In early 2018, the Centers for Medicare & Medicaid Services released the Medical Review of Evaluation and Management (E/M) Documentation, which allows supervising teaching physicians to rely on a medical student's documentation to support billing for E/M services. This change has potential to enhance education, clinical documentation quality, and the satisfaction of students, postgraduate trainees, and teaching physicians. However, its practical adoption presents many challenges that must be navigated successfully to realize these important goals in compliance with federal and local requirements, while avoiding unintended downstream problems. Implementation requires careful planning, policy creation, education, and monitoring, all with collaboration between institutional leaders, compliance and information technology professionals, educators, and learners. In this paper, we review the 2018 Centers for Medicare & Medicaid Services rule change, address common questions and potential impacts, outline practical workflows to meet the supervision requirement, and discuss steps for successful implementation.

Providing guideline-concordant management of pulmonary nodules can present challenges when a patient's anxiety about cancer or fear of invasive procedures colors judgment. The way in which providers discuss and make decisions about how to evaluate a pulmonary nodule can affect patient satisfaction, distress, and adherence to evaluation. This article discusses the complexity of tailoring patient-provider communication, decision-making, and implementation of guidelines for pulmonary nodule evaluation to the individual patient, emphasizing the importance of how information is conveyed and the value of listening to and addressing patients' concerns. We summarize the relevant guideline recommendations and literature, and provide two case scenarios to illustrate a patient-centered approach to discussing and managing pulmonary nodules from our perspectives as a pulmonologist and thoracic surgeon.

Idiopathic inflammatory myopathies are autoimmune processes that are characterized by skeletal muscle inflammation. The lung is the most commonly involved extramuscular organ, and, when present, pulmonary disease drives morbidity and mortality. A subset of patients can present with rapidly progressive hypoxemic respiratory failure due to myositis-related interstitial lung disease. Confirmatory autoantibody testing requires sending samples to a reference laboratory; thus, diagnosis of rapidly progressive myositis-associated interstitial lung disease relies on a high index of suspicion and careful history and physical examination. Although the cornerstone of therapy for these patients remains multimodality immunosuppression, emerging data support a role for advanced therapies (including extracorporeal membrane oxygenation and lung transplantation) in appropriately selected patients. It is hoped that greater awareness of the clinical features of this syndrome will allow for appropriate diagnosis and treatment of these potentially treatable patients, as well as raise awareness of the need for multicenter collaboration to prospectively study how to manage this complex disease.

There is increasing evidence that COPD is a disease of accelerated lung aging, with the accumulation of senescent cells that lose their ability to repair and secrete multiple inflammatory proteins known as the senescence-associated secretory phenotype (SASP), which mimic the profile of inflammatory mediators secreted in COPD. This review discusses novel drugs (senotherapies) that target cellular senescence and which may be a promising therapeutic approach to prevent currently unaddressed disease progression and mortality in COPD. A major pathway leading to senescence is via the activation of phosphoinositide-3-kinase/mammalian target of rapamycin signaling. Existing drugs, such as rapamycin and metformin, target this pathway. Mitochondrial oxidative stress is a key driving mechanism for this pathway, and mitochondria-targeted antioxidants are promising. A key finding in COPD is loss of antiaging molecules such as sirtuin-1 and sirtuin-6, which are reduced by phosphoinositide-3-kinase/mammalian target of rapamycin signaling through microRNA-34a. Sirtuin activators are in development, and inhibiting microRNA-34a restores sirtuin expression experimentally in COPD cells. Senolytic therapies induce apoptosis and removal of senescent cells and reduce the senescence-associated secretory phenotype response in animal models of aging and in pilot clinical studies of other age-related diseases. A combination of senolytics and senostatics (drugs that inhibit cellular senescence) may be a valuable new approach to COPD, especially if started early in the disease process. Furthermore, COPD is associated with several comorbidities that share the same aging pathways which may be spread by extracellular vesicles, and thus a single treatment for all these diseases is feasible in the future to extend health span.

