0

Current Issue

Editorials

Chest. 2015;147(3):585-586. doi:10.1378/chest.14-2701

ARDS is a complex syndrome, characterized by damage to the alveolar-capillary barrier resulting in increased permeability in the setting of an amplified inflammatory response. The role of the activation of clotting pathways in this process has been increasingly recognized, including the significant impact of platelets on ARDS pathogenesis.1-3 In a steady state, inactive platelets circulate in blood and promote endothelial barrier integrity.4 However, in the setting of critical illnesses (eg, sepsis), several overlapping mechanisms activate platelets, resulting in platelet aggregation, platelet-leukocyte complex formation, and release of the granule contents of the platelet cell, including molecules that enhance inflammation and cell adhesion. While platelet-mediated thrombosis in the lungs has been implicated in ARDS pathogenesis, the activation of circulating platelets results in a host of other inflammatory effects contributing to ARDS development, including augmented neutrophil migration and increased endothelial barrier permeability.3

Chest. 2015;147(3):586-588. doi:10.1378/chest.14-2081

Heart failure (HF) and COPD are major and increasing public health problems worldwide. In the United States, HF affects > 5 million adults and results in > 1 million hospitalizations annually.1 Despite advances in the treatment of chronic HF, outcomes following acute HF hospitalization remain poor.1 Given the neutral results of most recent HF trials, there is a need for a critical reappraisal of strategies to improve outcomes.2 COPD affects > 15 million Americans, commonly occurs in patients with HF, and is associated with significant morbidity and mortality.3-5 Recognition of the impact of comorbid conditions such as COPD on the characteristics and outcomes of patients with HF may represent a first step to identify strategies to improve outcomes.6 It is in this context that Fisher et al7 assessed the patient phenotype, management, and long-term outcomes of hospitalized patients with HF and COPD in this issue of CHEST (see page 637).

Chest. 2015;147(3):589-590. doi:10.1378/chest.14-2170

Treatment of patients with VTE, whether determining setting or intensity of care or duration of secondary prevention, is shifting from a disease-specific to an individualized approach. Current evidence-based treatment guidelines are fairly straightforward for some patients, such as those who present with isolated DVT or hemodynamic shock or sudden cardiac death.1 There is growing recognition, however, that patients with acute pulmonary embolism (PE) who are hemodynamically stable are not homogeneous. Some of these patients, particularly those with evidence of higher clot burden and right ventricular strain, might benefit from more aggressive care, to include ICU admission and the consideration of thrombolytic therapy. Other patients may suffer minimal physiologic consequences from the acute clot and could potentially be treated in the outpatient environment.2

Chest. 2015;147(3):590-592. doi:10.1378/chest.14-2202

Alveolar-pleural fistula (APF) and bronchopleural fistula (BPF) are uncommon yet frustrating medical and surgical problems with high morbidity and mortality. They may originate spontaneously or be encountered after bronchoscopy or thoracic surgery. However, they are almost always caused by an underlying pulmonary pathology, which seems to be the most important prognostic factor.

New Associate Editors

Chest. 2015;147(3):593. doi:10.1378/chest.15-0039
FREE TO VIEW

We are pleased to announce the appointment of Reena Mehra, MD, FCCP, as Associate Editor for CHEST. As Associate Editor with a 3-year term, she joins the existing Associate Editor group in providing guidance for the future direction of the Journal.

Point and Counterpoint

Chest. 2015;147(3):594-595. doi:10.1378/chest.14-2838
FREE TO VIEW

The model of health-care delivery in the United States is evolving to endorse collaborative and multidisciplinary care delivered to more people with fewer complications at a lower cost. In response to the nation’s demand for health-care reform, the Institute of Medicine (IOM) produced the landmark report, The Future of Nursing: Leading Change, Advancing Health.1 Herein, the IOM sounded a clarion call for nurses to practice to the full extent of their education and training. Can nurse practitioners (NPs) do transbronchial biopsies? Yes. Should they? According to the IOM, if they can, they should. This is consistent with the balanced ideals of quality, access, and cost which must be given due consideration in any theoretical debate about delivery of health care.2

Chest. 2015;147(3):596-597. doi:10.1378/chest.14-2840
FREE TO VIEW

I (C. B. S.) was flying home from a conference in a Boeing 787 when I first began to write this editorial and wondered about the analogous questions from other industries. Did I really want a trained pilot in the cockpit? Could not anyone train on simulators enough to achieve competence in handling any airplane? What if someone put in sufficient hours of simulator and supervised flight time, might they then be given the controls of my 787? And the answer was that with enough training anyone can become sufficiently competent to perform any procedure in medicine.

Chest. 2015;147(3):597-598. doi:10.1378/chest.14-2839
FREE TO VIEW

The question is not, as Drs Pastis and Strange1 have suggested, about the best interest of the medical profession; rather, it is about what is in the best interest of the patients. A decade ago, Barber and colleagues2 published their experience in developing the first nurse-led bronchoscopy practice in the United Kingdom. Inspiration to establish this practice was drawn from concerns about inconsistency and rapid turnover of medical trainees, the multiple competing priorities of attending physicians, and the business practicalities associated with facilitating interventional techniques. In other words, they were seeking to optimize quality, access, and cost in the bronchoscopy suite. The curriculum and practical training were deemed to be “safe, well supervised, rigorous and formal.” Eight months after the program was completed, an audit was performed to evaluate the first nurse bronchoscopist’s safety and efficacy. With no adverse events and a 95% histology hit rate, findings compared favorably with published physician bronchoscopists’ results and the standards set forth by the British Thoracic Society. Regardless of the bronchoscopist’s discipline, these findings are consistent with the advice from Ernst and colleagues3 who suggested that procedural volume would beget safety and mastery.

Chest. 2015;147(3):598-599. doi:10.1378/chest.14-2841
FREE TO VIEW

As I reflect on my most recent episode of life-threatening hemoptysis after transbronchial lung biopsies (TBLBs), I compare it to an episode from earlier in my career. Even in the busiest bronchoscopy suites, these events are rare, and a year or more may pass between episodes. My first episode occurred after performing biopsies on a morbidly obese patient with multiple comorbidities, and I was terrified. Ultimately and with difficulty, an airway was established, and the nonbleeding lung was isolated with the endotracheal tube. After 2 days in the ICU, she was safe to discharge home. During my most recent episode 12 years later, our bronchoscopy staff and I were like a well-oiled machine. Within minutes, not only was an airway established, but an endobronchial blocker was placed deftly into the left lower lobe bronchus, and we were calmly updating the family.

Commentary

Chest. 2015;147(3):600-606. doi:10.1378/chest.14-1648

Because of the rapid increase in the volume and costs of polysomnography and other sleep medicine diagnostic services, the Centers for Medicare & Medicaid Services (CMS) recently commissioned the Office of Inspector General (OIG) to review claims submitted for these services. The OIG found numerous cases of inappropriate payment for submitted claims and recommended significant changes in the CMS auditing process for polysomnography claims review. Additionally, a local Medicare Administrative Contractor released the most specific rules and regulations to date regarding billing and payment for sleep medicine services. These regulations specify covered diagnoses for submitted claims for both facility-based polysomnograms and unattended home sleep tests (HSTs) and list noncovered diagnoses that cannot be used to document medical necessity for such studies. The proposed rules specify minimum credentials for technologists performing polysomnograms and HSTs, mandate education prior to application of HST devices, demand a follow-up visit to discuss results after studies, and elaborate new requirements for physicians interpreting these studies. Providers of sleep medicine services must be prepared to provide documentation of diagnoses and indications when submitting claims for sleep services, and they can expect to be required to produce evidence of accreditation of the physicians and technologists providing services and the credentials of the sleep center. These changes will dramatically affect sleep medicine practitioners who order sleep studies and positive airway pressure therapies. Successful sleep medicine centers and sleep physicians alike will need to develop strategies to meet these new challenges.

