Ventilator-associated pneumonia (VAP) is a common cause of hospital-related morbidity in critically ill patients. The efficacy of prophylactic antibiotics in the prevention of VAP has been the subject of several studies in recent years. Three large randomized controlled trials, all published since late 2022, have investigated whether antibiotics can prevent VAP and the optimal method of antibiotic administration.
In the AMIKINHAL trial, patients intubated for at least 72 hours in 19 ICUs in France received inhaled amikacin at a dose of 20 mg/kg/day for 3 days.1 Compared with placebo, there was a statistically significant, 7% absolute risk reduction in rate of VAP at 28 days.
In the SUDDICU trial, patients suspected to be intubated for at least 48 hours in 19 ICUs in Australia received a combination of oral paste and gastric suspension containing colistin, tobramycin, and nystatin every 6 hours along with 4 days of intravenous antibiotics.2 There was no difference in the primary outcome of 90-day all-cause mortality; however, there was a statistically significant, 12% reduction in the isolation of antibiotic-resistant organisms in cultures.
In the PROPHY-VAP trial, patients with acute brain injury (Glasgow Coma Scale score [GCS ] ≤12) intubated for at least 48 hours in 9 ICUs in France received a single dose of intravenous ceftriaxone (2 g) within 12 hours of intubation.3 There was an 18% absolute risk reduction in VAP from days 2 to 7 post-ventilation.
These trials, involving distinct patient populations and interventions, indicate that antibiotic prophylaxis may reduce VAP risk under specific circumstances, but its effect on overall outcomes is still uncertain. The understanding of prophylactic antibiotics in VAP prevention is rapidly evolving.
References
1. Ehrmann S, et al. N Engl J Med. 2023;389(22):2052-2062.
2. Myburgh JA, et al. JAMA. 2022;328(19):1911-1921.
3. Dahyot-Fizelier C, et al. Lancet Respir Med. 2024;S2213-2600(23):00471-X.
Ventilator-associated pneumonia (VAP) is a common cause of hospital-related morbidity in critically ill patients. The efficacy of prophylactic antibiotics in the prevention of VAP has been the subject of several studies in recent years. Three large randomized controlled trials, all published since late 2022, have investigated whether antibiotics can prevent VAP and the optimal method of antibiotic administration.
In the AMIKINHAL trial, patients intubated for at least 72 hours in 19 ICUs in France received inhaled amikacin at a dose of 20 mg/kg/day for 3 days.1 Compared with placebo, there was a statistically significant, 7% absolute risk reduction in rate of VAP at 28 days.
In the SUDDICU trial, patients suspected to be intubated for at least 48 hours in 19 ICUs in Australia received a combination of oral paste and gastric suspension containing colistin, tobramycin, and nystatin every 6 hours along with 4 days of intravenous antibiotics.2 There was no difference in the primary outcome of 90-day all-cause mortality; however, there was a statistically significant, 12% reduction in the isolation of antibiotic-resistant organisms in cultures.
In the PROPHY-VAP trial, patients with acute brain injury (Glasgow Coma Scale score [GCS ] ≤12) intubated for at least 48 hours in 9 ICUs in France received a single dose of intravenous ceftriaxone (2 g) within 12 hours of intubation.3 There was an 18% absolute risk reduction in VAP from days 2 to 7 post-ventilation.
These trials, involving distinct patient populations and interventions, indicate that antibiotic prophylaxis may reduce VAP risk under specific circumstances, but its effect on overall outcomes is still uncertain. The understanding of prophylactic antibiotics in VAP prevention is rapidly evolving.
References
1. Ehrmann S, et al. N Engl J Med. 2023;389(22):2052-2062.
2. Myburgh JA, et al. JAMA. 2022;328(19):1911-1921.
3. Dahyot-Fizelier C, et al. Lancet Respir Med. 2024;S2213-2600(23):00471-X.
CHEST
Dr. Reid Eggleston
Chest Infections and Disaster Response Network
Chest Infections Section
Ventilator-associated pneumonia (VAP) is a common cause of hospital-related morbidity in critically ill patients. The efficacy of prophylactic antibiotics in the prevention of VAP has been the subject of several studies in recent years. Three large randomized controlled trials, all published since late 2022, have investigated whether antibiotics can prevent VAP and the optimal method of antibiotic administration.
