A 3-month-old infant was brought to clinic for evaluation of recurrent apparent life-threatening events (ALTEs). Two ALTE episodes occurred while the infant was sleeping in a safety car seat. The first one occurred when he was 4 weeks old. His mother noticed that he was not breathing; he appeared limp with full body cyanosis. His mother picked him up from the car seat, and he started breathing spontaneously and without any sign of distress. His skin color returned to normal. He was evaluated at the ED where the physical examination was normal. He was hospitalized 1 day for observation. During this time, workup, including ECG and chest radiograph, was normal. The parents were instructed on cardiorespiratory resuscitation and recommended to change car seats. The infant was discharged with an apnea monitor. He wore the apnea monitor while in the car seat. A second similar episode occurred at 10 weeks of age for which he was seen at the ED and referred to our clinic for further evaluation. Neither episode was related to feeding.

A 15-year-old boy presented for evaluation of snoring and sleep-disordered breathing. The parents noted that the patient snored every night and that he had episodes when he stopped breathing, ending with gasping for air. He had no history of sleep walking, night terrors, tongue biting, or seizures. The patient had two healthy siblings, but he had a history of intellectual disability and developmental delay. The patient had a history of adenotonsillectomy.

A 66-year-old woman presented with acute onset of fever, chills, and productive cough associated with right-sided chest pain. During a recent hospitalization for dyspnea, she had been diagnosed with Coombs-positive autoimmune hemolytic anemia and had been taking a tapering dose of prednisone starting approximately 6 weeks prior to admission. In the interim, her dyspnea had resolved on treatment with steroids. At the time of presentation, her prednisone dose was 40 mg. Additional medical history included VTE, for which the patient was receiving anticoagulation therapy, and steroid-induced diabetes mellitus. Many years earlier, she had been treated for TB in her home country. The patient had immigrated to Queens, New York, from a Nepalese village 8 years prior. While still in Nepal, she had worked on a farm and had been in close proximity to cows. In Queens, she lived with her family in a house with a small garden but had no pets. Recent travel included a visit to Nepal 9 months ago and a trip to Syracuse, New York, one month prior to presentation. She was a never smoker and did not consume alcohol.

Diffuse alveolar hemorrhage (DAH) is a syndrome caused by different mechanisms, including capillary stress failure, diffuse alveolar damage, and capillaritis. Capillaritis is the most common cause and is often associated with systemic autoimmune disorders, most commonly antineutrophilic cytoplasmic antibody-associated vasculitis. The occurrence of DAH with underlying pulmonary capillaritis but without clinical or serologic findings of an associated underlying systemic disorder is known as isolated pauciimmune pulmonary capillaritis (IPPC), and only eight cases have been described in the literature. The mainstay of treatment of this rare condition has been cyclophosphamide and glucocorticoids. When cases are unresponsive to cyclophosphamide, there is no known alternative treatment. Herein, we describe a case of IPPC that failed cyclophosphamide treatment with recurrent DAH. Rituximab therapy was then initiated with no further evidence of recurrence. This case report suggests that rituximab could be considered an alternative therapy to induce remission in patients with IPPC.

Dronedarone is an amiodarone-like antiarrhythmic with a modified structure. The addition of a methyl sulfonyl group theoretically reduces the toxicity of amiodarone, specifically, adverse thyroid and pulmonary effects. Although animal studies have implicated dronedarone as a cause of lung injury, to date controlled trials in humans have not demonstrated an association. A 68-year-old woman developed a dry cough and worsening respiratory distress after receiving dronedarone for 6 months. Discontinuation of dronedarone therapy and subsequent steroid therapy led to a dramatic improvement of symptoms. Dronedarone may be associated with interstitial lung disease. We believe that patients receiving dronedarone should have their diffusing capacity of lung for carbon monoxide and lung volumes monitored prior to initiation of therapy and frequently thereafter.

Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with difficulty falling asleep, frequent nighttime awakenings with difficulty returning to sleep, and/or awakening earlier in the morning than desired. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment. The aims of this report are (1) to summarize current knowledge on the pathophysiology of insomnia and (2) to present a model of the pathophysiology of insomnia that considers evidence from various domains of research. Working within several models of insomnia, evidence for the pathophysiology of the disorder is presented across levels of analysis, from genetic to molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and self-report. We discuss the role of hyperarousal as an overarching theme that guides our conceptualization of insomnia. Finally, we propose a model of the pathophysiology of insomnia that integrates the various types of evidence presented.

Improving value within critical care remains a priority because it represents a significant portion of health-care spending, faces high rates of adverse events, and inconsistently delivers evidence-based practices. ICU directors are increasingly required to understand all aspects of the value provided by their units to inform local improvement efforts and relate effectively to external parties. A clear understanding of the overall process of measuring quality and value as well as the strengths, limitations, and potential application of individual metrics is critical to supporting this charge. In this review, we provide a conceptual framework for understanding value metrics, describe an approach to developing a value measurement program, and summarize common metrics to characterize ICU value. We first summarize how ICU value can be represented as a function of outcomes and costs. We expand this equation and relate it to both the classic structure-process-outcome framework for quality assessment and the Institute of Medicine's six aims of health care. We then describe how ICU leaders can develop their own value measurement process by identifying target areas, selecting appropriate measures, acquiring the necessary data, analyzing the data, and disseminating the findings. Within this measurement process, we summarize common metrics that can be used to characterize ICU value. As health care, in general, and critical care, in particular, changes and data become more available, it is increasingly important for ICU leaders to understand how to effectively acquire, evaluate, and apply data to improve the value of care provided to patients.

