Interventional Chest/Diagnostic Procedures

 

Interventional Chest/Diagnostic Procedures

Endobronchial valve therapy receives FDA approval for bronchoscopic LVR

Lung volume reduction surgery (LVRS) is an established approach to improve exercise capacity and lung function in patients with heterogeneous emphysema and may confer survival benefit in patients with apical-predominant disease (Fishman, et al. N Engl J Med. 2003;348[21]:2059). Despite this, LVRS case numbers remain low due to patient and procedural morbidity. Bronchoscopic alternatives for LVRS have advanced considerably over the last decade with endobronchial valve (EBV) therapy emerging as a viable option for select subsets of patients with heterogeneous emphysema. Endobronchial valves are removable devices placed in segmental/subsegmental airways, which allow efflux of air during exhalation but close during inspiration, resulting in distal atelectasis in the absence of collateral ventilation.

The LIBERATE study, a multicenter randomized controlled trial demonstrated improvement in FEV1 ≥15% in 48% of patients after EBV placement compared with 17% of patients receiving standard medical therapy has resulted in FDA approval (Criner G, et al. Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC. [Epub ahead of print]). Patients with EBV had improved subjective dyspnea scores, residual volume, and 6-minute walk distance; however, the pneumothorax rate was 27%.

All study patients with EBV underwent bronchoscopic evaluation for collateral ventilation using a proprietary digital system, which measures expiratory airflow in target airways to establish the presence of collateral ventilation. Previous data have demonstrated improved transplant-free survival when implanted EBVs result in atelectasis of the target lobe, which requires intact interlobar fissures (Garner, et al. Am J Respir Crit Care Med. 2016;194[4]:519). Ongoing clinical trials are attempting to clarify the role of EBV therapy in different phenotypes of COPD, including patients with homogenous emphysema. Long-term follow-up data will be important in determining the broader implementation of bronchoscopic lung volume reduction moving forward.

Vivek Murthy, MD
Jason A. Akulian, MD, FCCP
Steering Committee Members
 

Pediatric Chest Medicine

CFTR modulators

Cystic fibrosis (CF) is a progressive genetic disorder resulting in multiorgan disease with progressive respiratory decline. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This codes for the CFTR anion channel and contributes to the movement of salt in and out of the cell. CFTR dysfunction leads to thickened secretions in the lungs and other organs, such as the gut and pancreas. This leads to more lung infections and other organ dysfunction that ultimately leads to premature death.

Established CF treatments include pulmonary and nutritional interventions. CFTR modulators are recent novel therapies that improve the function of CFTR and target the basic defect. Two types of modulator drugs (potentiators and correctors) have been developed with effectiveness depending upon the kind of CF mutation the person has.

CFTR potentiators, such as Kalydeco® (ivacaftor monotherapy), increase the likelihood that the CFTR channel will transport ions through the cell membrane, ie, they increase the channel’s “open probability.” Kalydeco has been approved for patients 12 months or older with mutations that result in partial CFTR protein function in the cell membrane. CFTR correctors, such as lumacaftor and tezacaftor, increase the amount of normal or mutated CFTR protein that gets transported, increasing the amount of CFTR protein on the cell surface. Combination drugs such as Orkambi® (lumacaftor/ivacaftor) for patients 2 years and older, and Symdeko™ (tezacaftor/ivacaftor) for patients 12 years and older, are considered in patients homozygous for the F508del mutation.

Sumit Bhargava, MBBS, FCCP
Steering Committee Member

 

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

 

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair

 

Thoracic Oncology

Multiple tumor nodules in lung cancer diagnosis

Low dose CT (LDCT) scan screening for lung cancer is a recommended preventative modality for adults with a significant smoking history (Mayer et al. Ann Int Med. 2014;160(5):330). The screening approach aims to identify adults at significant risk for lung cancer. The goal is to discover lung cancers at low stage with benign mediastinal nodes for optimal treatment and potential for cure. In a minority, but significant number of cases, the LDCT demonstrates multiple lung nodules or masses confounding the attempt to adequately stage the tumor. Two tumors representing a primary cancer and separate malignant spread, namely, intra-pulmonary metastases, in the same lobe, different ipsilateral lobe, or contralateral lobe would be staged, respectively, as T3, T4, or M1a (Detterbeck et al. Chest. 2013;143(5):e191S). Clearly, if the two tumors are separate unique primary cancers, independent of one another, then at best they would be considered as multiple T1 tumors. The treatment modalities of and clinical survival outcomes for these multiple conditions would be markedly different.

