Current Issue


Chest. 2016;150(2):263-265. doi:10.1016/j.chest.2016.02.663

The cause of sarcoidosis remains elusive; however, most experts agree upon several “essential ingredients.” Strong evidence implicates genetic factors predisposing certain individuals to the development of sarcoidosis. The evolutionary factors driving these genetic characteristics are unclear, but a reasonable case could be made for the sarcoidosis genotype being protective against common human infections, including MycobacteriumTB. Many sarcoidosis patients are hyperresponsive to immunogenic TB antigens in the absence of active or latent TB infection. That said, the immune response is not TB-specific, because immune cells derived from patients with sarcoidosis produce abnormally high levels of Th1 cytokines under conditions modeling the immune response to antigens present in an array of bacteria and fungi. Thus, it is not surprising that numerous organisms (and molecules) are incriminated in the pathogenesis of sarcoidosis.

Chest. 2016;150(2):266-267. doi:10.1016/j.chest.2016.03.023

Prior studies estimate that it takes 17 years to turn efficacious interventions into effective ones: that is, to turn high-quality research evidence into real-world clinical practice. In the case of ARDS—a major cause of morbidity and mortality in the ICU—it has been exactly 16 years since the ARDS Network convincingly established the benefits of lung-protective ventilation. And, in line with those estimates, we continue to woefully underperform when it comes to identifying patients with ARDS and providing evidence-based care.

Chest. 2016;150(2):268-269. doi:10.1016/j.chest.2016.03.028

Hospitalized exacerbations are important events in patients with COPD because they are responsible for high costs and have great impact on patient’s symptoms and prognosis. Review of high-quality randomized clinical trials in patients hospitalized for COPD exacerbations has established that systemic steroids significantly reduced treatment failure, were associated with earlier improvement in lung function and dyspnea, and shortened hospital stay. However, beneficial effects of systemic steroids came with high rates of adverse effects (including hyperglycemia), with one extra adverse effect occurring for every six people treated. These conclusions were based on studies that have used various protocols for steroid administration, including studies that used very high doses of steroids and administration of steroids for up to 8 weeks. Subsequent studies have suggested that low-dose steroids (30-40 mg/d) administered orally were not associated with worse outcomes than high-dose intravenous therapy and that a shorter duration (5 days) of oral prednisone was noninferior to 14-day treatment. This led to current recommendations of using low-dose short-term oral steroids in patients hospitalized for COPD exacerbations with the aim of limiting adverse events, which still occurred in approximately one to ten patients. Because results of clinical trials provide only limited information on the individual likelihood of benefiting from or being harmed by a therapy, a more personalized approach of steroid prescription in COPD exacerbation is urgently required, with the aim of limiting steroid prescription to patients who may show high benefits and low rates of adverse effects.

Chest. 2016;150(2):270-272. doi:10.1016/j.chest.2016.04.008

For nearly 40 years following the release of the flexible bronchoscope, only a few procedures (BAL, transbronchial lung biopsies, and transbronchial needle aspiration) were available to diagnose pulmonary diseases. Since then, the most impactful advance in bronchoscopy has been the introduction of endobronchial ultrasound, which revolutionized the bronchoscopic approach to assessing mediastinal adenopathy. In patients with known or suspected lung cancer, the diagnostic yield approaches 90%, and the procedure is useful in diagnosing sarcoidosis and lymphoma., Could cryobiopsies be the next game changer by expanding the capability of transbronchial lung biopsies by providing tissue samples that rival surgical lung biopsies?

Topics: biopsy , bronchoscopy , ice

Editorials: Point and Counterpoint

Chest. 2016;150(2):273-275. doi:10.1016/j.chest.2016.04.034

The lack of medical options for the treatment of idiopathic pulmonary fibrosis (IPF) has long been a source of frustration and consternation for pulmonologists treating this deadly disorder. This previously led to the adoption of therapies with little supportive data, some of which have subsequently proved not only to be ineffective but also deleterious., The early 2000s heralded a new era in clinical trials for IPF, with multiple multicenter studies being successfully completed. A wealth of valuable information about the natural history of the disease, but few positive studies, emanated from these robust clinical trials. These studies also spawned a certain amount of controversy regarding suitable and acceptable end points for IPF clinical trials. The labor and commitment of many patients, physicians, principal investigators, research coordinators, pharmaceutical companies, and governmental agencies finally bore fruit with two drugs being approved for the treatment of IPF contemporaneously by the US Food and Drug Administration (FDA). This has marked a turning point and a new era in the management of these patients. Although the development of efficacious pharmacologic therapy for IPF has provided renewed hope for this deadly disease, it has also led to many questions regarding the optimal use of these agents. Who should be prescribed these medications, when should they be started, and when, if ever, should they be stopped?

Chest. 2016;150(2):276-278. doi:10.1016/j.chest.2016.04.036

The fall of 2014 marked a new era in the management of patients with idiopathic pulmonary fibrosis (IPF), with the US Food and Drug Administration approval of not one but two therapies for its treatment. This came on the heels of a recent issue of the New England Journal of Medicine that included the results of three separate late-phase interventional trials as well as an accompanying editorial.,,, This is truly a dramatic advance in what was once considered a disease too rare to ever be adequately studied.

Chest. 2016;150(2):278. doi:10.1016/j.chest.2016.04.035

We agree with Dr Brown’s philosophical approach, exemplified by his concluding comment that there should be “thoughtful and reasoned discussion between a patient and the physician about hopes and expectations for the future, the goals of treatment, and the risks and benefits of any chosen course.” However, the devil lies in the details of this discussion and how the choice is portrayed to the patient, since the consulting physician’s bias will inevitably influence the patient’s decision. As an example, on one end of the spectrum, the patient can be guided to a “no treatment” choice by the following “we have two new medications; both appear to slow the disease progression in some patients. However, it is uncertain how this might translate to other more meaningful benefits. Both drugs have significant side effects and are very expensive. You would not have been eligible for any of the trials that demonstrated that these drugs worked, so I cannot be sure that either will help you. Do you want to give either of these a try?” Any reasoned patient would likely respond, “heck no” to this preamble. A more favorably predisposed clinician might have a slightly different conversation with the same patient, “You have a disease with an average survival of only 2½ to 4 years. Unfortunately, we are unable to predict the course in individual patients, and even those with well-maintained lung function may have unpredictable precipitous declines. We have two drugs that slow the rate of loss of lung function. We know that patients who lose lung function over time have worse outcomes. Both drugs have some side effects, but not everyone experiences them and they are usually quite manageable. Although your profile does not fit exactly with those patients enrolled in the clinical trials, it is not unreasonable to assume that if they work in selected patients with idiopathic pulmonary fibrosis (IPF), they are likely to work in others as well. Do you want to try one of these?” A possible response to this might be “seems like a no-brainer.”


