Physician reporting of the service to insurance companies for reimbursement is multifaceted and perplexing to those who do not understand the factors to consider. Test selection should be individualized based on the patient's history and/or needs. Federal regulations concerning physician supervision of diagnostic tests mandate different levels of physician supervision based on the type and complexity of the test. Many factors play a key role in physician claim submission. These include testing location, component services, coding edits, and additional visits. Medical necessity of the service(s) must also be demonstrated for payer consideration and reimbursement. The following article reviews various tests for exercise-induced bronchospasm and focuses on issues to assist the physician in reporting the services accurately and appropriately.

The diagnosis of adrenal failure and the indications for corticosteroid therapy in critically ill patients are controversial. This controversy is fueled by the complexity of the issues and the paucity of data from high quality clinical trials. Nevertheless, while the use of high-dose corticosteroids in patients with severe sepsis and ARDS failed to improve outcome and was associated with increased complications, an extended course of stress-dose corticosteroids has been reported to increase the occurrence of ventilator-free days and survival in select groups of ICU patients. These patients typically have an exaggerated proinflammatory response. Until recently the exaggerated proinflammatory response that characterizes critically ill patients with systemic inflammation has focused on suppression of the hypothalamic-pituitary-adrenal axis and adrenal failure. However, experimental and clinical data suggest that glucocorticoid tissue resistance may also play an important role. This complex syndrome is referred to as critical illness-related corticosteroid insufficiency (CIRCI) and is defined as inadequate corticosteroid activity for the severity of the illness of a patient. The paper reviews cortisol physiology, CIRCI, and the role of corticosteroid therapy in critically ill patients.

There is increasing evidence for a close relationship between aging and chronic inflammatory diseases. COPD is a chronic inflammatory disease of the lungs, which progresses very slowly and the majority of patients are therefore elderly. We here review the evidence that accelerating aging of lung in response to oxidative stress is involved in the pathogenesis and progression of COPD, particularly emphysema. Aging is defined as the progressive decline of homeostasis that occurs after the reproductive phase of life is complete, leading to an increasing risk of disease or death. This results from a failure of organs to repair DNA damage by oxidative stress (nonprogrammed aging) and from telomere shortening as a result of repeated cell division (programmed aging). During aging, pulmonary function progressively deteriorates and pulmonary inflammation increases, accompanied by structural changes, which are described as senile emphysema. Environmental gases, such as cigarette smoke or other pollutants, may accelerate the aging of lung or worsen aging-related events in lung by defective resolution of inflammation, for example, by reducing antiaging molecules, such as histone deacetylases and sirtuins, and this consequently induces accelerated progression of COPD. Recent studies of the signal transduction mechanisms, such as protein acetylation pathways involved in aging, have identified novel antiaging molecules that may provide a new therapeutic approach to COPD.

Polysomnography has developed from our understanding of sleep and its associated physiologic processes. This important tool extends the clinical examination into dynamic states that typically do not permit intrusive inspection. The two critical components of polysomnography are the determination of sleep-wake stage and identification of related bodily processes. In this article, the authors review the current standards for clinical polysomnography and discuss technical considerations that influence the accuracy of recorded data.

In contrast to spirometry, airflow resistance determinations provide an effort independent measure of the airway status and allow measurement in individuals unable or unwilling to provide adequate effort during spirometry. Resistance measurements may be performed using an esophageal balloon, airflow perturbation techniques (including interrupter and oscillatory techniques), or total-body plethysmography. Esophageal balloons are invasive, and airflow perturbation techniques are becoming more widely used. Airflow perturbation methods assess small airway dysfunction using frequency dependence of resistance, a surrogate for frequency dependence of compliance. Body plethysmography remains the "gold standard" for measuring airway resistance and is based on measures of pressure changes and flows with the patient enclosed in a body plethysmograph. While plethysmographic procedures may be completed rapidly, yielding multiple trials within preset repeatability criteria, the equipment is costly and the operator must be highly trained. Plethysmographic specific resistance loops have definite shapes (morphologies) indicative of specific airway disorders, which may be interpreted in a manner analogous to spirometry. Specific resistance and conductance assess the important effects of lung volumes. Reimbursement for resistance measurements varies depending on regional guidelines.

In November 2007, the Josiah Macy, Jr. Foundation convened a conference to address a number of complex issues concerning continuing education (CE) in the health professions. Participants concluded that CE, as currently practiced, does not focus adequately on improving clinician performance and patient care, is too dependent on lectures and too removed from the daily practice of clinicians, does not encourage or emphasize newer technologies and point-of-care learning, is poorly integrated across disciplines, and is inappropriately financed. Recommendations concerning educational methods, metrics, responsibilities, research in CE, financing, and oversight are reviewed. The relationship between the goals of improving clinician performance and patient care, while maintaining high standards of accountability and transparency, are reviewed.