The identification of additional tumors may be synchronous (at the same time of the primary discovery) or metachronous (at a later time than the primary discovery). The approach is basically the same. Two tumors with different histologic types, or having separate in-situ squamous cell carcinoma patterns, or disparate immunohistochemical or molecular expressions, or different genomic profiles or driver mutations may be considered as separate distinct primary malignancies (Detterbeck et al. J Thorac Oncol. 2016;11:639; Nicholson et al. J Thorac Oncol. 2017;13:205). Separate foci of ground-glass opacities with small solid central component indicative of minimally invasive adenocarcinoma may be designated as the highest T-stage. These cited and more challenging cases should be presented to a lung cancer tumor board with multiple specialties represented for analysis and judgment. The approach to diagnostic decision-making and clinical management should involve the expertise of all specialties in the lung cancer patient care team.

Arnold M. Schwartz, MD, PhD, FCCP
Steering Committee Member


















 

 

Interventional Chest/Diagnostic Procedures

Endobronchial valve therapy receives FDA approval for bronchoscopic LVR

Lung volume reduction surgery (LVRS) is an established approach to improve exercise capacity and lung function in patients with heterogeneous emphysema and may confer survival benefit in patients with apical-predominant disease (Fishman, et al. N Engl J Med. 2003;348[21]:2059). Despite this, LVRS case numbers remain low due to patient and procedural morbidity. Bronchoscopic alternatives for LVRS have advanced considerably over the last decade with endobronchial valve (EBV) therapy emerging as a viable option for select subsets of patients with heterogeneous emphysema. Endobronchial valves are removable devices placed in segmental/subsegmental airways, which allow efflux of air during exhalation but close during inspiration, resulting in distal atelectasis in the absence of collateral ventilation.

The LIBERATE study, a multicenter randomized controlled trial demonstrated improvement in FEV1 ≥15% in 48% of patients after EBV placement compared with 17% of patients receiving standard medical therapy has resulted in FDA approval (Criner G, et al. Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC. [Epub ahead of print]). Patients with EBV had improved subjective dyspnea scores, residual volume, and 6-minute walk distance; however, the pneumothorax rate was 27%.

All study patients with EBV underwent bronchoscopic evaluation for collateral ventilation using a proprietary digital system, which measures expiratory airflow in target airways to establish the presence of collateral ventilation. Previous data have demonstrated improved transplant-free survival when implanted EBVs result in atelectasis of the target lobe, which requires intact interlobar fissures (Garner, et al. Am J Respir Crit Care Med. 2016;194[4]:519). Ongoing clinical trials are attempting to clarify the role of EBV therapy in different phenotypes of COPD, including patients with homogenous emphysema. Long-term follow-up data will be important in determining the broader implementation of bronchoscopic lung volume reduction moving forward.

Vivek Murthy, MD
Jason A. Akulian, MD, FCCP
Steering Committee Members
 

Pediatric Chest Medicine

CFTR modulators

Cystic fibrosis (CF) is a progressive genetic disorder resulting in multiorgan disease with progressive respiratory decline. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This codes for the CFTR anion channel and contributes to the movement of salt in and out of the cell. CFTR dysfunction leads to thickened secretions in the lungs and other organs, such as the gut and pancreas. This leads to more lung infections and other organ dysfunction that ultimately leads to premature death.

Established CF treatments include pulmonary and nutritional interventions. CFTR modulators are recent novel therapies that improve the function of CFTR and target the basic defect. Two types of modulator drugs (potentiators and correctors) have been developed with effectiveness depending upon the kind of CF mutation the person has.

