Specialty Sections From CHEST® Physician

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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.

Eggleston_Reid_web.jpg

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.

Eggleston_Reid_web.jpg

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.

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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.

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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.

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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.

DiRienzo_Vincent_web.jpg

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.

Kapoor_Aanchal_web.jpg

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.

DiRienzo_Vincent_web.jpg

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.

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.

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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.

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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.

Shah_Sadia_Z_web.jpg

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.

Sandborn_David_web.jpg

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.

Shah_Sadia_Z_web.jpg

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.

Sandborn_David_web.jpg

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.

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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.

Losier_Ashley_web.jpg

Threadgill_Ryan_S_web.jpg

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.

Losier_Ashley_web.jpg

Threadgill_Ryan_S_web.jpg

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.

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.

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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.

Warner_Mark_2024_web.jpg

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.

Akkanti_Bindu_TEXAS_web.jpg

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.

Warner_Mark_2024_web.jpg

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.

Akkanti_Bindu_TEXAS_web.jpg

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.

Warner_Mark_2024_web.jpg

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.

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Evidence-based medicine (EBM) stems from making the best patient-centered decision from the highest-quality data available that comports with our understanding of pathophysiology. In some situations, clinicians are forced to draw conclusions from data that are imperfect and apply it to patients who are complex and dynamic. For most pathologies, available data provides some direction. There is, however, one pathophysiologic state that remains understudied, precarious, and common.

The Centers for Disease Control and Prevention (CDC) estimates that about 7.7% of the United States population has asthma. There were about 1 million ED visits in 2020, with asthma listed as the primary diagnosis, and only 94,000 required hospitalization.¹ There are many tools we employ that have greatly decreased inpatient admissions for asthma. The uptake of inhaled corticosteroids (ICS) has significantly reduced asthma-related morbidity and mortality and reduced exacerbations that require admission to a hospital. This treatment strategy is supported by the Global Initiative for Asthma (GINA) and National Asthma Education and Prevention Program (NAEPP) guidelines.^2,3 While we should celebrate the impact that EBM and ICS have had on asthma outcomes, we continue to struggle to control severe asthma.

Bronchodilator therapy in the hospital is ubiquitous. House staff and hospitalists click the bronchodilator order set early and often. However, the optimal frequency, dose, and duration of inhaled bronchodilator therapy for acute asthma exacerbation are unknown. Do frequency, dose, and duration change with exacerbation severity? Nothing gets ED, inpatient, or ICU physicians more jittery than the phrase “exacerbation of asthma on BiPap” or “intubated for asthma.” With its enormous clinical impact and notoriously difficult hospital and ICU course, the lack of evidence we have for managing these patients outside of the initial 24- to 48-hour visit is concerning. Neither NAEPP nor GINA provide management recommendations for the patient with severe asthma exacerbation that necessitates admission.

Albuterol is a commonly used medication for asthma and chronic obstructive airway disease. It is rapid acting and effective—few medications give patients (or clinicians) such instant satisfaction. As an internal medicine resident and pulmonary fellow, I ordered it countless times without ever looking at the dose. Sometimes, patients would come up from the emergency department after receiving a “continuous dose.” I would often wonder exactly what that meant. After some investigation, I found that in my hospital at the time, one dose of albuterol was 2.5 mg in 2 mL, and a continuous nebulization was four doses for a total of 10 mg.

Shrestha et al. found that high-dose albuterol (7.5 mg) administered continuously was superior to 2.5 mg albuterol delivered three times over 1.5 hours. There were demonstrable improvements in FEV₁ and no ICU admissions.⁴ This study is one of many that compared intermittent to continuous and high-dose vs low-dose albuterol in the emergency department. Most are small and occur over the first 24 hours of presentation to the hospital. They often use short-term changes in spirometry as their primary outcome measure. Being a pulmonary and critical care doctor, I see patients who require advanced rescue maneuvers such as noninvasive positive pressure ventilation (NIPPV) or other pharmacologic adjuncts, for which the current evidence is limited.

Because studies of inhaled bronchodilators in acute asthma exacerbation use spirometry as their primary outcome, those with more severe disease and higher acuity are excluded. Patients on NIPPV can’t perform spirometry. There is essentially no literature to guide treatment for a patient with asthma in the adult ICU. In pediatric intensive care units, there are some data to support either continuous or intermittent inhaled bronchodilator that extends beyond the initial ED visit up to about 60 hours.⁵ Much of the pediatric data revolve about the amount of albuterol given, which can be as high as 75 mg/hr though is typically closer to 10-20 mg/hr.⁶ This rate is continued until respiratory improvement occurs.

