There are no recommendations on how to measure arm exercise capacity in individuals with COPD. The objectives of this study were (1) to synthesize the literature on measures of arm exercise capacity in individuals with COPD, (2) to describe the psychometric properties and the target construct of each measure, and (3) to make recommendations for clinical practice and research.

To record sleep, actigraph devices are worn on the wrist and record movements that can be used to estimate sleep parameters with specialized algorithms in computer software programs. With the recent establishment of a Current Procedural Terminology code for wrist actigraphy, this technology is being used increasingly in clinical settings as actigraphy has the advantage of providing objective information on sleep habits in the patient's natural sleep environment. Actigraphy has been well validated for the estimation of nighttime sleep parameters across age groups, but the validity of the estimation of sleep-onset latency and daytime sleeping is limited. Clinical guidelines and research suggest that wrist actigraphy is particularly useful in the documentation of sleep patterns prior to a multiple sleep latency test, in the evaluation of circadian rhythm sleep disorders, to evaluate treatment outcomes, and as an adjunct to home monitoring of sleep-disordered breathing. Actigraphy has also been well studied in the evaluation of sleep in the context of depression and dementia. Although actigraphy should not be viewed as a substitute for clinical interviews, sleep diaries, or overnight polysomnography when indicated, it can provide useful information about sleep in the natural sleep environment and/or when extended monitoring is clinically indicated.

The complete type of anomalous systemic arterial supply to normal basal lung segments is characterized by anomalous systemic artery supply to all or some of the normal basal segments with an absent corresponding pulmonary artery. Surgical intervention generally is required. This study reports on four patients with this anomaly with hemoptysis or a combination of other symptoms who underwent successful transarterial embolization using metallic coils or an Amplatzer vascular plug. To our knowledge, only six such cases treated with transarterial embolization have been reported previously in adult patients.

Comprehensive pulmonary rehabilitation and respiratory therapy services benefit patients with chronic lung disease and other diseases of the lung by reducing symptoms and restoring independent function. Although the science of these therapies is not new, commercial payers and Medicare have generally been slow to support adequate coverage and reimbursement. These therapies are described as a multidisciplinary approach to individual patient care through a physician-supervised program that usually includes physician-prescribed exercise, education and/or training, psychosocial assessment, and an outcomes assessment comprehensively documented using an individualized treatment plan. This article includes a review of the requirements based on the July 2008 Congressional enactment of a new national policy for comprehensive pulmonary rehabilitation program coverage. Passage of Section 144 of the Medicare Improvements for Patients and Providers Act authorizes comprehensive pulmonary rehabilitation programs to be a covered Medicare benefit. Variability of coverage by various payers will be examined. Also discussed are various coding schema for the provision and reporting of comprehensive pulmonary rehabilitation and respiratory therapy services. The variability of requirements to establish medical necessity among several major payers of respiratory therapy services and comprehensive pulmonary rehabilitation programs will be explored. Despite these therapies being recognized universally as the standard of care for certain diseases and a new national mandate establishing coverage regulations, the continuation, expansion, and patient access for such therapies may be limited. Pitfalls and pluses are discussed.

Recent advances in basic science have greatly expanded our understanding of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR), the chloride and bicarbonate channel that is encoded by the gene, which is mutated in patients with CF. We review the structure, function, biosynthetic processing, and intracellular trafficking of CFTR and discuss the five classes of mutations and their impact on the CF phenotype. The therapeutic discussion is focused on the significant progress toward CFTR mutation-specific therapies. We review the results of encouraging clinical trials examining orally administered therapeutics, including agents that promote read-through of class I mutations (premature termination codons); correctors, which overcome the CFTR misfolding that characterizes the common class II mutation F508del; and potentiators, which enhance the function of class III or IV mutated CFTR at the plasma membrane. Long-term outcomes from successful mutation-specific treatments could finally answer the question that has been lingering since and even before the CFTR gene discovery: Will therapies that specifically restore CFTR-mediated chloride secretion slow or arrest the deleterious cascade of events leading to chronic infection, bronchiectasis, and end-stage lung disease?