CFTR potentiators, such as Kalydeco® (ivacaftor monotherapy), increase the likelihood that the CFTR channel will transport ions through the cell membrane, ie, they increase the channel’s “open probability.” Kalydeco has been approved for patients 12 months or older with mutations that result in partial CFTR protein function in the cell membrane. CFTR correctors, such as lumacaftor and tezacaftor, increase the amount of normal or mutated CFTR protein that gets transported, increasing the amount of CFTR protein on the cell surface. Combination drugs such as Orkambi® (lumacaftor/ivacaftor) for patients 2 years and older, and Symdeko™ (tezacaftor/ivacaftor) for patients 12 years and older, are considered in patients homozygous for the F508del mutation.

Sumit Bhargava, MBBS, FCCP
Steering Committee Member

 

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

 

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair

 

Thoracic Oncology

Multiple tumor nodules in lung cancer diagnosis

Low dose CT (LDCT) scan screening for lung cancer is a recommended preventative modality for adults with a significant smoking history (Mayer et al. Ann Int Med. 2014;160(5):330). The screening approach aims to identify adults at significant risk for lung cancer. The goal is to discover lung cancers at low stage with benign mediastinal nodes for optimal treatment and potential for cure. In a minority, but significant number of cases, the LDCT demonstrates multiple lung nodules or masses confounding the attempt to adequately stage the tumor. Two tumors representing a primary cancer and separate malignant spread, namely, intra-pulmonary metastases, in the same lobe, different ipsilateral lobe, or contralateral lobe would be staged, respectively, as T3, T4, or M1a (Detterbeck et al. Chest. 2013;143(5):e191S). Clearly, if the two tumors are separate unique primary cancers, independent of one another, then at best they would be considered as multiple T1 tumors. The treatment modalities of and clinical survival outcomes for these multiple conditions would be markedly different.

The identification of additional tumors may be synchronous (at the same time of the primary discovery) or metachronous (at a later time than the primary discovery). The approach is basically the same. Two tumors with different histologic types, or having separate in-situ squamous cell carcinoma patterns, or disparate immunohistochemical or molecular expressions, or different genomic profiles or driver mutations may be considered as separate distinct primary malignancies (Detterbeck et al. J Thorac Oncol. 2016;11:639; Nicholson et al. J Thorac Oncol. 2017;13:205). Separate foci of ground-glass opacities with small solid central component indicative of minimally invasive adenocarcinoma may be designated as the highest T-stage. These cited and more challenging cases should be presented to a lung cancer tumor board with multiple specialties represented for analysis and judgment. The approach to diagnostic decision-making and clinical management should involve the expertise of all specialties in the lung cancer patient care team.

Arnold M. Schwartz, MD, PhD, FCCP
Steering Committee Member


















 

 

Interventional Chest/Diagnostic Procedures

Endobronchial valve therapy receives FDA approval for bronchoscopic LVR

Lung volume reduction surgery (LVRS) is an established approach to improve exercise capacity and lung function in patients with heterogeneous emphysema and may confer survival benefit in patients with apical-predominant disease (Fishman, et al. N Engl J Med. 2003;348[21]:2059). Despite this, LVRS case numbers remain low due to patient and procedural morbidity. Bronchoscopic alternatives for LVRS have advanced considerably over the last decade with endobronchial valve (EBV) therapy emerging as a viable option for select subsets of patients with heterogeneous emphysema. Endobronchial valves are removable devices placed in segmental/subsegmental airways, which allow efflux of air during exhalation but close during inspiration, resulting in distal atelectasis in the absence of collateral ventilation.

The LIBERATE study, a multicenter randomized controlled trial demonstrated improvement in FEV1 ≥15% in 48% of patients after EBV placement compared with 17% of patients receiving standard medical therapy has resulted in FDA approval (Criner G, et al. Am J Respir Crit Care Med. 2018 May 22. doi: 10.1164/rccm.201803-0590OC. [Epub ahead of print]). Patients with EBV had improved subjective dyspnea scores, residual volume, and 6-minute walk distance; however, the pneumothorax rate was 27%.

