Aaron B. Holley, MD

Clinicians working within the U.S. health care system order CTs; it’s just what we do, and we do it a lot. This isn’t necessarily bad, but an inevitable byproduct is the pandemic of incidental findings. One underrecognized but frequent “incidentaloma” on CT is an interstitial lung abnormality (ILA). The Fleischner Society defines an ILA as honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone in a patient without a clinical diagnosis of interstitial lung disease (ILD). In essence, ILAs are both a radiographic and a clinical diagnosis.

ILAs are common. Depending on population characteristics, ILAs occur at a prevalence of up to 10%. With the advent of lung cancer screening and advances in CT technology, we’re now inundated with detailed images of lung parenchyma in older smokers who are at high risk for respiratory disease. The resulting opportunity for early identification of disease is as exciting as the risk for overdiagnosis, excessive testing, and unnecessary treatment is frightening. Early diagnosis remains critical for preventing irreversible respiratory disease. But as with any disease process, when we attempt to detect pathology before it has become apparent, the line between benign change and true abnormality is blurred.

Such is the challenge with ILAs. Past studies have shown an association between ILAs and morbidity and mortality, but considerable uncertainty persists over what the ILAs represent and how they should be managed. A recent study published in the American Journal of Respiratory and Critical Care Medicine  provides some clarity. The authors used data from the COPDGene cohort to correlate ILAs with lung testing, and functional and respiratory outcomes. As with other studies, they found that approximately 10% of the COPDGene patients that they examined had ILAs on CT and half of those met their criteria for “suspected ILD.” Suspected ILD was defined radiographically (definite fibrosis) and on lung function testing (abnormal forced vital capacity [FVC] or diffusing capacity of the lungs for carbon monoxide [DLCO]). The patients with suspected ILD had worse clinical outcomes; being a Black individual, pack-years of smoking, and GOLD stage on spirometry were independently associated with suspected ILD.

This type of study is urgently needed. Given their high prevalence, we’re in dire need of a valid model for risk stratifying ILAs. The authors of this study have moved us closer, but we’ve still got a long way to go. The study has significant limitations. First, although patients with previous documentation of ILD were excluded from COPDGene, no formal, multidisciplinary assessment was performed; therefore, some of the patients labeled as having ILA probably had diagnosable ILD. Their possible inclusion would falsely increase the prevalence of clinically important ILAs and exaggerate the relationship between ILAs and clinical outcomes.

The rhetorical gymnastics performed throughout the paper are necessary yet problematic. “Suspected ILD” is not a recognized diagnosis and the definition is therefore arbitrary. To the extent that “suspected ILD” requires an abnormality on spirometry or DLCO, one could argue it’s the lung function changes and not the radiographic findings that are driving the differences. In fact, “suspected ILD” was defined by lung function more often than radiographic criteria (16% had definite fibrosis on CT, 57% had an abnormal FVC, and 67% had an abnormal DLCO). Patients with ILAs without suspected ILD had outcomes that weren’t statistically different from those with no ILAs at all, implying that the lung testing and not the ILA is the better discriminator. Regardless, this leads us back to where we started before this paper was published: ILAs require lung function testing and referral to a pulmonologist for proper risk stratification. An accompanying editorial highlights these and other limitations.

One particular problem that isn’t addressed by the authors or the editorial is their findings on race. The authors concluded that Black persons with ILAs are more likely to have “suspected ILD.” However, their definition suffers from an insidious form of incorporation bias generated by the way they handled their DLCO reference values. The Global Lung Function Initiative equations they used were derived exclusively from White persons. In accordance with the recent American Thoracic Society/European Respiratory Society (ATS/ERS) statement on lung testing, the authors did not apply a fixed correction factor to adjust for race. Without such an adjustment, Black persons would be biased toward having lower percent predicted values for DLCO. In short, self-identified Black individuals would be more likely to have a predicted DLCO of less than 70% and to therefore meet criteria for “suspected ILD.” The resulting effects on biologic plausibility, causal inference, and the strength of the relationship between “suspected ILD” and clinical outcomes will vary by whether the association between race and lung function is considered a product of inherent biologic variability or a result of external (socioeconomic and environmental) effects.

In summary, ILAs remain a challenge for radiologists, primary care providers, pulmonologists, and anyone else who orders a CT of the lungs. Despite its limitations, I believe the recently published paper pushes us forward conceptually. Perhaps its most important contribution is showing that 50% of ILAs are clinically insignificant by definition. This offers further reassurance that a subset of ILAs can be dismissed. Now, all we need is an easy, cost-effective, and efficient way to identify this subset.
 

Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed ties to Metapharm Inc., CHEST College, and WebMD. A version of this article originally appeared on Medscape.com.

Clinicians working within the U.S. health care system order CTs; it’s just what we do, and we do it a lot. This isn’t necessarily bad, but an inevitable byproduct is the pandemic of incidental findings. One underrecognized but frequent “incidentaloma” on CT is an interstitial lung abnormality (ILA). The Fleischner Society defines an ILA as honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone in a patient without a clinical diagnosis of interstitial lung disease (ILD). In essence, ILAs are both a radiographic and a clinical diagnosis.

ILAs are common. Depending on population characteristics, ILAs occur at a prevalence of up to 10%. With the advent of lung cancer screening and advances in CT technology, we’re now inundated with detailed images of lung parenchyma in older smokers who are at high risk for respiratory disease. The resulting opportunity for early identification of disease is as exciting as the risk for overdiagnosis, excessive testing, and unnecessary treatment is frightening. Early diagnosis remains critical for preventing irreversible respiratory disease. But as with any disease process, when we attempt to detect pathology before it has become apparent, the line between benign change and true abnormality is blurred.

Such is the challenge with ILAs. Past studies have shown an association between ILAs and morbidity and mortality, but considerable uncertainty persists over what the ILAs represent and how they should be managed. A recent study published in the American Journal of Respiratory and Critical Care Medicine  provides some clarity. The authors used data from the COPDGene cohort to correlate ILAs with lung testing, and functional and respiratory outcomes. As with other studies, they found that approximately 10% of the COPDGene patients that they examined had ILAs on CT and half of those met their criteria for “suspected ILD.” Suspected ILD was defined radiographically (definite fibrosis) and on lung function testing (abnormal forced vital capacity [FVC] or diffusing capacity of the lungs for carbon monoxide [DLCO]). The patients with suspected ILD had worse clinical outcomes; being a Black individual, pack-years of smoking, and GOLD stage on spirometry were independently associated with suspected ILD.