Original Research: Critical Care

Chest. 2015;147(3):607-617. doi:10.1378/chest.14-1246

BACKGROUND:  Platelets are believed to be critical in pulmonary-origin ARDS as mediators of endothelial damage through their interactions with fibrinogen and multiple signal transduction pathways. A prior meta-analysis identified five loci for platelet count (PLT): BAD, LRRC16A, CD36, JMJD1C, and SLMO2. This study aims to validate the quantitative trait loci (QTLs) of PLT within BAD, LRRC16A, CD36, JMJD1C, and SLMO2 among critically ill patients and to investigate the associations of these QTLs with ARDS risk that may be mediated through PLT.

METHODS:  ARDS cases and at-risk control subjects were recruited from the intensive care unit of the Massachusetts General Hospital. Exome-wide genotyping data of 629 ARDS cases and 1,026 at-risk control subjects and genome-wide gene expression profiles of 18 at-risk control subjects were generated for analysis.

RESULTS:  Single-nucleotide polymorphism (SNP) rs7766874 within LRRC16A was a significant locus for PLT among at-risk control subjects (β = −13.00; 95% CI, −23.22 to −2.77; P = .013). This association was validated using LRRC16A gene expression data from at-risk control subjects (β = 77.03 per 1 SD increase of log2-transformed expression; 95% CI, 27.26-126.80; P = .005). Further, rs7766874 was associated with ARDS risk conditioned on PLT (OR = 0.68; 95% CI, 0.51-0.90; P = .007), interacting with PLT (OR = 1.15 per effect allele per 100 × 103/μL of PLT; 95% CI, 1.03-1.30; P = .015), and mediated through PLT (indirect OR = 1.045; 95% CI, 1.007-1.085; P = .021).

CONCLUSIONS:  Our findings support the role of LRRC16A in platelet formation and suggest the importance of LRRC16A in ARDS pathophysiology by interacting with, and being mediated through, platelets.

Chest. 2015;147(3):618-625. doi:10.1378/chest.14-1371

BACKGROUND:  Early differential diagnosis of acute lung injury (ALI) vs cardiogenic pulmonary edema (CPE) is important for selecting the most appropriate therapy, but the prognostic implications of this distinction have not been studied. Accurate prognostic information is essential for providing appropriate informed consent prior to initiation of mechanical ventilation.

METHODS:  This is a long-term follow-up study of a previously established population-based cohort of critically ill adult patients with acute pulmonary edema admitted at a tertiary-care center during 2006 to 2009, in which post hoc expert review had established ALI vs CPE diagnosis. Using logistic and Cox regression, hospital mortality and long-term survival were compared in patients with ALI vs patients with CPE.

RESULTS:  Of 328 patients (ALI = 155, CPE = 173), 240 patients (73%) died during a median follow-up of 160 days. After adjusting for confounders, patients with ALI were significantly more likely to die in the hospital (OR = 4.2, 95% CI = 2.3-7.8, n = 325, P < .001), but among hospital survivors the risk of death during follow-up was the same in both groups (hazard ratio = 1.13, 95% CI = 0.79-1.62, n = 229, P = .50). Independent predictors of mortality included age and APACHE (Acute Physiology and Chronic Health Evaluation) III score. Results were similar when restricting patients with ALI to the subset with ARDS (Berlin definition). In post hoc analyses, the mortality rate in hospital survivors compared with the general US population was significantly higher during the first 2 years but essentially converged by year five.

CONCLUSIONS:  Although hospital mortality is higher in patients with ALI/ARDS compared with patients with CPE, long-term survival is similar in hospital survivors from both groups.

Chest. 2015;147(3):626-636. doi:10.1378/chest.14-1060

BACKGROUND:  ICU readmissions are associated with increased mortality and costs; however, it is unclear whether these outcomes are caused by readmissions or by residual confounding by illness severity. An assessment of temporal changes in ICU readmission in response to a specific policy change could help disentangle these possibilities. We sought to determine whether ICU readmission rates changed after 2003 Accreditation Council for Graduate Medical Education Resident Duty Hours reform (“reform”) and whether there were temporally corresponding changes in other ICU outcomes.

METHODS:  We used a difference-in-differences approach using Project IMPACT (Improved Methods of Patient Information Access of Core Clinical Tasks). Piecewise regression models estimated changes in outcomes immediately before and after reform in 274,491 critically ill medical and surgical patients in 151 community and academic US ICUs. Outcome measures included ICU readmission, ICU mortality, and in-hospital post-ICU-discharge mortality.

RESULTS:  In ICUs with residents, ICU readmissions increased before reform (OR, 1.5; 95% CI, 1.22-1.84; P < .01), and decreased after (OR, 0.85; 95% CI, 0.73-0.98; P = .03). This abrupt decline in ICU readmissions after reform differed significantly from an increase in readmissions observed in ICUs without residents at this time (difference-in-differences P < .01). No comparable changes in mortality were observed between ICUs with vs without residents.

CONCLUSIONS:  The changes in ICU readmission rates after reform, without corresponding changes in mortality, suggest that ICU readmissions are not causally related to other untoward patient outcomes. Instead, ICU readmission rates likely reflect operational aspects of care that are not patient-centered, making them less useful indicators of ICU quality.

Original Research: COPD

Chest. 2015;147(3):637-645. doi:10.1378/chest.14-0607

BACKGROUND:  COPD is a common comorbidity in patients with heart failure, yet little is known about the impact of this condition in patients with acute decompensated heart failure (ADHF), especially from a more generalizable, community-based perspective. The primary objective of this study was to describe the in-hospital and postdischarge mortality and treatment of patients hospitalized with ADHF according to COPD status.

METHODS:  The study population consisted of patients hospitalized with ADHF at all 11 medical centers in central Massachusetts during four study years: 1995, 2000, 2002, and 2004. Patients were followed through 2010 for determination of their vital status.

RESULTS:  Of the 9,748 patients hospitalized with ADHF during the years under study, 35.9% had a history of COPD. The average age of this population was 76.1 years, 43.9% were men, and 93.3% were white. At the time of hospital discharge, patients with COPD were less likely to have received evidence-based heart failure medications, including β-blockers and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, than patients without COPD. Multivariable, adjusted in-hospital death rates were similar for patients with and without COPD. However, among patients who survived to hospital discharge, patients with COPD had a significantly higher risk of dying at 1 year (adjusted relative risk [RR], 1.10; 95% CI, 1.06-1.14) and 5 years (adjusted RR, 1.40; 95% CI, 1.28-1.52) after hospital discharge than patients who were not previously diagnosed with COPD.

CONCLUSIONS:  COPD is a common comorbidity in patients hospitalized with ADHF and is associated with a worse long-term prognosis. Further research is required to understand the complex interactions of these diseases and ensure that patients with ADHF and COPD receive optimal treatment modalities.

