Asthma and COPD Section

Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with chronic obstructive pulmonary disease (COPD). Type 2 inflammation has been recognized as an important phenotypic pathway in asthma. However, its role in COPD has been much less clear, which had been largely associated with innate immune response.1

Activation of Interleukin (IL)-25, IL-33, thymic stromal lymphopoietin [TSLP] produces type 2 cytokines IL-4, IL-5, and IL-13, either by binding to ILC2 or by direct Th2 cells resulting in elevated eosinophils in sputum, lungs, and blood, as well as fractional exhaled nitric oxide.2 The combined inflammation from this pathway underpins the pathological changes seen in airway mucosa, causing mucous hypersecretion and hyperresponsiveness.

Prior trials delineating the role of biologics, such as mepolizumab and benralizumab, showed variable results with possible benefit of add-on biologics on the annual COPD exacerbations among patients with eosinophilic phenotype of COPD.3

More recently, the BOREAS trial evaluated the role of dupilumab as an add-on therapy for patients with type 2 inflammation-driven COPD established using blood eosinophil count of at least 300/mL at initial screening.4 Dupilumab is a human monoclonal antibody that blocks combined IL-4 and IL-13 pathways with a broader effect on the type 2 inflammation. It included patients with moderate to severe exacerbations despite maximal triple inhaler therapy with blood eosinophilia. Patients with asthma were excluded. This 52-week trial showed reduction in annual moderate to severe COPD exacerbations, sustained lung function improvement as measured by prebronchodilator FEV1, and improvement in patient-reported respiratory symptoms.4 Evaluation of sustainability of these results with therapy step-down approaches should be explored.

Maria Azhar, MD, Section Fellow-in-Training

Abdullah Alismail, PhD, RRT, FCCP, Section Member

Raghav Gupta, MD, FCCP, Section Member


1. Scanlon & McKenzie. 2012.

2. Brussell, et al. 2013.

3. Pavord, et al. 2017.

4. Bhatt, et al. 2023.


Disaster Response and Global Health Section

Viral infections frequently cause acute respiratory failure requiring ICU admission. In the United States, influenza causes over 50,000 deaths annually and SARS-CoV2 resulted in 170,000 hospitalizations in December 2023 alone.1 2 RSV lacks precise incidence data due to inconsistent testing but is increasingly implicated in respiratory failure.

Patients with underlying pulmonary comorbidities are at increased risk of severe infection. RSV induces bronchospasm and increases the risk for severe infection in patients with obstructive lung disease.3 Additionally, COPD patients with viral respiratory infections have higher rates of ICU admission, mechanical ventilation, and death compared with similar patients admitted for other etiologies.4

Diagnosis typically is achieved with nasopharyngeal PCR swabs. Positive viral swabs correlate with higher ICU admission and ventilation rates in patients with COPD.4 Coinfection with multiple respiratory viruses leads to higher mortality rates and bacterial and fungal coinfection further increases morbidity and mortality.5

Treatment includes respiratory support with noninvasive ventilation and high-flow nasal cannula, reducing the need for mechanical ventilation.6 Inhaled bronchodilators are particularly beneficial in patients with RSV infection.5 Oseltamivir reduces mortality in severe influenza cases, while remdesivir shows efficacy in SARS-CoV2 infection not requiring invasive ventilation.7 Severe SARS-CoV2 infection can be treated with immunomodulators. However, their availability is limited. Corticosteroids reduce mortality and mechanical ventilation in patients with SARS-CoV2; however, their use is associated with worse outcomes in influenza and RSV.7 8

Vaccination remains crucial for prevention of severe disease. RSV vaccination, in addition to influenza and SARS-CoV2 immunization, presents an opportunity to reduce morbidity and mortality.

Zein Kattih, MD, Section Fellow-in-Training

Kathryn Hughes, MD

Brian Tran, MD


1. Troeger C, et al. Lancet Infect Dis. 2028;18(11):1191-1210.

2. WHO COVID-19 Epidemilogical Update, 2024.

3. Coussement J, et al. Chest. 2022;161(6):1475-1484.

4. Mulpuru S, et al. Influenza Other Respir Viruses. 2022;16(6):1172-1182.

5. Saura O, et al. Expert Rev Anti Infect Ther. 2022;20(12):1537-1550.

6. Inglis R, Ayebale E, Shultz MJ. Curr Opin Crit Care. 2019;25(1):45-53.

7. O’Driscoll LS, Martin-Loeches I. Semin Respir Crit Care Med. 2021;42(6):771-787.

8. Bhimraj A, et al. Clin Inf Dis. 2022.


Palliative & End-of-Life Section

For providers caring for critically ill patients, navigating death and dying in the intensive care unit (ICU) with proficiency and empathy is essential. Approximately 20% of deaths in the United States occur during or shortly after a stay in the ICU and approximately 40% of ICU deaths involve withdrawal of artificial life support (WOALS) or compassionate extubation.

This is a complex process that may involve advanced communication with family, expertise in mechanical ventilation, vasopressors, dialysis, and complex symptom management. Importantly, surrogate medical decision-making for a critically ill patient can be a challenging experience associated with anxiety and depression. How the team approaches WOALS can make a difference to both patients and decision-makers. Unfortunately, there is striking variation in practice and lack of guidance in navigating issues that arise at end-of-life in the ICU. One study of 2814 hospitals in the US with ICU beds found that 52% had intensivists while 48% did not.2 This highlights the importance of developing resources focusing on end-of-life care in the ICU setting regardless of the providers’ educational training.