This type of study is urgently needed. Given their high prevalence, we’re in dire need of a valid model for risk stratifying ILAs. The authors of this study have moved us closer, but we’ve still got a long way to go. The study has significant limitations. First, although patients with previous documentation of ILD were excluded from COPDGene, no formal, multidisciplinary assessment was performed; therefore, some of the patients labeled as having ILA probably had diagnosable ILD. Their possible inclusion would falsely increase the prevalence of clinically important ILAs and exaggerate the relationship between ILAs and clinical outcomes.

The rhetorical gymnastics performed throughout the paper are necessary yet problematic. “Suspected ILD” is not a recognized diagnosis and the definition is therefore arbitrary. To the extent that “suspected ILD” requires an abnormality on spirometry or DLCO, one could argue it’s the lung function changes and not the radiographic findings that are driving the differences. In fact, “suspected ILD” was defined by lung function more often than radiographic criteria (16% had definite fibrosis on CT, 57% had an abnormal FVC, and 67% had an abnormal DLCO). Patients with ILAs without suspected ILD had outcomes that weren’t statistically different from those with no ILAs at all, implying that the lung testing and not the ILA is the better discriminator. Regardless, this leads us back to where we started before this paper was published: ILAs require lung function testing and referral to a pulmonologist for proper risk stratification. An accompanying editorial highlights these and other limitations.

One particular problem that isn’t addressed by the authors or the editorial is their findings on race. The authors concluded that Black persons with ILAs are more likely to have “suspected ILD.” However, their definition suffers from an insidious form of incorporation bias generated by the way they handled their DLCO reference values. The Global Lung Function Initiative equations they used were derived exclusively from White persons. In accordance with the recent American Thoracic Society/European Respiratory Society (ATS/ERS) statement on lung testing, the authors did not apply a fixed correction factor to adjust for race. Without such an adjustment, Black persons would be biased toward having lower percent predicted values for DLCO. In short, self-identified Black individuals would be more likely to have a predicted DLCO of less than 70% and to therefore meet criteria for “suspected ILD.” The resulting effects on biologic plausibility, causal inference, and the strength of the relationship between “suspected ILD” and clinical outcomes will vary by whether the association between race and lung function is considered a product of inherent biologic variability or a result of external (socioeconomic and environmental) effects.

In summary, ILAs remain a challenge for radiologists, primary care providers, pulmonologists, and anyone else who orders a CT of the lungs. Despite its limitations, I believe the recently published paper pushes us forward conceptually. Perhaps its most important contribution is showing that 50% of ILAs are clinically insignificant by definition. This offers further reassurance that a subset of ILAs can be dismissed. Now, all we need is an easy, cost-effective, and efficient way to identify this subset.
 

Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed ties to Metapharm Inc., CHEST College, and WebMD. A version of this article originally appeared on Medscape.com.

Clinicians working within the U.S. health care system order CTs; it’s just what we do, and we do it a lot. This isn’t necessarily bad, but an inevitable byproduct is the pandemic of incidental findings. One underrecognized but frequent “incidentaloma” on CT is an interstitial lung abnormality (ILA). The Fleischner Society defines an ILA as honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone in a patient without a clinical diagnosis of interstitial lung disease (ILD). In essence, ILAs are both a radiographic and a clinical diagnosis.

ILAs are common. Depending on population characteristics, ILAs occur at a prevalence of up to 10%. With the advent of lung cancer screening and advances in CT technology, we’re now inundated with detailed images of lung parenchyma in older smokers who are at high risk for respiratory disease. The resulting opportunity for early identification of disease is as exciting as the risk for overdiagnosis, excessive testing, and unnecessary treatment is frightening. Early diagnosis remains critical for preventing irreversible respiratory disease. But as with any disease process, when we attempt to detect pathology before it has become apparent, the line between benign change and true abnormality is blurred.

Such is the challenge with ILAs. Past studies have shown an association between ILAs and morbidity and mortality, but considerable uncertainty persists over what the ILAs represent and how they should be managed. A recent study published in the American Journal of Respiratory and Critical Care Medicine  provides some clarity. The authors used data from the COPDGene cohort to correlate ILAs with lung testing, and functional and respiratory outcomes. As with other studies, they found that approximately 10% of the COPDGene patients that they examined had ILAs on CT and half of those met their criteria for “suspected ILD.” Suspected ILD was defined radiographically (definite fibrosis) and on lung function testing (abnormal forced vital capacity [FVC] or diffusing capacity of the lungs for carbon monoxide [DLCO]). The patients with suspected ILD had worse clinical outcomes; being a Black individual, pack-years of smoking, and GOLD stage on spirometry were independently associated with suspected ILD.

This type of study is urgently needed. Given their high prevalence, we’re in dire need of a valid model for risk stratifying ILAs. The authors of this study have moved us closer, but we’ve still got a long way to go. The study has significant limitations. First, although patients with previous documentation of ILD were excluded from COPDGene, no formal, multidisciplinary assessment was performed; therefore, some of the patients labeled as having ILA probably had diagnosable ILD. Their possible inclusion would falsely increase the prevalence of clinically important ILAs and exaggerate the relationship between ILAs and clinical outcomes.

The rhetorical gymnastics performed throughout the paper are necessary yet problematic. “Suspected ILD” is not a recognized diagnosis and the definition is therefore arbitrary. To the extent that “suspected ILD” requires an abnormality on spirometry or DLCO, one could argue it’s the lung function changes and not the radiographic findings that are driving the differences. In fact, “suspected ILD” was defined by lung function more often than radiographic criteria (16% had definite fibrosis on CT, 57% had an abnormal FVC, and 67% had an abnormal DLCO). Patients with ILAs without suspected ILD had outcomes that weren’t statistically different from those with no ILAs at all, implying that the lung testing and not the ILA is the better discriminator. Regardless, this leads us back to where we started before this paper was published: ILAs require lung function testing and referral to a pulmonologist for proper risk stratification. An accompanying editorial highlights these and other limitations.