Guidelines for clinical documentation of evaluation and management face-to-face services were developed > 20 years ago. Recently, the Centers for Medicare & Medicaid Services (CMS) have addressed office and other outpatient services and the corresponding reimbursement, intending to reduce the amount of required documentation and to alleviate clerical burden. A CMS final rule for 2021 will eliminate the history and physical examination as criteria for level of service, allow time or medical decision-making to be used as coding criteria, and will recognize a code for prolonged service. The net effect of these changes may be some decrease in documentation burden, a change in the composition of clinical notes, and greater recognition by CMS of primary care and those who see highly complex patients requiring prolonged services.

Pulmonary arterial hypertension (PAH) is a rare disease with high mortality despite therapeutic advances. Clinical management of children with PAH is particularly challenging because of increased complexity of disease etiology and clinical presentation, and the lack of data from pediatric-specific clinical trials. In children, PAH often develops in association with congenital heart disease and other developmental disorders. Emerging data from genetic studies of pediatric-onset PAH indicate that the genetic basis is different than that of adults. There is a greater genetic burden in children, with rare genetic factors contributing to at least 35% of pediatric-onset idiopathic PAH (IPAH) compared with approximately 11% of adult-onset IPAH. De novo variants are the most frequent monogenetic cause of PAH in children, likely contributing to approximately 15% of all cases. Rare deleterious variants in BMPR2 contribute to pediatric-onset IPAH and familial PAH with similar frequency as adult-onset disease but rarely explain cases of PAH associated with other diseases. Rare deleterious variants in developmental genes-including TBX4, SOX17, and other genes requiring confirmation in larger cohorts-are emerging as important contributors to pediatric-onset disease. Because each causal gene contributes to only a small number of cases, large cohorts of pediatric-onset PAH are needed to further identify the unique etiologic differences of PAH in children. We propose a genetics-first approach followed by focused phenotyping of pediatric patients grouped by genetic diagnosis to define endophenotypes that can be used to improve risk stratification and treatment.

Smoking continues to be a burden to economies and health-care systems across the world. One proposed solution to the problem has been e-cigarettes; however, because they are a relatively new product in the market, little is known about their potential health impacts. Furthermore, e-cigarettes continue to evolve at a rapid rate, making it necessary to regularly review and summarize available studies. Although e-cigarettes are marketed as a smoking cessation tool by some manufacturers, the reality is that many nonsmokers, including youth, are using them. This review focuses on two major demographic groups (smokers and nonsmokers) and evaluates the most recent data (early 2017 to mid 2019) regarding the potential health effects of e-cigarettes. We assessed peer-reviewed studies on the health impacts of e-cigarettes, with a particular focus on common questions asked by policy makers, clinicians, and scientists: (1) What are the effects of e-cigarettes compared with air/not smoking?; (2) Is there any direct evidence of harm or benefit to humans?; (3) Is there a risk from secondhand exposure?; (4) What are the risks and/or benefits of e-cigarettes compared with tobacco cigarette use?; (5) Are there risks or benefits to specific populations (eg, people with COPD or asthma, pregnant women [and their offspring])?; (6) What are the effects of flavoring chemicals?; (7) What are the effects of including nicotine in e-liquids?; (8) How often is nicotine concentration labeling incorrect?; and (9) What are the risks when e-cigarettes explode?

IV fluids are recommended during the initial management of sepsis, but the quality of evidence is low, and clinical equipoise exists. We aimed to assess patient-important benefits and harms of lower vs higher fluid volumes in adult patients with sepsis.

COPD is a common respiratory disorder that poses a major health-care burden with societal and financial ramifications. Although effective inhaled therapies are available, nonadherence is common among patients with COPD and potentially contributes to the burden of this disease. Electronic inhaler monitoring (EIM) is a novel modality that enables real-time assessment of adherence to inhaled therapy and informs the assessment of treatment effectiveness. EIM can be combined with physician feedback, automated audiovisual reminders, and text messaging to bolster adherence. Clinical studies have suggested that EIM can diagnose nonadherence, improve adherence, and predict exacerbations. Using an EIM-guided protocol has the potential to avoid treatment escalation in the nonadherent. Coupling EIM to behavioral intervention is an area of ongoing research with mixed results, with some studies showing benefit and others showing minimal or no significant change in clinical outcomes. Further investigation is necessary to understand the incremental benefits of EIM features, delineate optimal program implementation, and target patient populations that would benefit the most from monitoring.

