Networks

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Lung Transplant Section

Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Typically presenting within 2 weeks post transplant, HALT manifests as elevated serum ammonia levels with symptoms ranging from encephalopathy to seizures and cerebral edema. Early recognition is crucial, as mortality rates can reach 75%.¹

CHEST

HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.² Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.

CHEST

References

1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234

2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
 

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Lung Transplant Section

Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Typically presenting within 2 weeks post transplant, HALT manifests as elevated serum ammonia levels with symptoms ranging from encephalopathy to seizures and cerebral edema. Early recognition is crucial, as mortality rates can reach 75%.¹

CHEST

HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.² Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.

CHEST

References

1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234

2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
 

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Lung Transplant Section

Hyperammonemia after lung transplantation (HALT) is a rare but serious complication occurring in 1% to 4% of patients with high morbidity and mortality. Typically presenting within 2 weeks post transplant, HALT manifests as elevated serum ammonia levels with symptoms ranging from encephalopathy to seizures and cerebral edema. Early recognition is crucial, as mortality rates can reach 75%.¹

CHEST

HALT arises from excess ammonia production or decreased clearance and is often linked to infections by urea-splitting organisms, including mycoplasma and ureaplasma. Prompt, aggressive treatment is essential and typically includes dietary protein restriction, renal replacement therapy (ideally intermittent hemodialysis), bowel decontamination (lactulose, rifaximin, metronidazole, or neomycin), amino acids (arginine and levocarnitine), nitrogen scavengers (sodium phenylbutyrate or glycerol phenylbutyrate), and empiric antimicrobial coverage for urea-splitting organisms.² Given concerns for calcineurin inhibitor-induced hyperammonemia, transition to an alternative agent may be considered.

CHEST

References

1. Leger RF, Silverman MS, Hauck ES, Guvakova KD. Hyperammonemia post lung transplantation: a review. Clin Med Insights Circ Respir Pulm Med. 2020;14:1179548420966234. doi:10.1177/1179548420966234

2. Chen C, Bain KB, Luppa JA. Hyperammonemia syndrome after lung transplantation: a single center experience. Transplantation. 2016;100(3):678-684. doi:10.1097/TP.0000000000000868
 

CRITICAL CARE NETWORK

Nonrespiratory Critical Care Section

Nutrition plays an important role in the management and recovery of critically ill patients admitted to the ICU. Major guidelines recommend that critically ill patients should receive 1.2 to 2.0 g/kg/day of protein, with an emphasis on early (within 48 hours of ICU admission) enteral nutrition.^1-3

In a randomized controlled trial involving 173 critically ill patients who stayed in the ICU in Zhejiang, China, Wang and colleagues studied the impact of early high protein intake (1.5 g/kg/day vs 0.8 g/kg/day).⁴ The primary outcome of 28-day mortality was lower among the high protein intake group (8.14% vs 19.54%). Still, this intention-to-treat analysis did not reach a statistical significance (P = .051). However, a time-to-event analysis using the Cox proportional hazard model showed that the high protein intake group had a significantly lower 28-day mortality rate, shorter ICU stays, and improved nutritional status, particularly in patients with sepsis (P = .045).

CHEST

CHEST

References

1. Taylor BE, McClave SA, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). Crit Care Med. 2016;44(2):390-438. doi:10.1097/CCM.0000000000001525

2. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive care unit. Clin Nutr. 2019;38(1):48-79. doi:10.1016/j.clnu.2018.08.037

3. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). JJPEN J Parenter Enteral Nutr. 2016;40(2):159-211. doi:10.1177/0148607115621863

4. Wang Y, Ye Y, Xuan L, et al. Impact of early high protein intake in critically ill patients: a randomized controlled trial. Nutr Metab. 2024;21(1):39. doi.org/10.1186/s12986-024-00818-8

5. Lee ZY, Yap CSL, Hasan MS, et al. The effect of higher versus lower protein delivery in critically ill patients: a systematic review and meta-analysis of randomized controlled trials. Crit Care. 2021;25(1):260. doi.org/10.1186/s13054-021-03693-4

6. Stoppe C, Patel JJ, Zarbock A, et al. The impact of higher protein dosing on outcomes in critically ill patients with acute kidney injury: a post hoc analysis of the EFFORT protein trial. Crit Care. 2023;27(1):399. doi.org/10.1186/s13054-023-04663-8
 

CRITICAL CARE NETWORK

Nonrespiratory Critical Care Section

Nutrition plays an important role in the management and recovery of critically ill patients admitted to the ICU. Major guidelines recommend that critically ill patients should receive 1.2 to 2.0 g/kg/day of protein, with an emphasis on early (within 48 hours of ICU admission) enteral nutrition.^1-3

In a randomized controlled trial involving 173 critically ill patients who stayed in the ICU in Zhejiang, China, Wang and colleagues studied the impact of early high protein intake (1.5 g/kg/day vs 0.8 g/kg/day).⁴ The primary outcome of 28-day mortality was lower among the high protein intake group (8.14% vs 19.54%). Still, this intention-to-treat analysis did not reach a statistical significance (P = .051). However, a time-to-event analysis using the Cox proportional hazard model showed that the high protein intake group had a significantly lower 28-day mortality rate, shorter ICU stays, and improved nutritional status, particularly in patients with sepsis (P = .045).