With poor evidence to guide us and no specific direction from major guidelines, how should providers manage severe asthma exacerbation? The amount of drug deposited in the lung varies by the device used to deliver it. For nebulization, only about 10% of the nebulized amount reaches the lungs for effect; this is a smaller amount compared with all other devices one could use, such as MDI or DPI.⁷ Once a patient with asthma reaches the emergency department, that person is usually placed on some form of nebulizer treatment. But based on local hospital protocols, the amount and duration can vary widely. Sometimes, in patients with severe exacerbation, there is trepidation to continuing albuterol therapy due to ongoing tachycardia. This seems reasonable given increased albuterol administration could beget an ongoing cycle of dyspnea and anxiety. It could also lead to choosing therapies that are less evidence based.

In closing, this seemingly mundane topic takes on new meaning when a patient is in severe exacerbation. Fortunately, providers are not often faced with the decision to wade into the evidence-free territory of severe asthma exacerbation that is unresponsive to first-line treatments. This narrative should serve as a general alert that this pathophysiologic state is understudied. When encountered, thoughtful consideration of pathology, physiology, and pharmacology is required to reverse it.

References

1. Centers for Disease Control and Prevention. (2023, May 10). Most recent national asthma data. Centers for Disease Control and Prevention. https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm

2. Global Initiative for Asthma - GINA. (2023, August 15). 2023 GINA Main Report - Global Initiative for Asthma - GINA. https://ginasthma.org/2023-gina-main-report/

3. Kiley J, Mensah GA, Boyce CA, et al (A Report from the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group). 2020 Focused updates to the: Asthma Management Guidelines. US Department of Health and Human Services, NIH, NHLBI 2020.

4. Shrestha M, Bidadi K, Gourlay S, Hayes J. Continuous vs intermittent albuterol, at high and low doses, in the treatment of severe acute asthma in adults. Chest. 1996 Jul;110(1):42-7. doi: 10.1378/chest.110.1.42. PMID: 8681661.

5. Kulalert P, Phinyo P, Patumanond J, Smathakanee C, Chuenjit W, Nanthapisal S. Continuous versus intermittent short-acting β2-agonists nebulization as first-line therapy in hospitalized children with severe asthma exacerbation: a propensity score matching analysis. Asthma Res Pract. 2020 Jul 2;6:6. doi: 10.1186/s40733-020-00059-5. PMID: 32632352; PMCID: PMC7329360.

6. Phumeetham S, Bahk TJ, Abd-Allah S, Mathur M. Effect of high-dose continuous albuterol nebulization on clinical variables in children with status asthmaticus. Pediatr Crit Care Med. 2015 Feb;16(2):e41-6. doi: 10.1097/PCC.0000000000000314. PMID: 25560428.

7. Gardenhire DS, Burnett D, Strickland S, Myers, TR. A guide to aerosol delivery devices for respiratory therapists. American Association for Respiratory Care, Dallas, Texas 2017.

Ghionni_Nicholas_E_BALT_web.jpg

Evidence-based medicine (EBM) stems from making the best patient-centered decision from the highest-quality data available that comports with our understanding of pathophysiology. In some situations, clinicians are forced to draw conclusions from data that are imperfect and apply it to patients who are complex and dynamic. For most pathologies, available data provides some direction. There is, however, one pathophysiologic state that remains understudied, precarious, and common.

The Centers for Disease Control and Prevention (CDC) estimates that about 7.7% of the United States population has asthma. There were about 1 million ED visits in 2020, with asthma listed as the primary diagnosis, and only 94,000 required hospitalization.¹ There are many tools we employ that have greatly decreased inpatient admissions for asthma. The uptake of inhaled corticosteroids (ICS) has significantly reduced asthma-related morbidity and mortality and reduced exacerbations that require admission to a hospital. This treatment strategy is supported by the Global Initiative for Asthma (GINA) and National Asthma Education and Prevention Program (NAEPP) guidelines.^2,3 While we should celebrate the impact that EBM and ICS have had on asthma outcomes, we continue to struggle to control severe asthma.