In the AMIKINHAL trial, patients intubated for at least 72 hours in 19 ICUs in France received inhaled amikacin at a dose of 20 mg/kg/day for 3 days.1 Compared with placebo, there was a statistically significant, 7% absolute risk reduction in rate of VAP at 28 days.
In the SUDDICU trial, patients suspected to be intubated for at least 48 hours in 19 ICUs in Australia received a combination of oral paste and gastric suspension containing colistin, tobramycin, and nystatin every 6 hours along with 4 days of intravenous antibiotics.2 There was no difference in the primary outcome of 90-day all-cause mortality; however, there was a statistically significant, 12% reduction in the isolation of antibiotic-resistant organisms in cultures.
In the PROPHY-VAP trial, patients with acute brain injury (Glasgow Coma Scale score [GCS ] ≤12) intubated for at least 48 hours in 9 ICUs in France received a single dose of intravenous ceftriaxone (2 g) within 12 hours of intubation.3 There was an 18% absolute risk reduction in VAP from days 2 to 7 post-ventilation.
These trials, involving distinct patient populations and interventions, indicate that antibiotic prophylaxis may reduce VAP risk under specific circumstances, but its effect on overall outcomes is still uncertain. The understanding of prophylactic antibiotics in VAP prevention is rapidly evolving.
References
1. Ehrmann S, et al. N Engl J Med. 2023;389(22):2052-2062.
2. Myburgh JA, et al. JAMA. 2022;328(19):1911-1921.
3. Dahyot-Fizelier C, et al. Lancet Respir Med. 2024;S2213-2600(23):00471-X.
In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.
CHEST
Vincent DiRienzo
Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.
In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.
CHEST
Vincent DiRienzo
Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.
CHEST
Dr. Aanchal Kapoor
Critical Care Network
Nonrespiratory Critical Care Section
In patients with decompensated cirrhosis, there are multiple intrahepatic and extrahepatic factors contributing to hemodynamic alterations at baseline, including endothelial cell dysfunction, hepatic stellate cell activation promoting increase in vasoconstrictors, decrease in vasodilators, and angiogenesis leading to worsening of portal hypertension. Increased resistance to hepatic blood flow leads to increased production of nitric oxide and other vasodilators leading to splanchnic vasodilation, decreased effective blood volume, activation of the renin angiotensin system, sodium, and water retention. In addition to portal hypertension and splanchnic vasodilation, there is a decrease in systemic vascular resistance and hyperdynamic circulation with increased cardiac output. As cirrhosis progresses to the decompensated stage, patients may develop cirrhotic cardiomyopathy, characterized by impaired cardiac response to stress, manifesting as systolic and diastolic dysfunction, and electrophysiological abnormalities such as QT prolongation leading to hypotension and dysregulated response to fluid resuscitation.
CHEST
Vincent DiRienzo
Early recognition of septic shock in these patients can be challenging when using traditional criteria due to their baseline hypotension, tachycardia, systemic vasodilation, and propensity for volume overload with fluid resuscitation. Elevated lactate levels in acutely ill patients are an independent risk factor for mortality in patients with cirrhosis. However, lactate levels >2mmol/L need not necessarily define sepsis in these patients, as these patients have decreased lactate clearance. Understanding the intricate interplay between the cardiac pump, vascular tone, and afterload is essential in managing shock in these individuals. Aggressive volume resuscitation may not be well tolerated, emphasizing the need for frequent hemodynamic assessments and prompt initiation of vasopressors when indicated.
Chronic lung allograft dysfunction (CLAD) remains the leading cause of morbidity and mortality in lung transplant recipients (LTRs), accounting for around 40% of deaths.1 LTRs are typically maintained on a three-drug immunosuppressive regimen—a calcineurin inhibitor, antimetabolite agent, and corticosteroid—in order to prevent rejection. Strong randomized controlled trial-generated evidence guiding the choice of immunosuppressive therapy for LTRs is generally lacking.
CHEST
Dr. Sadia Z. Shah
A recent large, multicentered, randomized controlled trial in Scandinavia compared outcomes between once daily extended-release tacrolimus and twice daily cyclosporin.2 The target trough for cyclosporin was 250 to 300 ng/mL (0 to 3 months), 200 to 250 ng/mL (3 to 6 months), 150 to 200 ng/mL (6 to 12 months), and 100 to 150 ng/mL beyond 12 months. The trough target for tacrolimus was 10 to 14 ng/mL (0 to 3 months), 8 to 12 ng/mL (3 to 6 months), 8 to 10 ng/mL (6 to 12 months), and 6 to 8 ng/mL beyond 12 months.
