Faculty Bibliography

ABSTRACT/UNASSIGNED:The current global health crisis due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has prompted the medical community to investigate the effects of underlying medical conditions, including sleep-disordered breathing, on inpatient care. Obstructive sleep apnea (OSA) is a common form of sleep-disordered breathing that may complicate numerous acquired conditions, particularly in inpatient and critical care settings. Viral pneumonia is a major contributor to intensive care unit (ICU) admissions and often presents more severely in patients with underlying pulmonary disease, especially those with obesity and OSA. This review summarizes the most recent data regarding complications of both OSA and obesity and highlights their impact on clinical outcomes in hospitalized patients. Additionally, it will highlight pertinent evidence for the complications of OSA in an organ-systems approach. Finally, this review will also discuss impatient treatment approaches for OSA, particularly in relation to the SARS-CoV-2 pandemic.

Coronavirus disease (COVID-19), the clinical syndrome caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is currently a global health pandemic with substantial morbidity and mortality. COVID-19 has cast a shadow on nearly every aspect of society, straining health systems and economies across the world. Although it is widely accepted that a close relationship exists between obesity, cardiovascular disease, and metabolic disorders on infection, we are only beginning to understand ways in which the immunological sequelae of obesity functions as a predisposing factor related to poor clinical outcomes in COVID-19. As both the innate and adaptive immune systems are each primed by obesity, the alteration of key pathways results in both an immunosuppressed and hyperinflammatory state. The present review will discuss the cellular and molecular immunology of obesity in the context of its role as a risk factor for severe COVID-19, discuss the role of cytokine storm, and draw parallels to prior viral epidemics such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and 2009 H1N1.

INTRODUCTION:Lung cancer is the leading cause of cancer death in the USA, claiming more than 140,000 deaths annually. Delays in diagnosis and treatment can lead to missed opportunities for both curative and life prolonging therapies. This study aimed to evaluate duration of time to diagnosis and first treatment, as well as investigate reasons for delays in care. METHODS:This retrospective study included all lung cancer cases diagnosed by Stony Brook's Lung Cancer Evaluation Center (LCEC) between 2013 and 2019. Demographic, radiologic, pathologic and clinical variables were investigated, including cancer staging, histology, and medical and family histories. Evaluations included the determination of median time from initial encounter to diagnosis, median time from diagnosis to start of treatment and an exploration of the factors that influence possible causes for delays in care. RESULTS:The LCEC's comprehensive multidisciplinary lung nodule program yielded a median length of time from CT to PET of 11 days, PET to procedure of 13 days, procedure to treatment consult of 9 days, and from consult to treatment of 9 days. LCEC patients experienced an overall median of 44 days from initial presentation to first treatment compared to the national ideal of 62 days, thereby representing a 29% reduction in time from first CT to onset of treatment. CONCLUSION:Delays in lung cancer diagnosis and treatment can negatively impact patient morbidity and mortality. This study suggests that a coordinated multidisciplinary lung cancer program may reduce delays in care, thereby improving patient outcomes.

OBJECTIVES/OBJECTIVE:The National Lung Screening Trial (NLST) demonstrated a 20% reduction in mortality with low-dose computed tomography (CT) for lung cancer screening (LCS). The NLST found the greatest benefit to LCS for patients who underwent annual screening for a full 3-year follow-up period. The adherence to serial imaging in the NLST was 95%. METHODS:We conducted a prospective study of 268 patients who presented for LCS and who were not enrolled in a research study to determine the adherence to recommended follow-up imaging and biopsy at a single center. We evaluated the correlations among sociodemographic characteristics, Lung Imaging and Reporting Data System, and adherence. RESULTS:Only 48% of the patient population received recommended follow-up (either imaging or biopsy) after their referent LCS. Patients with abnormal LCS (Lung Imaging and Reporting Data System 3 or 4) were more likely to adhere to the recommended follow-up (additional imaging or biopsy) compared with those with negative screens. Sex, ethnicity, smoking status, and household income were not correlated with adherence to screening and biopsy. CONCLUSIONS:The benefits from LCS observed in the NLST may be undermined by low adherence to follow-up screening. Studies targeting LCS patients to bolster adherence to follow-up are needed.

This prospective investigation derived a prediction model for identifying risk of incident lung cancer among patients with visible lung nodules identified on computed tomography (CT). Among 2,924 eligible patients referred for evaluation of a pulmonary nodule to the Stony Brook Lung Cancer Evaluation Center between January 1, 2002 and December 31, 2015, 171 developed incident lung cancer during the observation period. Cox proportional hazard models were used to model time until disease onset. The sample was randomly divided into discovery (n = 1,469) and replication (n = 1,455) samples. In the replication sample, concordance was computed to indicate predictive accuracy and risk scores were calculated using the linear predictions. Youden index was used to identify high-risk versus low-risk patients and cumulative lung cancer incidence was examined for high-risk and low-risk groups. Multivariable analyses identified a combination of clinical and radiologic predictors for incident lung cancer including ln-age, ln-pack-years smoking, a history of cancer, chronic obstructive pulmonary disease, and several radiologic markers including spiculation, ground glass opacity, and nodule size. The final model reliably detected patients who developed lung cancer in the replication sample (C = 0.86, sensitivity/specificity = 0.73/0.81). Cumulative incidence of lung cancer was elevated in high-risk versus low-risk groups [HR = 14.34; 95% confidence interval (CI), 8.17-25.18]. Quantification of reliable risk scores has high clinical utility, enabling physicians to better stratify treatment protocols to manage patient care. The final model is among the first tools developed to predict incident lung cancer in patients presenting with a concerning pulmonary nodule.

An understanding of thoracic computed tomographic anatomy is vital for procedural planning in bronchoscopy. When reviewing computed tomographic images in preparation for endobronchial ultrasound-directed staging for lung cancer, the presence of fluid in pericardial recesses can often be mistaken for mediastinal lymphadenopathy, potentially causing pitfalls in radiologic interpretation. We describe 2 cases of a high-riding superior aortic recess extending into right paratracheal lymph node station mimicking paratracheal lymphadenopathy. We review the anatomy and imaging characteristics of pericardial recesses with emphasis on differentiating these findings from mediastinal lymphadenopathy.

Sepsis is not only a significant cause of mortality worldwide but has particularly devastating effects on the central nervous system of survivors. It is therefore crucial to understand the molecular structure, physiology, and events involved in the pathogenesis of sepsis-associated encephalopathy, so that potential therapeutic advances can be achieved. A key determinant to the development of this type of encephalopathy is morphological and functional modification of the blood-brain barrier (BBB), whose function is to protect the CNS from pathogens and toxic threats. Key mediators of pathologic sequelae of sepsis in the brain include cytokines, including TNF-α, and sphingolipids, which are biologically active components of cellular membranes that possess diverse functions. Emerging data demonstrated an essential role for sphingolipids in the pulmonary vascular endothelium. This raises the question of whether endothelial stability in other organs systems such as the CNS may also be mediated by sphingolipids and their receptors. In this review, we will model the structure and vulnerability of the BBB and hypothesize mechanisms for therapeutic stabilization and repair following a confrontation with sepsis-induced inflammation.