Tremendous advances have occurred in the care of patients with HIV/AIDS resulting from the advent of highly active antiretroviral therapy (HAART). This has led to differences in the presentations of HIV-related pulmonary disease. Infections such as bacterial pneumonias, particularly Streptococcus pneumoniae, remain commonplace, while opportunistic agents such as Pneumocystis jirovecii remain a concern in patients without adequate access to optimal medical care. The tuberculosis epidemic, once thought to be slowing, has been re-energized by the spread of HIV, particularly in sub-Saharan Africa. Unusual inflammatory responses due to a phenomenon of immune reconstitution, are now recognized as a consequence of HAART, with a reported incidence of IRIS in this setting ranges from 7 to 45% in retrospective reviews. Noninfectious pulmonary conditions such as chronic obstructive lung disease and pulmonary malignancies are gaining prominence as patients are accessing antiretroviral care and enjoying significantly extended survival.

The mainstay of current drug therapy is long-acting bronchodilators; several longer acting inhaled beta(2)-agonists and muscarinic antagonists (and combinations) are now in development. No treatments have so far been shown to reduce the progression or suppress the inflammation of COPD. With better understanding of the inflammatory and destructive processes in the pathophysiology of COPD, several new targets have been identified. Several mediator antagonists tested in COPD patients have so far been disappointing, but CXC receptor 2 antagonists that block pulmonary neutrophil and monocyte recruitment may be more promising. Broad-spectrum antiinflammatory drugs, including inhibitors of the enzymes phosphodiesterase 4, p38 mitogen-activated protein kinase, nuclear factor-kappaB, and phosphoinositide-3-kinase-gamma, may be more effective, but the side effects will be a major limitation so that inhaled delivery may be necessary. Perhaps the most promising approach is the reversal of corticosteroid resistance through increasing histone deacetylase-2 activity. This might be achieved by theophylline-like drugs, more effective antioxidants, and nonantibiotic macrolide agents.

Pulmonary arterial hypertension (PAH) is characterized by abnormal remodeling of small, peripheral resistance vessels in the lung involving proliferation and migration of vascular smooth muscle, endothelial cell and fibroblasts. The increase in pulmonary vascular resistance leads to right heart failure, and, without treatment, death occurs within 3 years of diagnosis. The etiology of PAH is multifactorial. In some patients, there is a major genetic predisposition in the form of heterozygous germline mutations in a transforming growth factor-beta superfamily receptor, the bone morphogenetic type II receptor (BMPR-II). In addition, it is likely that additional factors, such as inflammation, are important to manifest disease. The currently available treatments for PAH were developed mainly as vasodilators, and although they improve symptoms they have limited impact on survival. This review examines the role of the BMPR-II signaling pathway in the process of pulmonary vascular remodeling. We discuss the ways in which manipulation of BMPR-II signaling might be targeted with the aim of preventing or reversing vascular remodeling and improving survival in patients with PAH.

Few admissions to the ICU present a greater clinical challenge than the patient with acute liver failure (ALF), the syndrome of abrupt loss of liver function in a previously unaffected individual. Although advances in the intensive care management of patients with ALF have improved survival, the prognosis of ALF remains poor, with a 33% mortality rate and a 25% liver transplant rate in the United States. ALF adversely affects nearly every organ system, with most deaths occurring from sepsis and subsequent multiorgan system failure, and cerebral edema, resulting in intracranial hypertension (ICH) and brainstem herniation. Unfortunately, the optimal management of ALF remains poorly defined, and practices are often based on local experience and case reports rather than on randomized, controlled clinical trials. The paramount question in any patient presenting with ALF remains defining an etiology, since specific antidotes can save lives and spare the liver. This article will consider recent advances in the assignment of an etiology, the administration of etiology-specific treatment to abate the liver injury, and the management of complications (eg, infection, cerebral edema, and the bleeding diathesis) in patients with ALF. New data on the administration of N-acetylcysteine to patients with non-acetaminophen ALF, the treatment of ICH, and assessment of the need for liver transplantation will also be presented.

Medical malpractice with its associated costs, including insurance premiums, impact on practice, consequences for career and insurability, and emotional toll, is a reality of practicing medicine in the United States. Understanding the types of claims that may be asserted, the issues to consider when securing insurance coverage, how to manage the cost of insurance, the nuances of the claims process, and the implications of the claims process are critical to the successful management of this aspect of medical practice. This article provides a guide for practicing physicians on the legal, financial, and practical considerations involved.

The US malpractice system is based on tort law, which holds physicians responsible for not harming patients intentionally or through negligence. Malpractice claims are brought against physicians from most medical disciplines in proportion to their numbers in practice and to the frequency with which they perform procedures. Claims against chest physicians most commonly allege injuries caused by the following: (1) errors in diagnosis, (2) improper performance of procedures, (3) failure to supervise or monitor care, (4) medication errors, and (5) failure to recognize the complications of treatment. Most of these injuries occur in hospitals, and many of the injured patients die. The social goals of the medical malpractice system include the following: (1) compensating patients injured through negligence, (2) exacting corrective justice, and (3) deterring unsafe practices by creating an economic incentive to take greater precautions. Some patients injured through negligence are compensated, but most are not. Claims are brought against some negligent physicians but also some who are not negligent, and being negligent does not guarantee that a claim will be brought. The deterrent effect of medical malpractice is unproven, and the malpractice system may prompt defensive medicine and increase health-care costs. And by stressing individual accountability, it conflicts with a systems-oriented approach to reducing medical errors.