Chest. 2016;150(2):279-282. doi:10.1016/j.chest.2016.05.005

This article provides an update on progress toward establishing pulmonary and critical care medicine (PCCM) fellowship training as one of the first four subspecialties to be recognized and supported by the Chinese government. Designed and implemented throughout 2013 and 2014 by a collaborative effort of the Chinese Thoracic Society (CTS) and the American College of Chest Physicians (CHEST), 12 leading Chinese hospitals enrolled a total of 64 fellows into standardized PCCM training programs with common curricula, educational activities, and assessment measures. Supplemental educational materials, online assessment tools, and institutional site visits designed to evaluate and provide feedback on the programs’ progress are being provided by CHEST. As a result of this initial progress, the Chinese government, through the Chinese Medical Doctor’s Association, endorsed the concept of subspecialty fellowship training in China, with PCCM as one of the four pilot subspecialties to be operationalized nationwide in 2016, followed by implementation across other subspecialties by 2020. This article also reflects on the achievements of the training sites and the challenges they face and outlines plans to enhance and expand PCCM training and practice in China.

Commentary: Ahead of the Curve

Chest. 2016;150(2):283-288. doi:10.1016/j.chest.2016.05.035

New treatments are needed for patients with asthma who are refractory to standard therapies, such as individuals with a phenotype of “type 2-low” inflammation. This important clinical problem could potentially be addressed by the development of apolipoprotein A-I (apoA-I) mimetic peptides. ApoA-I interacts with its cellular receptor, the ATP-binding cassette subfamily A, member 1 (ABCA1), to facilitate cholesterol efflux out of cells to form nascent high-density lipoprotein particles. The ability of the apoA-I/ABCA1 pathway to promote cholesterol efflux from cells that mediate adaptive immunity, such as antigen-presenting cells, can attenuate their function. Data from experimental murine models have shown that the apoA-I/ABCA1 pathway can reduce neutrophilic airway inflammation, primarily by suppressing the production of granulocyte-colony stimulating factor. Furthermore, administration of apoA-I mimetic peptides to experimental murine models of allergic asthma has decreased both neutrophilic and eosinophilic airway inflammation, as well as airway hyperresponsiveness and mucous cell metaplasia. Higher serum levels of apoA-I have also been associated with less severe airflow obstruction in patients with asthma. Collectively, these results suggest that the apoA-I/ABCA1 pathway may have a protective effect in asthma, and support the concept of advancing inhaled apoA-I mimetic peptides to clinical trials that can assess their safety and effectiveness. Thus, we propose that the development of inhaled apoA-I mimetic peptides as a new treatment could represent a clinical advance for patients with severe asthma who are unresponsive to other therapies.

Original Research: Diffuse Lung Disease

Chest. 2016;150(2):289-298. doi:10.1016/j.chest.2016.01.020

Background  Sarcoidosis is a disease that is associated with occupational and environmental antigens, in the setting of a susceptible host. The aim of this study was to examine the association between sarcoidosis mortality and previously reported occupational exposures based on sex and race.

Methods  The decedents enrolled in this study were derived from United States death certificates from 1988-1999. Cause of death was coded according to ICD-9 and ICD-10. The usual occupation was coded with Bureau of the Census Occupation Codes. Mortality odds ratio (MOR) were determined and multiple Poisson regression were performed to evaluate the independent exposure effects after adjustment for age, sex, race and other occupational exposures.

Results  Of the 7,118,535 decedents in our study, 3,393 were identified as sarcoidosis-related, including 1,579 identified as sarcoidosis being the underlying cause of death. The sarcoidosis-related MOR of any occupational exposure was 1.52 (95% CI, 1.35-1.71). Women with any exposure demonstrated an increased MOR compared to women without (MOR 1.65, 95% CI, 1.45-1.89). The mortality risk was significantly elevated in those with employment involving metal working, health care, teaching, sales, banking, and administration. Higher sarcoidosis-related mortality risks associated with specific exposures were noted in women vs men and blacks vs whites.

Conclusions  Findings of prior occupations and risk of sarcoidosis were verified using sarcoidosis mortality rates. There were significant differences in risk for sarcoidosis mortality by occupational exposures based on sex and race.

Chest. 2016;150(2):299-306. doi:10.1016/j.chest.2016.03.004

Objective  Markers for early identification of progressive interstitial lung disease (ILD) in systemic sclerosis (SSc) are in demand. Chemokine CCL18, which has been linked to pulmonary inflammation, is an interesting candidate, but data have not been consistent. We aimed to assess CCL18 levels in a large, prospective, unselected SSc cohort with longitudinal, paired data sets on pulmonary function and lung fibrosis.

Methods  Sera from the Oslo University Hospital SSc cohort (n = 298) and healthy control subjects (n = 100) were analyzed for CCL18 by enzyme immunoassay. High CCL18 (>53 ng/mL) was defined using the mean value plus 2 SD in sera obtained from healthy control subjects as the cutoff.

Results  High serum CCL18 was identified in 35% (105 of 298). Annual decline in FVC differed significantly between high and low CCL18 subsets (13.3% and 4.7%; P = .016), as did the annual progression rate of lung fibrosis (0.9% [SD, 2.9] and 0.2% [SD, 1.9]). Highest rates of annual FVC decline > 10% (21%) and annual fibrosis progression (1.2%) were seen in patients with high CCL18 and early disease (< 3 years). In multivariate analyses, CCL18 was associated with annual FVC decline > 10% (OR, 1.1; 95% CI, 1.01-1.11) and FVC < 70% at follow-up (OR, 3.1; 95% CI, 1.08-8.83). Survival analyses showed that patients with high CCL18 had reduced 5- and 10-year cumulative survival compared with patients with low CCL18 (85% and 74%, compared with 97% and 89%, respectively; P = .001).

Conclusions  The results from this prospective cohort reinforce the notion that high CCL18 may serve as a marker for early identification of progressive ILD in SSc.

Original Research: Critical Care

Chest. 2016;150(2):307-313. doi:10.1016/j.chest.2016.01.003

Background  ARDS is an important clinical problem. The definition of ARDS requires testing of arterial blood gas to define the ratio of Pao2 to Fio2 (Pao2/Fio2 ratio). However, many patients with ARDS do not undergo blood gas measurement, which may result in underdiagnosis of the condition. As a consequence, a method for estimating Pao2 on the basis of noninvasive measurements is desirable.

Methods  Using data from three ARDS Network studies, we analyzed the enrollment arterial blood gas measurements to compare nonlinear with linear and log-linear imputation methods of estimating Pao2 from percent saturation of hemoglobin with oxygen as measured by pulse oximetry (Spo2). We compared mortality on the basis of various measured and imputed Pao2/Fio2 ratio cutoffs to ensure clinical equivalence.

