1378/chest.13-1273
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I remember waking up early that morning.
You, still sound asleep, deserving a few moments longer.
Lord knows you had taken care of me all those months.
Ever since Dr. H. told us “we” had cancer -
lung cancer - stage IV – all the way to the brain.
I blamed myself for putting you through this.
How long did it take me to give them up?
But you stayed with me,
held my hand, tightly, as Dr. H. repeated those words,
making sure we understood.
We did.
And there we were.
Knowing the end would be sooner, rather than later.
I worried about you being alone.
You said there was time to think about that.
For now, it was about me;
the symptoms, treatment, side effects … our cancer.
Even though we knew it would never be enough –
that soon I would be gone.
You made me the focus and I let you.
It was your gift to me you said.
I accepted that.
Yet, here I am two years later.
Me, still surviving.
I’ve had good care.
Now and everyday
remembering back to that morning
I let you sleep a bit longer –
the only gift I could give in return
but, you were not asleep at all.

Chest. 2014;145(4):924. doi:10.1378/chest.13-2147
FREE TO VIEW

Marsha said she’d appear on Sunday and we would go to the
store and buy cases of electrolyte drinks – although I remain
unclear about what electrolytes actually are and why I have
ended up in the ER because my electrolytes were horrendously
disheveled – one time by ambulance which was a kind of public
display of my failures to be a healthy human being that I work
on avoiding – not successfully that time – the hospital allowed
five liters of electrolyte liquid and then put me on a bus back
to my house on another dark night – another night because
nights are always dark so it is not necessary to repeat the
obvious – unless the lights are turned on yet still there’s that
suggestion in the background that now is night and you had
better be either dancing or sleeping.

Chest. 2014;145(4):924. doi:10.1378/chest.13-2156
FREE TO VIEW

The sweet dreams of needles plunged into meridian points that
connect to the earth and stars giving away that quiver of qi up
your arms into the cavern where a heart used to be and actually
still is but the cave seems larger with steep walls climbing
higher than the sky although to pierce a necessary point while
you lie on the table and feel the plunge. The plant in your
bedroom has big leaves and an arrogant attitude. Objects
abound. The book on shoes you bought because you had to,
because you did not buy it before and thought about it and felt
it as loss, suddenly now the book reappears and that loss can be
filled perfectly. Unlike. Unlike.
How much needs to be explained about loss remaining loss?
The earth as burial for secrets, the stories never told and only
one person knows and will not say but asks for the needles to
dream and break the narration.

Correspondence

Chest. 2014;145(4):925. doi:10.1378/chest.13-2764
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Chest. 2014;145(4):925-926. doi:10.1378/chest.13-2857
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Chest. 2014;145(4):926-927. doi:10.1378/chest.13-2978
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Chest. 2014;145(4):927. doi:10.1378/chest.14-0098
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Chest. 2014;145(4):927-928. doi:10.1378/chest.13-2971
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Chest. 2014;145(4):928. doi:10.1378/chest.14-0178
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Errata

Chest. 2014;145(4):929. doi:10.1378/chest.14-0489
FREE TO VIEW

An error appeared in the title of: “Detection of COPD Exacerbations and Compliance With Patient-Reported Daily Symptom Diaries” published in August 2013 (Chest. 2013; 144(2): 507-514.)

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  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543