CHEST

CHEST

References

1. Taylor BE, McClave SA, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). Crit Care Med. 2016;44(2):390-438. doi:10.1097/CCM.0000000000001525

2. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive care unit. Clin Nutr. 2019;38(1):48-79. doi:10.1016/j.clnu.2018.08.037

3. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). JJPEN J Parenter Enteral Nutr. 2016;40(2):159-211. doi:10.1177/0148607115621863

4. Wang Y, Ye Y, Xuan L, et al. Impact of early high protein intake in critically ill patients: a randomized controlled trial. Nutr Metab. 2024;21(1):39. doi.org/10.1186/s12986-024-00818-8

5. Lee ZY, Yap CSL, Hasan MS, et al. The effect of higher versus lower protein delivery in critically ill patients: a systematic review and meta-analysis of randomized controlled trials. Crit Care. 2021;25(1):260. doi.org/10.1186/s13054-021-03693-4

6. Stoppe C, Patel JJ, Zarbock A, et al. The impact of higher protein dosing on outcomes in critically ill patients with acute kidney injury: a post hoc analysis of the EFFORT protein trial. Crit Care. 2023;27(1):399. doi.org/10.1186/s13054-023-04663-8
 

CRITICAL CARE NETWORK

Nonrespiratory Critical Care Section

Nutrition plays an important role in the management and recovery of critically ill patients admitted to the ICU. Major guidelines recommend that critically ill patients should receive 1.2 to 2.0 g/kg/day of protein, with an emphasis on early (within 48 hours of ICU admission) enteral nutrition.^1-3

In a randomized controlled trial involving 173 critically ill patients who stayed in the ICU in Zhejiang, China, Wang and colleagues studied the impact of early high protein intake (1.5 g/kg/day vs 0.8 g/kg/day).⁴ The primary outcome of 28-day mortality was lower among the high protein intake group (8.14% vs 19.54%). Still, this intention-to-treat analysis did not reach a statistical significance (P = .051). However, a time-to-event analysis using the Cox proportional hazard model showed that the high protein intake group had a significantly lower 28-day mortality rate, shorter ICU stays, and improved nutritional status, particularly in patients with sepsis (P = .045).

CHEST

CHEST

References

1. Taylor BE, McClave SA, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). Crit Care Med. 2016;44(2):390-438. doi:10.1097/CCM.0000000000001525

2. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive care unit. Clin Nutr. 2019;38(1):48-79. doi:10.1016/j.clnu.2018.08.037

3. McClave SA, Taylor BE, Martindale RG, et al. Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (ASPEN). JJPEN J Parenter Enteral Nutr. 2016;40(2):159-211. doi:10.1177/0148607115621863

4. Wang Y, Ye Y, Xuan L, et al. Impact of early high protein intake in critically ill patients: a randomized controlled trial. Nutr Metab. 2024;21(1):39. doi.org/10.1186/s12986-024-00818-8

5. Lee ZY, Yap CSL, Hasan MS, et al. The effect of higher versus lower protein delivery in critically ill patients: a systematic review and meta-analysis of randomized controlled trials. Crit Care. 2021;25(1):260. doi.org/10.1186/s13054-021-03693-4

6. Stoppe C, Patel JJ, Zarbock A, et al. The impact of higher protein dosing on outcomes in critically ill patients with acute kidney injury: a post hoc analysis of the EFFORT protein trial. Crit Care. 2023;27(1):399. doi.org/10.1186/s13054-023-04663-8
 

PULMONARY VASCULAR AND CARDIOVASCULAR NETWORK

Cardiovascular Medicine and Surgery Section

Patients with intermediate-risk pulmonary embolism (IRPE), or those with right ventricular dysfunction without overt hemodynamic instability, represent a heterogenous population with short-term mortality ranging from 2% to 17%.¹ While systemic anticoagulation is the mainstay therapy, select individuals may benefit from more immediate reperfusion. Catheter-based therapies (CBT), including thrombus aspiration, fragmentation, or catheter-directed thrombolysis, have seen rapid uptake over the last decade, with promising retrospective data. Unfortunately, only small, randomized trials exploring surrogate outcomes are available to guide modality and patient selection.²

CHEST

To better define which patients with IRPE are best managed with which therapy, several large-scale randomized controlled trials are underway. PE-TRACT, a study funded by the National Institutes of Health, aims to randomize 500 patients with IRPE to anticoagulation alone vs one of several modalities of CBT with a focus on long-term functional outcomes, including peak oxygen consumption at 3 months and functional class at 1 year. Aspiration thrombectomy with the FlowTriever^® device is being compared with anticoagulation alone in a study of 1,200 patients examining short-term composite end points.

CHEST

References

1. Fernández C, Bova C, Sanchez O, et al. Validation of a model for identification of patients at intermediate to high risk for complications associated with acute symptomatic pulmonary embolism. Chest. 2015;148(1):211-218. doi:10.1378/chest.14-2551

2. Yuriditsky E, Horowitz JM. The role of the PERT in the management and therapeutic decision-making in pulmonary embolism. Eur Heart J Acute Cardiovasc Care. 2022;11(9):693-694. doi:10.1093/ehjacc/zuac102

3. National Library of Medicine (US). A Randomized Trial of Ultrasound-facilitated, Catheter-directed, Thrombolysis Versus Anticoagulation for Acute Intermediate-high Risk Pulmonary Embolism: The Higher-risk Pulmonary Embolism Thrombolysis Study. Updated July 16, 2024. https://clinicaltrials.gov/study/NCT04790370

4. National Library of Medicine (US). PEERLESS II: RCT of FlowTriever vs. Anticoagulation Alone in Pulmonary Embolism. Updated July 17, 2024. https://clinicaltrials.gov/study/NCT06055920

5. National Library of Medicine (US). A Reduced Dose of Thrombolytic Treatment for Patients With Intermediate High-risk Acute Pulmonary Embolism: a Randomized Controled Trial. Updated July 17, 2024. https://clinicaltrials.gov/study/NCT04430569