Chest. 2015;147(3):646-661. doi:10.1378/chest.14-1658

BACKGROUND:  Self-management (SM) reduces hospital admissions in patients with stable COPD. However, its role immediately post-acute exacerbation (AE) is unclear. The objectives of this review were to describe SM interventions delivered immediately following an AE of COPD (AECOPD) and to conduct a systematic review with meta-analysis of its impact on health-care utilization and health outcomes.

METHODS:  Randomized controlled trials reporting on SM interventions delivered during hospitalization for an AECOPD or within 1 month of hospital discharge were included. Seven articles were identified. Data were extracted and assessed for quality by two researchers.

RESULTS:  By definition, all interventions included action plans, education, and at least two SM skills. Nurses were responsible for providing all SM interventions. The delivery and follow-up periods varied widely. At 12 months, there were no significant differences between those who completed the SM intervention and control subjects in the number of patients readmitted to hospital (P = .38), or in health-related quality of life (P = .27). No effects were found on rate of mortality, depressive symptoms, primary care usage, or exercise capacity. Minimal effects were found on self-efficacy, anxiety symptoms, and health promoting behavior. SM was associated with positive effects on knowledge and management of an AECOPD.

CONCLUSIONS:  SM interventions delivered immediately post-AE vary widely and outcome measures are inconsistent, making it difficult to draw strong recommendations regarding its effectiveness. The evaluation of SM interventions, delivered by trained health-care professionals to selected patients and which offer structured follow-up, appears necessary.

Chest. 2015;147(3):662-672. doi:10.1378/chest.14-1488

BACKGROUND:  Involving family as part of the patient’s rehabilitation plan of care might enhance the management of COPD. The primary aim of this study was to investigate the impact of a family-based pulmonary rehabilitation (PR) program on patients and family members’ coping strategies to manage COPD.

METHODS:  Family dyads (patient and family member) were randomly assigned to family-based (experimental) or conventional (control) PR. Patients from both groups underwent exercise training three times a week and psychosocial support and education once a week, during 12 weeks. Family members of the family-based PR attended the psychosocial support and education sessions together with patients. In the conventional PR, family members did not participate. Family coping and psychosocial adjustment to illness were assessed in patients and family members of both groups. Patients’ exercise tolerance, functional balance, muscle strength, and health-related quality of life were also measured. All measures were collected pre/post-program.

RESULTS:  Forty-two dyads participated (patients: FEV1, 70.4% ± 22.1% predicted). Patients (P = .048) and family members (P = .004) in the family-based PR had significantly greater improvements in family coping than the control group. Family members of the family-based PR had significantly greater changes in sexual relationships (P = .026) and in psychologic distress (P = .033) compared with the control group. Patients from both groups experienced significant improvements in exercise tolerance, functional balance, knee extensors strength, and health-related quality of life after intervention (P < .001).

CONCLUSIONS:  This research supports family-based PR programs to enhance coping and psychosocial adjustment to illness of the family system.

TRIAL REGISTRY:  ClinicalTrials.gov; No.: NCT02048306; URL: www.clinicaltrials.gov

Chest. 2015;147(3):673-684. doi:10.1378/chest.14-1079

BACKGROUND:  Although the aerobic profile of the quadriceps muscle is reduced in COPD, there is conflicting evidence regarding whether this leads to reduced quadriceps muscle endurance. We, therefore, performed a systematic review of studies comparing quadriceps endurance in individuals with COPD with that in healthy control subjects.

METHODS:  Relevant studies were identified by searching six electronic databases (1946-2011). Full-text articles were obtained after two researchers independently reviewed the abstracts. The results were combined in a random effects meta-analysis, and metaregression models were fitted to assess the influence of the type of measurement.

RESULTS:  Data were extracted from 21 studies involving 728 individuals with COPD and 440 healthy control subjects. Quadriceps endurance was reduced in those with COPD compared with healthy control subjects (standardized mean difference, 1.16 [95% CI, 1.02-1.30]; P < .001) with a 44.5 s (4.5-84.5 s; P = .029) reduction in COPD (large effect size) when measured using a nonvolitional technique. The relationship between quadriceps endurance in those with COPD and control subjects did not differ when comparing nonvolitional and volitional techniques (P = .22) or when high- or low-intensity tasks (P = .44) were undertaken.

CONCLUSIONS:  Quadriceps endurance is reduced in individuals with COPD compared with healthy control subjects, independent of the type of task performed.

Original Research: Pulmonary Vascular Disease

Chest. 2015;147(3):685-694. doi:10.1378/chest.14-0700

BACKGROUND:  Elevated cardiac troponin levels have been shown to be associated with adverse outcomes in patients with acute pulmonary embolism (PE). However, few data address the management implications of undetectable cardiac troponin I (cTnI) using a highly sensitive assay. We hypothesized that undetectable cTnI predicts very low in-hospital adverse event rates.

METHODS:  In a retrospective cohort study, we classified patients with confirmed acute PE according to cTnI detectability into cTnI+ (≥ 0.012 ng/mL) and cTnI− (< 0.012 ng/mL) groups. The Pulmonary Embolism Severity Index (PESI) was used for clinical risk determination. The primary outcome was a composite of hard events defined as in-hospital death, CPR, or thrombolytic therapy. The secondary outcome was a composite of soft events defined as ICU admission or inferior vena cava filter placement.

RESULTS:  Among 298 consecutive patients with confirmed acute PE, 161 (55%) were cTnI+ and 137 (45%) cTnI−. No deaths occurred in the cTnI− group vs nine (6%) in the cTnI+ group (P = .004). No hard events were observed in the cTnI− group vs 15 (9%) in the cTnI+ group (P < .001). Soft events were observed at a lower rate in the cTnI– group (21[15%] vs 69 [43%], P < .001). Patients in the cTnI− group had a higher survival rate free of hard (P = .001) or soft (P < .001) events, irrespective of clinical risk. Furthermore, cTnI provided incremental prognostic value beyond clinical, ECG, and imaging data (P < .001).

CONCLUSIONS:  Highly sensitive cTnI assay provides an excellent prognostic negative predictive value; thus, it plays a role in identifying candidates for out-of-hospital treatment of acute PE.

Original Research: Pulmonary Procedures

Chest. 2015;147(3):695-699. doi:10.1378/chest.14-0823

BACKGROUND:  Alveolar-pleural fistula with persistent air leak is a common problem causing significant morbidity, prolonged hospital stay, and increased health-care costs. When conventional therapy fails, an alternative to prolonged chest-tube drainage or surgery is needed. New bronchoscopic techniques have been developed to close the air leak by reducing the flow of air through the leak. The objective of this study was to analyze our experience with bronchoscopic application of a synthetic hydrogel for the treatment of such fistulas.

METHODS:  We conducted a retrospective study of patients with alveolar-pleural fistula with persistent air leaks treated with synthetic hydrogel application via flexible bronchoscopy. Patient characteristics, underlying disease, and outcome of endoscopic treatment were analyzed.

RESULTS:  Between January 2009 and December 2013, 22 patients (14 men, eight women; mean age ± SD, 62 ± 10 years) were treated with one to three applications of a synthetic hydrogel per patient. The primary etiology of persistent air leak was necrotizing pneumonia (n = 8), post-thoracic surgery (n = 6), bullous emphysema (n = 5), idiopathic interstitial pneumonia (n = 2), and sarcoidosis (n = 1). Nineteen patients (86%) had complete resolution of the air leak, leading to successful removal of chest tube a mean ( ± SD) of 4.3 ± 0.9 days after last bronchoscopic application. The procedure was very well tolerated, with two patients coughing up the hydrogel and one having hypoxemia requiring bronchoscopic suctioning.

