CHEST NetWorks Submassive PE, antibiotic resistance, advanced practice providers

 

Cardiovascular Medicine and Surgery

Catch 22 of Submassive Pulmonary Emboli

Venous thromboembolism (including deep vein thrombosis (DVT) and pulmonary embolism [PE]) occurs in approximately 1 per 1,000 patients (Piran S, Schulman S. Thromb J. 2016;14[S1]:23) and can be fatal. Pulmonary embolus severity is classified as low risk, intermediate-risk/submassive PE, and massive PE. There is significant controversy about the management of submassive PE, which is defined as PE with right-sided heart strain (elevated troponin or B-type natriuretic peptide, right-axis deviation on ECG, or e

vidence of RV dysfunction on CT or echocardiogram), and the absence of hypotension (systolic blood pressure > 90 mm Hg). In addition to the acute manifestations of VTE, there are potential long-term complications, including postthrombotic syndrome and chronic thromboembolic pulmonary hypertension. Several trials have examined the utility of systemic thrombolysis in submassive PE (MAPPET-3 [Konstantinides, et al. N Engl J Med. 2002;347:1143], PEITHO (Meyer, et al. N Engl J Med. 2014;370:1402; Konstantinides, et al. JACC. 2017;69[12]:1536); MOPETT (Sharifi, et al. Am J Cardiol. 2013;111:273); and TOPCOAT (Kline, et al. J Thromb Haemost. 2014;12:459), but all have failed to establish a mortality benefit. However, thrombolytics demonstrated decreased clinical deterioration and may mitigate the development of postthrombotic syndrome. Yet thrombolysis has been associated with increased bleeding (PEITHO: 11.5% vs 2.4% had major bleeding, and 2% vs 0.2% experienced hemorrhagic stroke). Current CHEST guidelines (Kearon, et al. Chest. 2016;149[2]:3150) recommend against the use of thrombolytics in submassive PE without hypotension. Treatment of intermediate-risk PE remains an enigma for physicians, but it is hoped that with further investigation, optimal management will be elucidated.

David J. Nagel, MD

Steering Committee Member

Olivier Axler, MD, FCCP

Vice-Chair

Chest Infections

Antibiotic Resistance

One-hundred years ago, infectious diseases caused 5 of the 10 most common causes of deaths in the United States. In 2016, only one infection remained on this list (influenza/pneumonia) (MMWR Morb Mortal Wkly Rep. 2017;66:413).

How medicine has improved with antibiotics. An unfortunate and unintended consequence of widespread antibiotic use has been the progressive resistance to these drugs. It is estimated that, if current trends continue, 10 million lives a year will be at risk from resistant organisms by 2050 (O’Neill, J. (2016). https://amr-review.org/sites/default/files/160518_Final%20paper_with%20cover.pdf).

Pathogens acquire antibiotic resistance by passing genetic material to one another through plasmids, bacteriophages, or naked DNA. Once acquired, resistance manifests via a number of mechanisms under the stress imposed by antibiotics (Levy SB, et al. Nat Med. 2004;10:S122).

Among the best studied is enzymatic degradation of the antibiotic. This occurs when beta-lactamases degrade penicillin. A second mechanism alters cell transport, thereby blocking cell entry or actively ejecting the antibiotic from the cell. Finally, overexpression or alteration of the antibiotic target may render a drug ineffective at inhibiting any vital cell function.

At the pace with which resistance now develops, the medical community faces a crisis, whereby infections caused by evolving superbugs are no longer effectively controlled by the available menu of antimicrobial agents.

This challenge must be met collectively by the more prudent prescribing of antibiotics, potentially with the help of rapid diagnostics; isolation of patients potentially infected with resistant organisms; and a focus on developing newer drugs that defy known resistant mechanisms.

Marc Feinstein, MD, FCCP

Steering Committee Member

Clinical Pulmonary Medicine

COPD and sleep-disordered breathing; A missing comorbid condition

Subjective, as well as objective, sleep complaints are common in patients with COPD (Krachman S, et al. Proc Am Thorac Soc. 2008;5[4]:536), and sleeping difficulties are ranked the third most frequent complaint (behind dyspnea and fatigue) in patients with COPD (Kinsman RA, et al. Chest. 1983;83[5]:755). Also, sleep quality is poor, and patients with moderate to severe COPD may have higher-than-expected incidence of OSA (Soler X, et al. Ann Am Thorac Soc. 2015;12[8]:1219).