PULMONARY VASCULAR AND CARDIOVASCULAR NETWORK

Cardiovascular Medicine and Surgery Section

Patients with intermediate-risk pulmonary embolism (IRPE), or those with right ventricular dysfunction without overt hemodynamic instability, represent a heterogenous population with short-term mortality ranging from 2% to 17%.¹ While systemic anticoagulation is the mainstay therapy, select individuals may benefit from more immediate reperfusion. Catheter-based therapies (CBT), including thrombus aspiration, fragmentation, or catheter-directed thrombolysis, have seen rapid uptake over the last decade, with promising retrospective data. Unfortunately, only small, randomized trials exploring surrogate outcomes are available to guide modality and patient selection.²

CHEST

To better define which patients with IRPE are best managed with which therapy, several large-scale randomized controlled trials are underway. PE-TRACT, a study funded by the National Institutes of Health, aims to randomize 500 patients with IRPE to anticoagulation alone vs one of several modalities of CBT with a focus on long-term functional outcomes, including peak oxygen consumption at 3 months and functional class at 1 year. Aspiration thrombectomy with the FlowTriever^® device is being compared with anticoagulation alone in a study of 1,200 patients examining short-term composite end points.

CHEST

References

1. Fernández C, Bova C, Sanchez O, et al. Validation of a model for identification of patients at intermediate to high risk for complications associated with acute symptomatic pulmonary embolism. Chest. 2015;148(1):211-218. doi:10.1378/chest.14-2551

2. Yuriditsky E, Horowitz JM. The role of the PERT in the management and therapeutic decision-making in pulmonary embolism. Eur Heart J Acute Cardiovasc Care. 2022;11(9):693-694. doi:10.1093/ehjacc/zuac102

3. National Library of Medicine (US). A Randomized Trial of Ultrasound-facilitated, Catheter-directed, Thrombolysis Versus Anticoagulation for Acute Intermediate-high Risk Pulmonary Embolism: The Higher-risk Pulmonary Embolism Thrombolysis Study. Updated July 16, 2024. https://clinicaltrials.gov/study/NCT04790370

4. National Library of Medicine (US). PEERLESS II: RCT of FlowTriever vs. Anticoagulation Alone in Pulmonary Embolism. Updated July 17, 2024. https://clinicaltrials.gov/study/NCT06055920

5. National Library of Medicine (US). A Reduced Dose of Thrombolytic Treatment for Patients With Intermediate High-risk Acute Pulmonary Embolism: a Randomized Controled Trial. Updated July 17, 2024. https://clinicaltrials.gov/study/NCT04430569

PULMONARY VASCULAR AND CARDIOVASCULAR NETWORK

Cardiovascular Medicine and Surgery Section

Patients with intermediate-risk pulmonary embolism (IRPE), or those with right ventricular dysfunction without overt hemodynamic instability, represent a heterogenous population with short-term mortality ranging from 2% to 17%.¹ While systemic anticoagulation is the mainstay therapy, select individuals may benefit from more immediate reperfusion. Catheter-based therapies (CBT), including thrombus aspiration, fragmentation, or catheter-directed thrombolysis, have seen rapid uptake over the last decade, with promising retrospective data. Unfortunately, only small, randomized trials exploring surrogate outcomes are available to guide modality and patient selection.²

CHEST

To better define which patients with IRPE are best managed with which therapy, several large-scale randomized controlled trials are underway. PE-TRACT, a study funded by the National Institutes of Health, aims to randomize 500 patients with IRPE to anticoagulation alone vs one of several modalities of CBT with a focus on long-term functional outcomes, including peak oxygen consumption at 3 months and functional class at 1 year. Aspiration thrombectomy with the FlowTriever^® device is being compared with anticoagulation alone in a study of 1,200 patients examining short-term composite end points.

CHEST

References

1. Fernández C, Bova C, Sanchez O, et al. Validation of a model for identification of patients at intermediate to high risk for complications associated with acute symptomatic pulmonary embolism. Chest. 2015;148(1):211-218. doi:10.1378/chest.14-2551

2. Yuriditsky E, Horowitz JM. The role of the PERT in the management and therapeutic decision-making in pulmonary embolism. Eur Heart J Acute Cardiovasc Care. 2022;11(9):693-694. doi:10.1093/ehjacc/zuac102

3. National Library of Medicine (US). A Randomized Trial of Ultrasound-facilitated, Catheter-directed, Thrombolysis Versus Anticoagulation for Acute Intermediate-high Risk Pulmonary Embolism: The Higher-risk Pulmonary Embolism Thrombolysis Study. Updated July 16, 2024. https://clinicaltrials.gov/study/NCT04790370

4. National Library of Medicine (US). PEERLESS II: RCT of FlowTriever vs. Anticoagulation Alone in Pulmonary Embolism. Updated July 17, 2024. https://clinicaltrials.gov/study/NCT06055920

5. National Library of Medicine (US). A Reduced Dose of Thrombolytic Treatment for Patients With Intermediate High-risk Acute Pulmonary Embolism: a Randomized Controled Trial. Updated July 17, 2024. https://clinicaltrials.gov/study/NCT04430569

AIRWAYS DISORDERS NETWORK

Bronchiectasis Section

Bronchiectasis is an extremely heterogeneous airways disease, making it difficult to study. For years, the noncystic fibrosis (CF) bronchiectasis community has been trying to organize to provide better care for more than half a million adults with bronchiectasis in the United States. Internationally, the Europeans created the European Bronchiectasis Registry, which has been a powerful tool including nearly 20,000 patients, to answer important epidemiologic and management questions. We must do more for the bronchiectasis community.