Bronchodilator therapy in the hospital is ubiquitous. House staff and hospitalists click the bronchodilator order set early and often. However, the optimal frequency, dose, and duration of inhaled bronchodilator therapy for acute asthma exacerbation are unknown. Do frequency, dose, and duration change with exacerbation severity? Nothing gets ED, inpatient, or ICU physicians more jittery than the phrase “exacerbation of asthma on BiPap” or “intubated for asthma.” With its enormous clinical impact and notoriously difficult hospital and ICU course, the lack of evidence we have for managing these patients outside of the initial 24- to 48-hour visit is concerning. Neither NAEPP nor GINA provide management recommendations for the patient with severe asthma exacerbation that necessitates admission.

Albuterol is a commonly used medication for asthma and chronic obstructive airway disease. It is rapid acting and effective—few medications give patients (or clinicians) such instant satisfaction. As an internal medicine resident and pulmonary fellow, I ordered it countless times without ever looking at the dose. Sometimes, patients would come up from the emergency department after receiving a “continuous dose.” I would often wonder exactly what that meant. After some investigation, I found that in my hospital at the time, one dose of albuterol was 2.5 mg in 2 mL, and a continuous nebulization was four doses for a total of 10 mg.

Shrestha et al. found that high-dose albuterol (7.5 mg) administered continuously was superior to 2.5 mg albuterol delivered three times over 1.5 hours. There were demonstrable improvements in FEV₁ and no ICU admissions.⁴ This study is one of many that compared intermittent to continuous and high-dose vs low-dose albuterol in the emergency department. Most are small and occur over the first 24 hours of presentation to the hospital. They often use short-term changes in spirometry as their primary outcome measure. Being a pulmonary and critical care doctor, I see patients who require advanced rescue maneuvers such as noninvasive positive pressure ventilation (NIPPV) or other pharmacologic adjuncts, for which the current evidence is limited.

Because studies of inhaled bronchodilators in acute asthma exacerbation use spirometry as their primary outcome, those with more severe disease and higher acuity are excluded. Patients on NIPPV can’t perform spirometry. There is essentially no literature to guide treatment for a patient with asthma in the adult ICU. In pediatric intensive care units, there are some data to support either continuous or intermittent inhaled bronchodilator that extends beyond the initial ED visit up to about 60 hours.⁵ Much of the pediatric data revolve about the amount of albuterol given, which can be as high as 75 mg/hr though is typically closer to 10-20 mg/hr.⁶ This rate is continued until respiratory improvement occurs.

With poor evidence to guide us and no specific direction from major guidelines, how should providers manage severe asthma exacerbation? The amount of drug deposited in the lung varies by the device used to deliver it. For nebulization, only about 10% of the nebulized amount reaches the lungs for effect; this is a smaller amount compared with all other devices one could use, such as MDI or DPI.⁷ Once a patient with asthma reaches the emergency department, that person is usually placed on some form of nebulizer treatment. But based on local hospital protocols, the amount and duration can vary widely. Sometimes, in patients with severe exacerbation, there is trepidation to continuing albuterol therapy due to ongoing tachycardia. This seems reasonable given increased albuterol administration could beget an ongoing cycle of dyspnea and anxiety. It could also lead to choosing therapies that are less evidence based.

In closing, this seemingly mundane topic takes on new meaning when a patient is in severe exacerbation. Fortunately, providers are not often faced with the decision to wade into the evidence-free territory of severe asthma exacerbation that is unresponsive to first-line treatments. This narrative should serve as a general alert that this pathophysiologic state is understudied. When encountered, thoughtful consideration of pathology, physiology, and pharmacology is required to reverse it.

References

1. Centers for Disease Control and Prevention. (2023, May 10). Most recent national asthma data. Centers for Disease Control and Prevention. https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm

2. Global Initiative for Asthma - GINA. (2023, August 15). 2023 GINA Main Report - Global Initiative for Asthma - GINA. https://ginasthma.org/2023-gina-main-report/

3. Kiley J, Mensah GA, Boyce CA, et al (A Report from the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group). 2020 Focused updates to the: Asthma Management Guidelines. US Department of Health and Human Services, NIH, NHLBI 2020.

4. Shrestha M, Bidadi K, Gourlay S, Hayes J. Continuous vs intermittent albuterol, at high and low doses, in the treatment of severe acute asthma in adults. Chest. 1996 Jul;110(1):42-7. doi: 10.1378/chest.110.1.42. PMID: 8681661.