CHEST
Dr. David Sandborn
The study demonstrated that immunosuppressive regimens containing tacrolimus significantly reduced incidence of CLAD diagnosis at 36 months. The cumulative incidence of CLAD was 39% in the cyclosporin group vs 13% in the tacrolimus group (P < .0001), and the number needed to treat was 3.9 patients to prevent one case of CLAD with tacrolimus. While mortality was not significantly different between the two treatment groups in the intention to treat models, tacrolimus had a mortality benefit in the per protocol analysis.
While there is no consensus guideline recommending a first-line immunosuppression regimen following lung transplantation, the lung transplant steering committee believes that additional trials comparing existing agents are of critical importance to reduce CLAD incidence and improve long-term outcomes in LTRs.
References
1. Verleden GM, et al. J Heart Lung Transplant. 2019;38(5):493-503.
2. Dellgren G, et al. Lancet Respir Med. 2024;12(1):34-44.
Chronic lung allograft dysfunction (CLAD) remains the leading cause of morbidity and mortality in lung transplant recipients (LTRs), accounting for around 40% of deaths.1 LTRs are typically maintained on a three-drug immunosuppressive regimen—a calcineurin inhibitor, antimetabolite agent, and corticosteroid—in order to prevent rejection. Strong randomized controlled trial-generated evidence guiding the choice of immunosuppressive therapy for LTRs is generally lacking.
CHEST
Dr. Sadia Z. Shah
A recent large, multicentered, randomized controlled trial in Scandinavia compared outcomes between once daily extended-release tacrolimus and twice daily cyclosporin.2 The target trough for cyclosporin was 250 to 300 ng/mL (0 to 3 months), 200 to 250 ng/mL (3 to 6 months), 150 to 200 ng/mL (6 to 12 months), and 100 to 150 ng/mL beyond 12 months. The trough target for tacrolimus was 10 to 14 ng/mL (0 to 3 months), 8 to 12 ng/mL (3 to 6 months), 8 to 10 ng/mL (6 to 12 months), and 6 to 8 ng/mL beyond 12 months.
CHEST
Dr. David Sandborn
The study demonstrated that immunosuppressive regimens containing tacrolimus significantly reduced incidence of CLAD diagnosis at 36 months. The cumulative incidence of CLAD was 39% in the cyclosporin group vs 13% in the tacrolimus group (P < .0001), and the number needed to treat was 3.9 patients to prevent one case of CLAD with tacrolimus. While mortality was not significantly different between the two treatment groups in the intention to treat models, tacrolimus had a mortality benefit in the per protocol analysis.
While there is no consensus guideline recommending a first-line immunosuppression regimen following lung transplantation, the lung transplant steering committee believes that additional trials comparing existing agents are of critical importance to reduce CLAD incidence and improve long-term outcomes in LTRs.
References
1. Verleden GM, et al. J Heart Lung Transplant. 2019;38(5):493-503.
2. Dellgren G, et al. Lancet Respir Med. 2024;12(1):34-44.
Diffuse Lung Disease and Lung Transplant Network
Lung Transplant Section
Chronic lung allograft dysfunction (CLAD) remains the leading cause of morbidity and mortality in lung transplant recipients (LTRs), accounting for around 40% of deaths.1 LTRs are typically maintained on a three-drug immunosuppressive regimen—a calcineurin inhibitor, antimetabolite agent, and corticosteroid—in order to prevent rejection. Strong randomized controlled trial-generated evidence guiding the choice of immunosuppressive therapy for LTRs is generally lacking.
CHEST
Dr. Sadia Z. Shah
A recent large, multicentered, randomized controlled trial in Scandinavia compared outcomes between once daily extended-release tacrolimus and twice daily cyclosporin.2 The target trough for cyclosporin was 250 to 300 ng/mL (0 to 3 months), 200 to 250 ng/mL (3 to 6 months), 150 to 200 ng/mL (6 to 12 months), and 100 to 150 ng/mL beyond 12 months. The trough target for tacrolimus was 10 to 14 ng/mL (0 to 3 months), 8 to 12 ng/mL (3 to 6 months), 8 to 10 ng/mL (6 to 12 months), and 6 to 8 ng/mL beyond 12 months.