Clinicaltrials.gov indicates that there are 8 international phase 3 or 4 clinical trials that are currently enrolling; 3 of those have enrollment sites in the United States. One such study from University of North Carolina at Chapel Hill is looking at the use of nebulized hypertonic saline in patients with non-CF bronchiectasis to understand the effect it has on mucociliary clearance. Emory University is looking at the use of elexacaftor/tezacaftor/ivacaftor (Trikafta) in patients with non-CF bronchiectasis; these patients have only 1 targetable mutation and a phenotype that resembles CF. This 8-week, open-label, single-center study aims to measure both clinical and biomarker outcomes after treatment with Trikafta. Finally, a phase 3 trial out of Florida, the ICoN-1 study, is examining the efficacy and safety of inhaled clofazimine in the treatment of nontuberculous mycobacteria (NTM). This double-blind, randomized trial will look at culture conversion and quality of life measures. Additionally, the COPD Foundation has created the Bronchiectasis and NTM Research Registry, an American cohort containing more than 5,000 patients and data from 22 different sites, to answer some of the most important questions for clinicians and patients.

CHEST

We have made significant progress in bronchiectasis research; however, there is still much to learn. Together, we must make a concerted effort to enroll patients in clinical trials. Doing so will allow us to define our epidemiologic profile more precisely and explore new treatments and airway clearance techniques.

AIRWAYS DISORDERS NETWORK

Bronchiectasis Section

Bronchiectasis is an extremely heterogeneous airways disease, making it difficult to study. For years, the noncystic fibrosis (CF) bronchiectasis community has been trying to organize to provide better care for more than half a million adults with bronchiectasis in the United States. Internationally, the Europeans created the European Bronchiectasis Registry, which has been a powerful tool including nearly 20,000 patients, to answer important epidemiologic and management questions. We must do more for the bronchiectasis community.

Clinicaltrials.gov indicates that there are 8 international phase 3 or 4 clinical trials that are currently enrolling; 3 of those have enrollment sites in the United States. One such study from University of North Carolina at Chapel Hill is looking at the use of nebulized hypertonic saline in patients with non-CF bronchiectasis to understand the effect it has on mucociliary clearance. Emory University is looking at the use of elexacaftor/tezacaftor/ivacaftor (Trikafta) in patients with non-CF bronchiectasis; these patients have only 1 targetable mutation and a phenotype that resembles CF. This 8-week, open-label, single-center study aims to measure both clinical and biomarker outcomes after treatment with Trikafta. Finally, a phase 3 trial out of Florida, the ICoN-1 study, is examining the efficacy and safety of inhaled clofazimine in the treatment of nontuberculous mycobacteria (NTM). This double-blind, randomized trial will look at culture conversion and quality of life measures. Additionally, the COPD Foundation has created the Bronchiectasis and NTM Research Registry, an American cohort containing more than 5,000 patients and data from 22 different sites, to answer some of the most important questions for clinicians and patients.

CHEST

We have made significant progress in bronchiectasis research; however, there is still much to learn. Together, we must make a concerted effort to enroll patients in clinical trials. Doing so will allow us to define our epidemiologic profile more precisely and explore new treatments and airway clearance techniques.

AIRWAYS DISORDERS NETWORK

Bronchiectasis Section

Bronchiectasis is an extremely heterogeneous airways disease, making it difficult to study. For years, the noncystic fibrosis (CF) bronchiectasis community has been trying to organize to provide better care for more than half a million adults with bronchiectasis in the United States. Internationally, the Europeans created the European Bronchiectasis Registry, which has been a powerful tool including nearly 20,000 patients, to answer important epidemiologic and management questions. We must do more for the bronchiectasis community.

Clinicaltrials.gov indicates that there are 8 international phase 3 or 4 clinical trials that are currently enrolling; 3 of those have enrollment sites in the United States. One such study from University of North Carolina at Chapel Hill is looking at the use of nebulized hypertonic saline in patients with non-CF bronchiectasis to understand the effect it has on mucociliary clearance. Emory University is looking at the use of elexacaftor/tezacaftor/ivacaftor (Trikafta) in patients with non-CF bronchiectasis; these patients have only 1 targetable mutation and a phenotype that resembles CF. This 8-week, open-label, single-center study aims to measure both clinical and biomarker outcomes after treatment with Trikafta. Finally, a phase 3 trial out of Florida, the ICoN-1 study, is examining the efficacy and safety of inhaled clofazimine in the treatment of nontuberculous mycobacteria (NTM). This double-blind, randomized trial will look at culture conversion and quality of life measures. Additionally, the COPD Foundation has created the Bronchiectasis and NTM Research Registry, an American cohort containing more than 5,000 patients and data from 22 different sites, to answer some of the most important questions for clinicians and patients.

CHEST

We have made significant progress in bronchiectasis research; however, there is still much to learn. Together, we must make a concerted effort to enroll patients in clinical trials. Doing so will allow us to define our epidemiologic profile more precisely and explore new treatments and airway clearance techniques.

CHEST

CHEST INFECTIONS AND DISASTER RESPONSE NETWORK

Disaster Response and Global Health Section

Patients who are injured do better when treated at trauma centers.

During CHEST 2023 in Honolulu last year, the Disaster Response and Global Health Section hosted a presentation to a packed audience highlighting the history of the trauma model system in America. Attendees learned about the emergence of trauma systems in the US and the survival advantages that trauma centers offer to patients who are injured.

Inception of the first “trauma manual” was during President Lincoln’s term to address the need for a process to care for patients who were injured during the Civil War. By the time World War II occurred, hospitals had established the idea of emergency departments, and the foundations for an emergency medical system (EMS) emerged on the world scene. Eventually, the Hill-Burton Act of 1946 required hospitals to have emergency departments by incentivizing them with federal funding.

The Committee on Trauma was founded in the 1950s as an adaptation of the American College of Surgeons’ 1922 Committee on Fractures. Then, in 1966, the National Highway Traffic Safety Administration rolled out a federal initiative for all states to develop EMS programs. Additionally, the National Academy of Sciences published Accidental Death and Disability: The Neglected Disease of Modern Society, paving the way for the Emergency Medical Services Systems Act of 1973, along with the Wedworth-Townsend Paramedic Act in California.