Results  We studied 1,184 patients, in 707 of whom the Spo2 ≤ 96%. Nonlinear imputation from the Spo2/Fio2 ratio resulted in lower error than linear or log-linear imputation (P < .001) for patients with Spo2 ≤ 96% but was equivalent to log-linear imputation in all patients. Ninety-day hospital mortality was 26% to 30%, depending on the Pao2/Fio2 ratio, whether nonlinearly imputed or measured. On multivariate regression, the association between imputed and measured Pao2 varied by use of vasopressors and Spo2.

Conclusions  A nonlinear equation more accurately imputes Pao2/Fio2 from Spo2/Fio2 than linear or log-linear equations, with similar observed hospital mortality depending on Spo2/Fio2 ratio vs measured Pao2/Fio2 ratios. While further refinement through prospective validation is indicated, a nonlinear imputation appears superior to prior approaches to imputation.

Chest. 2016;150(2):314-319. doi:10.1016/j.chest.2016.03.030

Background  Studies have identified processes that are associated with more favorable length of stay (LOS) outcomes when an ICU telemedicine program is implemented. Despite these studies, the relation of the acceptance of ICU telemedicine management services by individual ICUs to LOS outcomes is unknown.

Methods  This is a single ICU telemedicine center study that compares LOS outcomes among three groups of intensivist-staffed mixed medical-surgical ICUs that used alternative comanagement strategies. The proportion of provider orders recorded by an ICU telemedicine provider to all recorded orders was compared among ICUs that used a monitor and notify comanagement approach, a direct intervention with timely notification process, and ICUs that used a mix of these two approaches. The primary outcome was acuity-adjusted hospital LOS.

Results  ICUs that used the direct intervention with timely notification strategy had a significantly larger proportion of provider orders recorded by ICU telemedicine physicians than the mixed methods of comanagement group, which had a larger proportion than ICUs that used the monitor and notify method (P < .001). Acuity-adjusted hospital LOS was significantly lower for the direct intervention with timely notification comanagement strategy (0.68; 0.65-0.70) compared with the mixed methods group (0.70 [0.69-0.72]; P = .01), which was significantly lower than the monitor and notify group (0.83 [0.80-0.86]; P < .001).

Conclusions  Direct intervention with timely notification strategies of ICU telemedicine comanagement were associated with shorter LOS outcomes than monitor and notify comanagement strategies.

Original Research: COPD

Chest. 2016;150(2):320-328. doi:10.1016/j.chest.2016.01.026

Background  Patients with moderate exacerbations of COPD and the eosinophilic phenotype have better outcomes with prednisolone. Whether this outcome is similar in patients hospitalized with a severe exacerbation of COPD is unclear. We investigated the rate of recovery of eosinophilic and noneosinophilic exacerbations in patients participating in a multicenter randomized controlled trial assessing health outcomes in hospitalized exacerbations.

Methods  Patients were recruited at presentation to the hospital with an exacerbation of COPD. They were stratified into groups according to eosinophilic exacerbations if the peripheral blood eosinophil count on admission was ≥ 200 cells/μL and/or ≥ 2% of the total leukocyte count. Admission details, serum C-reactive protein levels, length of stay, and subsequent rehospitalization data were compared between groups.

Results  A total of 243 patients with COPD (117 men) with a mean age of 71 years (range, 45-93 years) were recruited. The inpatient mortality rate was 3% (median time to death, 12 days; range, 9-16 days). The median absolute eosinophil count was 100 cells/μL (range, 10-1,500 cells/μL), and 25% met our criteria for an eosinophilic exacerbation; in this population, the mean length of stay (in days) was shorter than in patients with noneosinophilic exacerbations (5.0 [range, 1-19] vs 6.5 [range, 1-33]; P = .015) following treatment with oral corticosteroids and independent of treatment prior to admission. Readmission rates at 12 months were similar between groups.

Conclusions  The study patients presenting to the hospital with a severe eosinophilic exacerbation of COPD had a shorter length of stay. The exacerbations were usually not associated with elevated C-reactive protein levels, suggesting that better treatment stratification of exacerbations can be used.

Trial Registry  http://www.isrctn.com/ISRCTN05557928.

Original Research: Pulmonary Procedures

Chest. 2016;150(2):329-336. doi:10.1016/j.chest.2016.01.018

Background  Transbronchial forceps biopsy (FBx) has been the preferred method for obtaining bronchoscopic lung biopsy specimens. Cryoprobe biopsy (CBx) has been shown to obtain larger and higher quality samples, but is limited by its inability to retrieve the sample through the working channel of the bronchoscope, requiring the bronchoscope to leave the airway for sample retrieval.

Objective  We evaluated a novel device using a sheath cryobiopsy (SCBx). This method allows for specimen retrieval through the working channel of the bronchoscope, with the scope remaining inside the airway.

Methods  This prospective, randomized controlled, single-blinded porcine study compared a 1.1-mm SCBx probe, a 1.9-mm CBx probe, and 2.0-mm FBx forceps. Assessment of histologic accessibility, sample quantity and quality, number of attempts to acquire and retrieve samples, cryoprobe activation time, fluoroscopy activation time, technical feasibility, and complications were compared.

Results  Samples adequate for standard pathologic processing were retrieved with 82.1% of the SCBx specimens, 82.9%% of the CBx specimens, and 30% of the FBx specimens. The histologic accessibility of both SCBx (P = .0002) and CBx (P = .0003) was superior to FBx. Procedure time for FBx was faster than for both SCBx and CBx, but SCBx was significantly faster than CBx (P < .0001). Fluoroscopy time was lower for both SCBx and CBx compared with FBx. There were no significant bleeding events.

Conclusions  SCBx is a feasible technique providing a higher quality lung biopsy specimen compared with FBx and can successfully be retrieved through the working channel. Human studies are needed to further assess this technique with additional safety data.

Original Research: Sleep Disorders

Chest. 2016;150(2):337-345. doi:10.1016/j.chest.2016.03.019

Background  Motivational enhancement (ME) shows promise as a means of increasing adherence to CPAP for OSA.

Methods  We performed an open-label, parallel-arm, randomized controlled trial of CPAP only or CPAP + ME, recruiting individuals 45 to 75 years with moderate or severe OSA without marked sleepiness and with either established cardiovascular disease (CVD) or at risk for CVD. All participants received standardized CPAP support from a sleep technologist; those randomly assigned to CPAP + ME also received standardized ME delivered by a psychologist during two appointments and six phone calls over 32 weeks. Mixed-effect models with subject-specific intercepts and slopes were fitted to compare objective CPAP adherence between arms, adjusting for follow-up duration, randomization factors, and device manufacturer. All analyses were intention-to-treat.