Unfortunately, sleep is usually not assessed during a COPD evaluation. Up to 27% of patients with COPD without hypoxia during wakefulness can experience important desaturation during sleep, so called nocturnal oxygen desaturation (NOD) (Fletcher EC, et al. Chest. 1987;92[4]:604), that may lead to pulmonary hypertension (Chaouat A, et a

l. Am J Respir Crit Care Med. 1995;151[1]:82). Little is known about the pathophysiologic and clinical consequences of having concomitant COPD and OSA, but recent studies have demonstrated that patients with both disorders have a high risk of hospitalizations (30-day readmission rate for rehospitalization ranges from 20% to 39%), and death from acute exacerbations if OSA remains untreated (Marin JM, et al. Am J Respir Crit Care Med. 2010;182[3]:325; Machado MC, et al. Eur Respir J. 2010;35[1]:132). Another study has found that in patients with OSA, the presence of COPD increases the risk of death seven-fold (Lavie P, et al. J Sleep Res. 2007;16[1]:128).

Although identification and effective treatment of COPD comorbidities are becoming the cornerstone of COPD management, sleep-disordered breathing has not been identified in current guidelines yet as a true potential contributor in poor outcomes despite emergent clinical evidence. Multidisciplinary programs, such as pulmonary rehabilitation, that improve dyspnea, exercise capacity, and quality of life may also positively impact sleep (Soler X, et al. COPD. 2013;10[2]:156). Because of the background of the staff involved, the comprehensive approach to patient assessment, and access to number of COPD subjects, pulmonary rehabilitation may be an optimal opportunity to assess sleep and identify an important comorbid condition often overlooked in patients with more advanced COPD.

 

Xavier Soler, MD, PhD

Steering Committee Member

Interprofessional Team

Finding Home

Outside our internal medicine curriculum, there is no formal pulmonary training or post-masters fellowship in pulmonary medicine for Advanced Practice Providers (APPs). Because of this, APPs are left to their own devices to fill educational gaps. To perform at the level expected by the physicians I work for, journal reviews and memorizing guidelines were not going to be enough. Since there is no formal pulmonary APP society, there were no peers to reach out to either. Off to conferences I went.

At first, I found CHEST daunting. After all, it’s run by the American College of Chest “Physicians,” not Nurse Practitioners. I spent most of the first day with my nametag turned around worried I’d be found out as a nonphysician attendee who snuck in. And then the unthinkable happened, I ran into another unicorn—another APP seeking the same information, only her nametag was turned the right way. The best advice she gave was to attend the Interprofessional NetWork meeting. This was ground zero of the conference as far as I was concerned. There I found myself surrounded by RTs, RNs, NPs, PAs, and yes, even physicians.

Over the years, as I’ve gotten further involved with CHEST NetWorks, I have found from top to bottom CHEST striving to incorporate APPs and advance our education. From including us in the FCCP program, reducing conference pricing for APPs, and focusing this year’s conference theme around being team focused, CHEST is creating a home for APPs.

Corinne Preston Young, FNP, FCCP

Steering Committee Member

 

Cardiovascular Medicine and Surgery

Catch 22 of Submassive Pulmonary Emboli

Venous thromboembolism (including deep vein thrombosis (DVT) and pulmonary embolism [PE]) occurs in approximately 1 per 1,000 patients (Piran S, Schulman S. Thromb J. 2016;14[S1]:23) and can be fatal. Pulmonary embolus severity is classified as low risk, intermediate-risk/submassive PE, and massive PE. There is significant controversy about the management of submassive PE, which is defined as PE with right-sided heart strain (elevated troponin or B-type natriuretic peptide, right-axis deviation on ECG, or e

vidence of RV dysfunction on CT or echocardiogram), and the absence of hypotension (systolic blood pressure > 90 mm Hg). In addition to the acute manifestations of VTE, there are potential long-term complications, including postthrombotic syndrome and chronic thromboembolic pulmonary hypertension. Several trials have examined the utility of systemic thrombolysis in submassive PE (MAPPET-3 [Konstantinides, et al. N Engl J Med. 2002;347:1143], PEITHO (Meyer, et al. N Engl J Med. 2014;370:1402; Konstantinides, et al. JACC. 2017;69[12]:1536); MOPETT (Sharifi, et al. Am J Cardiol. 2013;111:273); and TOPCOAT (Kline, et al. J Thromb Haemost. 2014;12:459), but all have failed to establish a mortality benefit. However, thrombolytics demonstrated decreased clinical deterioration and may mitigate the development of postthrombotic syndrome. Yet thrombolysis has been associated with increased bleeding (PEITHO: 11.5% vs 2.4% had major bleeding, and 2% vs 0.2% experienced hemorrhagic stroke). Current CHEST guidelines (Kearon, et al. Chest. 2016;149[2]:3150) recommend against the use of thrombolytics in submassive PE without hypotension. Treatment of intermediate-risk PE remains an enigma for physicians, but it is hoped that with further investigation, optimal management will be elucidated.