The mitogen-activated protein kinase (MAPK) family includes the p38 kinases, which consist of highly conserved proline-directed serine-threonine protein kinases that are activated in response to inflammatory signals. Of the four isoforms, p38α is the most abundant in inflammatory cells and has been the most studied through mainly the availability of small molecule inhibitors. The p38 substrates include transcription factors; other protein kinases, which in turn phosphorylate transcription factors; cytoskeletal proteins and translational components; and other enzymes. Both asthma and COPD are characterized by chronic airflow obstruction, airway and lung remodeling, and chronic inflammation. p38 is involved in the inflammatory responses induced by cigarette smoke exposure, endotoxin, and oxidative stress through activation and release of proinflammatory cytokines/chemokines, posttranslational regulation of these genes, and activation of inflammatory cell migration. Inhibition of p38 MAPK prevented allergen-induced pulmonary eosinophilia, mucus hypersecretion, and airway hyperresponsiveness, effects that may partly result from p38 activation on eosinophil apoptosis and on airway smooth muscle cell production of cytokines/chemokines. In addition, p38 regulates the augmented contractile response induced by oxidative stress. The activation of p38 observed in epithelial cells and macrophages also may underlie corticosteroid insensitivity of severe asthma and COPD. Therefore, p38 inhibitors present a potential attractive treatment of these conditions. Second-generation p38 inhibitors have been disappointing in the treatment of rheumatoid arthritis. In two 6-week studies in patients with COPD, the results were encouraging. Side effects such as liver toxicity remain a possibility, and whether the beneficial effects of p38 inhibitors are clinically significant and sustained need to be determined.

This study compares, by meta-analysis, the use of anterior-posterior chest radiography (CR) with transthoracic ultrasonography for the diagnosis of pneumothorax.

There is now a new pathway and examination for sleep medicine, sponsored by the American Board of Internal Medicine, and a number of accredited sleep medicine fellowship programs through the Accreditation Council for Graduate Medical Education. This review takes an historical approach to discuss the process of education for sleep physiology and disorders not only in the postgraduate period but also at all levels of instruction. In reality, there is a continuum of knowledge that needs to be reinforced up and down the educational system, of which Sleep Medicine subspecialty training is just one part. Although progress has been made at all educational levels up to this point, the future of training and education will depend on a sustained effort at several levels from undergraduate to postgraduate continuing medical education and will be facilitated by professional societies and other specialties who will collectively promote the value of and outcomes for clinical sleep medicine.

Although early and appropriate antibiotic therapy remains the cornerstone of success for the treatment of septic shock, few data exist to guide antibiotic dose optimization in critically ill patients, particularly those with multiple organ dysfunction syndrome (MODS). It is well known that MODS significantly alters the patient's physiology, but the effects of these variations on pharmacokinetics have not been reviewed concisely. Therefore, the aims of this article are to summarize the disease-driven variations in pharmacokinetics and pharmacodynamics and to provide antibiotic dosing recommendations for critically ill patients with MODS. The main findings of this review are that the two parameters that vary with greatest significance in critically ill patients with MODS are drug volume of distribution and clearance. Disease- and clinician-driven changes lead to an increased volume of distribution and lower-than-expected plasma drug concentrations during the first day of therapy at least. Decreased antibiotic clearance is common and can lead to drug toxicity. In summary, "front-loaded" doses of antibiotic during the first 24 h of therapy should account for the likely increases in the antibiotic volume of distribution. Thereafter, maintenance dosing must be guided by drug clearance and adjusted to the degree of organ dysfunction.

Despite the increased use of CT imaging, chest radiography remains a very important diagnostic modality in the evaluation of lung parenchymal and mediastinal diseases, providing a vast amount of useful information. This information is generally derived from the relationships among the normal anatomic structures of the mediastinum, pleura, and lungs, which represent the basis of the "cardiac silhouette" and "mediastinal lines-and-stripes" concepts that potentially play an important role in the establishment of a diagnosis or a spectrum of diagnoses before proceeding to CT imaging. The capability of recognizing an abnormal chest radiograph on the basis of the displacement, deformation, or obscuration of one of these structures when compared with those in normal findings is often mandatory prior to requesting a potentially useful CT scan examination. Therefore, radiologists, trainees, and physicians must be familiar with the anatomic basis of those findings to be able to recognize the normal and abnormal appearance of structures when developing an appropriate differential diagnosis. In this review, we briefly describe the cardiac silhouette concepts and the mediastinal lines-and-stripes configurations as they relate to the radiographic and CT scan appearance of structures for a spectrum of pathologic diseases and list the possible underlying causes of the displacement, deformation, or obscuration of the structures.