CHEST
Dr. David Sandborn
The study demonstrated that immunosuppressive regimens containing tacrolimus significantly reduced incidence of CLAD diagnosis at 36 months. The cumulative incidence of CLAD was 39% in the cyclosporin group vs 13% in the tacrolimus group (P < .0001), and the number needed to treat was 3.9 patients to prevent one case of CLAD with tacrolimus. While mortality was not significantly different between the two treatment groups in the intention to treat models, tacrolimus had a mortality benefit in the per protocol analysis.
While there is no consensus guideline recommending a first-line immunosuppression regimen following lung transplantation, the lung transplant steering committee believes that additional trials comparing existing agents are of critical importance to reduce CLAD incidence and improve long-term outcomes in LTRs.
References
1. Verleden GM, et al. J Heart Lung Transplant. 2019;38(5):493-503.
2. Dellgren G, et al. Lancet Respir Med. 2024;12(1):34-44.
Bronchiectasis patients have dilated airways that are often colonized with bacteria, resulting in a vicious cycle of airway inflammation and progressive dilation. Pseudomonas aeruginosa is a frequent airway colonizer and is associated with increased morbidity and mortality in cystic fibrosis (CF) and noncystic fibrosis bronchiectasis (NCFB).1
Both CF and NCFB guidelines recommend eradication of P. aeruginosa upon detection.2 In CF, the guidelines suggest use of inhaled tobramycin, without systemic antibiotics.3 Optimal NCFB eradication regimens remain unknown, though recent studies demonstrated inhaled tobramycin is safe and effective for chronic P. aeruginosa infections in NCFB.4
The 2024 meta-analysis by Conceiçã et al. revealed that P. aeruginosa eradication endures more than 12 months in only 40% of NCFB cases, but that patients who received combined therapy—both systemic and inhaled therapies—had a higher eradication rate at 48% compared with 27% in those receiving only systemic antibiotics.5 They found that successful eradication reduced exacerbation rate by 0.91 exacerbations per year without changing hospitalization rate. They were unable to comment on optimal antibiotic selection or duration.
A take-home point from Conceiçã et al. suggests trying to eradicate P. aeruginosa with combined systemic and inhaled antibiotics if possible, but other clinical questions remain around initial antibiotic selection and how to treat persistent P. aeruginosa.
References
1. Finch, et al. Ann Am Thorac Soc. 2015;12(11):1602-1611.
2. Polverino, et al. Eur Respir J. 2017;50:1700629.
3. Mogayzel, et al. Ann ATS. 2014;11(10):1511-1761.
4. Guan, et al. CHEST. 2023;163(1):64-76.
5. Conceiçã, et al. Eur Respir Rev. 2024;33:230178.
Bronchiectasis patients have dilated airways that are often colonized with bacteria, resulting in a vicious cycle of airway inflammation and progressive dilation. Pseudomonas aeruginosa is a frequent airway colonizer and is associated with increased morbidity and mortality in cystic fibrosis (CF) and noncystic fibrosis bronchiectasis (NCFB).1
Both CF and NCFB guidelines recommend eradication of P. aeruginosa upon detection.2 In CF, the guidelines suggest use of inhaled tobramycin, without systemic antibiotics.3 Optimal NCFB eradication regimens remain unknown, though recent studies demonstrated inhaled tobramycin is safe and effective for chronic P. aeruginosa infections in NCFB.4
The 2024 meta-analysis by Conceiçã et al. revealed that P. aeruginosa eradication endures more than 12 months in only 40% of NCFB cases, but that patients who received combined therapy—both systemic and inhaled therapies—had a higher eradication rate at 48% compared with 27% in those receiving only systemic antibiotics.5 They found that successful eradication reduced exacerbation rate by 0.91 exacerbations per year without changing hospitalization rate. They were unable to comment on optimal antibiotic selection or duration.
A take-home point from Conceiçã et al. suggests trying to eradicate P. aeruginosa with combined systemic and inhaled antibiotics if possible, but other clinical questions remain around initial antibiotic selection and how to treat persistent P. aeruginosa.