Parasitoses are infectious diseases of global distribution, with predominance in areas of poor sanitation. Parasites cause damage through direct tissue injury and the inflammatory response generated by their migration and establishment in various organs. Thoracic involvement by parasitic disease can generate both specific and nonspecific clinical, laboratorial, and radiologic manifestations, which often makes their diagnosis challenging. The correct diagnosis is crucial for definition of treatment, which sometimes requires rapid intervention. Based on a literature review of the last few decades, this article aimed to characterize the main radiologic findings related to thoracic manifestations of parasitic diseases, correlating them with radiographic and tomographic images of patients with confirmed diagnosis of such pathologies. The included parasitic diseases are malaria, Chagas disease, toxoplasmosis, amoebiasis, ascariasis, toxocariasis, strongyloidiasis, dirofilariasis, cysticercosis, echinococcosis, schistosomiasis, and paragonimiasis.

Chronic hypersensitivity pneumonitis (CHP) is an immune-mediated interstitial lung disease (ILD) caused by inhalational exposure to environmental antigens, resulting in parenchymal fibrosis. By definition, a diagnosis of CHP assumes a history of antigen exposure, but only half of all patients eventually diagnosed with CHP will have a causative antigen identified. Individual clinician variation in eliciting a history of antigen exposure may affect the frequency and confidence of CHP diagnosis.

The concerns regarding air leak after lung surgery or spontaneous pneumothorax include detection and duration. Prior studies have suggested that digital drainage systems permit shorter chest tube duration and hospital length of stay (LOS) by earlier detection of air leak cessation. We conducted a systematic review to assess the impact of digital drainage on chest tube duration and hospital LOS after pulmonary surgery and spontaneous pneumothorax.

Central sleep apnea/Hunter-Cheyne-Stokes breathing (CSA/HCSB) is prevalent in patients with heart failure with reduced ejection fraction (HFrEF). The acute pathobiologic consequences of CSA/HSCB eventually lead to sustained sympathetic overactivity, repeated hospitalization, and premature mortality. A few randomized controlled trials (RCTs) have shown statistically significant and clinically important reduction in sympathetic activity when CSA/HCSB is attenuated by oxygen or PAP therapy. Yet, the two largest PAP RCTs in patients with HFrEF, one with CPAP and the other with adaptive servoventilation (ASV), were negative with respect to their primary outcomes, and both were associated with excess mortality. However, both trials suffered from significant deficiencies, casting doubt on their results. A second RCT evaluating an ASV device with an advanced algorithm is ongoing. A new modality of therapy, unilateral phrenic nerve stimulation, has undergone an RCT that demonstrated an improvement in CSA that was associated with a reduction in arousals, improvement in sleepiness, and improvement in quality of life. However, a long-term mortality trial has not been performed with this modality. Most recently, the National Institutes of Health has funded a long-term, phase 3 RCT of low-flow oxygen vs sham for the treatment of CSA/HCSB in HFrEF. The composite primary outcome includes all-cause mortality and hospitalization for worsening HF. In this article, we focus on various therapeutic options for the treatment of CSA/HCSB and, when appropriate, emphasize the importance of identifying CSA/HCSB phenotypes to tailor treatment.

In addition to affecting the oxygen supply to the brain, pulmonary function is a marker of multiple insults throughout life (including smoking, illness, and socioeconomic deprivation). In this meta-analysis of existing longitudinal studies, the hypothesis that lower pulmonary function and respiratory illness are linked to an elevated risk of dementia was tested.