Pseudomonas aeruginosa carries a notably higher mortality rate than other pneumonia pathogens. Because of its multiple mechanisms of antibiotic resistance, therapy has always been challenging. This problem has been magnified in recent years with the emergence of multidrug-resistant (MDR) pathogens often unharmed by almost all classes of antimicrobials. The objective of this article is to assess optimal antimicrobial therapy based on in vitro activity, animal studies, and pharmacokinetic/pharmacodynamic (PK/PD) observations so that evidence-based recommendations can be developed to maximize favorable clinical outcomes. Mechanisms of antimicrobial resistance of P aeruginosa are reviewed. A selective literature review of laboratory studies, PK/PD concepts, and controlled clinical trials of antibiotic therapy directed at P aeruginosa pneumonia was performed. P aeruginosa possesses multiple mechanisms for inducing antibiotic resistance to antimicrobial agents. Continuous infusion of antipseudomonal β-lactam antibiotics enhances bacterial killing. Although the advantages of combination therapy remain contentious, in vitro and animal model studies plus selected meta-analyses of clinical trials support its use, especially in the era of MDR. Colistin use and the role of antibiotic aerosolization are reviewed. An evidence-based algorithmic approach based on severity of illness, Clinical Pulmonary Infection Score, and combination antibiotic therapy is presented; clinical outcomes may be improved, and the emergence of MDR pathogens should be minimized with this approach.

Atopic asthma is the most common form of asthma, particularly during childhood, and in many cases it persists into adult life. Although atopy is clearly a risk factor for development of this disease, only a small subset of subjects sensitized to aeroallergens express persistent symptoms, suggesting that additional pathogenic mechanisms are involved. Recent studies have implicated respiratory viral infections as key cofactors in asthma development in atopic patients. In relation to initial expression of the asthma phenotype in early childhood, it has been shown that although both atopic sensitization and early severe lower respiratory tract infections can operate as independent asthma risk factors, the persistence of asthma is most frequent among children who experience both insults, suggesting that the relevant inflammatory pathways interact to maximally drive disease pathogenesis. Importantly, it has been established that both these factors must be operative contemporaneously for these interactions to occur (ie, the interactions are likely to be direct). Recent studies on viral-induced asthma exacerbations in atopic children have provided a plausible mechanism for these interactions. Notably, it has been demonstrated that signals triggered during the innate immune response to the virus can lead to the release of large numbers of migrating high-affinity IgE receptor-bearing bone marrow-derived precursors of mucosal dendritic cells into the blood. The subsequent trafficking of these cells to the infected airway mucosa where dendritic cell turnover is very high provides a potential mechanism for recruitment of underlying aeroallergen-specific T-helper 2 immunity into the already inflamed milieu in the infected airway mucosa.

Chronic smoking, theoretically, can interfere with warfarin metabolism through enzyme-inducing effects of polycyclic aromatic hydrocarbons. However, clinical evidence of interactions between warfarin and smoking are inconclusive. This study aimed to systematically review all relevant clinical evidence of this interaction.

Atelectasis is considered to be the most common cause of early postoperative fever (EPF) but the existing evidence is contradictory. We sought to determine if atelectasis is associated with EPF by analyzing the relevant published evidence.

A consultation service provides expert opinion or advice at the request of another provider. The Centers for Medicare and Medicaid Services (CMS) eliminated reimbursement for the outpatient and inpatient consultation codes traditionally used to report these services (CPT 99241-99245 and 99251-99255, respectively), and private payers are likely to follow suit. CMS has instead mandated that these services are mapped to new or established visit codes for outpatients (99201-99205 or 99212-99215) and to initial or subsequent hospital services codes for inpatients (99221-99223 or 99231-99233). This article reviews appropriate medical consultation and provides specific guidance for the reporting of these services to CMS and other payers not reimbursing consultation codes.

Although, to our knowledge, there has been no exhaustive or credible review of the evidence of the disease burden of COPD in China, COPD has become an increasing public health concern to the Chinese medical community. The purpose of this article is to review the evidence and evaluate and clarify the disease burden of COPD in China with the aim of improving effective management. We reviewed previous studies of COPD in China, which included data on prevalence, mortality, disease burden, risk factors, diagnosis, and management by searching related Web sites, including PubMed, ProQuest, and Thomson Reuters' Web of Knowledge, as well as major Chinese databases and government Web sites. Reported COPD prevalence varied between 5% and 13% in different provinces/cities across China. In 2008, COPD ranked fourth as a leading cause of death in urban areas and third in rural areas. In addition, COPD accounted for 1.6% of all hospital admissions in China in that year. The high prevalence of smoking and biomass fuel use acted as major contributors to the high occurrence of COPD in China. Management of COPD in China should focus on adjusting the distribution of medical resources and on addressing public health policies to facilitate earlier diagnosis in rural areas, aim to reduce smoking prevalence, improve patients' self-management, and keep physicians' knowledge up to date and consistent with current guidelines. COPD is one of the most challenging medical issues facing China because of its influence on both personal and public health and its impact on the economy. Optimal management strategies should be adopted and strengthened immediately.