Results  Overall, 83 participants (n = 42 CPAP only; n = 41 CPAP + ME) contributed 14,273 nights of data for 6 months. Participants were predominantly male (67%) and had a mean ± SD age of 63.9 ± 7.4 years, a BMI of 31.1 ± 5.2 kg/m2, and an apnea-hypopnea index of 26.2 ± 12.9 events/h. In our fully adjusted model, average nightly adherence for 6 months was 99.0 min/night higher with CPAP + ME compared with CPAP only (P = .003; primary analysis). A subset of 52 participants remained in the study for 12 months; modeling these data yielded a consistent difference in adherence between arms of 97 min/night (P = .006) favoring CPAP + ME.

Conclusions  ME delivered during brief appointments and phone calls resulted in a clinically significant increase in CPAP adherence. This strategy may represent a feasible approach for optimizing management of OSA.

Trial Registry  ClinicalTrials.gov; No.: NCT01261390; URL: www.clinicaltrials.gov.

Chest. 2016;150(2):346-352. doi:10.1016/j.chest.2016.03.005

Background  Obesity is known to be an important risk factor for OSA; however, OSA can also be seen in nonobese patients with a small maxilla and/or mandible as well as in all obese patients with such features. Thus, we hypothesized that regional factors, oropharyngeal crowding associated with fat deposition, and maxillomandibular enclosure size closely related to the severity of OSA.

Methods  A total of 703 male Japanese subjects were enrolled; theywere classified into obese (BMI ≥ 30 kg/m2; n = 158) and nonobese (BMI < 30 kg/m2; n = 545) groups. Using lateral cephalometric analysis, we measured the tongue size (TG), lower face cage (LFC), and TG/LFC ratio (ie, oropharyngeal crowding) to evaluate the state of upper airway crowding. The correlations between these cephalometric measurements and BMI, age, and the apnea-hypopnea index (AHI) were evaluated.

Results  In obese subjects, the TG/LFC ratio, BMI, and TG positively correlated with AHI, whereas, in nonobese subjects, age, BMI, and TG/LFC significantly correlated with AHI. Subsequent stepwise multiple linear regression analysis revealed that the variables associated with AHI differed between obese and nonobese OSA subjects, although BMI and TG/LFC were significantly associated with AHI in both groups. In particular, the contribution of TG/LFC to AHI was larger than that of BMI in the obese group.

Conclusions  Oropharyngeal crowding is a local anatomic factor that independently relates to the severity of OSA in both obese and nonobese patients; the more crowded the upper airway, the more severe the OSA.

Original Research: Pulmonary Vascular Disease

Chest. 2016;150(2):353-366. doi:10.1016/j.chest.2016.03.031

Background  Previous meta-analyses of pulmonary arterial hypertension (PAH)-specific therapy for PAH pooled PAH-specific combination therapy and monotherapy. This flaw may threaten the authenticity of their findings.

Methods  PubMed, Embase, and the Cochrane Library were searched for randomized controlled trials that evaluated any PAH-specific medications in the treatment of PAH. We calculated ORs with 95% CIs for dichotomous data and standardized mean differences for continuous data.

Results  In total, 35 randomized controlled trials involving 6,702 patients were included. In monotherapy vs placebo/conventional therapy, significance was obtained in mortality reduction (OR, 0.50 [95% CI, 0.33 to 0.76]; P = .001), 6-min walk test (mean difference, 31.10 m [95% CI, 25.40 to 36.80]; P < .00001), New York Heart Association/World Health Organization functional class (OR, 2.48 [95% CI, 1.51 to 4.07]; P = .0003), and hemodynamic status based on mean pulmonary artery pressure, pulmonary vascular resistance, cardiac index, and incidence of withdrawal due to adverse effects. In combination therapy vs monotherapy, significance was reached for the 6-min walk test (mean difference, 19.96 m [95% CI, 15.35 to 24.57]; P < .00001), functional class (OR, 1.65 [95% CI, 1.20 to 2.28]; P = .002), hemodynamic status, and incidence of withdrawal due to adverse effects (OR, 2.01 [95% CI, 1.54 to 2.61]; P < .00001) but not for mortality reduction (OR, 0.98 [95% CI, 0.57 to 1.68]; P = .94).

Conclusions  Our meta-analysis revealed that PAH-specific monotherapy could improve mortality, exercise capacity, functional class, and hemodynamic status compared with placebo or conventional therapy. However, combination therapy could further improve exercise capacity, functional class, and hemodynamic status compared with monotherapy, but it had no proven effect on mortality. Combination therapy had a much higher incidence of withdrawal due to adverse effects than monotherapy.

Chest. 2016;150(2):367-373. doi:10.1016/j.chest.2016.03.007

Background  This study aimed to show whether circulating bone morphogenetic proteins (BMPs) levels are associated with increased risk of mortality in patients with pulmonary arterial hypertension (PAH).

Methods  A total of 156 patients with PAH including 43 with heritable PAH (HPAH) and 113 with idiopathic PAH (IPAH) diagnosed by gene screening were enrolled in the study. Circulating BMPs were measured by ELISA in plasma samples from patients with HPAH (n = 43) and IPAH (n = 113) and from control subjects (n = 51). Clinical characteristics at baseline and long-term survival were compared according to the different BMP levels.

Results  Patients with HPAH had significantly higher BMP7 concentrations than patients with IPAH and control subjects (20.1 [interquartile range (IQR), 9.4, 55.2] vs 6.5 [IQR, 3.5, 11.7] and 2.5 [IQR, 0.9, 6.6] pg/mL, respectively; P < .001). Elevated plasma BMP7 were associated with a higher risk of mortality after adjustment for sex, 6-minute walk distance, mean right atrial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and cardiac output (HR, 1.904; 95% CI, 1.021-3.551; P = .043). Patients with IPAH with a BMP7 level > 7.85 pg/mL had a higher risk of mortality than those with a low BMP7 concentration (P = .042, log-rank test).

Conclusions  Levels of circulating BMP7 correlate with mortality in PAH, and may be a predictor of disease in patients with HPAH and IPAH.

Chest. 2016;150(2):374-383. doi:10.1016/j.chest.2016.03.046

Background  A comprehensive evaluation of temporal trends in the treatment of patients who have DVT may assist with identification of modifiable factors that contribute to short-term outcomes.

Methods  We assessed temporal trends in length of hospital stay and use of pharmacological and interventional therapies among 26,695 adults with DVT enrolled in the Registro Informatizado de la Enfermedad TromboEmbólica registry between 2001 and 2014. We also examined temporal trends in risk-adjusted rates of all-cause, pulmonary embolism-related, and bleeding-related death to 30 days after diagnosis.