The concept of today’s trauma centers started in 1966 at Cook County Hospital in Chicago and Shock Trauma Center in Baltimore.

CHEST

CHEST INFECTIONS AND DISASTER RESPONSE NETWORK

Disaster Response and Global Health Section

Patients who are injured do better when treated at trauma centers.

During CHEST 2023 in Honolulu last year, the Disaster Response and Global Health Section hosted a presentation to a packed audience highlighting the history of the trauma model system in America. Attendees learned about the emergence of trauma systems in the US and the survival advantages that trauma centers offer to patients who are injured.

Inception of the first “trauma manual” was during President Lincoln’s term to address the need for a process to care for patients who were injured during the Civil War. By the time World War II occurred, hospitals had established the idea of emergency departments, and the foundations for an emergency medical system (EMS) emerged on the world scene. Eventually, the Hill-Burton Act of 1946 required hospitals to have emergency departments by incentivizing them with federal funding.

The Committee on Trauma was founded in the 1950s as an adaptation of the American College of Surgeons’ 1922 Committee on Fractures. Then, in 1966, the National Highway Traffic Safety Administration rolled out a federal initiative for all states to develop EMS programs. Additionally, the National Academy of Sciences published Accidental Death and Disability: The Neglected Disease of Modern Society, paving the way for the Emergency Medical Services Systems Act of 1973, along with the Wedworth-Townsend Paramedic Act in California.

The concept of today’s trauma centers started in 1966 at Cook County Hospital in Chicago and Shock Trauma Center in Baltimore.

CHEST

CHEST INFECTIONS AND DISASTER RESPONSE NETWORK

Disaster Response and Global Health Section

Patients who are injured do better when treated at trauma centers.

During CHEST 2023 in Honolulu last year, the Disaster Response and Global Health Section hosted a presentation to a packed audience highlighting the history of the trauma model system in America. Attendees learned about the emergence of trauma systems in the US and the survival advantages that trauma centers offer to patients who are injured.

Inception of the first “trauma manual” was during President Lincoln’s term to address the need for a process to care for patients who were injured during the Civil War. By the time World War II occurred, hospitals had established the idea of emergency departments, and the foundations for an emergency medical system (EMS) emerged on the world scene. Eventually, the Hill-Burton Act of 1946 required hospitals to have emergency departments by incentivizing them with federal funding.

The Committee on Trauma was founded in the 1950s as an adaptation of the American College of Surgeons’ 1922 Committee on Fractures. Then, in 1966, the National Highway Traffic Safety Administration rolled out a federal initiative for all states to develop EMS programs. Additionally, the National Academy of Sciences published Accidental Death and Disability: The Neglected Disease of Modern Society, paving the way for the Emergency Medical Services Systems Act of 1973, along with the Wedworth-Townsend Paramedic Act in California.

The concept of today’s trauma centers started in 1966 at Cook County Hospital in Chicago and Shock Trauma Center in Baltimore.

CHEST

CRITICAL CARE NETWORK

Palliative and End-of-Life Care Section

As critical care medicine continues to advance understanding of ICU survivorship, thoughtful selection of medications in the acute setting can potentially mitigate long-term cognitive, physical, and affective effects.

As of yet, no significant studies have linked opioid use in critical care to new diagnoses of opioid use disorder, but the opioid epidemic has taught us that profligate use of opioids can have devastating effects despite best intentions. Continuous infusions of full agonist opioids for sedation remain an important tool in management of sedation. For acute pain, buprenorphine represents an attractive alternative for patients who are both intubated and nonintubated. It provides equal pain relief as full agonist opioids while causing less respiratory depression, less delirium, less nausea, less constipation, less euphoria, and less misuse potential. Its unique partial mu-opioid agonism is responsible for the improved nausea, constipation, and respiratory depression, while the kappa and delta receptor antagonisms are responsible for antidepressant effects as well as lessened opioid craving, sedation, and dysphoria. Given the variety of doses and routes for buprenorphine, palliative medicine consults can help navigate preventing precipitated withdrawal in patients who are opioid-tolerant and the variety of available dosing and routes.

It is a testament to the growth of critical care medicine that we now have the privilege and responsibility to account for long-term sequelae of our lifesaving interventions, rather than the old model of “prevent death at all costs.” Continued integration of high-quality symptom management into critical care offers an opportunity to better balance life-prolonging treatment and optimize quality of life.

References

1. Neale KJ, Weimer MB, Davis MP, et al. Top ten tips palliative care clinicians should know about buprenorphine. J Palliat Med. 2023;26(1):120-130. doi: 10.1089/jpm.2022.0399
 

CHEST

CRITICAL CARE NETWORK

Palliative and End-of-Life Care Section

As critical care medicine continues to advance understanding of ICU survivorship, thoughtful selection of medications in the acute setting can potentially mitigate long-term cognitive, physical, and affective effects.

As of yet, no significant studies have linked opioid use in critical care to new diagnoses of opioid use disorder, but the opioid epidemic has taught us that profligate use of opioids can have devastating effects despite best intentions. Continuous infusions of full agonist opioids for sedation remain an important tool in management of sedation. For acute pain, buprenorphine represents an attractive alternative for patients who are both intubated and nonintubated. It provides equal pain relief as full agonist opioids while causing less respiratory depression, less delirium, less nausea, less constipation, less euphoria, and less misuse potential. Its unique partial mu-opioid agonism is responsible for the improved nausea, constipation, and respiratory depression, while the kappa and delta receptor antagonisms are responsible for antidepressant effects as well as lessened opioid craving, sedation, and dysphoria. Given the variety of doses and routes for buprenorphine, palliative medicine consults can help navigate preventing precipitated withdrawal in patients who are opioid-tolerant and the variety of available dosing and routes.