COPD is a heterogeneous syndrome. Many COPD subtypes have been proposed, but there is not yet consensus on how many COPD subtypes there are and how they should be defined. The COPD Genetic Epidemiology Study (COPDGene), which has generated 10-year longitudinal chest imaging, spirometry, and molecular data, is a rich resource for relating COPD phenotypes to underlying genetic and molecular mechanisms. In this article, we place COPDGene clustering studies in context with other highly cited COPD clustering studies, and summarize the main COPD subtype findings from COPDGene. First, most manifestations of COPD occur along a continuum, which explains why continuous aspects of COPD or disease axes may be more accurate and reproducible than subtypes identified through clustering methods. Second, continuous COPD-related measures can be used to create subgroups through the use of predictive models to define cut-points, and we review COPDGene research on blood eosinophil count thresholds as a specific example. Third, COPD phenotypes identified or prioritized through machine learning methods have led to novel biological discoveries, including novel emphysema genetic risk variants and systemic inflammatory subtypes of COPD. Fourth, trajectory-based COPD subtyping captures differences in the longitudinal evolution of COPD, addressing a major limitation of clustering analyses that are confounded by disease severity. Ongoing longitudinal characterization of subjects in COPDGene will provide useful insights about the relationship between lung imaging parameters, molecular markers, and COPD progression that will enable the identification of subtypes based on underlying disease processes and distinct patterns of disease progression, with the potential to improve the clinical relevance and reproducibility of COPD subtypes.

Sleep is important to health and well-being, and studies in healthy adults have demonstrated that sleep deprivation impacts respiratory, immune, and cognitive function. Historically, because of the nature of critical illness, sleep has not been considered a priority for patient care in the ICU. More recently, research has demonstrated that sleep is markedly abnormal in patients who are critically ill. In addition, there is often disruption of circadian rhythms. Delirium is a syndrome of acute alteration in mental status that occurs in the setting of contributing factors such as serious illness, medication, and drug or alcohol intoxication or withdrawal. Delirium is a frequent occurrence in critical illness, and research has demonstrated several adverse outcomes associated with delirium including persistent cognitive impairment and increased mortality. Sleep deprivation and delirium share many common symptoms. The similarity in symptoms between sleep disruption and delirium have prompted experts to draw links between the two and question both the relationship and its direction. In addition, the inclusion of sleep disturbance to the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition in its constellation of symptoms used in diagnosing delirium has increased awareness of the link between sleep and delirium. This paper will review the literature on sleep in critical illness and the potential mechanisms and pathways that may connect sleep and delirium.

Sleep health is a multidimensional construct that includes adequate duration, quality, and appropriately timed sleep that may be influenced by environmental factors. In this review, we focus on how an individual's living and sleeping environment, both the surrounding neighborhood physical and social features and the atmosphere around them, may impact their sleep health. We explore the associations of the physical environment (urban density, recreational facilities, green space, mixed land use, and healthy food stores), neighborhood deprivation (disadvantage and disorder), and the social environment (social cohesion, safety, and stigma) with sleep in both adult and pediatric populations. We investigate how physical and social environmental features may lead to alterations in the timing, duration, and quality of sleep and contribute to the most prevalent sleep disorders: insomnia, sleep apnea, and circadian rhythm disorders. We also review how ambient factors such as artificial light, environmental noise, and air pollution may contribute to sleep pathology. We have included key studies and recent emerging data regarding how the differential distribution of environmental factors that may affect sleep health may contribute to sleep health disparities.

Accurate diagnosis is crucial to improve the treatment and prognosis of respiratory disease, especially lung cancer. Tumors and lesions located deep in the lung are directly accessible via dendritic tracheal bronchus, thereby opening a new way to tackle respiratory disease. Intratracheal delivery is an innovative, noninvasive approach for imaging and treating respiratory disease efficiently, when compared with other delivery methods. Intratracheal delivery of nano- and microparticles and hyperpolarized gases offers valuable clinical advantages, such as assessing lung function, monitoring ventilation and perfusion, controlling disease progression, and inhibiting tumor growth. Especially, versatile nanosized particles have enormous potential to benefit precision imaging and therapy at the molecular level. Here we discuss advances of intratracheal delivery of nano- and microparticles and hyperpolarized gases for respiratory disease imaging and treatment, with an emphasis on intratracheal nanoparticles delivery for pulmonary imaging, which has extremely valuable clinical applications in precise theranostics for respiratory disease.