References
1. Finch, et al. Ann Am Thorac Soc. 2015;12(11):1602-1611.
2. Polverino, et al. Eur Respir J. 2017;50:1700629.
3. Mogayzel, et al. Ann ATS. 2014;11(10):1511-1761.
4. Guan, et al. CHEST. 2023;163(1):64-76.
5. Conceiçã, et al. Eur Respir Rev. 2024;33:230178.
CHEST
Dr. Ashley Losier
CHEST
Dr. Ryan S. Threadgill
Airways Disorders Network
Bronchiectasis Section
Bronchiectasis patients have dilated airways that are often colonized with bacteria, resulting in a vicious cycle of airway inflammation and progressive dilation. Pseudomonas aeruginosa is a frequent airway colonizer and is associated with increased morbidity and mortality in cystic fibrosis (CF) and noncystic fibrosis bronchiectasis (NCFB).1
Both CF and NCFB guidelines recommend eradication of P. aeruginosa upon detection.2 In CF, the guidelines suggest use of inhaled tobramycin, without systemic antibiotics.3 Optimal NCFB eradication regimens remain unknown, though recent studies demonstrated inhaled tobramycin is safe and effective for chronic P. aeruginosa infections in NCFB.4
The 2024 meta-analysis by Conceiçã et al. revealed that P. aeruginosa eradication endures more than 12 months in only 40% of NCFB cases, but that patients who received combined therapy—both systemic and inhaled therapies—had a higher eradication rate at 48% compared with 27% in those receiving only systemic antibiotics.5 They found that successful eradication reduced exacerbation rate by 0.91 exacerbations per year without changing hospitalization rate. They were unable to comment on optimal antibiotic selection or duration.
A take-home point from Conceiçã et al. suggests trying to eradicate P. aeruginosa with combined systemic and inhaled antibiotics if possible, but other clinical questions remain around initial antibiotic selection and how to treat persistent P. aeruginosa.
References
1. Finch, et al. Ann Am Thorac Soc. 2015;12(11):1602-1611.
2. Polverino, et al. Eur Respir J. 2017;50:1700629.
3. Mogayzel, et al. Ann ATS. 2014;11(10):1511-1761.
4. Guan, et al. CHEST. 2023;163(1):64-76.
5. Conceiçã, et al. Eur Respir Rev. 2024;33:230178.
Intensive care physicians around the nation are pivotal in improving shock-related patient outcomes. At present time, there is still a dearth of available dual-boarded cardiology and intensive care physicians around the country, and advanced heart failure fellowship positions continue to be unfilled in the NRMP match. Most intensive care units (academic and nonacademic) are currently managed by intensive care physicians, and a large majority of these physicians are either pulmonary/critical care, emergency medicine critical care, surgery critical care, or medicine/critical care.
CHEST
Dr. Bindu Akkanti
There is lack of systematic training in cardiogenic shock across the board in these specialties as it relates to management of patients supported on extracorporeal membrane oxygenation (ECMO), left ventricular assist devices (LVADs), percutaneous devices, and intermediate devices such as centrimag devices.
CHEST
Dr. Mark Warner
By integrating comprehensive systematic training on cardiogenic shock recognition and management into educational initiatives, fellowship programs that are noncardiology-based can empower health care providers to make informed decisions and expedite life-saving interventions for patients in need of advanced cardiac support. Furthermore, the next generation of intensive care physicians may require ongoing education in the cardiac space, including additional training in point-of-care ultrasound, transesophageal echocardiography (TEE), and advanced hemodynamics, including management of alarms related to percutaneous and durable devices. Through continuous education and training both at conferences and at the simulation center in Glenview, Illinois, CHEST is especially suited to aid intensive care physicians to navigate the evolving landscape of mechanical circulatory support critical care and improve outcomes for patients in need of mechanical circulatory support.
Intensive care physicians around the nation are pivotal in improving shock-related patient outcomes. At present time, there is still a dearth of available dual-boarded cardiology and intensive care physicians around the country, and advanced heart failure fellowship positions continue to be unfilled in the NRMP match. Most intensive care units (academic and nonacademic) are currently managed by intensive care physicians, and a large majority of these physicians are either pulmonary/critical care, emergency medicine critical care, surgery critical care, or medicine/critical care.
CHEST
Dr. Bindu Akkanti
There is lack of systematic training in cardiogenic shock across the board in these specialties as it relates to management of patients supported on extracorporeal membrane oxygenation (ECMO), left ventricular assist devices (LVADs), percutaneous devices, and intermediate devices such as centrimag devices.