One particular problem that isn’t addressed by the authors or the editorial is their findings on race. The authors concluded that Black persons with ILAs are more likely to have “suspected ILD.” However, their definition suffers from an insidious form of incorporation bias generated by the way they handled their DLCO reference values. The Global Lung Function Initiative equations they used were derived exclusively from White persons. In accordance with the recent American Thoracic Society/European Respiratory Society (ATS/ERS) statement on lung testing, the authors did not apply a fixed correction factor to adjust for race. Without such an adjustment, Black persons would be biased toward having lower percent predicted values for DLCO. In short, self-identified Black individuals would be more likely to have a predicted DLCO of less than 70% and to therefore meet criteria for “suspected ILD.” The resulting effects on biologic plausibility, causal inference, and the strength of the relationship between “suspected ILD” and clinical outcomes will vary by whether the association between race and lung function is considered a product of inherent biologic variability or a result of external (socioeconomic and environmental) effects.

In summary, ILAs remain a challenge for radiologists, primary care providers, pulmonologists, and anyone else who orders a CT of the lungs. Despite its limitations, I believe the recently published paper pushes us forward conceptually. Perhaps its most important contribution is showing that 50% of ILAs are clinically insignificant by definition. This offers further reassurance that a subset of ILAs can be dismissed. Now, all we need is an easy, cost-effective, and efficient way to identify this subset.
 

Dr. Holley is professor of medicine at Uniformed Services University in Bethesda, Md., and a pulmonary/sleep and critical care medicine physician at MedStar Washington Hospital Center in Washington. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed ties to Metapharm Inc., CHEST College, and WebMD. A version of this article originally appeared on Medscape.com.

The European Respiratory Society (ERS) and the American Thoracic Society (ATS) just published an updated technical standard on lung function interpretation. It’s a critically important document written by a “Who’s Who” in the lung function world. It’s impossible to review in its entirety without more space, so I’ll settle for covering what the authors say about bronchodilator testing. But before I do that, it’s worth reviewing what we think we know about having a patient perform spirometry, inhale a bronchodilator, and then repeat it. This is colloquially referred to as pre- and postbronchodilator testing.

Administering a bronchodilator and measuring changes in lung function seems simple and intuitive. It is biologically plausible that improvement would predict treatment response. It should allow for phenotyping airway diseases and quantifying exacerbation risk. It is easy to perform and can be done in the clinic. But in practice it falls short of its purpose, in part because of technical factors but also because it doesn’t really have a purpose.

The last interpretative strategies document from the ERS/ATS was published in 2005. Reading it many years ago, I was struck by the contrast between our reliance on bronchodilator response and its lack of standardization. It seemed that there was none. After making statements like, “There is no consensus on what constitutes reversibility in subjects with airflow obstruction” and “There is no consensus on how a bronchodilator response should be expressed, the variables to be used, and finally, the kind, dose, and inhalation mode of bronchodilator agent,” the 2005 ERS/ATS authors suggest using the criteria most clinicians are familiar with: A change of 12% and 200 cc in FEV₁ or FVC marks a “significant” bronchodilator response. Four puffs of albuterol (100 mcg each for a total of 400 mcg) with a 15- to 20-minute wait before repeat spirometry is also suggested.

The 2005 iteration acknowledges that a significant bronchodilator response isn’t a very accurate predictor of, well, anything. It doesn’t reliably differentiate COPD from asthma and it’s never been as sensitive as bronchoprovocation testing for diagnosing airway reactivity. The absence of a significant bronchodilator response does not preclude a 2-month trial of the same medicine used to test for response. Given these problems with standardization and accuracy, I was left wondering why anyone bothers ordering the test at all.

In my own practice, I continued to order, conduct, and interpret bronchodilator response according to the suggestions made by the ERS/ATS in 2005 when trying to diagnose asthma. I recognized that a nonsignificant response meant nothing, but bronchodilator response testing was easier to obtain than bronchoprovocation at my hospital. It was a matter of convenience for me and the patient. According to the Global Initiative for Asthma (GINA) Guidelines, a significant bronchodilator response conducted and interpreted as recommended by the ERS/ATS 2005 standard provides objective confirmation of asthma in the presence of characteristic clinical symptoms.

The headline from the ERS/ATS 2022 Technical Standard is that the 12% and 200-cc criteria suggested in 2005 are being retired. Why? Well, much of the variability in the 2005 criteria is explained by height, age, sex, and baseline lung function. These factors obscure change related to intrinsic airway abnormalities. Instead, the authors suggest using a threshold change in the predicted values of FEV₁ and FVC to determine a significant response. Because predicted values incorporate age, height, and sex, the impact from these variables is minimized. Using a percent predicted (PPD) threshold will also minimize the effect from the inverse relationship between measured values and bronchodilator response.

A 10% change in the PPD value for either FEV₁ or FVC constitutes a significant bronchodilator response. Ten percent was chosen because it represents the statistically defined upper limit of normal response; and a greater than 8% change in bronchodilator response is associated with mortality, implying that values above this threshold connote disease. The technical standard seems to be on solid ground here; the rationale is mathematically appropriate and evidence based. The new definition will certainly improve precision.

There’s really no progress on accuracy, though. There are no comments on the protocol to be followed or clinical indications. The reader is referred to the ERS/ATS 2019 technical statement on standardization of spirometry. The statement on standardization is short on details, too, and refers the reader to an online supplement for a suggested protocol. The suggested protocol is identical to that suggested in 2005.

In summary, not a lot is different in the world of bronchodilator response testing. The definition is different now, and though it’s likely to be more precise, we still don’t know enough about accuracy. It’s nice to know that the new criteria will predict mortality, but in clinical practice we don’t use the test for that purpose. The 2022 technical standard acknowledges this and other limitations in a “future directions” paragraph. Perhaps we’ll know more when the next iteration is published.

Dr. Holley is a professor of medicine at Uniformed Services University of the Health Sciences. Bethesda, Md., and a pulmonary medicine/critical care physician at MedStar Washington Hospital Center, Washington. He reported conflicts of interest with Metapharm and the American College of Chest Physicians. A version of this article first appeared on Medscape.com.