CONCLUSIONS:  Bronchoscopic administration of a synthetic hydrogel is an effective, nonsurgical, minimally invasive intervention for patients with persistent pulmonary air leaks secondary to alveolar-pleural fistula.

Chest. 2015;147(3):700-707. doi:10.1378/chest.14-0724

BACKGROUND:  Bronchoscopic transparenchymal nodule access (BTPNA) is a novel approach to accessing pulmonary nodules. This real-time, image-guided approach was evaluated for safety, accuracy, and yield in the healthy canine model.

METHODS:  A novel, inorganic model of subcentimeter pulmonary nodules was developed, consisting of 0.25-cc aliquots of calcium hydroxylapatite (Radiesse) implanted via transbronchial access in airways seven generations beyond the main bronchi to represent targets for evaluation of accuracy and yield. Thoracic CT scans were acquired for each subject, and from these CT scans LungPoint Virtual Bronchoscopic Navigation software provided guidance to the region of interest. Novel transparenchymal nodule access software algorithms automatically generated point-of-entry recommendations, registered CT images, and real-time fluoroscopic images and overlaid guidance onto live bronchoscopic and fluoroscopic video to achieve a vessel-free, straight-line path from a central airway through parenchymal tissue for access to peripheral lesions.

RESULTS:  In a nine-canine cohort, the BTPNA procedure was performed to sample 31 implanted Radiesse targets, implanted to simulate pulmonary nodules, via biopsy forceps through a specially designed sheath. The mean length of the 31 tunnels was 35 mm (20.5-50.3-mm range). Mean tunnel creation time was 16:52 min, and diagnostic yield was 90.3% (28 of 31). No significant adverse events were noted in the status of any of the canine subjects post BTPNA, with no pneumothoraces and minimal bleeding (all bleeding events < 2 mL in volume).

CONCLUSIONS:  These canine studies demonstrate that BTPNA has the potential to achieve the high yield of transthoracic needle aspiration with the low complication profile associated with traditional bronchoscopy. These results merit further study in humans.

Original Research: Sleep Disorders

Chest. 2015;147(3):708-718. doi:10.1378/chest.14-1634

BACKGROUND:  The impact of OSA treatment with CPAP on percutaneous coronary intervention (PCI) outcomes remains largely unknown.

METHODS:  Between 2002 and 2012, we identified 390 patients with OSA who had undergone PCI. OSA was diagnosed through in-laboratory sleep studies and defined by an apnea-hypopnea index ≥ 5 events/h. The cohort was divided into three groups: (1) moderate-severe OSA successfully treated with CPAP (n = 128), (2) untreated moderate-severe OSA (n = 167), and (3) untreated mild OSA (n = 95). Main outcomes included repeat revascularization, major adverse cardiac events (MACEs) (ie, death, nonfatal myocardial infarction, repeat revascularization), and major adverse cardiac or cerebrovascular events (MACCEs). The median follow-up period was 4.8 years (interquartile range, 3.0-7.1).

RESULTS:  The untreated moderate-severe OSA group had a higher incidence of repeat revascularization than the treated moderate-severe OSA group (25.1% vs 14.1%, P = .019). There were no differences in mortality (P = .64), MACE (P = .33), and MACCE (P = .76) among the groups. In multivariate analysis adjusted for potential confounders, untreated moderate-severe OSA was associated with increased risk of repeat revascularization (hazard ratio, 2.13; 95% CI, 1.19-3.81; P = .011).

CONCLUSIONS:  Untreated moderate-severe OSA was independently associated with a significant increased risk of repeat revascularization after PCI. CPAP treatment reduced this risk.

Chest. 2015;147(3):719-727. doi:10.1378/chest.14-0929

BACKGROUND:  The advent of home sleep testing has allowed for the development of an ambulatory care model for OSA that most health-care providers can easily deploy. Although automated algorithms that accompany home sleep monitors can identify and classify disordered breathing events, it is unclear whether manual scoring followed by expert review of home sleep recordings is of any value. Thus, this study examined the agreement between automated and manual scoring of home sleep recordings.

METHODS:  Two type 3 monitors (ApneaLink Plus [ResMed] and Embletta [Embla Systems]) were examined in distinct study samples. Data from manual and automated scoring were available for 200 subjects. Two thresholds for oxygen desaturation (≥ 3% and ≥ 4%) were used to define disordered breathing events. Agreement between manual and automated scoring was examined using Pearson correlation coefficients and Bland-Altman analyses.

RESULTS:  Automated scoring consistently underscored disordered breathing events compared with manual scoring for both sleep monitors irrespective of whether a ≥ 3% or ≥ 4% oxygen desaturation threshold was used to define the apnea-hypopnea index (AHI). For the ApneaLink Plus monitor, Bland-Altman analyses revealed an average AHI difference between manual and automated scoring of 6.1 (95% CI, 4.9-7.3) and 4.6 (95% CI, 3.5-5.6) events/h for the ≥ 3% and ≥ 4% oxygen desaturation thresholds, respectively. Similarly for the Embletta monitor, the average difference between manual and automated scoring was 5.3 (95% CI, 3.2-7.3) and 8.4 (95% CI, 7.2-9.6) events/h, respectively.

CONCLUSIONS:  Although agreement between automated and manual scoring of home sleep recordings varies based on the device used, modest agreement was observed between the two approaches. However, manual review of home sleep test recordings can decrease the misclassification of OSA severity, particularly for those with mild disease.

TRIAL REGISTRY:  ClinicalTrials.gov; No.: NCT01503164; www.clinicaltrials.gov

Chest. 2015;147(3):728-734. doi:10.1378/chest.14-1187

BACKGROUND:  Excess sitting is emerging as a novel risk factor for cardiovascular disease, diabetes, mental illness, and all-cause mortality. Physical activity, distinct from sitting, is associated with better sleep and lower risk for OSA, yet relationships among sitting behaviors and sleep/OSA remain unknown. We examined whether total sitting time and sitting while viewing television were associated with sleep duration and quality, OSA risk, and sleepiness.

METHODS:  The 2013 National Sleep Foundation Sleep in America Poll was a cross-sectional study of 1,000 adults aged 23 to 60 years. Total sitting time, time watching television while sitting, sleep duration and quality, OSA risk, and daytime sleepiness were assessed.

RESULTS:  After adjusting for confounding factors (including BMI and physical activity), each additional hour per day of total sitting was associated with greater odds of poor sleep quality (OR [95% CI] = 1.06 [1.01, 1.11]) but not with other sleep metrics (including sleep duration), OSA risk, or daytime sleepiness. For television viewing while sitting, each additional hour per day was associated with greater odds of long sleep onset latency (≥ 30 min) (OR = 1.15 [1.04, 1.27]), waking up too early in the morning (OR = 1.12 [1.03, 1.23]), poor sleep quality (OR = 1.12 [1.02, 1.24]), and “high risk” for OSA (OR = 1.15 [1.04, 1.28]). Based upon an interaction analysis, regular physical activity was protective against OSA risk associated with television viewing (P = .04).

CONCLUSIONS:  Excess sitting was associated with relatively poor sleep quality. Sitting while watching television was associated with relatively poor sleep quality and OSA risk and may be an important risk factor for sleep disturbance and apnea risk.