It is a testament to the growth of critical care medicine that we now have the privilege and responsibility to account for long-term sequelae of our lifesaving interventions, rather than the old model of “prevent death at all costs.” Continued integration of high-quality symptom management into critical care offers an opportunity to better balance life-prolonging treatment and optimize quality of life.

References

1. Neale KJ, Weimer MB, Davis MP, et al. Top ten tips palliative care clinicians should know about buprenorphine. J Palliat Med. 2023;26(1):120-130. doi: 10.1089/jpm.2022.0399
 

CHEST

CRITICAL CARE NETWORK

Palliative and End-of-Life Care Section

As critical care medicine continues to advance understanding of ICU survivorship, thoughtful selection of medications in the acute setting can potentially mitigate long-term cognitive, physical, and affective effects.

As of yet, no significant studies have linked opioid use in critical care to new diagnoses of opioid use disorder, but the opioid epidemic has taught us that profligate use of opioids can have devastating effects despite best intentions. Continuous infusions of full agonist opioids for sedation remain an important tool in management of sedation. For acute pain, buprenorphine represents an attractive alternative for patients who are both intubated and nonintubated. It provides equal pain relief as full agonist opioids while causing less respiratory depression, less delirium, less nausea, less constipation, less euphoria, and less misuse potential. Its unique partial mu-opioid agonism is responsible for the improved nausea, constipation, and respiratory depression, while the kappa and delta receptor antagonisms are responsible for antidepressant effects as well as lessened opioid craving, sedation, and dysphoria. Given the variety of doses and routes for buprenorphine, palliative medicine consults can help navigate preventing precipitated withdrawal in patients who are opioid-tolerant and the variety of available dosing and routes.

It is a testament to the growth of critical care medicine that we now have the privilege and responsibility to account for long-term sequelae of our lifesaving interventions, rather than the old model of “prevent death at all costs.” Continued integration of high-quality symptom management into critical care offers an opportunity to better balance life-prolonging treatment and optimize quality of life.

References

1. Neale KJ, Weimer MB, Davis MP, et al. Top ten tips palliative care clinicians should know about buprenorphine. J Palliat Med. 2023;26(1):120-130. doi: 10.1089/jpm.2022.0399
 

CHEST

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Lung Cancer Section

Since the American College of Radiology (ACR) updated its Lung CT Screening Reporting & Data System (Lung-RADS) to include atypical pulmonary cysts in 2022, there has been little discussion among chest physicians regarding the significance of pulmonary cysts and why these changes were made.

Lung-RADS 2022 defined atypical pulmonary cysts as single, unilocular cysts with a wall thickness greater than 2 mm or any multilocular cysts. These can be uniform, asymmetric, or have a focal nodularity. This change was prompted by data derived from multiple studies. First, a finding that 3.6% of lung cancers were associated with cysts at baseline.¹ This was followed by a reanalysis of the NELSON trial’s missed cancers showing 22% of those overlooked during initial screening had findings of cystic disease, reaffirming the significance of atypical pulmonary cysts.² Though the number is low, we now know 1.1% of all cancers present as an atypical cyst, with 4.7% of them being malignant.³
 

Based on these studies, cysts are a baseline Lung-RADS 4A—a finding that correlates to a higher risk and needs to be followed with a short-term CT scan in 3 months vs a PET. ACR does recommend reserving PET scans for wall thickness > 8 mm. If the repeat CT scan is stable, then the Lung-RADS designation is dropped to a 3 for follow-up.

References

1. Farooqi AO, Cham M, Zhang L, et al. Lung cancer associated with cystic airspaces. AJR Am J Roentgenol. 2012;199(4):781-786.

2. Scholten ET, Horeweg N, Koning HJ, et al. Computed tomographic characteristics of interval and post screen carcinomas in lung cancer screening. Eur Radiol. 2015;25(1):81-88.

3. Mascalchi M, Attinà D, Bertelli E, et al. Lung cancer associated with cystic airspaces. J Comput Assist Tomogr. 2015;39(1):102-108.

CHEST

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Lung Cancer Section

Since the American College of Radiology (ACR) updated its Lung CT Screening Reporting & Data System (Lung-RADS) to include atypical pulmonary cysts in 2022, there has been little discussion among chest physicians regarding the significance of pulmonary cysts and why these changes were made.

Lung-RADS 2022 defined atypical pulmonary cysts as single, unilocular cysts with a wall thickness greater than 2 mm or any multilocular cysts. These can be uniform, asymmetric, or have a focal nodularity. This change was prompted by data derived from multiple studies. First, a finding that 3.6% of lung cancers were associated with cysts at baseline.¹ This was followed by a reanalysis of the NELSON trial’s missed cancers showing 22% of those overlooked during initial screening had findings of cystic disease, reaffirming the significance of atypical pulmonary cysts.² Though the number is low, we now know 1.1% of all cancers present as an atypical cyst, with 4.7% of them being malignant.³
 

Based on these studies, cysts are a baseline Lung-RADS 4A—a finding that correlates to a higher risk and needs to be followed with a short-term CT scan in 3 months vs a PET. ACR does recommend reserving PET scans for wall thickness > 8 mm. If the repeat CT scan is stable, then the Lung-RADS designation is dropped to a 3 for follow-up.

References

1. Farooqi AO, Cham M, Zhang L, et al. Lung cancer associated with cystic airspaces. AJR Am J Roentgenol. 2012;199(4):781-786.

2. Scholten ET, Horeweg N, Koning HJ, et al. Computed tomographic characteristics of interval and post screen carcinomas in lung cancer screening. Eur Radiol. 2015;25(1):81-88.