Results  The mean length of hospital stay decreased from 9.0 days in 2001 to 2005 to 7.6 days in 2010 to 2014 (P < .01). For initial DVT treatment, the use of low-molecular-weight heparin decreased from 98% to 90% (P < .01). Direct oral anticoagulants use increased from 0.5% in 2010 to 13.4% in 2014 (P < .001). Risk-adjusted rates of 30-day all-cause mortality decreased from 3.9% in 2001 to 2005 to 2.7% in 2010 to 2014 (adjusted rate ratio per year, 0.84; 95% CI, 0.74-0.96; P < .01). VTE-related mortality showed a nonstatistically significant downward trend (adjusted rate ratio per year, 0.70; 95% CI, 0.44-1.10; P = .13), whereas 30-day bleeding-related mortality significantly decreased from 0.5% in 2001 to 2005 to 0.1% in 2010-2014 (adjusted rate ratio per year, 0.55; 95% CI, 0.40-0.77; P < .01).

Conclusions  This international registry-based temporal analysis identified reductions in length of stay for adults hospitalized for DVT. The study also found a decreasing trend in adjusted rates of all-cause and bleeding-related mortality.

Chest. 2016;150(2):384-393. doi:10.1016/j.chest.2016.03.011

Background  Integrating newly developed tests and treatments for severe pulmonary embolism (PE) into clinical care requires coordinated multispecialty collaboration. To meet this need, we developed a new paradigm: a multidisciplinary Pulmonary Embolism Response Team (PERT). In this report, we provide the first longitudinal analysis of patients treated by a PERT.

Methods  Our PERT includes specialists in cardiovascular medicine and surgery, emergency medicine, hematology, pulmonary/critical care, and radiology, and is organized as a rapid response team. We prospectively captured clinical, therapeutic, and outcome data at PERT activation and during follow-up periods up to 365 days. We analyzed data collectively, and as five mutually exclusive 6-month periods. We performed Fisher exact tests and regression analysis to test for trend.

Results  In 30 months, there were 394 unique PERT activations, 314 (80%) for confirmed PE. PERT activations increased by 16% every 6 months. Most confirmed PEs were submassive (n = 143, 46%) or massive (n = 80, 26%). The PERT treated a relatively large proportion of patients with PE and systemic or catheter-directed thrombolysis (n = 35, 11%), though the most common treatment was anticoagulation alone (n = 215, 69%). Hemorrhagic complications were rare overall, especially among patients treated with catheter-directed thrombolysis. The all-cause 30-day mortality of PERT patients with confirmed PE was 12%.

Conclusions  We report our initial 30-month experience with a novel multidisciplinary PERT that rapidly engages multiple specialists to deliver efficient, organized, and evidence-based care to patients with high-risk PE. The PERT paradigm was rapidly adopted and may become a new standard of care for patients with PE.

Original Research: Respiratory Care

Chest. 2016;150(2):394-406. doi:10.1016/j.chest.2016.03.041

Background  Problems with the use of inhalers by patients were noted shortly after the launch of the metered-dose inhaler (MDI) and persist today. We aimed to assess the most common errors in inhaler use over the past 40 years in patients treated with MDIs or dry powder inhalers (DPIs).

Methods  A systematic search for articles reporting direct observation of inhaler technique by trained personnel covered the period from 1975 to 2014. Outcomes were the nature and frequencies of the three most common errors; the percentage of patients demonstrating correct, acceptable, or poor technique; and variations in these outcomes over these 40 years and when partitioned into years 1 to 20 and years 21 to 40. Analyses were conducted in accordance with recommendations from Preferred Reporting Items for Systematic Reviews and Meta-Analyses and Strengthening the Reporting of Observational Studies in Epidemiology.

Results  Data were extracted from 144 articles reporting on a total number of 54,354 subjects performing 59,584 observed tests of technique. The most frequent MDI errors were in coordination (45%; 95% CI, 41%-49%), speed and/or depth of inspiration (44%; 40%-47%), and no postinhalation breath-hold (46%; 42%-49%). Frequent DPI errors were incorrect preparation in 29% (26%-33%), no full expiration before inhalation in 46% (42%-50%), and no postinhalation breath-hold in 37% (33%-40%). The overall prevalence of correct technique was 31% (28%-35%); of acceptable, 41% (36%-47%); and of poor, 31% (27%-36%). There were no significant differences between the first and second 20-year periods of scrutiny.

Conclusions  Incorrect inhaler technique is unacceptably frequent and has not improved over the past 40 years, pointing to an urgent need for new approaches to education and drug delivery.

Topics: inhaler
Chest. 2016;150(2):407-414. doi:10.1016/j.chest.2016.03.035

Background  Little is known about the effects of long-term nasal low-flow oxygen (NLFO) on mucus and symptoms and how this variable is affected by dry or cold humidified gas. The aim of this study was to investigate the effects of dry-NLFO and cold bubble humidified-NLFO on nasal mucociliary clearance (MCC), mucus properties, inflammation, and symptoms in subjects with chronic hypoxemia requiring long-term domiciliary oxygen therapy.

Methods  Eighteen subjects (mean age, 68 years; 7 male; 66% with COPD) initiating NLFO were randomized to receive dry-NLFO (n = 10) or humidified-NLFO (n = 8). Subjects were assessed at baseline, 12 h, 7 days, 30 days, 12 months, and 24 months by measuring nasal MCC using the saccharin transit test, mucus contact angle (surface tension), inflammation (cells and cytokine concentration in nasal lavage), and symptoms according to the Sino-Nasal Outcome Test–20.

Results  Nasal MCC decreased significantly (40% longer saccharin transit times) and similarly in both groups over the study period. There was a significant association between impaired nasal MCC and decline in lung function. Nasal lavage revealed an increased proportion of macrophages, interleukin-8, and epidermal growth factor concentrations with decreased interleukin-10 during the study. No changes in the proportion of ciliated cells or contact angle were observed. Coughing and sleep symptoms decreased similarly in both groups. There were no outcome differences comparing dry vs cold bubble humidified NLFO.

Conclusions  In subjects receiving chronic NLFO, cold bubble humidification does not adequately humidify inspired oxygen to prevent deterioration of MCC, mucus hydration, and pulmonary function. The unheated bubble humidification performed no better than no humidification.

Trial Registry  ClinicalTrials.gov; No.: NCT02515786; URL: www.clinicaltrials.gov.

Original Research: Chest Infections

Chest. 2016;150(2):415-425. doi:10.1016/j.chest.2016.03.042

Background  Pseudomonas aeruginosa is not a frequent pathogen in community-acquired pneumonia (CAP). However, in patients with severe CAP, P aeruginosa can be the etiology in 1.8% to 8.3% of patients, with a case-fatality rate of 50% to 100%. We describe the prevalence, clinical characteristics, outcomes, and risk factors associated with CAP resulting from multidrug-resistant (MDR) and non-MDR P aeruginosa.

Methods  Prospective observational study of 2,023 consecutive adult patients with CAP with definitive etiology.