Original Research: Asthma

Chest. 2015;147(3):735-744. doi:10.1378/chest.14-1119

BACKGROUND:  Cigarette smoking is associated with worse symptoms in asthma and abnormal segmental airways in healthy subjects. We tested the hypothesis that current symptom control in smokers with asthma is associated with altered segmental airway dimensions measured by CT scan.

METHODS:  In 93 subjects with mild, moderate, and severe asthma (smokers and never smokers), we recorded Asthma Control Questionnaire-6 (ACQ-6) score, spirometry (FEV1; forced expiratory flow rate, midexpiratory phase [FEF25%-75%]), residual volume (RV), total lung capacity (TLC), and CT scan measures of the right bronchial (RB) and left bronchial (LB) segmental airway dimensions (wall thickness, mm; lumen area, mm2) in the RB3/LB3, RB6/LB6, and RB10/LB10 (smaller) airways.

RESULTS:  The CT scan segmental airway (RB10 and LB10) lumen area was reduced in smokers with asthma compared with never smokers with asthma; RB10, 16.6 mm2 (interquartile range, 12.4-19.2 mm2) vs 19.6 mm2 (14.7-24.2 mm2) (P = .01); LB10, 14.8 mm2 (12.1-19.0 mm2) vs 19.9 mm2 (14.5-25.0 mm2) (P = .003), particularly in severe disease, with no differences in wall thickness or in larger airway (RB3 and LB3) dimensions. In smokers with asthma, a reduced lumen area in fifth-generation airways (RB10 or LB10) was associated with poor symptom control (higher ACQ-6 score) (−0.463 [−0.666 to −0.196], P = .001, and −0.401 [−0.619 to −0.126], P = .007, respectively) and reduced postbronchodilator FEF25%-75% (0.521 [0.292-0.694], P < .001, and [0.471 [0.236-0.654], P = .001, respectively) and higher RV/TLC %.

CONCLUSIONS:  The CT scan segmental airway lumen area is reduced in smokers with asthma compared with never smokers with asthma, particularly in severe disease, and is associated with worse current symptom control and small airway dysfunction.

Original Research: Signs and Symptoms of Chest Diseases

Chest. 2015;147(3):745-753. doi:10.1378/chest.14-2155

BACKGROUND:  Chronic cough is associated with poor quality of life and may signify a serious underlying disease. Differentiating nonspecific cough (when watchful waiting can be safely undertaken) from specific cough (treatment and further investigations are beneficial) would be clinically useful. In 326 children, we aimed to (1) determine how well cough pointers (used in guidelines) differentiate specific from nonspecific cough and (2) describe the clinical profile of children whose cough resolved without medications (spontaneous resolution).

METHODS:  A dataset from a multicenter study involving children newly referred for chronic cough (median duration, 3-4 months) was used to determine the sensitivity, specificity, predictive values, and likelihood ratios (LRs) of cough pointers (symptoms, signs, and simple investigations [chest radiography, spirometry]) recommended in guidelines.

RESULTS:  The pretest probability of specific cough was 88%. The absence of false-positive results meant that most pointers had strongly positive LRs. The most sensitive pointer (wet cough) had a positive LR of 26.2 (95% CI, 3.8-181.5). Although the absence of other individual pointers did not change the pretest probability much (negative LR close to 1), the absence of all pointers had a strongly negative LR of 0 (95% CI, 0-0.03). Children in the resolved spontaneously group were significantly more likely to be older, to be non-Indigenous, and to have a dry cough and a normal chest radiograph.

CONCLUSIONS:  Children with chronic dry cough without any cough pointers can be safely managed using the watchful waiting approach. The high pretest probability and high positive LRs of cough pointers support the use of individual cough pointers to identify high risk of specific cough in pediatric chronic cough guidelines.

TRIAL REGISTRY:  Australian New Zealand Clinical Trials Registry; No.: 12607000526471; URL: www.anzctr.org.au

Original Research: Education, Research, and Quality Improvement

Chest. 2015;147(3):754-763. doi:10.1378/chest.14-1366

BACKGROUND:  Bridging the gap between clinical research and everyday health-care practice requires effective communication strategies. To address current shortcomings in conveying practice recommendations and supporting evidence, we are creating and testing presentation formats for clinical practice guidelines (CPGs).

METHODS:  We carried out multiple cycles of brainstorming and sketching, developing a prototype. Physicians participating in the user testing viewed CPG formats linked to clinical scenarios and engaged in semistructured interviews applying a think-aloud method for exploring important aspects of user experience.

RESULTS:  We developed a multilayered presentation format that allows clinicians to successively view more in-depth information. Starting with the recommendations, clinicians can, on demand, access a rationale and a key information section containing statements on quality of the evidence, balance between desirable and undesirable consequences, values and preferences, and resource considerations. We collected feedback from 27 stakeholders and performed user testing with 47 practicing physicians from six countries. Advisory group feedback and user testing of the first version revealed problems with conceptual understanding of underlying CPG methodology, as well as difficulties with the complexity of the layout and content. Extensive revisions made before the second round of user testing resulted in most participants expressing overall satisfaction with the final presentation format.

CONCLUSIONS:  We have developed an electronic, multilayered, CPG format that enhances the usability of CPGs for frontline clinicians. We have implemented the format in electronic guideline tools that guideline organizations can now use when authoring and publishing their guidelines.

Original Research: Pediatrics

Chest. 2015;147(3):764-770. doi:10.1378/chest.13-2913

BACKGROUND:  Cilia line the surface of the respiratory tract and beat in a coordinated wave to protect the lungs against infection. Bardet Biedl Syndrome (BBS) is a rare condition attributed to cilia dysfunction. Murine models of BBS suggest a respiratory phenotype; however, no reports have studied the translation of these findings in patients.

METHODS:  We assessed the clinical symptoms of motile cilia dysfunction and the histology of ciliated respiratory epithelium in patients with BBS.

RESULTS:  We report an increased prevalence of neonatal respiratory distress at birth (12%), general practitioner-diagnosed asthma (21%), otitis media (33%), and rhinitis (36%) in patients with BBS. These symptoms, however, occurred at a significantly reduced prevalence compared with patients with known motile cilia dysfunction (primary ciliary dyskinesia). Respiratory epithelial assessment revealed cellular damage, significant ciliary depletion (on 60% of ciliated cells), and goblet cell hyperplasia in patients with BBS (50% goblet cells). These findings were quantifiably similar to those of patients with asthma (P > .05). Surprisingly, motile cilia function and ultrastructure were grossly normal with the exception of occasional unique inclusions within the ciliary membrane.

CONCLUSIONS:  In conclusion, motile ciliary structure and function are essentially normal in patients with BBS.

Original Research: Diffuse Lung Disease

Chest. 2015;147(3):771-777. doi:10.1378/chest.14-0380

BACKGROUND:  Lymphangioleiomyomatosis (LAM) is characterized by the proliferation in the lung, axial lymphatics (eg, lymphangioleiomyomas), and kidney (eg, angiomyolipomas) of abnormal smooth muscle-like LAM cells, which express melanoma antigens such as Pmel17/gp100 and have dysfunctional tumor suppressor tuberous sclerosis complex (TSC) genes TSC2 or TSC1. Histopathologic diagnosis of LAM in lung specimens is based on identification of the Pmel17 protein with the monoclonal antibody HMB-45.

METHODS:  We compared the sensitivity of HMB-45 to that of antipeptide antibody αPEP13h, which reacts with a C-terminal peptide of Pmel17. LAM lung nodules were laser-capture microdissected to identify proteins by Western blotting.