All study patients with EBV underwent bronchoscopic evaluation for collateral ventilation using a proprietary digital system, which measures expiratory airflow in target airways to establish the presence of collateral ventilation. Previous data have demonstrated improved transplant-free survival when implanted EBVs result in atelectasis of the target lobe, which requires intact interlobar fissures (Garner, et al. Am J Respir Crit Care Med. 2016;194[4]:519). Ongoing clinical trials are attempting to clarify the role of EBV therapy in different phenotypes of COPD, including patients with homogenous emphysema. Long-term follow-up data will be important in determining the broader implementation of bronchoscopic lung volume reduction moving forward.

Vivek Murthy, MD
Jason A. Akulian, MD, FCCP
Steering Committee Members
 

Pediatric Chest Medicine

CFTR modulators

Cystic fibrosis (CF) is a progressive genetic disorder resulting in multiorgan disease with progressive respiratory decline. CF is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This codes for the CFTR anion channel and contributes to the movement of salt in and out of the cell. CFTR dysfunction leads to thickened secretions in the lungs and other organs, such as the gut and pancreas. This leads to more lung infections and other organ dysfunction that ultimately leads to premature death.

Established CF treatments include pulmonary and nutritional interventions. CFTR modulators are recent novel therapies that improve the function of CFTR and target the basic defect. Two types of modulator drugs (potentiators and correctors) have been developed with effectiveness depending upon the kind of CF mutation the person has.

CFTR potentiators, such as Kalydeco® (ivacaftor monotherapy), increase the likelihood that the CFTR channel will transport ions through the cell membrane, ie, they increase the channel’s “open probability.” Kalydeco has been approved for patients 12 months or older with mutations that result in partial CFTR protein function in the cell membrane. CFTR correctors, such as lumacaftor and tezacaftor, increase the amount of normal or mutated CFTR protein that gets transported, increasing the amount of CFTR protein on the cell surface. Combination drugs such as Orkambi® (lumacaftor/ivacaftor) for patients 2 years and older, and Symdeko™ (tezacaftor/ivacaftor) for patients 12 years and older, are considered in patients homozygous for the F508del mutation.

Sumit Bhargava, MBBS, FCCP
Steering Committee Member

 

Pulmonary Physiology, Function, and Rehabilitation

Wildfires, particulate matter, and lung function

In the last 3 decades, human-caused climate change contributed to wildfires in an additional 4.2 million hectares of land across the western US alone. Human impact on climate is responsible for nearly doubling the expected wildfire area (Abatzoglou, et al. PNAS. 2016;113:11770). Year 2017 saw the most destructive wildfires in California recorded to date, and over $2 billion dollars was spent by the US Forest Service, the most-expensive on record. Besides the devastating effects on the forestry and nearby communities, wildfires also generate a large amount of particulate matter (PM). In western US, wildfires contributed to 71.3% of total PM2.5 on days exceeding regulatory PM2.5 standards during 2004-2009 (Liu et al. Clim Change. 2016;138:655). Acute PM exposure is associated with respiratory health effects, such as exacerbation of asthma and COPD, increased ED visits and hospitalization for pneumonia, and increased mortality. Chronic PM2.5 exposure may also affect lung function. Cross-shift and cross-season FEV1 declined by 0.150 L and 0.104 L, respectively in forest firefighters (Betchley, et al. Am. J Ind Med. 1997;31:503). The Children’s Health Study conducted in California found that subjects who were exposed to the highest level of exposure to PM2.5 were five times more likely to have an FEV1 less than 80% of expected FEV1 when they reached 18 years of age than subjects exposed to the lowest level of PM2.5 (Gauderman et al. N Engl J Med. 2004;351:1057). Clinicians should educate patients and the public how to protect our environment and, when wildfires occur, how to protect themselves from exposure to PM.