The European Respiratory Society (ERS) and the American Thoracic Society (ATS) just published an updated technical standard on lung function interpretation. It’s a critically important document written by a “Who’s Who” in the lung function world. It’s impossible to review in its entirety without more space, so I’ll settle for covering what the authors say about bronchodilator testing. But before I do that, it’s worth reviewing what we think we know about having a patient perform spirometry, inhale a bronchodilator, and then repeat it. This is colloquially referred to as pre- and postbronchodilator testing.

Administering a bronchodilator and measuring changes in lung function seems simple and intuitive. It is biologically plausible that improvement would predict treatment response. It should allow for phenotyping airway diseases and quantifying exacerbation risk. It is easy to perform and can be done in the clinic. But in practice it falls short of its purpose, in part because of technical factors but also because it doesn’t really have a purpose.

The last interpretative strategies document from the ERS/ATS was published in 2005. Reading it many years ago, I was struck by the contrast between our reliance on bronchodilator response and its lack of standardization. It seemed that there was none. After making statements like, “There is no consensus on what constitutes reversibility in subjects with airflow obstruction” and “There is no consensus on how a bronchodilator response should be expressed, the variables to be used, and finally, the kind, dose, and inhalation mode of bronchodilator agent,” the 2005 ERS/ATS authors suggest using the criteria most clinicians are familiar with: A change of 12% and 200 cc in FEV₁ or FVC marks a “significant” bronchodilator response. Four puffs of albuterol (100 mcg each for a total of 400 mcg) with a 15- to 20-minute wait before repeat spirometry is also suggested.

The 2005 iteration acknowledges that a significant bronchodilator response isn’t a very accurate predictor of, well, anything. It doesn’t reliably differentiate COPD from asthma and it’s never been as sensitive as bronchoprovocation testing for diagnosing airway reactivity. The absence of a significant bronchodilator response does not preclude a 2-month trial of the same medicine used to test for response. Given these problems with standardization and accuracy, I was left wondering why anyone bothers ordering the test at all.

In my own practice, I continued to order, conduct, and interpret bronchodilator response according to the suggestions made by the ERS/ATS in 2005 when trying to diagnose asthma. I recognized that a nonsignificant response meant nothing, but bronchodilator response testing was easier to obtain than bronchoprovocation at my hospital. It was a matter of convenience for me and the patient. According to the Global Initiative for Asthma (GINA) Guidelines, a significant bronchodilator response conducted and interpreted as recommended by the ERS/ATS 2005 standard provides objective confirmation of asthma in the presence of characteristic clinical symptoms.

The headline from the ERS/ATS 2022 Technical Standard is that the 12% and 200-cc criteria suggested in 2005 are being retired. Why? Well, much of the variability in the 2005 criteria is explained by height, age, sex, and baseline lung function. These factors obscure change related to intrinsic airway abnormalities. Instead, the authors suggest using a threshold change in the predicted values of FEV₁ and FVC to determine a significant response. Because predicted values incorporate age, height, and sex, the impact from these variables is minimized. Using a percent predicted (PPD) threshold will also minimize the effect from the inverse relationship between measured values and bronchodilator response.

A 10% change in the PPD value for either FEV₁ or FVC constitutes a significant bronchodilator response. Ten percent was chosen because it represents the statistically defined upper limit of normal response; and a greater than 8% change in bronchodilator response is associated with mortality, implying that values above this threshold connote disease. The technical standard seems to be on solid ground here; the rationale is mathematically appropriate and evidence based. The new definition will certainly improve precision.

There’s really no progress on accuracy, though. There are no comments on the protocol to be followed or clinical indications. The reader is referred to the ERS/ATS 2019 technical statement on standardization of spirometry. The statement on standardization is short on details, too, and refers the reader to an online supplement for a suggested protocol. The suggested protocol is identical to that suggested in 2005.

In summary, not a lot is different in the world of bronchodilator response testing. The definition is different now, and though it’s likely to be more precise, we still don’t know enough about accuracy. It’s nice to know that the new criteria will predict mortality, but in clinical practice we don’t use the test for that purpose. The 2022 technical standard acknowledges this and other limitations in a “future directions” paragraph. Perhaps we’ll know more when the next iteration is published.

Dr. Holley is a professor of medicine at Uniformed Services University of the Health Sciences. Bethesda, Md., and a pulmonary medicine/critical care physician at MedStar Washington Hospital Center, Washington. He reported conflicts of interest with Metapharm and the American College of Chest Physicians. A version of this article first appeared on Medscape.com.

The European Respiratory Society (ERS) and the American Thoracic Society (ATS) just published an updated technical standard on lung function interpretation. It’s a critically important document written by a “Who’s Who” in the lung function world. It’s impossible to review in its entirety without more space, so I’ll settle for covering what the authors say about bronchodilator testing. But before I do that, it’s worth reviewing what we think we know about having a patient perform spirometry, inhale a bronchodilator, and then repeat it. This is colloquially referred to as pre- and postbronchodilator testing.

Administering a bronchodilator and measuring changes in lung function seems simple and intuitive. It is biologically plausible that improvement would predict treatment response. It should allow for phenotyping airway diseases and quantifying exacerbation risk. It is easy to perform and can be done in the clinic. But in practice it falls short of its purpose, in part because of technical factors but also because it doesn’t really have a purpose.

The last interpretative strategies document from the ERS/ATS was published in 2005. Reading it many years ago, I was struck by the contrast between our reliance on bronchodilator response and its lack of standardization. It seemed that there was none. After making statements like, “There is no consensus on what constitutes reversibility in subjects with airflow obstruction” and “There is no consensus on how a bronchodilator response should be expressed, the variables to be used, and finally, the kind, dose, and inhalation mode of bronchodilator agent,” the 2005 ERS/ATS authors suggest using the criteria most clinicians are familiar with: A change of 12% and 200 cc in FEV₁ or FVC marks a “significant” bronchodilator response. Four puffs of albuterol (100 mcg each for a total of 400 mcg) with a 15- to 20-minute wait before repeat spirometry is also suggested.

The 2005 iteration acknowledges that a significant bronchodilator response isn’t a very accurate predictor of, well, anything. It doesn’t reliably differentiate COPD from asthma and it’s never been as sensitive as bronchoprovocation testing for diagnosing airway reactivity. The absence of a significant bronchodilator response does not preclude a 2-month trial of the same medicine used to test for response. Given these problems with standardization and accuracy, I was left wondering why anyone bothers ordering the test at all.