RESULTS:  HMB-45 recognized approximately 25% of LAM cells within the LAM lung nodules, whereas αPEP13h identified > 82% of LAM cells within these structures in approximately 90% of patients. Whereas HMB-45 reacted with epithelioid but not with spindle-shaped LAM cells, αPEP13h identified both spindle-shaped and epithelioid LAM cells, providing greater sensitivity for detection of all types of LAM cells. HMB-45 recognized Pmel17 in premelanosomal organelles; αPEP13h recognized proteins in the cytoplasm as well as in premelanosomal organelles. Both antibodies recognized a Pmel17 variant of approximately 50 kDa.

CONCLUSIONS:  Based on its sensitivity and specificity, αPEP13h may be useful in the diagnosis of LAM and more sensitive than HMB-45.

Chest. 2015;147(3):778-791. doi:10.1378/chest.14-1475

BACKGROUND:  An increased cancer risk in patients with sarcoidosis has been suggested, although results are conflicting in a number of case-control and cohort studies. We conducted a systematic review of all available data and performed a meta-analysis to better define and quantify the association between sarcoidosis and cancer.

METHODS:  We searched Medline and Embase for all original articles on cancer and sarcoidosis published up to January 2013. Two independent authors reviewed all titles/abstracts to identify studies according to predefined selection criteria. We derived summary estimates using a random-effects model and reported them as relative risk (RR). Publication bias was evaluated using a funnel plot and was quantified by the Egger test.

RESULTS:  Sixteen original studies, involving > 25,000 patients, were included in the present review. The summary RR to develop all invasive cancers was 1.19 (95% CI, 1.07-1.32). The results for selected cancer sites indicated a significantly increased risk of skin (RR, 2.00; 95% CI, 1.69-2.36), hematopoietic (RR, 1.92; 95% CI, 1.41-2.62), upper digestive tract (RR, 1.73; 95% CI, 1.07-2.79), kidney (RR, 1.55; 95% CI, 1.21-1.99), liver (RR, 1.79; 95% CI, 1.03-3.11), and colorectal cancers (RR, 1.33; 95% CI, 1.07-1.67). There was no evidence of publication bias for all cancers (P = .9), nor for any specific cancer site.

CONCLUSIONS:  The present meta-analysis suggests a significant, though moderate, association between sarcoidosis and malignancy.

Original Research: Pulmonary Physiology

Chest. 2015;147(3):792-797. doi:10.1378/chest.14-1365

BACKGROUND:  Most but not all data from different ethnic groups fit the Global Lung Function Initiative (GLI) spirometric reference model. This study investigates to what extent discrepancies are caused by secular changes in body proportions.

METHODS:  FEV1 and FVC from 20,336 healthy Japanese subjects (13,492 women) aged 17 to 95 years were compared with GLI-2012 reference values for Europeans. Data on the sitting height/standing height ratio (Cormic index) in 17-year-old students, collected from 1949 to 2012 in successive birth cohorts, were used to assess secular changes in body frame. The cohort-specific Cormic index was used to assess how variation in body frame affected pulmonary function.

RESULTS:  FEV1 and FVC were lower than GLI-2012 reference values, with values progressively falling until age 35 to 40 years and then rising to European levels in the elderly. The Cormic index rose until 1942, then fell, with a nadir in the 1970s, before rising again until 1995. Nearly one-half of the spirometric variability from predicted values could be explained by differences in the Cormic index between birth cohorts.

CONCLUSIONS:  In low-income countries, improving health conditions are likely to drive increases in height and changes in relative leg length similar to those observed in Japan and, thus, to a change in body frame. This implies that height-based prediction equations for such populations will need to be periodically updated.

Translating Basic Research into Clinical Practice

Chest. 2015;147(3):798-803. doi:10.1378/chest.14-1142

Recent work has demonstrated that mechanical forces occurring in the airway as a consequence of bronchoconstriction are sufficient to not only induce symptoms but also influence airway biology. Animal and human in vitro and in vivo work demonstrates that the airways are structurally and functionally altered by mechanical stress induced by bronchoconstriction. Compression of the airway epithelium and mechanosensing by the airway smooth muscle trigger the activation and release of growth factors, causing cell proliferation, extracellular matrix protein accumulation, and goblet cell differentiation. These effects of bronchoconstriction are of major importance to asthma pathophysiology and appear sufficient to induce remodeling independent of the inflammatory response. We review these findings in detail and discuss previous studies in light of this new evidence regarding the influence of mechanical forces in the airways. Furthermore, we highlight potential impacts of therapies influencing mechanical forces on airway structure and function in asthma.

Evidence-Based Medicine

Chest. 2015;147(3):804-814. doi:10.1378/chest.14-2506
FREE TO VIEW

BACKGROUND:  Since the publication of the 2006 American College of Chest Physicians (CHEST) cough guidelines, a variety of tools has been developed or further refined for assessing cough. The purpose of the present committee was to evaluate instruments used by investigators performing clinical research on chronic cough. The specific aims were to (1) assess the performance of tools designed to measure cough frequency, severity, and impact in adults, adolescents, and children with chronic cough and (2) make recommendations or suggestions related to these findings.

METHODS:  By following the CHEST methodologic guidelines, the CHEST Expert Cough Panel based its recommendations and suggestions on a recently published comparative effectiveness review commissioned by the US Agency for Healthcare Research and Quality, a corresponding summary published in CHEST, and an updated systematic review through November 2013. Recommendations or suggestions based on these data were discussed, graded, and voted on during a meeting of the Expert Cough Panel.

RESULTS:  We recommend for adults, adolescents (≥ 14 years of age), and children complaining of chronic cough that validated and reliable health-related quality-of-life (QoL) questionnaires be used as the measurement of choice to assess the impact of cough, such as the Leicester Cough Questionnaire and the Cough-Specific Quality-of-Life Questionnaire in adult and adolescent patients and the Parent Cough-Specific Quality of Life Questionnaire in children. We recommend acoustic cough counting to assess cough frequency but not cough severity. Limited data exist regarding the performance of visual analog scales, numeric rating scales, and tussigenic challenges.

CONCLUSIONS:  Validated and reliable cough-specific health-related QoL questionnaires are recommended as the measurement of choice to assess the impact of cough on patients. How they compare is yet to be determined. When used, the reporting of cough severity by visual analog or numeric rating scales should be standardized. Previously validated QoL questionnaires or other cough assessments should not be modified unless the new version has been shown to be reliable and valid. Finally, in research settings, tussigenic challenges play a role in understanding mechanisms of cough.

Recent Advances in Chest Medicine

Chest. 2015;147(3):815-823. doi:10.1378/chest.14-1049

Aspiration of foreign matter into the airways and lungs can cause a wide spectrum of pulmonary disorders with various presentations. The type of syndrome resulting from aspiration depends on the quantity and nature of the aspirated material, the chronicity, and the host responses. Aspiration is most likely to occur in subjects with a decreased level of consciousness, compromised airway defense mechanisms, dysphagia, gastroesophageal reflux, and recurrent vomiting. These aspiration-related syndromes can be categorized into airway disorders, including vocal cord dysfunction, large airway obstruction with a foreign body, bronchiectasis, bronchoconstriction, and diffuse aspiration bronchiolitis, or parenchymal disorders, including aspiration pneumonitis, aspiration pneumonia, and exogenous lipoid pneumonia. In idiopathic pulmonary fibrosis, aspiration has been implicated in disease progression and acute exacerbation. Aspiration may increase the risk of bronchiolitis obliterans syndrome in patients who have undergone a lung transplant. Accumulating evidence suggests that a causative role for aspiration is often unsuspected in patients presenting with aspiration-related pulmonary diseases; thus, many cases go undiagnosed. Herein, we discuss the broadening spectrum of these pulmonary syndromes with a focus on presenting features and diagnostic aspects.