3. Mascalchi M, Attinà D, Bertelli E, et al. Lung cancer associated with cystic airspaces. J Comput Assist Tomogr. 2015;39(1):102-108.

CHEST

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Lung Cancer Section

Since the American College of Radiology (ACR) updated its Lung CT Screening Reporting & Data System (Lung-RADS) to include atypical pulmonary cysts in 2022, there has been little discussion among chest physicians regarding the significance of pulmonary cysts and why these changes were made.

Lung-RADS 2022 defined atypical pulmonary cysts as single, unilocular cysts with a wall thickness greater than 2 mm or any multilocular cysts. These can be uniform, asymmetric, or have a focal nodularity. This change was prompted by data derived from multiple studies. First, a finding that 3.6% of lung cancers were associated with cysts at baseline.¹ This was followed by a reanalysis of the NELSON trial’s missed cancers showing 22% of those overlooked during initial screening had findings of cystic disease, reaffirming the significance of atypical pulmonary cysts.² Though the number is low, we now know 1.1% of all cancers present as an atypical cyst, with 4.7% of them being malignant.³
 

Based on these studies, cysts are a baseline Lung-RADS 4A—a finding that correlates to a higher risk and needs to be followed with a short-term CT scan in 3 months vs a PET. ACR does recommend reserving PET scans for wall thickness > 8 mm. If the repeat CT scan is stable, then the Lung-RADS designation is dropped to a 3 for follow-up.

References

1. Farooqi AO, Cham M, Zhang L, et al. Lung cancer associated with cystic airspaces. AJR Am J Roentgenol. 2012;199(4):781-786.

2. Scholten ET, Horeweg N, Koning HJ, et al. Computed tomographic characteristics of interval and post screen carcinomas in lung cancer screening. Eur Radiol. 2015;25(1):81-88.

3. Mascalchi M, Attinà D, Bertelli E, et al. Lung cancer associated with cystic airspaces. J Comput Assist Tomogr. 2015;39(1):102-108.

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Interventional Procedures Section

More than 1.5 million Americans are diagnosed with an incidental CT scan-detected lung nodule annually. Advanced bronchoscopy, as a diagnostic tool for evaluation of these nodules, has evolved rapidly, incorporating a range of techniques and tools beyond CT scan-guided biopsies to assess peripheral lesions. The primary goal is to provide patients with accurate benign or malignant diagnoses. However, accurately determining the effectiveness of innovative technologies in providing a diagnosis remains challenging, in part due to limitations in study design and outcome reporting, along with the scarcity of comparative and randomized controlled studies.^1,2 Current literature shows significant variability in diagnostic yield definition, lacking generalizability.

CHEST

To address this issue, an official research statement by the American Thoracic Society and CHEST defines the diagnostic yield as “the proportion of all individuals undergoing the diagnostic procedure under evaluation in whom a specific malignant or benign diagnosis is established.”³ To achieve this measure, the numerator includes all patients with lung nodules in whom the result of a diagnostic procedure establishes a specific benign or malignant diagnosis that is readily sufficient to inform patient care without additional diagnostic workup, and the denominator should include all patients in whom the procedure was attempted or performed. This standardized definition is crucial for ensuring consistency across studies, allowing for comparison or pooling of results, enhancing the reliability of diagnostic yield data, and informing clinical decisions.

CHEST

References

1. Tanner NT, Yarmus L, Chen A, et al. Standard bronchoscopy with fluoroscopy vs thin bronchoscopy and radial endobronchial ultrasound for biopsy of pulmonary lesions: a multicenter, prospective, randomized trial. Chest. 2018;154(5):1035-1043.

2. Ost DE, Ernst A, Lei X, et al. Diagnostic yield and complications of bronchoscopy for peripheral lung lesions. Results of the AQuIRE Registry. Am J Resp Crit Care Med. 2016;193(1):68-77.

3. Gonzalez AV, Silvestri GA, Korevaar DA, et al. Assessment of advanced diagnostic bronchoscopy outcomes for peripheral lung lesions: a Delphi consensus definition of diagnostic yield and recommendations for patient-centered study designs. An official American Thoracic Society/American College of Chest Physicians research statement. Am J Respir Crit Care Med. 2024;209(6):634-646.

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Interventional Procedures Section

More than 1.5 million Americans are diagnosed with an incidental CT scan-detected lung nodule annually. Advanced bronchoscopy, as a diagnostic tool for evaluation of these nodules, has evolved rapidly, incorporating a range of techniques and tools beyond CT scan-guided biopsies to assess peripheral lesions. The primary goal is to provide patients with accurate benign or malignant diagnoses. However, accurately determining the effectiveness of innovative technologies in providing a diagnosis remains challenging, in part due to limitations in study design and outcome reporting, along with the scarcity of comparative and randomized controlled studies.^1,2 Current literature shows significant variability in diagnostic yield definition, lacking generalizability.

CHEST

To address this issue, an official research statement by the American Thoracic Society and CHEST defines the diagnostic yield as “the proportion of all individuals undergoing the diagnostic procedure under evaluation in whom a specific malignant or benign diagnosis is established.”³ To achieve this measure, the numerator includes all patients with lung nodules in whom the result of a diagnostic procedure establishes a specific benign or malignant diagnosis that is readily sufficient to inform patient care without additional diagnostic workup, and the denominator should include all patients in whom the procedure was attempted or performed. This standardized definition is crucial for ensuring consistency across studies, allowing for comparison or pooling of results, enhancing the reliability of diagnostic yield data, and informing clinical decisions.

CHEST

References

1. Tanner NT, Yarmus L, Chen A, et al. Standard bronchoscopy with fluoroscopy vs thin bronchoscopy and radial endobronchial ultrasound for biopsy of pulmonary lesions: a multicenter, prospective, randomized trial. Chest. 2018;154(5):1035-1043.