In my own practice, I continued to order, conduct, and interpret bronchodilator response according to the suggestions made by the ERS/ATS in 2005 when trying to diagnose asthma. I recognized that a nonsignificant response meant nothing, but bronchodilator response testing was easier to obtain than bronchoprovocation at my hospital. It was a matter of convenience for me and the patient. According to the Global Initiative for Asthma (GINA) Guidelines, a significant bronchodilator response conducted and interpreted as recommended by the ERS/ATS 2005 standard provides objective confirmation of asthma in the presence of characteristic clinical symptoms.

The headline from the ERS/ATS 2022 Technical Standard is that the 12% and 200-cc criteria suggested in 2005 are being retired. Why? Well, much of the variability in the 2005 criteria is explained by height, age, sex, and baseline lung function. These factors obscure change related to intrinsic airway abnormalities. Instead, the authors suggest using a threshold change in the predicted values of FEV₁ and FVC to determine a significant response. Because predicted values incorporate age, height, and sex, the impact from these variables is minimized. Using a percent predicted (PPD) threshold will also minimize the effect from the inverse relationship between measured values and bronchodilator response.

A 10% change in the PPD value for either FEV₁ or FVC constitutes a significant bronchodilator response. Ten percent was chosen because it represents the statistically defined upper limit of normal response; and a greater than 8% change in bronchodilator response is associated with mortality, implying that values above this threshold connote disease. The technical standard seems to be on solid ground here; the rationale is mathematically appropriate and evidence based. The new definition will certainly improve precision.

There’s really no progress on accuracy, though. There are no comments on the protocol to be followed or clinical indications. The reader is referred to the ERS/ATS 2019 technical statement on standardization of spirometry. The statement on standardization is short on details, too, and refers the reader to an online supplement for a suggested protocol. The suggested protocol is identical to that suggested in 2005.

In summary, not a lot is different in the world of bronchodilator response testing. The definition is different now, and though it’s likely to be more precise, we still don’t know enough about accuracy. It’s nice to know that the new criteria will predict mortality, but in clinical practice we don’t use the test for that purpose. The 2022 technical standard acknowledges this and other limitations in a “future directions” paragraph. Perhaps we’ll know more when the next iteration is published.

Dr. Holley is a professor of medicine at Uniformed Services University of the Health Sciences. Bethesda, Md., and a pulmonary medicine/critical care physician at MedStar Washington Hospital Center, Washington. He reported conflicts of interest with Metapharm and the American College of Chest Physicians. A version of this article first appeared on Medscape.com.

In 2002, two landmark trials found that targeted temperature management (TTM) after out-of-hospital cardiac arrest led to improvements in neurologic outcomes. The larger of the two trials found a reduction in mortality. Such treatment benefits are hard to come by in critical care in general and in out-of-hospital cardiac arrest in particular. With the therapeutic overconfidence typical of our profession, my institution embraced TTM quickly and completely soon after these trials were published. Remember, this was “back in the day” when sepsis management included drotrecogin alfa, Cortrosyn stim tests, tight glucose control (90-120 mg/dL), and horrible over-resuscitation via the early goal-directed therapy paradigm.

If you’ve been practicing critical care medicine for more than a few years, you already know where I’m going. Most of the interventions in the preceding paragraph were adopted but discarded before 2010. Though TTM has managed to stand the test of time, our confidence in its benefit has waned since 2002. Hypothermia – temperature management with a goal of 32-36° C – has been struggling to stay relevant ever since the publication of the TTM randomized controlled trial (RCT) in 2013. Then came the HYPERION trial, which brought the 32-36° C target back from the dead (pun definitely intended) in 2019. This is critical care medicine: Today’s life-saving intervention proves harmful tomorrow, but withholding it may constitute malpractice a few months down the road.

So where are we now? Good question. I’ve had seasoned neurointensivists insist that 33° C remains the standard of care and others who’ve endorsed normothermia. So much for finding an answer via my more specialized colleagues.

Let’s go to the guidelines then. Prompted largely by HYPERION, a temperature target of 32-36° C was endorsed in 2020 and 2021. Then came publication of the TTM2 trial, the largest temperature management RCT to date, which found no benefit to targeting 33° C. A network meta-analysis published in 2021 reached a similar conclusion. A recently released update by the same international guideline group now recommends targeting normothermia (< 37.7° C) and avoiding fever, and it specifically says that there is insufficient evidence to support a 32-36° C target. Okay, everyone tracking all that?

Lest I sound overly catty and nihilistic, I see all this in a positive light. Huge credit goes to the critical care medicine academic community for putting together so many RCTs. The scientific reality is that it takes “a lotta” sample size to clarify the effects of an intervention. Throw in the inevitable bevy of confounders (in- vs. out-of-hospital cardiac arrest, resuscitation time, initial rhythm, and so on), and you get a feel for the work required to understand a treatment’s true effects.

Advances in guideline science and the hard, often unpaid work of panels are also important. The guideline panel I’ve been citing came out for aggressive temperature control (32-36° C) a few months before the TTM2 RCT was published. In the past, they updated their recommendations every 5 years, but this time, they were out with a new manuscript that incorporated TTM2 in less than a year. If you’ve been involved at any level with producing guidelines, you can appreciate this achievement. Assuming that aggressive hypothermia is truly harmful, waiting 5 years to incorporate TTM2 could have led to significant morbidity.

I do take issue with you early adopters, though. Given the litany of failed therapies that have shown initial promise, and the well-documented human tendency to underestimate the impact of sample size, your rapid implementation of major interventions is puzzling. One might think you’d learned your lessons after seeing drotrecogin alfa, Cortrosyn stim tests, tight glucose control, early goal-directed therapy, and aggressive TTM come and go. Your recent enthusiasm for vitamin C after publication of a single before-after study suggests that you haven’t.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center, Bethesda, Md. He has received a research grant from Fisher-Paykel.

A version of this article first appeared on Medscape.com.

In 2002, two landmark trials found that targeted temperature management (TTM) after out-of-hospital cardiac arrest led to improvements in neurologic outcomes. The larger of the two trials found a reduction in mortality. Such treatment benefits are hard to come by in critical care in general and in out-of-hospital cardiac arrest in particular. With the therapeutic overconfidence typical of our profession, my institution embraced TTM quickly and completely soon after these trials were published. Remember, this was “back in the day” when sepsis management included drotrecogin alfa, Cortrosyn stim tests, tight glucose control (90-120 mg/dL), and horrible over-resuscitation via the early goal-directed therapy paradigm.