Medical Ethics

Chest. 2015;147(3):824-834. doi:10.1378/chest.14-1696

Stem cell research and related initiatives in regenerative medicine, cell-based therapy, and tissue engineering have generated considerable scientific and public interest. Researchers are applying stem cell technologies to chest medicine in a variety of ways: using stem cells as models for drug discovery, testing stem cell-based therapies for conditions as diverse as COPD and cystic fibrosis, and producing functional lung and tracheal tissue for physiologic modeling and potential transplantation. Although significant scientific obstacles remain, it is likely that stem cell-based regenerative medicine will have a significant clinical impact in chest medicine. However, stem cell research has also generated substantial controversy, posing a variety of ethical and regulatory challenges for research and clinical practice. Some of the most prominent ethical questions related to the use of stem cell technologies in chest medicine include (1) implications for donors, (2) scientific prerequisites for clinical testing and use, (3) stem cell tourism, (4) innovation and clinical use of emerging stem cell-based interventions, (5) responsible translation of stem cell-based therapies to clinical use, and (6) appropriate and equitable access to emerging therapies. Having a sense of these issues should help to put emerging scientific advances into appropriate context and to ensure the responsible clinical translation of promising therapeutics.

Contemporary Reviews in Critical Care Medicine

Chest. 2015;147(3):835-846. doi:10.1378/chest.14-1335

In critically ill patients, the right ventricle is susceptible to dysfunction due to increased afterload, decreased contractility, or alterations in preload. With the increased use of point-of-care ultrasonography and a decline in the use of pulmonary artery catheters, echocardiography can be the ideal tool for evaluation and to guide hemodynamic and respiratory therapy. We review the epidemiology of right ventricular failure in critically ill patients; echocardiographic parameters for evaluating the right ventricle; and the impact of mechanical ventilation, fluid therapy, and vasoactive infusions on the right ventricle. Finally, we summarize the principles of management in the context of right ventricular dysfunction and provide recommendations for echocardiography-guided management.

Contemporary Reviews in Sleep Medicine

Chest. 2015;147(3):847-861. doi:10.1378/chest.14-0614

OSA is a common yet underdiagnosed disorder encountered in everyday practice. The disease is a unique physiologic stressor that contributes to the development or progression of many other disorders, particularly cardiovascular conditions. The pulmonary circulation is specifically affected by the intermittent hypoxic apneas associated with OSA. The general consensus has been that OSA is associated with pulmonary hypertension (PH), but only in a minority of OSA patients and generally of a mild degree. Consequently, there has been no sense of urgency to screen for either condition when evaluating the other. In this review, we explore available evidence describing the interaction between OSA and PH and seek to better understand underlying pathophysiology. We describe certain groups of patients who have a particular preponderance of OSA and PH. Failure to recognize the mutual additive effects of these disorders can lead to suboptimal patient outcomes. Among patients with PH and OSA, CPAP, the mainstay treatment for OSA, may ameliorate pulmonary pressure elevations, but has not been studied adequately. Conversely, among patients with OSA, PH significantly limits functional capacity and potentially shortens survival; yet, there is no routine screening for PH in patients with OSA. We think it is time to study the interaction between OSA and PH more carefully to identify high-risk subgroups. These would be screened for the presence of combined disorders, facilitating earlier institution of therapy and improving outcomes.

Pectoriloquy

Chest. 2015;147(3):862. doi:10.1378/chest.14-2084
FREE TO VIEW

I might be okay.
I might even be okay again,
when the heroes arrive,
wearing sincerity on their
starched white sleeves and
dispensing courage in place
of drugs that never seem to
work anyway. It’s all
a matter of perspective, says
the artist, gazing at the ceiling
as empty and white and
sterile as an unblemished
canvas ready for the first
vibrant swirls of color or
viewing jagged shards of
pain in the reflecting pool
that is life unlived.
All that remains is reassurance,
a seemingly abundant commodity
for which there is no billing code.
It gushes like tap water through
the lips of the well-meaning, who
know full well there is no medical
term for certainty and no medical
cure for certain death.

Chest. 2015;147(3):862. doi:10.1378/chest.14-2085
FREE TO VIEW

The eyes will tell
the story if you let them.
The eyes that have seen
everything and
now see nothing.
Shine the light
and watch. Do
the pupils, black
and deep as a
starless night,
sharpen to a pinpoint
to mitigate the assault?
The heart beats on.
The chest rises rhythmically
with each mechanical whisper
of the ventilator. An
involuntary twitch of
a muscle heralds the miracle
that never comes. All lies.
If you really want
to know the truth,
it’s in the eyes.

Chest. 2015;147(3):863-864. doi:10.1378/chest.14-2103
FREE TO VIEW

Little Max, I’m so short-ranged.
   So dense. The dog
eloquence of your urine is wasted on me.
Still you rise on hind legs in a circus pose,
   settle at my feet, and I feel clean.
Today’s early September breeze is fine.
   The clarity of light helps me
perceive and perceive and perceive –
the blending of your brown, black and white
hairs, the way your ears respond, creased at times
   like paper boats. I see patterns – a tan
stripe down the underside of your tail
   expanding to a loopy trident
   at the base. The center tine
divides your balls – your unabashed
   and humorous balls.
* * * * * *
   Humor, Max. Humor.
Some people persist on faith. But you’ve
got to have humor, and it’s obvious – you have the knack.
You should see yourself – asleep on your back,
faintly snoring in the plush dog bed!
   Maurice, of all people, nudges me –
wants me to look without waking you.
Your rear legs are splayed and the front ones
stick up, bent at the hocks – ebony nails pointing
at your belly. You’re like a cartoon, Max.
   You remind me of the carrots.
* * * * * *
See, last year I got rheumatoid arthritis.
   The pain from my swollen joints
was yellowish, blaring – almost nauseous.
Then the meds gave me pneumonia, with fevers
   and anemia. At night that summer,
I woke almost every hour. My pillows were soaked
with sweat. My mouth was sticky and dry,
   yet I dreaded sitting up
   to reach my water. My wrists
and elbows were sore, so I had to heave up from
the hip – I couldn’t press the mattress without gasping.
   The lurch upright brought on a wild
   tachycardia. And that thumping –
the anarchy in my chest – brought on fear.
   That’s something I couldn’t get out
from under, Max. I was afraid one of those times
   my heartbeat wouldn’t settle.
Afraid I’d never be well again.
* * * * *
   One night I gave up on sleep,
and limped across the hall to the computer. There was
mail from my sister – Subject: Obscene carrots.
   I clicked it open. The screen filled
with an orange host of un-sellable carrots,
shaped like genitals and fat, crossed legs. They looked
unconcerned, sturdy – sporting root hairs and dirt.
   Those ridiculous, lewd roots almost winked!
   Max, I laughed and laughed, though
laughing uses oxygen. Because who ever knows
what comes next? I wasn’t healed – in fact
I ended up in the hospital – but for the first time
   in weeks I felt clean.