Results  P aeruginosa was found in 77 (4%) of the 2,023 cases with microbial etiology. In 22 (32%) of the 68 cases of P aeruginosa with antibiogram data, the isolates were MDR. Inappropriate therapy was present in 49 (64%) cases of P aeruginosa CAP, including 17/22 (77%) cases of MDR P aeruginosa CAP. Male sex, chronic respiratory disease, C-reactive protein <12.35 mg/dL, and pneumonia severity index risk class IV to V were independently associated with P aeruginosa CAP. Prior antibiotic treatment was more frequent in MDR P aeruginosa CAP compared with non-MDR P aeruginosa (58% vs 29%, P = .029), and was the only risk factor associated with CAP resulting from MDR P aeruginosa. In the multivariate analysis, age ≥65 years, CAP resulting from P aeruginosa, chronic liver disease, neurologic disease, nursing home, criteria of ARDS, acute renal failure, ICU admission, and inappropriate empiric treatment were the factors associated with 30-day mortality.

Conclusions  P aeruginosa is an individual risk factor associated with mortality in CAP. The risk factors described can help clinicians to suspect P aeruginosa and MDR P aeruginosa.

Recent Advances in Chest Medicine

Chest. 2016;150(2):426-441. doi:10.1016/j.chest.2016.02.001

The purpose of this article is to provide an update on methods for palliating symptoms in patients with histologically benign and malignant central airway obstruction. We review the published literature within the past decade on postintubation, posttracheostomy, and TB- and transplant-related airway strictures; tracheobronchomalacia; and malignant airway obstruction. We review terminology, classification systems, and parameters that impact treatment decisions. The focus is on how airway stent insertion fits into the best algorithm of care. Several case series and cohort studies demonstrate that airway stents improve dyspnea, lung function, and quality of life in patients with airway obstruction. Airway stenting, however, is associated with high rates of adverse events and should be used only when curative open surgical interventions are not feasible or are contraindicated.

Contemporary Reviews in Critical Care Medicine

Chest. 2016;150(2):442-450. doi:10.1016/j.chest.2016.02.656

Lung transplantation (LTx) has become an accepted treatment for carefully selected patients with end-stage lung disease. Critical care issues have gained importance concerning bridging of candidates by mechanical respiratory support and are involved in the care after transplantation. The nature of respiratory support varies from oxygen supply and noninvasive ventilation, to mechanical respiratory support either by mechanical ventilation and/or extracorporeal life support. Recent innovations in extracorporeal life support technology have resulted in its more widespread use. Retrospective studies have demonstrated promising outcomes in candidates on mechanical respiratory support as a bridge to lung transplantation. The role of mechanical respiratory support has influenced the selection criteria for LTx, although bridging remains technically and ethically challenging. Critical care is integral to manage and prevent postoperative complications of LTx. Primary graft dysfunction and prolonged mechanical ventilation are major obstacles to hospital survival after LTx. Clear evidence is lacking on how to ventilate and optimally manage patients after LTx. Prolonged extracorporeal life support after LTx may improve outcome in selected patients with a primary graft dysfunction.

Contemporary Reviews in Sleep Medicine

Chest. 2016;150(2):451-463. doi:10.1016/j.chest.2016.04.029

Despite the undeniable medical advances achieved in recent decades, cancer remains one of the main causes of mortality. It is thus extremely important to make every effort to discover new risk factors for this disease, particularly ones that can be treated or modified. Various pathophysiologic pathways have been postulated as possible causes of cancer or its increased aggressiveness, and also of greater resistance to antitumoral treatment, in the presence of both intermittent hypoxia and sleep fragmentation (both inherent to sleep apnea). Thus far, these biological hypotheses have been supported by various experimental studies in animals. Meanwhile, recent human studies drawing on preexisting databases have observed an increase in cancer incidence and mortality in patients with a greater severity of sleep-disordered breathing. However, the methodologic limitations of these studies (which are mostly retrospective and lack any measurement of direct markers of intermittent hypoxia or sleep fragmentation) highlight the need for controlled, prospective studies that would provide stronger scientific evidence regarding the existence of this association and its main characteristics, as well as explore its nature and origin in greater depth. The great epidemiologic impact of both cancer and sleep apnea and the potential for clinical treatment make this field of research an exciting challenge.

Topics: cancer


Chest. 2016;150(2):464. doi:10.1016/j.chest.2016.02.679

    I'm resident and active; billion-copied, systemic,
    So myriad now I'm potentially epidemic
    She's infectious, her symptoms unveiled
    painful expansion, with volume inhaled

    Each inhalation, takes her breath away
    with difficulty her thoughts cast the day
    sense the ballooning within, intercostals complaining
    then exhalation and relief from constraining

    Mucosa inflamed now in throat and nose
    I move rapidly to claim more beyond those
    my infection races on soundless
    my infectivity seems boundless

    In her upper airway I begin to be heard
    now increasingly sore with a tickle
    then full-throated cough, air jetting in
    it's unpredictable and fickle

    I'll stay for the duration, as long as I can – her immune response is my foe
    It will get me in time for she's fit, she's healthy, strong from top to toe
    my kin engulfed, my virulence diminished
    She'll recover, more immunity acquired; re-infection effectively finished

    I'll overcome the resistance of the young, the old,
    and multiply with persistence 'til they fold
    With their cough, their fever I'll inflame their contagion
    And open the floodgates for pneumococcal invasion

    And so I will spread, sparing few their infection
    my ancient properties so refined by selection
    Neither race nor religion a barrier will be
    I'm a breathtaking virus for sure -that's me!

Chest. 2016;150(2):465-466. doi:10.1016/j.chest.2016.03.006

    For there will be the laying on of hands and the letting go

    It was 6:17 on my first week of nights when I was called
    not sweetly, the low incessant beep of my pager
    but a whispered yell, an urgency atypical
    on this floor of sweet, demented adult-children
    (women who kissed my hands and held them to their cheeks,
    men who told me I looked like their wives after the war)
    my name, over and over.

    I keep thinking about his eyes, how they
    how I stopped,
    how she looked at me, the veteran nurse,
    wildness in her eyes like I’ve never seen before
    “should I start CPR?”
    And I, feeling until this moment a small, smart girl
    realize how crazy it is they gave me this position
    an imposter in navy blue scrubs
    a frantic nurse
    a small, staring man
    and the silence.

    (My whole body shaking, I wanted to say
    but there is no room for not knowing in crisis).