David J. Nagel, MD

Steering Committee Member

Olivier Axler, MD, FCCP

Vice-Chair

Chest Infections

Antibiotic Resistance

One-hundred years ago, infectious diseases caused 5 of the 10 most common causes of deaths in the United States. In 2016, only one infection remained on this list (influenza/pneumonia) (MMWR Morb Mortal Wkly Rep. 2017;66:413).

How medicine has improved with antibiotics. An unfortunate and unintended consequence of widespread antibiotic use has been the progressive resistance to these drugs. It is estimated that, if current trends continue, 10 million lives a year will be at risk from resistant organisms by 2050 (O’Neill, J. (2016). https://amr-review.org/sites/default/files/160518_Final%20paper_with%20cover.pdf).

Pathogens acquire antibiotic resistance by passing genetic material to one another through plasmids, bacteriophages, or naked DNA. Once acquired, resistance manifests via a number of mechanisms under the stress imposed by antibiotics (Levy SB, et al. Nat Med. 2004;10:S122).

Among the best studied is enzymatic degradation of the antibiotic. This occurs when beta-lactamases degrade penicillin. A second mechanism alters cell transport, thereby blocking cell entry or actively ejecting the antibiotic from the cell. Finally, overexpression or alteration of the antibiotic target may render a drug ineffective at inhibiting any vital cell function.

At the pace with which resistance now develops, the medical community faces a crisis, whereby infections caused by evolving superbugs are no longer effectively controlled by the available menu of antimicrobial agents.

This challenge must be met collectively by the more prudent prescribing of antibiotics, potentially with the help of rapid diagnostics; isolation of patients potentially infected with resistant organisms; and a focus on developing newer drugs that defy known resistant mechanisms.

Marc Feinstein, MD, FCCP

Steering Committee Member

Clinical Pulmonary Medicine

COPD and sleep-disordered breathing; A missing comorbid condition

Subjective, as well as objective, sleep complaints are common in patients with COPD (Krachman S, et al. Proc Am Thorac Soc. 2008;5[4]:536), and sleeping difficulties are ranked the third most frequent complaint (behind dyspnea and fatigue) in patients with COPD (Kinsman RA, et al. Chest. 1983;83[5]:755). Also, sleep quality is poor, and patients with moderate to severe COPD may have higher-than-expected incidence of OSA (Soler X, et al. Ann Am Thorac Soc. 2015;12[8]:1219).

Unfortunately, sleep is usually not assessed during a COPD evaluation. Up to 27% of patients with COPD without hypoxia during wakefulness can experience important desaturation during sleep, so called nocturnal oxygen desaturation (NOD) (Fletcher EC, et al. Chest. 1987;92[4]:604), that may lead to pulmonary hypertension (Chaouat A, et a

l. Am J Respir Crit Care Med. 1995;151[1]:82). Little is known about the pathophysiologic and clinical consequences of having concomitant COPD and OSA, but recent studies have demonstrated that patients with both disorders have a high risk of hospitalizations (30-day readmission rate for rehospitalization ranges from 20% to 39%), and death from acute exacerbations if OSA remains untreated (Marin JM, et al. Am J Respir Crit Care Med. 2010;182[3]:325; Machado MC, et al. Eur Respir J. 2010;35[1]:132). Another study has found that in patients with OSA, the presence of COPD increases the risk of death seven-fold (Lavie P, et al. J Sleep Res. 2007;16[1]:128).

Although identification and effective treatment of COPD comorbidities are becoming the cornerstone of COPD management, sleep-disordered breathing has not been identified in current guidelines yet as a true potential contributor in poor outcomes despite emergent clinical evidence. Multidisciplinary programs, such as pulmonary rehabilitation, that improve dyspnea, exercise capacity, and quality of life may also positively impact sleep (Soler X, et al. COPD. 2013;10[2]:156). Because of the background of the staff involved, the comprehensive approach to patient assessment, and access to number of COPD subjects, pulmonary rehabilitation may be an optimal opportunity to assess sleep and identify an important comorbid condition often overlooked in patients with more advanced COPD.