If you’ve been practicing critical care medicine for more than a few years, you already know where I’m going. Most of the interventions in the preceding paragraph were adopted but discarded before 2010. Though TTM has managed to stand the test of time, our confidence in its benefit has waned since 2002. Hypothermia – temperature management with a goal of 32-36° C – has been struggling to stay relevant ever since the publication of the TTM randomized controlled trial (RCT) in 2013. Then came the HYPERION trial, which brought the 32-36° C target back from the dead (pun definitely intended) in 2019. This is critical care medicine: Today’s life-saving intervention proves harmful tomorrow, but withholding it may constitute malpractice a few months down the road.

So where are we now? Good question. I’ve had seasoned neurointensivists insist that 33° C remains the standard of care and others who’ve endorsed normothermia. So much for finding an answer via my more specialized colleagues.

Let’s go to the guidelines then. Prompted largely by HYPERION, a temperature target of 32-36° C was endorsed in 2020 and 2021. Then came publication of the TTM2 trial, the largest temperature management RCT to date, which found no benefit to targeting 33° C. A network meta-analysis published in 2021 reached a similar conclusion. A recently released update by the same international guideline group now recommends targeting normothermia (< 37.7° C) and avoiding fever, and it specifically says that there is insufficient evidence to support a 32-36° C target. Okay, everyone tracking all that?

Lest I sound overly catty and nihilistic, I see all this in a positive light. Huge credit goes to the critical care medicine academic community for putting together so many RCTs. The scientific reality is that it takes “a lotta” sample size to clarify the effects of an intervention. Throw in the inevitable bevy of confounders (in- vs. out-of-hospital cardiac arrest, resuscitation time, initial rhythm, and so on), and you get a feel for the work required to understand a treatment’s true effects.

Advances in guideline science and the hard, often unpaid work of panels are also important. The guideline panel I’ve been citing came out for aggressive temperature control (32-36° C) a few months before the TTM2 RCT was published. In the past, they updated their recommendations every 5 years, but this time, they were out with a new manuscript that incorporated TTM2 in less than a year. If you’ve been involved at any level with producing guidelines, you can appreciate this achievement. Assuming that aggressive hypothermia is truly harmful, waiting 5 years to incorporate TTM2 could have led to significant morbidity.

I do take issue with you early adopters, though. Given the litany of failed therapies that have shown initial promise, and the well-documented human tendency to underestimate the impact of sample size, your rapid implementation of major interventions is puzzling. One might think you’d learned your lessons after seeing drotrecogin alfa, Cortrosyn stim tests, tight glucose control, early goal-directed therapy, and aggressive TTM come and go. Your recent enthusiasm for vitamin C after publication of a single before-after study suggests that you haven’t.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center, Bethesda, Md. He has received a research grant from Fisher-Paykel.

A version of this article first appeared on Medscape.com.

In 2002, two landmark trials found that targeted temperature management (TTM) after out-of-hospital cardiac arrest led to improvements in neurologic outcomes. The larger of the two trials found a reduction in mortality. Such treatment benefits are hard to come by in critical care in general and in out-of-hospital cardiac arrest in particular. With the therapeutic overconfidence typical of our profession, my institution embraced TTM quickly and completely soon after these trials were published. Remember, this was “back in the day” when sepsis management included drotrecogin alfa, Cortrosyn stim tests, tight glucose control (90-120 mg/dL), and horrible over-resuscitation via the early goal-directed therapy paradigm.

If you’ve been practicing critical care medicine for more than a few years, you already know where I’m going. Most of the interventions in the preceding paragraph were adopted but discarded before 2010. Though TTM has managed to stand the test of time, our confidence in its benefit has waned since 2002. Hypothermia – temperature management with a goal of 32-36° C – has been struggling to stay relevant ever since the publication of the TTM randomized controlled trial (RCT) in 2013. Then came the HYPERION trial, which brought the 32-36° C target back from the dead (pun definitely intended) in 2019. This is critical care medicine: Today’s life-saving intervention proves harmful tomorrow, but withholding it may constitute malpractice a few months down the road.

So where are we now? Good question. I’ve had seasoned neurointensivists insist that 33° C remains the standard of care and others who’ve endorsed normothermia. So much for finding an answer via my more specialized colleagues.

Let’s go to the guidelines then. Prompted largely by HYPERION, a temperature target of 32-36° C was endorsed in 2020 and 2021. Then came publication of the TTM2 trial, the largest temperature management RCT to date, which found no benefit to targeting 33° C. A network meta-analysis published in 2021 reached a similar conclusion. A recently released update by the same international guideline group now recommends targeting normothermia (< 37.7° C) and avoiding fever, and it specifically says that there is insufficient evidence to support a 32-36° C target. Okay, everyone tracking all that?

Lest I sound overly catty and nihilistic, I see all this in a positive light. Huge credit goes to the critical care medicine academic community for putting together so many RCTs. The scientific reality is that it takes “a lotta” sample size to clarify the effects of an intervention. Throw in the inevitable bevy of confounders (in- vs. out-of-hospital cardiac arrest, resuscitation time, initial rhythm, and so on), and you get a feel for the work required to understand a treatment’s true effects.

Advances in guideline science and the hard, often unpaid work of panels are also important. The guideline panel I’ve been citing came out for aggressive temperature control (32-36° C) a few months before the TTM2 RCT was published. In the past, they updated their recommendations every 5 years, but this time, they were out with a new manuscript that incorporated TTM2 in less than a year. If you’ve been involved at any level with producing guidelines, you can appreciate this achievement. Assuming that aggressive hypothermia is truly harmful, waiting 5 years to incorporate TTM2 could have led to significant morbidity.

I do take issue with you early adopters, though. Given the litany of failed therapies that have shown initial promise, and the well-documented human tendency to underestimate the impact of sample size, your rapid implementation of major interventions is puzzling. One might think you’d learned your lessons after seeing drotrecogin alfa, Cortrosyn stim tests, tight glucose control, early goal-directed therapy, and aggressive TTM come and go. Your recent enthusiasm for vitamin C after publication of a single before-after study suggests that you haven’t.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center, Bethesda, Md. He has received a research grant from Fisher-Paykel.