2. Ost DE, Ernst A, Lei X, et al. Diagnostic yield and complications of bronchoscopy for peripheral lung lesions. Results of the AQuIRE Registry. Am J Resp Crit Care Med. 2016;193(1):68-77.

3. Gonzalez AV, Silvestri GA, Korevaar DA, et al. Assessment of advanced diagnostic bronchoscopy outcomes for peripheral lung lesions: a Delphi consensus definition of diagnostic yield and recommendations for patient-centered study designs. An official American Thoracic Society/American College of Chest Physicians research statement. Am J Respir Crit Care Med. 2024;209(6):634-646.

THORACIC ONCOLOGY AND CHEST PROCEDURES NETWORK

Interventional Procedures Section

More than 1.5 million Americans are diagnosed with an incidental CT scan-detected lung nodule annually. Advanced bronchoscopy, as a diagnostic tool for evaluation of these nodules, has evolved rapidly, incorporating a range of techniques and tools beyond CT scan-guided biopsies to assess peripheral lesions. The primary goal is to provide patients with accurate benign or malignant diagnoses. However, accurately determining the effectiveness of innovative technologies in providing a diagnosis remains challenging, in part due to limitations in study design and outcome reporting, along with the scarcity of comparative and randomized controlled studies.^1,2 Current literature shows significant variability in diagnostic yield definition, lacking generalizability.

CHEST

To address this issue, an official research statement by the American Thoracic Society and CHEST defines the diagnostic yield as “the proportion of all individuals undergoing the diagnostic procedure under evaluation in whom a specific malignant or benign diagnosis is established.”³ To achieve this measure, the numerator includes all patients with lung nodules in whom the result of a diagnostic procedure establishes a specific benign or malignant diagnosis that is readily sufficient to inform patient care without additional diagnostic workup, and the denominator should include all patients in whom the procedure was attempted or performed. This standardized definition is crucial for ensuring consistency across studies, allowing for comparison or pooling of results, enhancing the reliability of diagnostic yield data, and informing clinical decisions.

CHEST

References

1. Tanner NT, Yarmus L, Chen A, et al. Standard bronchoscopy with fluoroscopy vs thin bronchoscopy and radial endobronchial ultrasound for biopsy of pulmonary lesions: a multicenter, prospective, randomized trial. Chest. 2018;154(5):1035-1043.

2. Ost DE, Ernst A, Lei X, et al. Diagnostic yield and complications of bronchoscopy for peripheral lung lesions. Results of the AQuIRE Registry. Am J Resp Crit Care Med. 2016;193(1):68-77.

3. Gonzalez AV, Silvestri GA, Korevaar DA, et al. Assessment of advanced diagnostic bronchoscopy outcomes for peripheral lung lesions: a Delphi consensus definition of diagnostic yield and recommendations for patient-centered study designs. An official American Thoracic Society/American College of Chest Physicians research statement. Am J Respir Crit Care Med. 2024;209(6):634-646.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.¹ We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.² Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.³ When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.¹ We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.² Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.³ When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

SLEEP MEDICINE NETWORK

Nonrespiratory Sleep Section

There has been a recent interest in post–intensive care syndrome (PICS), as an increasing number of patients are surviving critical illness. PICS is defined as “new onset or worsening of impairments in physical, cognitive, and/or mental health that arises after an ICU stay and persists beyond hospital discharge.¹ We know that poor sleep is a common occurrence in the ICU, which can contribute to cognitive impairment and could be due to various risk factors, including age, individual comorbidities, reason for admission, and ICU interventions.² Sleep impairment after hospital discharge is highly prevalent for up to 1 year after hospitalization.

CHEST

The most common sleep impairment described after hospital discharge from the ICU is insomnia, which coexists with anxiety, depression, and posttraumatic stress disorder.³ When patients are seen in a post-ICU clinic, a multimodal strategy is needed for the treatment of insomnia, which includes practicing good sleep hygiene, cognitive behavioral therapy for insomnia (CBT-I), and pharmacotherapy if indicated.

CHEST

References

1. Rawal G, Yadav S, Kumar R. Post-intensive care syndrome: an overview. J Transl Int Med. 2017;5(2):90-92.

2. Zampieri FG, et al. Ann Am Thorac Soc. 2023;20(11):1558-1560.

3. Altman MT, Knauert MP, Pisani MA. Sleep disturbance after hospitalization and critical illness: a systematic review. Ann Am Thorac Soc. 2017;14(9):1457-1468.

4. Edinger JD, Arnedt JT, Bertisch SM, et al. Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2021;17(2):255-262.

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Interstitial Lung Disease Section

Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.

CHEST

Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).

CHEST

References

1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Interstitial Lung Disease Section

Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.

CHEST

Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).

CHEST

References

1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.

DIFFUSE LUNG DISEASE AND LUNG TRANSPLANT NETWORK

Interstitial Lung Disease Section

Interstitial lung diseases (ILDs) are a diverse group of relentlessly progressive fibroinflammatory disorders. Pharmacotherapy includes antifibrotics and immunosuppressants as foundational strategies to mitigate loss of lung function. There has been a growing interest in telomere length and its response to immunosuppression in the ILD community.

CHEST

Telomeres are repetitive nucleotide sequences that “cap” chromosomes and protect against chromosomal shortening during cell replication. Genetic and environmental factors can lead to premature shortening of telomeres. Once a critical length is reached, the cell enters senescence. Short telomere length has been linked to rapid progression, worse outcomes, and poor response to immunosuppressants in idiopathic pulmonary fibrosis (IPF).

CHEST

References

1. Zhang D, Adegunsoye A, Oldham JM, et al. Telomere length and immunosuppression in non-idiopathic pulmonary fibrosis interstitial lung disease. Eur Respir J. 2023;62(5):2300441.