Pseudomonas aeruginosa is an uncommon cause of community-acquired pneumonia (CAP), but a common cause of hospital-acquired pneumonia. Controversies exist for diagnostic methods and antibiotic therapy. We review the epidemiology of CAP, including that in patients with HIV and also in hospital-acquired pneumonia, including ventilator-associated pneumonia (VAP) and bronchoscope-associated pneumonia. We performed a literature review of clinical studies involving P aeruginosa pneumonia with an emphasis on treatment and prevention. Pneumonia due to P aeruginosa occurs in several distinct syndromes: (1) CAP, usually in patients with chronic lung disease; (2) hospital-acquired pneumonia, usually occurring in the ICU; and (3) bacteremic P aeruginosa pneumonia, usually in the neutropenic host. Radiologic manifestations are nonspecific. Colonization with P aeruginosa in COPD and in hospitalized patients is a well established phenomenon such that treatment based on respiratory tract cultures may lead to overtreatment. We present circumstantial evidence that the incidence of P aeruginosa has been overestimated for hospital-acquired pneumonia and reflex administration of empirical antipseudomonal antibiotic therapy may be unnecessary. A diagnostic approach with BAL and protected specimen brush using quantitative cultures for patients with VAP led to a decrease in broad-spectrum antibiotic use and improved outcome. Endotracheal aspirate cultures with quantitative counts are commonly used, but validation is lacking. An empirical approach using the Clinical Pulmonary Infection Score is a pragmatic approach that minimizes antibiotic resistance and leads to decreased mortality in patients in the ICU. The source of the P aeruginosa may be endogenous (from respiratory or GI tract colonization) or exogenous from tap water in hospital-acquired pneumonia. The latter source is amenable to preventive measures.

Increasing awareness of the role of intestinal commensal bacteria in the development and modulation of the immune system has led to great interest in the therapeutic potential of probiotics and other bacteria-based strategies for a range of immune-related disorders. Studies in animal models have identified strong immunomodulatory effects of many nonpathogenic bacteria and provided evidence that intestinal microbes can activate a common mucosal immune response and, thus, influence sites distant to the intestine, including the respiratory tract. Respiratory effects of probiotics in animal models have included attenuating allergic airway responses and protecting against respiratory pathogens. Dendritic cells appear central to directing the beneficial immune response to probiotic bacteria and in translating microbial signals from the innate to the adaptive immune system, whereas regulatory T cells are emerging as potentially key effectors of probiotic-mediated responses, particularly in the reduction of allergic inflammation. Despite progress in basic research, clinical trials of probiotics in allergy/asthma and respiratory infection have been highly variable at best, leading to an undermining of confidence in this potential therapeutic strategy. It is clear that there is still much to learn regarding the determinants of the diverse immune responses elicited by different bacterial strains. A deeper knowledge of the interactions between administered probiotics and the existing microbiota, together with an understanding of how the dialogue between microbes and the innate immune system is translated into beneficial/protective responses, will be required before we can achieve clinically effective bacteria-based strategies that maintain and promote respiratory health.

Apologizing to patients and their families for medical mistakes is an increasingly accepted practice. Overlooked is the need to apologize to other members of the treatment team or patients for humiliations inflicted in medical practice, independent of medical mistakes. A humiliated treatment team member or patient is apt to undermine optimal care, particularly when teamwork or patient adherence to treatment is required. This article describes the psychology of humiliation and the history of humiliation in medical practice, including why doctors and patients are vulnerable to being humiliated. Several humiliation narratives are presented. This article presents empirical data based on a sample of 355 subjects that analyze what the offended party seeks in an apology and the magnitude of the importance of each of these desires. The restoration of dignity in response to humiliation emerges as one of the most important functions of apologies. Finally, this article identifies 15 healing forces of apology, a combination of which is necessary for healing any given offense. The final challenge is educating individuals as to how to apply these findings to healing after a humiliating offense.

The measurement of hydrogen peroxide (H(2)O(2)) in exhaled breath condensate (EBC) has been proposed as a noninvasive way of monitoring airway inflammation. However, results from individual studies on EBC H(2)O(2) evaluation of asthma are conflicting. The purpose of this study was to explore whether EBC H(2)O(2) is elevated in people with asthma and whether it reflects disease severity and disease control or responds to corticosteroid treatment.