CHEST
Dr. Mark Warner
By integrating comprehensive systematic training on cardiogenic shock recognition and management into educational initiatives, fellowship programs that are noncardiology-based can empower health care providers to make informed decisions and expedite life-saving interventions for patients in need of advanced cardiac support. Furthermore, the next generation of intensive care physicians may require ongoing education in the cardiac space, including additional training in point-of-care ultrasound, transesophageal echocardiography (TEE), and advanced hemodynamics, including management of alarms related to percutaneous and durable devices. Through continuous education and training both at conferences and at the simulation center in Glenview, Illinois, CHEST is especially suited to aid intensive care physicians to navigate the evolving landscape of mechanical circulatory support critical care and improve outcomes for patients in need of mechanical circulatory support.
Pulmonary Vascular and Cardiovascular Network
Cardiovascular Medicine and Surgery Section
Intensive care physicians around the nation are pivotal in improving shock-related patient outcomes. At present time, there is still a dearth of available dual-boarded cardiology and intensive care physicians around the country, and advanced heart failure fellowship positions continue to be unfilled in the NRMP match. Most intensive care units (academic and nonacademic) are currently managed by intensive care physicians, and a large majority of these physicians are either pulmonary/critical care, emergency medicine critical care, surgery critical care, or medicine/critical care.
CHEST
Dr. Bindu Akkanti
There is lack of systematic training in cardiogenic shock across the board in these specialties as it relates to management of patients supported on extracorporeal membrane oxygenation (ECMO), left ventricular assist devices (LVADs), percutaneous devices, and intermediate devices such as centrimag devices.
CHEST
Dr. Mark Warner
By integrating comprehensive systematic training on cardiogenic shock recognition and management into educational initiatives, fellowship programs that are noncardiology-based can empower health care providers to make informed decisions and expedite life-saving interventions for patients in need of advanced cardiac support. Furthermore, the next generation of intensive care physicians may require ongoing education in the cardiac space, including additional training in point-of-care ultrasound, transesophageal echocardiography (TEE), and advanced hemodynamics, including management of alarms related to percutaneous and durable devices. Through continuous education and training both at conferences and at the simulation center in Glenview, Illinois, CHEST is especially suited to aid intensive care physicians to navigate the evolving landscape of mechanical circulatory support critical care and improve outcomes for patients in need of mechanical circulatory support.
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, 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. 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.
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, 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. 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.
References
1. Dresler et al. Lung Cancer. 2003.
2. J Cancer Educ. 2018;33[5].
3. Addiction. 2023.
Thoracic Oncology And Chest Procedures Network
Lung Cancer Section
Stella Ogake, MD, FCCP
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, 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. 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.
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.
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.
Sleep Medicine Network
Nonrespiratory Sleep Section
Dr. Vineet Arora
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.
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 2,814 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.
References
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.
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 2,814 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.
References
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.
Critical Care Network
Palliative and End-of-Life Care Section
Angela Birdwell, DO, MA
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 2,814 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.
References
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.
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.
References
1. Troeger C, et al. Lancet Infect Dis. 2018;18[11]:1191-1210.
2. WHO COVID-19 Epidemiological 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, Schultz 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.
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.
References
1. Troeger C, et al. Lancet Infect Dis. 2018;18[11]:1191-1210.
2. WHO COVID-19 Epidemiological 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, Schultz 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.
Chest Infections and Disaster Response Network
Disaster Response and Global Health Section
Zein Kattih, MD
Kathryn Hughes, MD
Brian Tran, MD
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.
References
1. Troeger C, et al. Lancet Infect Dis. 2018;18[11]:1191-1210.
2. WHO COVID-19 Epidemiological 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, Schultz 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.
Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with 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.
Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with 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.
References
1. Scanlon & McKenzie, 2012.
2. Brusselle et al, 2013.
3. Pavord et al, 2017.
4. Bhatt et al, 2023.
Airways Disorders Network
Asthma and COPD Section
Maria Azhar, MD
Abdullah Alismail, PhD, RRT, FCCP
Raghav Gupta, MD, FCCP
Remodeling of airways and destruction of parenchyma by immune and inflammatory mechanisms are the leading cause of lung function decline in patients with 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.