A version of this article first appeared on Medscape.com.

Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to noxious air particles. The physiologic results include varying degrees of gas-exchange abnormality and mechanical respiratory limitation, often in the form of dynamic hyperinflation. There’s a third major contributor, though – skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.

When your patients with COPD report dyspnea or exercise intolerance, what do you do? Do you attempt to determine its character to pinpoint its origin? Do you quiz them about their baseline activity levels to quantify their conditioning? I bet you get right to the point and order a cardiopulmonary exercise test (CPET). That way you’ll be able to tease out all the contributors. Nah. Most likely you add an inhaler before continuing to rush through your COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Smoking cessation? Check.

The physiology of dyspnea and exercise limitation in COPD has been extensively studied. Work-of-breathing, dynamic hyperinflation, and gas-exchange inefficiencies interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies the existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (AECOPD) and oral corticosteroids further aggravate skeletal muscle dysfunction.

The Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) Report directs clinicians to use inhalers to manage dyspnea. If they’re already on one inhaler, they get another. This continues until they’re stabilized on a long-acting beta-agonist (LABA), long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B through D disease. Unfortunately, the pulmonary rehabilitation recommendation is buried in the text and doesn’t appear within the popularized pharmacologic algorithms in the report’s figures.

The data for adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QOL) are good. However, although GOLD tells us to keep adding inhalers for the dyspneic patient with COPD, the authors acknowledge that this hasn’t been systematically tested. It’s important to remember that GOLD is a “statement” as opposed to a clinical practice guideline. The difference? A statement doesn’t require the same formal, rigorous scientific analysis known as the GRADE approach. Using this kind of analysis, a recent clinical practice guideline by the American Thoracic Society found no benefit in dyspnea or respiratory QOL with step-up from inhaler monotherapy.

Inhalers won’t do anything for gas-exchange inefficiencies and deconditioning, at least not directly. A recent CPET study from the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2-4 COPD patients. The numbers were higher for those who reported dyspnea. Skeletal muscle dysfunction rates are equally high.

Thus, dyspnea and exercise intolerance are major determinants of QOL in COPD, but inhalers will only get you so far. At a minimum, make sure you get an activity/exercise history from your patients with COPD. For those who are sedentary, provide an exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the complaint before doubling down. Finally, try to get the patient into a good pulmonary rehabilitation program. They’ll thank you afterwards.

Dr. Holley is Associate Professor, department of medicine, Uniformed Services University of the Health Sciences and Program Director, Pulmonary and Critical Care Medical Fellowship, department of medicine, Walter Reed National Military Medical Center, both in Bethesda, Md. He reported receiving research grants from Fisher-Paykel and receiving income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to noxious air particles. The physiologic results include varying degrees of gas-exchange abnormality and mechanical respiratory limitation, often in the form of dynamic hyperinflation. There’s a third major contributor, though – skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.

When your patients with COPD report dyspnea or exercise intolerance, what do you do? Do you attempt to determine its character to pinpoint its origin? Do you quiz them about their baseline activity levels to quantify their conditioning? I bet you get right to the point and order a cardiopulmonary exercise test (CPET). That way you’ll be able to tease out all the contributors. Nah. Most likely you add an inhaler before continuing to rush through your COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Smoking cessation? Check.

The physiology of dyspnea and exercise limitation in COPD has been extensively studied. Work-of-breathing, dynamic hyperinflation, and gas-exchange inefficiencies interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies the existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (AECOPD) and oral corticosteroids further aggravate skeletal muscle dysfunction.

The Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) Report directs clinicians to use inhalers to manage dyspnea. If they’re already on one inhaler, they get another. This continues until they’re stabilized on a long-acting beta-agonist (LABA), long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B through D disease. Unfortunately, the pulmonary rehabilitation recommendation is buried in the text and doesn’t appear within the popularized pharmacologic algorithms in the report’s figures.

The data for adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QOL) are good. However, although GOLD tells us to keep adding inhalers for the dyspneic patient with COPD, the authors acknowledge that this hasn’t been systematically tested. It’s important to remember that GOLD is a “statement” as opposed to a clinical practice guideline. The difference? A statement doesn’t require the same formal, rigorous scientific analysis known as the GRADE approach. Using this kind of analysis, a recent clinical practice guideline by the American Thoracic Society found no benefit in dyspnea or respiratory QOL with step-up from inhaler monotherapy.

Inhalers won’t do anything for gas-exchange inefficiencies and deconditioning, at least not directly. A recent CPET study from the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2-4 COPD patients. The numbers were higher for those who reported dyspnea. Skeletal muscle dysfunction rates are equally high.

Thus, dyspnea and exercise intolerance are major determinants of QOL in COPD, but inhalers will only get you so far. At a minimum, make sure you get an activity/exercise history from your patients with COPD. For those who are sedentary, provide an exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the complaint before doubling down. Finally, try to get the patient into a good pulmonary rehabilitation program. They’ll thank you afterwards.

Dr. Holley is Associate Professor, department of medicine, Uniformed Services University of the Health Sciences and Program Director, Pulmonary and Critical Care Medical Fellowship, department of medicine, Walter Reed National Military Medical Center, both in Bethesda, Md. He reported receiving research grants from Fisher-Paykel and receiving income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

Chronic obstructive pulmonary disease (COPD) is defined by airway obstruction and alveolar damage caused by exposure to noxious air particles. The physiologic results include varying degrees of gas-exchange abnormality and mechanical respiratory limitation, often in the form of dynamic hyperinflation. There’s a third major contributor, though – skeletal muscle deconditioning. Only one of these abnormalities responds to inhalers.

When your patients with COPD report dyspnea or exercise intolerance, what do you do? Do you attempt to determine its character to pinpoint its origin? Do you quiz them about their baseline activity levels to quantify their conditioning? I bet you get right to the point and order a cardiopulmonary exercise test (CPET). That way you’ll be able to tease out all the contributors. Nah. Most likely you add an inhaler before continuing to rush through your COPD quality metrics: Vaccines? Check. Lung cancer screening? Check. Smoking cessation? Check.