    There’s no pulse, I said
    Yes, I said
    Call the code, I said
    Call my senior, I said
    Get the code cart, I said
    Help me, I didn’t say

    I ran back to get my stethoscope, as if
    listening to the static in your frail chest,
    the empty airwaves where once an irregular consistency lived
    might help bring you back from the dead.
    And I stood there, stethoscope in hand
    frantically trying to remember if we give Epinephrine
    and at what dose
    and at what point someone else would take over
    (be it a senior resident or God)
    and watched the fluid slosh out of your mouth
    as she pushed your whole body into the bed
    and you rose back up.

    and then the rush of cool breeze
    a wave of a dozen people
    and someone asked the air “what’s his code status?”
    And I then I knew I had failed.
    Because he, the former doctor, had told me “all of this,
    all of this is too much” and to just let him be
    and I looked down at my hands and saw it, in red letters
    Stop, I said
    He’s DNR, I said
    I’m so sorry, I said
    over and over and over.

    I didn’t stop shaking for the next hour.
    Everyone left, and we cleaned everything up
    calmed down the nurse,
    called his wife, who cried, at 84, but didn’t sound surprised,
    filled out the death paperwork
    brought in mint scents
    and I sat there, in the chair next to his bed,
    behind the closed door everyone was avoiding
    and held his hand and cried.

    The doctor who couldn’t save him;
    the intern who didn’t know what to do to let him go.

    The Lord being his heritage, let him rest in peace
    And so I name you, student of Freud,
    he who taught me to do a radial artery stick on his own wrist
    who diagnosed his own atelectasis
    but was blind to his own cancer.
    I name you, and I pray for your rest,
    and as the intern who only knows to lay on hands
    and not yet how to let go;

    And let us say, Amen


Chest. 2016;150(2):467. doi:10.1016/j.chest.2016.03.064

The recent publication by Smith et al in CHEST (July 2016) entitled “Analysis of National Trends in Admissions for Pulmonary Embolism” was a thought-provoking examination of national trends in the management of pulmonary embolism. There are, however, several significant issues that were not addressed by the authors that warrant explanation.

Chest. 2016;150(2):467-468. doi:10.1016/j.chest.2016.04.038

Recently, we read with great interest the paper entitled “Various Mechanistic Pathways Representing the Aging Process Are Altered in COPD” in CHEST (January 2016) by Rutten et al, in which the authors showed in an excellent work that several biomedical signaling pathways were probably involved in the aging process of patients with COPD. Interestingly, soluble klotho significantly decreased in patients with COPD compared with those in the smoking or nonsmoking control groups. It has been widely recognized that klotho has two subunits consisting of α-klotho and β-klotho that separately trigger distinct physiological actions by binding to its coreceptors fibroblast growth factor (FGF) 23 and FGF21. Although FGF23 and FGF21 are individually implicated in the pathogenesis of chronic kidney disease and obesity, it cannot be ignored that abnormalities in FGF23 or FGF21, or both, would also be implicated in the underlying mechanisms of the aging process in COPD. More importantly, klotho deficiency may elicit a vicious result of resistance of FGF 23 and FGF21, since decreased klotho could not provide adequate binding sites for FGF 23 and FGF21., Relative increased levels of FGF23 and FGF21 would exert deletion effects on physiological functions. Based on these findings, we suggest that excessive levels of FGF23 or FGF21, or both, are also probably involved in the mechanisms of the COPD-related aging process. It is likely, therefore, that detecting levels of FGF23 or FGF21, or both, may favor the observation of the aging process of individuals with COPD. To the best of our knowledge, there is no study reporting the role of FGF23 or FGF21 in COPD. Subsequent investigations on the role of FGF-klotho signaling in the COPD-associated aging process are needed.

Chest. 2016;150(2):468-469. doi:10.1016/j.chest.2016.04.037

Respiratory failure is a frequent cause of death that is increased in the absence of ventilatory support. Noninvasive ventilation (NIV) is succesfully used to improve gas exchange, avoid endotracheal intubation, and reduce mortality in respiratory failure., There is good evidence to support NIV use as the first-line treatment in respiratory failure due to COPD exacerbations, but the evidence for use in acute asthma attacks is less compelling.

Chest. 2016;150(2):469-470. doi:10.1016/j.chest.2016.06.007

We thank Drs Takir and Esquinas for their insightful commentary regarding our findings. In our study, we analyzed data from the electronic medical records of 58 hospitals. We adjusted for patient case mix and several variables indicative of disease severity, including the Laboratory Acute Physiological Score, which integrates 14 laboratory tests, including arterial blood gas, and for prior noninvasive ventilation (NIV) or invasive ventilation (intermittent mandatory ventilation [IMV]). The models predicting NIV and IMV use had strong discriminatory ability with c-statistics > 0.78 using only patient-level variables as fixed effects. Patient characteristics did not differ according to hospital quartiles of adjusted NIV rates. Moreover, we performed a hospital-level rather than patient-level analysis, which greatly reduces the risk of confounding by indication. Nevertheless, we agree that a study limitation is its lack of information about prior pulmonary function test results.

Chest. 2016;150(2):470-471. doi:10.1016/j.chest.2016.04.033

Dyspnea affects approximately 50% of patients admitted to hospitals. Prompt identification of its correct cause may optimize the management and improve outcomes. Lung ultrasound (LUS) is emerging as a bedside tool that could discriminate different causes of dyspnea even by nonphysicians.

Chest. 2016;150(2):471-473. doi:10.1016/j.chest.2016.05.031

Castro-Grattoni et al should be congratulated for their article published in CHEST (June 2016) demonstrating in a mouse model of sleep apnea (OSA) that intermittent hypoxia (IH)-induced cardiovascular remodeling is reversed after removal of IH exposure (mimicking OSA treatment by CPAP). We would like to contribute to this important topic by providing additional data and comments.

Chest. 2016;150(2):473-474. doi:10.1016/j.chest.2016.05.032

We have read with great interest the article by Mackay et al published in CHEST (May 2016) entitled “Airway Surfactant Protein D Deficiency in Adults with Severe Asthma.” As elegantly shown, serum surfactant protein D (SP-D) concentrations were significantly lower in individuals with severe asthma as opposed to individuals with mild asthma and healthy control subjects, and SP-D levels were significantly higher in the BAL of patients with severe asthma compared with those with mild asthma. On this basis, the authors propose that serum SP-D could serve as a biomarker of the most severe forms of asthma. In their article, Mackay et al state that “To the best of our knowledge, this study is the first to investigate the relationship between asthma and SP-D concentration in patients with such severe disease.” We respectfully disagree with this statement, since we recently reported that indeed serum SP-D concentrations are significantly higher in individuals with severe asthma as opposed to healthy control subjects and individuals with mild asthma, and their levels correlate with the degree of airway obstruction. In our study, we hypothesized that serum SP-D could increase as a result of inflammation-induced permeability of the bronchial microvasculature, which allows the passage of large macromolecules, such as hydrophilic surfactant proteins, from lung to blood. However, the increased levels of surfactant proteins in serum could also be explained by an increased local synthesis of surfactant proteins induced by local inflammation.