Chest. 2015;147(3):865. doi:10.1378/chest.14-2072
FREE TO VIEW

The Drug Rehab Counselor said, Draw a bridge!
The inmates started sketching. Grand bridges,
stone and concrete bridges, massive draw bridges
opening for ships heavy with goods.
Off to the left, one inmate’s face is inches
from his pad. He’s drawing the bridge
of the rented violin when he was ten; a bridge
that carried four strings; a slow sound, screechy sometimes,
sometimes deep and strong. From heaven, his mom said.
So he’d practice till heaven came over that bridge.
Heaven came best when he closed his eyes.
So he drew that bridge.
When the Drug Rehab Counselor said, Pencils down!
the inmates put their pencils down, turned their papers in.
Leafing through, she offered commendations all around.
Such detail, such realism! And you know, she said, we are
each of us responsible for building bridges just like these.
We are each of us connected in some way, after all.
But her voice dropped when she got to the violin bridge.
She frowned, shook her head. You’ll never learn
to follow directions, she said. He turned his face from hers
to the cinderblock wall. No difference. All he could do
was whisper, Nope.

Selected Reports

Chest. 2015;147(3):e76-e78. doi:10.1378/chest.14-1503

Small pulmonary lesions can be difficult to locate intraoperatively. Preoperative CT scan-guided localization, for example with hookwire, is a popular method to help localize such lesions. However, the delay between CT scan localization with hookwire and surgery can lead to risks of pneumothorax and wire dislodgement. We describe a 56-year-old woman who underwent DynaCT-guided hookwire localization of a ground-glass opacity in the hybrid operating room followed immediately by single-port video-assisted thoracic surgery lobectomy. The advantages, disadvantages, and special considerations in adopting this approach are discussed.

Topics: lobectomy
Chest. 2015;147(3):e79-e82. doi:10.1378/chest.14-1198

The underlying cause of cystic fibrosis (CF) is the loss of epithelial chloride and bicarbonate transport due to mutations in the CF transmembrane conductance regulator (CFTR) gene encoding the CFTR protein. Ivacaftor is a gene-specific CFTR potentiator that augments in vivo chloride transport in CFTR mutations affecting channel gating. Originally approved for the G511D CFTR mutation, ivacaftor is now approved for eight additional alleles exhibiting gating defects and has also been tested in R117H, a CFTR mutation with residual function that exhibits abnormal gating. P67L is a class 4 conductance (nongating) mutation exhibiting residual CFTR function. We report marked clinical improvement, normalization of spirometry, and dramatic reduction in radiographic structural airway changes after > 1 year of treatment with ivacaftor in a young adult with the compound heterozygous genotype P67L/F508del CFTR. The case suggests that ivacaftor may have a potential benefit for patients with CF with nongating mutations.

Ultrasound Corner

Chest. 2015;147(3):e83-e85. doi:10.1378/chest.14-1416
Topics: hypoxemia , dyspnea

Pulmonary, Critical Care, and Sleep Pearls

Chest. 2015;147(3):e86-e89. doi:10.1378/chest.14-1572

A 51-year-old man was admitted for evaluation of new-onset generalized seizures in the context of progressive and significant behavioral change. His medical history was only notable for previous outbreaks of genital herpes. He took no medications. He had occasional social alcohol use and no illicit drug use but was a 35-pack-year current smoker. The patient had no relevant occupational exposure history but had recently traveled to Panama. Initially, the patient’s significant other noticed a progressive flattening of his affect. The patient then started to experience episodes of “passing out” that led to injuries prompting ED visits. He was prescribed antiseizure medications and scheduled for an outpatient workup. However, with progressive gait instability, lethargy, and an increase in frequency of generalized seizures, the patient was admitted for treatment of suspected viral encephalitis. Despite initiation of antimicrobial and antiviral therapy, the patient’s level of alertness continued to decline, ultimately leading to intubation for airway protection.

Chest. 2015;147(3):e90-e94. doi:10.1378/chest.14-1100

A 62-year-old man developed a scalp rash 2 months ago, followed by bilateral eyelid swelling. The nonpruritic rash then spread to involve most of his skin. He also had fatigue, muscle weakness, mild muscle soreness with activity, and dysphagia for solid foods for the last 3 weeks. He had no other symptoms. He had a 50 pack-year history of smoking and drank two to three shots of alcohol daily.

Chest. 2015;147(3):e95-e99. doi:10.1378/chest.14-1054

A healthy 55-year-old man without known medical problems presented for a routine physical examination and was found to have an abnormal ECG. He denied chest pain, dyspnea, palpitations, dizziness, or syncopal episodes. He also denied orthopnea, paroxysmal nocturnal dyspnea, and lower-extremity edema. His exercise capacity had been excellent. He was a lifelong nonsmoker and never had lung problems.

Chest. 2015;147(3):e100-e104. doi:10.1378/chest.14-1391

A teenager was admitted to an outside hospital ED following an episode of melena. He had been complaining of intermittent abdominal pain, nausea, malaise, and easy fatigability for 2 months, with significant worsening of symptoms 2 weeks prior to this episode. He had no significant medical, surgical, or family history. On presentation at the outside ED, he was found to be profoundly icteric and encephalopathic. Initial laboratories suggested anemia, acute kidney injury, and acute liver failure, leading to a presumptive diagnosis of acute fulminant liver failure necessitating transfer to our institution.

Correspondence

Chest. 2015;147(3):e105. doi:10.1378/chest.14-2682
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e105-e106. doi:10.1378/chest.14-2859
FREE TO VIEW
Chest. 2015;147(3):e107. doi:10.1378/chest.14-2735
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e107-e108. doi:10.1378/chest.14-2831
FREE TO VIEW
Chest. 2015;147(3):e109. doi:10.1378/chest.14-2523
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e109-e110. doi:10.1378/chest.14-2802
FREE TO VIEW
Chest. 2015;147(3):e111-e112. doi:10.1378/chest.14-2465
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e112. doi:10.1378/chest.14-2855
FREE TO VIEW
Chest. 2015;147(3):e113-e114. doi:10.1378/chest.14-2705
FREE TO VIEW
Chest. 2015;147(3):e115-e116. doi:10.1378/chest.14-2697
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e116-e117. doi:10.1378/chest.14-2892
FREE TO VIEW
Chest. 2015;147(3):e118. doi:10.1378/chest.14-2740
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e119. doi:10.1378/chest.14-2996
FREE TO VIEW
Chest. 2015;147(3):e120. doi:10.1378/chest.14-2826
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e120-e121. doi:10.1378/chest.14-2993
FREE TO VIEW
Chest. 2015;147(3):e122. doi:10.1378/chest.14-2577
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e122-e123. doi:10.1378/chest.14-3079
FREE TO VIEW
Chest. 2015;147(3):e124. doi:10.1378/chest.14-2651
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e124-e126. doi:10.1378/chest.14-3041
FREE TO VIEW
Chest. 2015;147(3):e127-e128. doi:10.1378/chest.14-2378
FREE TO VIEW
ResponseResponse ONLINE EXCLUSIVES
Chest. 2015;147(3):e128-e129. doi:10.1378/chest.14-2635
FREE TO VIEW
Chest. 2015;147(3):e130. doi:10.1378/chest.14-2755
FREE TO VIEW

Sign In to Access Full Content

Don't have an account?

Register for a FREE personal account to access these and other personalization features:

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