5. Kulalert P, Phinyo P, Patumanond J, Smathakanee C, Chuenjit W, Nanthapisal S. Continuous versus intermittent short-acting β2-agonists nebulization as first-line therapy in hospitalized children with severe asthma exacerbation: a propensity score matching analysis. Asthma Res Pract. 2020 Jul 2;6:6. doi: 10.1186/s40733-020-00059-5. PMID: 32632352; PMCID: PMC7329360.

6. Phumeetham S, Bahk TJ, Abd-Allah S, Mathur M. Effect of high-dose continuous albuterol nebulization on clinical variables in children with status asthmaticus. Pediatr Crit Care Med. 2015 Feb;16(2):e41-6. doi: 10.1097/PCC.0000000000000314. PMID: 25560428.

7. Gardenhire DS, Burnett D, Strickland S, Myers, TR. A guide to aerosol delivery devices for respiratory therapists. American Association for Respiratory Care, Dallas, Texas 2017.

Ghionni_Nicholas_E_BALT_web.jpg

Evidence-based medicine (EBM) stems from making the best patient-centered decision from the highest-quality data available that comports with our understanding of pathophysiology. In some situations, clinicians are forced to draw conclusions from data that are imperfect and apply it to patients who are complex and dynamic. For most pathologies, available data provides some direction. There is, however, one pathophysiologic state that remains understudied, precarious, and common.

The Centers for Disease Control and Prevention (CDC) estimates that about 7.7% of the United States population has asthma. There were about 1 million ED visits in 2020, with asthma listed as the primary diagnosis, and only 94,000 required hospitalization.¹ There are many tools we employ that have greatly decreased inpatient admissions for asthma. The uptake of inhaled corticosteroids (ICS) has significantly reduced asthma-related morbidity and mortality and reduced exacerbations that require admission to a hospital. This treatment strategy is supported by the Global Initiative for Asthma (GINA) and National Asthma Education and Prevention Program (NAEPP) guidelines.^2,3 While we should celebrate the impact that EBM and ICS have had on asthma outcomes, we continue to struggle to control severe asthma.

Bronchodilator therapy in the hospital is ubiquitous. House staff and hospitalists click the bronchodilator order set early and often. However, the optimal frequency, dose, and duration of inhaled bronchodilator therapy for acute asthma exacerbation are unknown. Do frequency, dose, and duration change with exacerbation severity? Nothing gets ED, inpatient, or ICU physicians more jittery than the phrase “exacerbation of asthma on BiPap” or “intubated for asthma.” With its enormous clinical impact and notoriously difficult hospital and ICU course, the lack of evidence we have for managing these patients outside of the initial 24- to 48-hour visit is concerning. Neither NAEPP nor GINA provide management recommendations for the patient with severe asthma exacerbation that necessitates admission.

Albuterol is a commonly used medication for asthma and chronic obstructive airway disease. It is rapid acting and effective—few medications give patients (or clinicians) such instant satisfaction. As an internal medicine resident and pulmonary fellow, I ordered it countless times without ever looking at the dose. Sometimes, patients would come up from the emergency department after receiving a “continuous dose.” I would often wonder exactly what that meant. After some investigation, I found that in my hospital at the time, one dose of albuterol was 2.5 mg in 2 mL, and a continuous nebulization was four doses for a total of 10 mg.

Shrestha et al. found that high-dose albuterol (7.5 mg) administered continuously was superior to 2.5 mg albuterol delivered three times over 1.5 hours. There were demonstrable improvements in FEV₁ and no ICU admissions.⁴ This study is one of many that compared intermittent to continuous and high-dose vs low-dose albuterol in the emergency department. Most are small and occur over the first 24 hours of presentation to the hospital. They often use short-term changes in spirometry as their primary outcome measure. Being a pulmonary and critical care doctor, I see patients who require advanced rescue maneuvers such as noninvasive positive pressure ventilation (NIPPV) or other pharmacologic adjuncts, for which the current evidence is limited.

Because studies of inhaled bronchodilators in acute asthma exacerbation use spirometry as their primary outcome, those with more severe disease and higher acuity are excluded. Patients on NIPPV can’t perform spirometry. There is essentially no literature to guide treatment for a patient with asthma in the adult ICU. In pediatric intensive care units, there are some data to support either continuous or intermittent inhaled bronchodilator that extends beyond the initial ED visit up to about 60 hours.⁵ Much of the pediatric data revolve about the amount of albuterol given, which can be as high as 75 mg/hr though is typically closer to 10-20 mg/hr.⁶ This rate is continued until respiratory improvement occurs.