Air pollution exposure is a well-established risk factor for several adverse respiratory outcomes, including airways diseases and lung cancer. Few studies have investigated the relationship between air pollution and interstitial lung disease (ILD) despite many forms of ILD arising from environmental exposures. There are potential mechanisms by which air pollution could cause, exacerbate, or accelerate the progression of certain forms of ILD via pulmonary and systemic inflammation as well as oxidative stress. This article will review the current epidemiologic and translational data supporting the plausibility of this relationship and propose a new conceptual framework for characterizing novel environmental risk factors for these forms of lung disease.

Electronic health records (EHRs) have the potential to improve health-care quality by allowing providers to make better decisions at the point of care based on electronically aggregated data and by facilitating clinical research. These goals are easier to achieve when key, disease-specific clinical information is documented as structured data elements (SDEs) that computers can understand and process, rather than as free-text/natural-language narrative. This article reviews the benefits of capturing disease-specific SDEs. It highlights several design and implementation considerations, including the impact on efficiency and expressivity of clinical documentation and the importance of adhering to data standards when available. Pulmonary disease-specific examples of collection instruments are provided from two commonly used commercial EHRs. Future developments that can leverage SDEs to improve clinical quality and research are discussed.

A 13-year-old patient named Jahi McMath was determined to be dead by neurologic criteria following cardiopulmonary arrest and resuscitation at a hospital in Oakland, California. Her family did not agree that she was dead and refused to allow her ventilator to be removed. The family's attorney stated in the media that families, rather than physicians, should decide whether patients are dead and argued in the courts that the families' constitutional rights of religion and privacy would be violated otherwise. Ultimately, a judge agreed that the patient was dead in keeping with California law, but the constitutional issue was undecided. The patient was then transferred to a hospital in New Jersey, a state whose laws allow families to require on religious grounds that death be determined by cardiopulmonary criteria. Although cases such as this are uncommon, they demonstrate public confusion about the concept of neurologic death and the rejection of this concept by some families. The confusion may be caused in part by a lack of uniformity in state laws regarding the legal basis of death, as reflected in the differences between New Jersey and California statutes. Families who reject the determination of death by neurologic criteria on religious grounds should be given reasonable accommodation in all states, but society should not pay for costly treatments for patients who meet these criteria unless the state requires it, as only New Jersey does. Laws that give physicians the right to determine death by neurologic criteria in other states probably can survive a constitutional challenge. Physicians and hospitals faced with similar cases in the future should follow state laws and work through the courts if necessary.

Physicians are more and more often challenged by difficult-to-treat cases of TB. They include patients infected by strains of Mycobacterium tuberculosis that are resistant to at least isoniazid and rifampicin (multidrug-resistant TB) or to at least one fluoroquinolone (FQ) and one injectable, second-line anti-TB drug in addition to isoniazid and rifampicin (extensively drug-resistant TB). The drug treatment of these cases is very long, toxic, and expensive, and, unfortunately, the proportion of unsatisfactory outcomes is still considerably high. Although FQs and pyrazinamide (PZA) are backbone drugs in the available anti-TB regimens, several uncertainties remain about their mechanisms of action and even more remain about the mechanisms leading to drug resistance. From a clinical point of view, a better understanding of the genetic basis of drug resistance will aid (1) clinicians to provide quality clinical management to both drug-susceptible and drug-resistant TB cases (while preventing emergence of further resistance), and (2) developers of new molecular-based diagnostic assays to better direct their research efforts toward a new generation of sensitive, specific, cheap, and easy-to-use point-of-care diagnostics. In this review we provide an update on the molecular mechanisms leading to FQ- and PZA-resistance in M tuberculosis.

Pulmonary hypertension (PH) is a common complication of numerous diseases, including left-sided heart diseases and chronic lung diseases and/or hypoxia, where PH is associated with exercise limitation and a worse prognosis. Other forms of PH include pulmonary arterial hypertension (PAH), chronic thromboembolic PH (CTEPH), and PH with unclear multifactorial mechanisms. Over the past decade, it has been documented that systolic pulmonary artery pressure (sPAP) may help estimate mean pulmonary artery pressure (mPAP) in adults with high accuracy and reasonably good precision (mPAP = 0.61 sPAP + 2 mm Hg). This strong linear relationship between sPAP and mPAP was unexpected from a classic physiologic point of view. Consistent results have been obtained from independent teams using either high-fidelity micromanometer-tipped PA catheters or fluid-filled catheters. Overall, the strong link between sPAP and mPAP has been documented over a wide range of PAPs, heart rate, cardiac output, wedge pressure, and causes of PH, during changes in posture and activity, and irrespective of patient's sex, age, and BMI. A review of available invasive data confirms that patients with CTEPH and idiopathic PAH matched for their mPAP exhibit essentially similar sPAP. Pressure redundancy may be explained by the dependence of PA compliance upon mPAP. The 25 mm Hg threshold used to define PH accurately corresponds to an sPAP of 38 mm Hg. Although the limits of the echocardiographic estimation of sPAP are widely documented, results from invasive studies may furnish an evidence-based sPAP-derived mPAP value, potentially useful in the multiparameter echocardiographic approach currently used to diagnose and follow patients with PH.