Thomas W. DeCato, MD
Fellow-in-Training Committee Member

Yuh-Chin T. Huang, MD, FCCP
Steering Committee Member
 

Pulmonary Vascular Disease

Small increases in pulmonary pressures—big impact

Pulmonary hypertension (PH) is a progressive, life-limiting pulmonary vascular disease that is diagnosed hemodynamically by right-sided heart catheterization (RHC) and defined by a mean pulmonary artery pressure (mPAP) >25 mm Hg (Hoeper MM, et al. JACC. 2013;62(25 Suppl):D42).

 

The impact of PH on survival both in its “pure” form, pulmonary arterial hypertension, and in the setting of underlying cardiopulmonary disease, is well established. However, the clinical relevance of mildly elevated mPAP, defined as mPAP between 18 and 24 mm Hg, has been unclear until recently. Two large cohort studies have suggested that mild increases in mPAP are clinically relevant. A large retrospective analysis of hemodynamic data from 21,727 US veterans found mildly increased mPAP (19-24 mm Hg) was associated with increased hospitalization and decreased survival (Maron, et al. Circulation. 2016;133:1240).

While this population was skewed toward elderly men, a study from Vanderbilt University that included equal numbers of men and women showed similar results. Patients with mPAP 19-24 mm Hg experienced incrementally increased mortality (HR:1.31, P=.001). Importantly, in the subset of patients who underwent a repeat RHC in follow-up, 61% developed progressive increases of pulmonary pressures (>25 mm Hg) on follow-up RHC suggesting that the disease process may progress in a substantial proportion of patients (Assad, et al. JAMA Cardiol. 2017;2[1]):1361). Combined with prior data from smaller cohorts, these studies highlight the impact of mildly increased pulmonary pressures on outcomes. Given the dearth of available data regarding interventions for these patients, there is an urgent need to study to role of specific therapy for mildly elevated pulmonary pressures.

Vijay Balasubramanian, MD, FCCP
Steering Committee Member

Jean Elwing, MD, FCCP
Steering Committee Vice-Chair

 

Thoracic Oncology

Multiple tumor nodules in lung cancer diagnosis

Low dose CT (LDCT) scan screening for lung cancer is a recommended preventative modality for adults with a significant smoking history (Mayer et al. Ann Int Med. 2014;160(5):330). The screening approach aims to identify adults at significant risk for lung cancer. The goal is to discover lung cancers at low stage with benign mediastinal nodes for optimal treatment and potential for cure. In a minority, but significant number of cases, the LDCT demonstrates multiple lung nodules or masses confounding the attempt to adequately stage the tumor. Two tumors representing a primary cancer and separate malignant spread, namely, intra-pulmonary metastases, in the same lobe, different ipsilateral lobe, or contralateral lobe would be staged, respectively, as T3, T4, or M1a (Detterbeck et al. Chest. 2013;143(5):e191S). Clearly, if the two tumors are separate unique primary cancers, independent of one another, then at best they would be considered as multiple T1 tumors. The treatment modalities of and clinical survival outcomes for these multiple conditions would be markedly different.

The identification of additional tumors may be synchronous (at the same time of the primary discovery) or metachronous (at a later time than the primary discovery). The approach is basically the same. Two tumors with different histologic types, or having separate in-situ squamous cell carcinoma patterns, or disparate immunohistochemical or molecular expressions, or different genomic profiles or driver mutations may be considered as separate distinct primary malignancies (Detterbeck et al. J Thorac Oncol. 2016;11:639; Nicholson et al. J Thorac Oncol. 2017;13:205). Separate foci of ground-glass opacities with small solid central component indicative of minimally invasive adenocarcinoma may be designated as the highest T-stage. These cited and more challenging cases should be presented to a lung cancer tumor board with multiple specialties represented for analysis and judgment. The approach to diagnostic decision-making and clinical management should involve the expertise of all specialties in the lung cancer patient care team.

Arnold M. Schwartz, MD, PhD, FCCP
Steering Committee Member