With poor evidence to guide us and no specific direction from major guidelines, how should providers manage severe asthma exacerbation? The amount of drug deposited in the lung varies by the device used to deliver it. For nebulization, only about 10% of the nebulized amount reaches the lungs for effect; this is a smaller amount compared with all other devices one could use, such as MDI or DPI.⁷ Once a patient with asthma reaches the emergency department, that person is usually placed on some form of nebulizer treatment. But based on local hospital protocols, the amount and duration can vary widely. Sometimes, in patients with severe exacerbation, there is trepidation to continuing albuterol therapy due to ongoing tachycardia. This seems reasonable given increased albuterol administration could beget an ongoing cycle of dyspnea and anxiety. It could also lead to choosing therapies that are less evidence based.

In closing, this seemingly mundane topic takes on new meaning when a patient is in severe exacerbation. Fortunately, providers are not often faced with the decision to wade into the evidence-free territory of severe asthma exacerbation that is unresponsive to first-line treatments. This narrative should serve as a general alert that this pathophysiologic state is understudied. When encountered, thoughtful consideration of pathology, physiology, and pharmacology is required to reverse it.

References

1. Centers for Disease Control and Prevention. (2023, May 10). Most recent national asthma data. Centers for Disease Control and Prevention. https://www.cdc.gov/asthma/most_recent_national_asthma_data.htm

2. Global Initiative for Asthma - GINA. (2023, August 15). 2023 GINA Main Report - Global Initiative for Asthma - GINA. https://ginasthma.org/2023-gina-main-report/

3. Kiley J, Mensah GA, Boyce CA, et al (A Report from the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group). 2020 Focused updates to the: Asthma Management Guidelines. US Department of Health and Human Services, NIH, NHLBI 2020.

4. Shrestha M, Bidadi K, Gourlay S, Hayes J. Continuous vs intermittent albuterol, at high and low doses, in the treatment of severe acute asthma in adults. Chest. 1996 Jul;110(1):42-7. doi: 10.1378/chest.110.1.42. PMID: 8681661.

5. Kulalert P, Phinyo P, Patumanond J, Smathakanee C, Chuenjit W, Nanthapisal S. Continuous versus intermittent short-acting β2-agonists nebulization as first-line therapy in hospitalized children with severe asthma exacerbation: a propensity score matching analysis. Asthma Res Pract. 2020 Jul 2;6:6. doi: 10.1186/s40733-020-00059-5. PMID: 32632352; PMCID: PMC7329360.

6. Phumeetham S, Bahk TJ, Abd-Allah S, Mathur M. Effect of high-dose continuous albuterol nebulization on clinical variables in children with status asthmaticus. Pediatr Crit Care Med. 2015 Feb;16(2):e41-6. doi: 10.1097/PCC.0000000000000314. PMID: 25560428.

7. Gardenhire DS, Burnett D, Strickland S, Myers, TR. A guide to aerosol delivery devices for respiratory therapists. American Association for Respiratory Care, Dallas, Texas 2017.

Thoracic Oncology And Chest Procedures Network

Lung Cancer Section

Ogake_Stella_web.jpg

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

Ogake_Stella_web.jpg

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

Ogake_Stella_web.jpg

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.

Sleep Medicine Network

Nonrespiratory Sleep Section

Arora_Vineet_web.jpg

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

Arora_Vineet_web.jpg

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

Arora_Vineet_web.jpg

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.

Critical Care Network

Palliative and End-of-Life Care Section

Birdwell_Angela_web.jpg

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

Birdwell_Angela_web.jpg

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

Birdwell_Angela_web.jpg

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.

 

Chest Infections and Disaster Response Network

Disaster Response and Global Health Section    

 

Kattih_Zein_web.jpg

Kathryn_Hughes_web.jpg

Brian_Tran_web.jpg

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    

 

Kattih_Zein_web.jpg

Kathryn_Hughes_web.jpg

Brian_Tran_web.jpg

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    

 

Kattih_Zein_web.jpg

Kathryn_Hughes_web.jpg

Brian_Tran_web.jpg

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.