Asthma, allergic rhinitis, nasal polyposis, chronic rhinosinusitis, and related forms of upper and lower airway diseases are often characterized by eosinophilic and basophilic inflammation, involving systemic processes. Eosinophil/basophil (Eo/B) lineage-committed progenitor cells in cord blood, peripheral blood, bone marrow, lung tissue, and sputum are up-regulated in the above conditions, and respond to allergen and other stimuli with increased differentiative and migratory capacity. A considerable body of evidence now exists showing that activation of such Eo/B-selective hemopoietic processes is not only associated with the onset and maintenance of allergic inflammation in atopic adults, but also with the development of the allergic diathesis. Moreover, eosinophilopoietic processes within hemopoietic compartments and, importantly, at mucosal tissue sites during an allergic inflammatory response provide novel targets for the treatment of allergy as a systemic process and disease.

Approximately 60 million people in the United States live with one of four chronic conditions: heart disease, diabetes, chronic respiratory disease, and major depression. Anxiety and depression are very common comorbidities in COPD and have significant impact on patients, their families, society, and the course of the disease.

Excessive daytime sleepiness and fatigue are common complaints in the sleep clinic. The objective evaluation and quantification of these symptoms is important for both the diagnosis of underlying health problems and for gauging treatment response. The multiple sleep latency test measures physiologic sleepiness, whereas the maintenance of wakefulness test (MWT) aims to measure manifest sleepiness. Neither test correlates well with subjective measures of sleep such as the Epworth sleepiness scale and the Stanford sleepiness scale. Although in the past methodological testing differences existed, in 2005 updated practice parameters were published, promoting the standardization of testing procedures. In recent years, there has been an effort to document daytime sleepiness when associated with occupational risk. However, these laboratory-based tests may not reflect or predict real-life experience. Normative data for both tests, particularly the MWT, are limited, and are inadequate for the evaluation of pediatric patients, shift workers, and others.

Because most critically ill patients lack decision-making capacity, physicians often ask family members to act as surrogates for the patient in discussions about the goals of care. Therefore, clinician-family communication is a central component of medical decision making in the ICU, and the quality of this communication has direct bearing on decisions made regarding care for critically ill patients. In addition, studies suggest that clinician-family communication can also have profound effects on the experiences and long-term mental health of family members. The purpose of this narrative review is to provide a context and rationale for improving the quality of communication with family members and to provide practical, evidence-based guidance on how to conduct this communication in the ICU setting. We emphasize the importance of discussing prognosis effectively, the key role of the integrated interdisciplinary team in this communication, and the importance of assessing spiritual needs and addressing barriers that can be raised by cross-cultural communication. We also discuss the potential value of protocols to encourage communication and the potential role of quality improvement for enhancing communication with family members. Last, we review issues regarding physician reimbursement for communication with family members within the context of the US health-care system. Communication with family members in the ICU setting is complex, and high-quality communication requires training and collaboration of a well-functioning interdisciplinary team. This communication also requires a balance between adhering to processes of care that are associated with improved outcomes and individualizing communication to the unique needs of the family.

The use of IV augmentation therapy with plasma-derived alpha1-antitrypsin (AAT) has become the standard of care for the treatment of pulmonary disease associated with the severe genetic deficiency of AAT. The Medical and Scientific Advisory Committee of the Alpha-1 Foundation has become aware that physicians are prescribing this expensive blood product for the treatment of individuals with a single abnormal AAT gene, primarily the PI*MZ genotype. We are aware of no evidence that such therapy is effective in this patient population. The most important therapeutic interventions in such patients remain smoking cessation and elimination of other risk factors for lung disease. This commentary discusses the treatment of AAT deficiency and the concerns regarding treatment of PI*MZ individuals. We conclude that clinicians should avoid prescribing augmentation therapy for this heterozygote population.

Bronchiectasis, which was once thought to be an orphan disease, is now being recognized with increasing frequency around the world. Patients with bronchiectasis have chronic cough and sputum production, and bacterial infections develop in them that result in the loss of lung function. Bronchiectasis occurs in patients across the spectrum of age and gender, but the highest prevalence is in older women. The diagnosis of bronchiectasis is made by high-resolution CT scans. Bronchiectasis, which can be focal or diffuse, may occur without antecedent disease but is often a complication of previous lung infection or injury or is due to underlying systemic illnesses. Patients with bronchiectasis may have predisposing congenital disease, immune disorders, or inflammatory disease. The treatment of bronchiectasis is multimodality, and includes therapy with antibiotics, antiinflammatory agents, and airway clearance. Resectional surgery and lung transplantation are rarely required. The prognosis for patients with bronchiectasis is variable given the heterogeneous nature of the disease. A tailored, patient-focused approach is needed to optimally evaluate and treat individuals with bronchiectasis.