 

Xavier Soler, MD, PhD

Steering Committee Member

Interprofessional Team

Finding Home

Outside our internal medicine curriculum, there is no formal pulmonary training or post-masters fellowship in pulmonary medicine for Advanced Practice Providers (APPs). Because of this, APPs are left to their own devices to fill educational gaps. To perform at the level expected by the physicians I work for, journal reviews and memorizing guidelines were not going to be enough. Since there is no formal pulmonary APP society, there were no peers to reach out to either. Off to conferences I went.

At first, I found CHEST daunting. After all, it’s run by the American College of Chest “Physicians,” not Nurse Practitioners. I spent most of the first day with my nametag turned around worried I’d be found out as a nonphysician attendee who snuck in. And then the unthinkable happened, I ran into another unicorn—another APP seeking the same information, only her nametag was turned the right way. The best advice she gave was to attend the Interprofessional NetWork meeting. This was ground zero of the conference as far as I was concerned. There I found myself surrounded by RTs, RNs, NPs, PAs, and yes, even physicians.

Over the years, as I’ve gotten further involved with CHEST NetWorks, I have found from top to bottom CHEST striving to incorporate APPs and advance our education. From including us in the FCCP program, reducing conference pricing for APPs, and focusing this year’s conference theme around being team focused, CHEST is creating a home for APPs.

Corinne Preston Young, FNP, FCCP

Steering Committee Member

 

Cardiovascular Medicine and Surgery

Catch 22 of Submassive Pulmonary Emboli

Venous thromboembolism (including deep vein thrombosis (DVT) and pulmonary embolism [PE]) occurs in approximately 1 per 1,000 patients (Piran S, Schulman S. Thromb J. 2016;14[S1]:23) and can be fatal. Pulmonary embolus severity is classified as low risk, intermediate-risk/submassive PE, and massive PE. There is significant controversy about the management of submassive PE, which is defined as PE with right-sided heart strain (elevated troponin or B-type natriuretic peptide, right-axis deviation on ECG, or e

vidence of RV dysfunction on CT or echocardiogram), and the absence of hypotension (systolic blood pressure > 90 mm Hg). In addition to the acute manifestations of VTE, there are potential long-term complications, including postthrombotic syndrome and chronic thromboembolic pulmonary hypertension. Several trials have examined the utility of systemic thrombolysis in submassive PE (MAPPET-3 [Konstantinides, et al. N Engl J Med. 2002;347:1143], PEITHO (Meyer, et al. N Engl J Med. 2014;370:1402; Konstantinides, et al. JACC. 2017;69[12]:1536); MOPETT (Sharifi, et al. Am J Cardiol. 2013;111:273); and TOPCOAT (Kline, et al. J Thromb Haemost. 2014;12:459), but all have failed to establish a mortality benefit. However, thrombolytics demonstrated decreased clinical deterioration and may mitigate the development of postthrombotic syndrome. Yet thrombolysis has been associated with increased bleeding (PEITHO: 11.5% vs 2.4% had major bleeding, and 2% vs 0.2% experienced hemorrhagic stroke). Current CHEST guidelines (Kearon, et al. Chest. 2016;149[2]:3150) recommend against the use of thrombolytics in submassive PE without hypotension. Treatment of intermediate-risk PE remains an enigma for physicians, but it is hoped that with further investigation, optimal management will be elucidated.

David J. Nagel, MD

Steering Committee Member

Olivier Axler, MD, FCCP

Vice-Chair

Chest Infections

Antibiotic Resistance

One-hundred years ago, infectious diseases caused 5 of the 10 most common causes of deaths in the United States. In 2016, only one infection remained on this list (influenza/pneumonia) (MMWR Morb Mortal Wkly Rep. 2017;66:413).

How medicine has improved with antibiotics. An unfortunate and unintended consequence of widespread antibiotic use has been the progressive resistance to these drugs. It is estimated that, if current trends continue, 10 million lives a year will be at risk from resistant organisms by 2050 (O’Neill, J. (2016). https://amr-review.org/sites/default/files/160518_Final%20paper_with%20cover.pdf).

Pathogens acquire antibiotic resistance by passing genetic material to one another through plasmids, bacteriophages, or naked DNA. Once acquired, resistance manifests via a number of mechanisms under the stress imposed by antibiotics (Levy SB, et al. Nat Med. 2004;10:S122).