Chest. 2016;150(2):474. doi:10.1016/j.chest.2016.05.033

We thank Dr Benfante et al for their letter. We are delighted that they have been able to replicate our findings reported in CHEST and add to our data that serum surfactant protein D (SP-D) is elevated in severe asthma and as such may act as a biomarker of small airway events. This was indicated by our identification of reduced concentrations of SP-D in BAL, which has implications for small airway function and innate immune defense. Benfante et al questioned our statement that “To the best of our knowledge, this study is the first to investigate the relationship between asthma and SP-D concentration in patients with such severe disease.” They respectfully disagree with our statement, referring to their recent report that serum SP-D concentrations are significantly higher in patients with severe asthma as opposed to healthy control subjects and individuals with mild asthma and that their levels correlate with the degree of airflow obstruction. However, our CHEST publication, first available as an e-publication in January 2016, predated their e-publication in March 2016, and as such our statement is correct. However, this is not of scientific importance; we highlight this only to provide the correct information and make the record clear. Of more importance is their validation of our findings and considerations about future work to understand the implications and the value of serum SP-D as a biomarker to potentially monitor the impact of therapy on the distal airways. This correspondence brings together similar research at separate sites and highlights the need for further research to investigate possible mechanisms of airway SP-D deficiency in severe asthma. As such, we welcome possible collaborations into understanding the underlying causes. A recent review has highlighted several important areas of further investigation, for example, are the low levels in the airway a result of consumption or cleavage associated with increased airway infection? We recognize that the airways are not sterile and that there is an altered colonization in severe asthma. We have recently reported that some bacterial strains may shield core structures in the lipopolysaccharide, which are targets for SP-D binding by the carbohydrate recognition domain; proteases present in severe asthma may cleave SP-D within the carbohydrate recognition domain and inhibit these innate immune defense functions, contributing to ongoing inflammation and low SP-D levels in the BAL.

Selected Reports

Chest. 2016;150(2):e29-e32. doi:10.1016/j.chest.2016.02.654

A young woman received a diagnosis of abdominal, sporadic lymphangioleiomyomatosis (LAM) and multiple abdominal lymphangioleiomyomas and was referred for recurrent chylous ascites responding only to a fat-free diet. On admission, pulmonary function test (PFT) results showed a moderate reduction in the transfer factor for carbon monoxide with normal exercise performance. The serum vascular endothelial growth factor D (VEGF-D) level was 2,209 pg/mL. DNA sequences, amplified at loci kg8, D16S3395, D16S3024, D16S521, and D16S291 on chromosome 16p13.3, showed a loss of heterozygosity (LOH) only for kg8. Fat-free total parenteral nutrition in association with sirolimus (2 mg po daily) was initiated. Serum sirolimus levels were maintained at concentrations between 5 and 15 ng/mL. After 1 month, reintroduction of a low-fat oral feeding was achieved without recurrence of ascites. PFT results were stable. Interestingly, clinical improvement was associated with a reduction in the VEGF-D serum level (1,558 pg/mL). LOH at the kg8 biomarker in blood LAM cells was no longer detected.

Ultrasound Corner

Chest. 2016;150(2):e33-e35. doi:10.1016/j.chest.2016.02.690

A 56-year-old woman was transferred to the ED after high-energy thoracic trauma with multiple bilateral rib fractures resulting from a car accident. Because of bilateral hemopneumothorax, bilateral chest tubes were placed and mechanical ventilation was started. As the patient recovered, weaning from mechanical ventilation was initiated. Drainage stopped and chest tubes were removed a few days later. During a weaning trial, a severe flail chest that impaired respiratory efforts became apparent. Surgical stabilization of the chest cage was made with titanium clips. Finally, the patient was successfully weaned from the ventilator. Ten days later, respiratory failure gradually developed. On physical examination, no crepitation or collection was found near the surgical incision. On the auscultation of the left hemithorax, breath sounds were absent. A chest radiograph study showed opacification of the left hemithorax (Fig 1). Further evaluation with chest ultrasonography (US) was performed (Video 1).

Chest. 2016;150(2):e37-e40. doi:10.1016/j.chest.2016.02.689

A 66-year-old man was undergoing transesophageal echocardiography in preparation for valve surgery for aortic stenosis when he experienced respiratory arrest during the procedure. The transesophageal echocardiography probe was withdrawn, and his ventilation was assisted using a bag-valve mask. The patient then experienced significant bradycardia with hypotension and a code blue was activated within the hospital. On arrival, the code team noted an agonal rhythm on telemetry. Blood pressure and oxygen saturation readings were unable to be obtained. A pocket-sized ultrasonographic device (Vscan, GE Healthcare) carried by a cardiologist responding to the code recorded subcostal views intermittently throughout the resuscitation (Video 1).

Chest Imaging and Pathology for Clinicians

Chest. 2016;150(2):e41-e47. doi:10.1016/j.chest.2016.02.680

A 57-year-old man with a history of DVT and pulmonary embolism, transient ischemic attacks, prior 60 pack-year smoking history, and oxygen-dependent COPD presented with insidiously worsening dyspnea associated with new pleuritic chest and back pain.

Pulmonary, Critical Care, and Sleep Pearls

Chest. 2016;150(2):e49-e52. doi:10.1016/j.chest.2016.02.668

A 44-year-old man from Connecticut with no significant past medical history presented to the ED with a 2-week history of sore throat and fatigue, subsequently developing cough, dyspnea, fevers, and chills. The patient reported buying an old camper van and noticed a large infestation of rodent droppings, which he had cleaned thoroughly from the cabin. He used the camper van on several camping trips in Vermont, and symptoms started on his return.

Topics: fatigue , sore throat
Chest. 2016;150(2):e53-e57. doi:10.1016/j.chest.2016.02.681

A 29-year-old woman presented with a 1-week history of fever, weakness, anorexia, darkened urine, and mild cough. The patient described her cough as nonproductive and without hemoptysis. She had no chest pain. The patient’s medical history was significant for x-linked hypophosphatemia, renal stones, migraine headaches, and chronic back pain managed on prescribed oral opiates for some time. She reported regular cigarette smoking, but denied illicit or IV drug use or any recent travel or sick contacts. The patient also had no known pertinent family history.

Chest. 2016;150(2):e59-e64. doi:10.1016/j.chest.2016.02.686

A 51-year-old woman with a personal history of vitiligo, normal thyroid hormone studies, a simple hysterectomy for multiple uterine myomas at age 35 years, and childhood adenotonsillectomy was seen for progressive hearing loss. She reported mild asthenia, cold intolerance, mild dysphagia with frequent choking while eating and drinking, and a progressive increase in inspiratory effort, especially in the supine position. Her partner described a progressively worsening history of snoring and witnessed apneic episodes, mostly in the supine position. Mild to moderate daytime sleepiness was also present.

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