Important elements could include the role for protocol-based WOALS, use of oxygen, selection and dosing strategy of comfort-focused medications, establishing expectations, and addressing uncertainties. This would be meaningful in providing effective, ethical end-of-life care based on evidence-based strategies. While death may be unavoidable, a thoughtful approach can allow providers to bring dignity to the dying process and lessen the burden of an already difficult experience for patients and families alike.

Angela L. Birdwell, DO, MA, Section Chair

Nehan Sher, MD, Section Member


1. Curtis JR, et al. Am J Respir Crit Care Med. 2012;186(7):587-592.

2. Halpern NA, et al. Crit Care Med. 2019;47(4):517-525.


Nonrespiratory Sleep Section

Q: Are there interventions that can be readily implemented to improve sleep quality for hospitalized patients?

Dr. Arora: A patient’s first night in the hospital is probably not the night to liberalize sleep; you’re still figuring out whether they’re stable. But by the second or third day, you should be questioning – do you need vitals at night? Do you need a 4 AM blood draw?

We did an intervention called SIESTA that included both staff education about batching care and system-wide, electronic health record-based interventions to remind clinicians that as patients get better, you can deintensify their care. And we’re currently doing a randomized controlled trial of educating and empowering patients to ask their teams to help them get better sleep.

Q: Does hospital sleep deprivation affect patients after discharge?

Dr. Arora: Absolutely. “Posthospital syndrome” is the idea that 30 days after discharge, you’re vulnerable to getting readmitted – not because of the disease you came in with, but something else. And people who report sleep complaints in the hospital are more likely to be readmitted.

When people are acutely sleep deprived, their blood pressure is higher. Their blood sugar is higher. Their cytokine response and immune function are blunted. And our work shows that sleep deficits from the hospital continue even when you go home. Fatigue becomes a very real issue. And when you’re super fatigued, are you going to want to do your physical therapy? Will you be able to take care of yourself? Will you be able to learn and understand your discharge instructions?

We have such a huge gap to improve sleep. It’s of interest to people, but they are struggling with how to do it. And that’s where I think empowering frontline clinicians to take the lead is a great project for people to take on.

Vineet Arora, MD, MAPP, is the Dean for Medical Education at the University of Chicago and an academic hospitalist who specializes in the quality, safety, and experience of care delivered to hospitalized adults.

Alison Szabo, MD

Lisa Wolfe, MD, Section Member


Lung Cancer Section

Lung cancer stands as the leading cause of cancer-related deaths globally, with its prevalence casting a long and challenging shadow. The most important risk factor for lung cancer is tobacco use, a relationship strongly substantiated by data. The impact of smoking cessation to reduce lung cancer incidence is underscored by the US Preventive Services Task Force (USPSTF), which mandates that smoking cessation services be an integral component of lung cancer screening programs.

However, beneath the surface of this overarching concern lies a web of factors contributing to racial and ethnic disparities in smoking cessation. Cultural intricacies play a pivotal role in shaping these disparities. Despite higher instances of light or intermediate smoking, racially ethnic minority groups in the general population often face greater challenges in achieving smoking cessation, as highlighted by Bacio, et al (Addict Behav. 2014). Adding another layer to this complex scenario is the profound impact of sustained smoking during cancer treatment. Research suggests that for individuals diagnosed with lung cancer, smoking cessation can markedly boost treatment efficacy, reduce the risk of secondary tumors, and even double the chances of survival.1

A study by Harris, et al. delving into the preferences of current smokers within a lung cancer screening setting uncovered noteworthy insights.2 White participants exhibited a fourfold greater likelihood of favoring a digital format for receiving smoking cessation information, while their Black counterparts expressed a preference for face-to-face support, phone assistance, or printed materials.

Moreover, a meta-analysis conducted by Jabari, et al. sheds light on the efficacy of culturally targeted smoking interventions.3 This comprehensive review describes a dual-level approach to tailoring smoking cessation health interventions: surface and deep. Surface adaptations encompass elements like language and imagery, which aim to enhance the acceptability of interventions within specific communities. Simultaneously, deep-tailored elements identify culturally significant factors that can fundamentally influence the behavior of the target population. The findings of this meta-analysis reveal that the integration of culturally tailored components into standard interventions significantly enhances their efficacy in facilitating smoking cessation.

In conclusion, sustained smoking cessation is a crucial element in combating the global burden of lung cancer. Recognizing the importance of individualized approaches in health care, it is imperative to tailor smoking cessation communications and interventions to diverse cultural influences and socioeconomic factors. Culturally tailored smoking cessation programs that account for nuances specific to each community have the potential to significantly enhance their effectiveness. This necessitates a shift towards individualized smoking cessation care, with a targeted focus on increasing cessation rates among racial and ethnic minority groups. In doing so, we take a step closer to a more equitable landscape in the battle against lung cancer.

Stella Ogake, MD, FCCP, Section Member


1. Dresler, et al. Lung Cancer. 2003.

2. J Cancer Educ. 2018;33(5).

3. Addiction. 2023.

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