Among the best studied is enzymatic degradation of the antibiotic. This occurs when beta-lactamases degrade penicillin. A second mechanism alters cell transport, thereby blocking cell entry or actively ejecting the antibiotic from the cell. Finally, overexpression or alteration of the antibiotic target may render a drug ineffective at inhibiting any vital cell function.

At the pace with which resistance now develops, the medical community faces a crisis, whereby infections caused by evolving superbugs are no longer effectively controlled by the available menu of antimicrobial agents.

This challenge must be met collectively by the more prudent prescribing of antibiotics, potentially with the help of rapid diagnostics; isolation of patients potentially infected with resistant organisms; and a focus on developing newer drugs that defy known resistant mechanisms.

Marc Feinstein, MD, FCCP

Steering Committee Member

Clinical Pulmonary Medicine

COPD and sleep-disordered breathing; A missing comorbid condition

Subjective, as well as objective, sleep complaints are common in patients with COPD (Krachman S, et al. Proc Am Thorac Soc. 2008;5[4]:536), and sleeping difficulties are ranked the third most frequent complaint (behind dyspnea and fatigue) in patients with COPD (Kinsman RA, et al. Chest. 1983;83[5]:755). Also, sleep quality is poor, and patients with moderate to severe COPD may have higher-than-expected incidence of OSA (Soler X, et al. Ann Am Thorac Soc. 2015;12[8]:1219).

Unfortunately, sleep is usually not assessed during a COPD evaluation. Up to 27% of patients with COPD without hypoxia during wakefulness can experience important desaturation during sleep, so called nocturnal oxygen desaturation (NOD) (Fletcher EC, et al. Chest. 1987;92[4]:604), that may lead to pulmonary hypertension (Chaouat A, et a

l. Am J Respir Crit Care Med. 1995;151[1]:82). Little is known about the pathophysiologic and clinical consequences of having concomitant COPD and OSA, but recent studies have demonstrated that patients with both disorders have a high risk of hospitalizations (30-day readmission rate for rehospitalization ranges from 20% to 39%), and death from acute exacerbations if OSA remains untreated (Marin JM, et al. Am J Respir Crit Care Med. 2010;182[3]:325; Machado MC, et al. Eur Respir J. 2010;35[1]:132). Another study has found that in patients with OSA, the presence of COPD increases the risk of death seven-fold (Lavie P, et al. J Sleep Res. 2007;16[1]:128).

Although identification and effective treatment of COPD comorbidities are becoming the cornerstone of COPD management, sleep-disordered breathing has not been identified in current guidelines yet as a true potential contributor in poor outcomes despite emergent clinical evidence. Multidisciplinary programs, such as pulmonary rehabilitation, that improve dyspnea, exercise capacity, and quality of life may also positively impact sleep (Soler X, et al. COPD. 2013;10[2]:156). Because of the background of the staff involved, the comprehensive approach to patient assessment, and access to number of COPD subjects, pulmonary rehabilitation may be an optimal opportunity to assess sleep and identify an important comorbid condition often overlooked in patients with more advanced COPD.

 

Xavier Soler, MD, PhD

Steering Committee Member

Interprofessional Team

Finding Home

Outside our internal medicine curriculum, there is no formal pulmonary training or post-masters fellowship in pulmonary medicine for Advanced Practice Providers (APPs). Because of this, APPs are left to their own devices to fill educational gaps. To perform at the level expected by the physicians I work for, journal reviews and memorizing guidelines were not going to be enough. Since there is no formal pulmonary APP society, there were no peers to reach out to either. Off to conferences I went.

At first, I found CHEST daunting. After all, it’s run by the American College of Chest “Physicians,” not Nurse Practitioners. I spent most of the first day with my nametag turned around worried I’d be found out as a nonphysician attendee who snuck in. And then the unthinkable happened, I ran into another unicorn—another APP seeking the same information, only her nametag was turned the right way. The best advice she gave was to attend the Interprofessional NetWork meeting. This was ground zero of the conference as far as I was concerned. There I found myself surrounded by RTs, RNs, NPs, PAs, and yes, even physicians.

Over the years, as I’ve gotten further involved with CHEST NetWorks, I have found from top to bottom CHEST striving to incorporate APPs and advance our education. From including us in the FCCP program, reducing conference pricing for APPs, and focusing this year’s conference theme around being team focused, CHEST is creating a home for APPs.

Corinne Preston Young, FNP, FCCP

Steering Committee Member