The physiology of dyspnea and exercise limitation in COPD has been extensively studied. Work-of-breathing, dynamic hyperinflation, and gas-exchange inefficiencies interact with each other in complex ways to produce symptoms. The presence of deconditioning simply magnifies the existing abnormalities within the respiratory system by creating more strain at lower work rates. Acute exacerbations (AECOPD) and oral corticosteroids further aggravate skeletal muscle dysfunction.

The Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) Report directs clinicians to use inhalers to manage dyspnea. If they’re already on one inhaler, they get another. This continues until they’re stabilized on a long-acting beta-agonist (LABA), long-acting muscarinic antagonist (LAMA), and an inhaled corticosteroid (ICS). The GOLD report also advises pulmonary rehabilitation for any patient with grade B through D disease. Unfortunately, the pulmonary rehabilitation recommendation is buried in the text and doesn’t appear within the popularized pharmacologic algorithms in the report’s figures.

The data for adding inhalers on top of each other to reduce AECOPD and improve overall quality of life (QOL) are good. However, although GOLD tells us to keep adding inhalers for the dyspneic patient with COPD, the authors acknowledge that this hasn’t been systematically tested. It’s important to remember that GOLD is a “statement” as opposed to a clinical practice guideline. The difference? A statement doesn’t require the same formal, rigorous scientific analysis known as the GRADE approach. Using this kind of analysis, a recent clinical practice guideline by the American Thoracic Society found no benefit in dyspnea or respiratory QOL with step-up from inhaler monotherapy.

Inhalers won’t do anything for gas-exchange inefficiencies and deconditioning, at least not directly. A recent CPET study from the CanCOLD network found ventilatory inefficiency in 23% of GOLD 1 and 26% of GOLD 2-4 COPD patients. The numbers were higher for those who reported dyspnea. Skeletal muscle dysfunction rates are equally high.

Thus, dyspnea and exercise intolerance are major determinants of QOL in COPD, but inhalers will only get you so far. At a minimum, make sure you get an activity/exercise history from your patients with COPD. For those who are sedentary, provide an exercise prescription (really, it’s not that hard to do). If dyspnea persists despite LABA or LAMA monotherapy, clarify the complaint before doubling down. Finally, try to get the patient into a good pulmonary rehabilitation program. They’ll thank you afterwards.

Dr. Holley is Associate Professor, department of medicine, Uniformed Services University of the Health Sciences and Program Director, Pulmonary and Critical Care Medical Fellowship, department of medicine, Walter Reed National Military Medical Center, both in Bethesda, Md. He reported receiving research grants from Fisher-Paykel and receiving income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

Hemodynamic instability is rewarded with a sojourn in the intensive care unit (ICU). When the intensivists see it, they’re going to throw fluids at it. Most likely a crystalloid of some type. This has been true for decades, centuries even. When I was a medical student, which was decades but not centuries ago, I used crystalloids every day on the surgical wards, in the operating room, in the emergency department, or on the medicine wards. Medicine docs preferred normal saline (NS) and surgeons used lactated Ringer’s solution (LR). I never gave this a second thought.

During medical school, I was drawn to internal medicine by the heavy emphasis on evidence-based medicine in the field. Prior to 2015 though, there wasn’t much data to support using one crystalloid formulation over another. Pre-2010, we had an American Thoracic Society (ATS) consensus statement on using crystalloid vs. colloid, making recommendations largely drawn from the SAFE trial. The ATS statement also suggested starches may be harmful, a view that was confirmed in a series of articles published in 2012 and 2013. There was less discussion about what type of crystalloid was best.

In 2014, I finally read a paper that compared crystalloid formulations. It was a network meta-analysis, which is “statistician speak” for combining disparate trials to make indirect comparisons. In the absence of large, randomized trials, this approach was a welcome addition to the data we had at the time. The authors concluded that “balanced” (typically LR or Plasma-Lyte) are superior to “unbalanced” (another term for NS) crystalloids. Balanced fluids typically have acetate or lactate and have a higher pH and lower chloride than NS. I found the signal for balanced fluids interesting at the time but promptly forgot about it.

Since 2015, the critical care community has rallied to produce a bevy of large trials comparing balanced vs. unbalanced crystalloids. The first was the SPLIT trial, which showed equivalence. Then came the SMART trial in 2018, which showed balanced fluids were better. Of note, another trial with an identical design (SALT-ED) was published in the same issue of The New England Journal of Medicine as SMART. SALT-ED enrolled patients in the emergency department, not the ICU, but also found benefit to using balanced fluids, albeit not for their primary outcome. I admit, after SMART and SALT-ED were published, I made the switch to LR. A secondary analysis of patients with sepsis pushed me further toward LR, while others withheld judgment.

Then we saw publication of the BaSICs trial, another large, randomized study evaluating crystalloid composition. I was hoping this one might put the issue to rest. That nephrologist who perseverated on every patient’s chloride during morning report would be vindicated. NS would prove to be too unbalanced and would finally be retired. No such luck. This is critical care medicine, where the initial signal is rarely confirmed in the follow-up trials. BaSICs found no difference between crystalloids for most important outcomes. The study did find balanced fluids may worsen outcomes for patients with head injuries.

Finally, there’s the PLUS trial, a large, multicenter randomized controlled trial comparing Plasma-Lyte vs. NS in the ICU. I could make the argument that this trial was the best of the bunch, and it was negative. The researchers did an excellent job of showing that serum pH and chloride levels did vary by fluid composition, but despite this, mortality and renal outcomes did not differ. Case closed? Crystalloid composition doesn’t matter, right?

An editorial that accompanies the BaSICs trial does an outstanding job of reviewing SPLIT, SMART, and BaSICs. The authors discuss design and population differences that may have led to differing results, and there are many. They conclude for most patients in the ICU, there’s no compelling reason to choose one crystalloid over another. Perhaps they’re right.

An updated meta-analysis that included all the studies I’ve mentioned concluded there was an 89% probability that balanced fluid reduces mortality for ICU patients. How could the meta-analysis authors reach this conclusion given all the negative trials? It has to do with their statistical methods – they performed both standard, frequentist (if statistical significance isn’t reached the study, is considered negative) and Bayesian analyses (posterior probability of benefit is calculated, regardless of P value). The frequentist approach was negative, but the posterior probability for benefit remained high.

Personally, I see no reason not to favor LR when resuscitating ICU patients without head injuries. In particular, it seems that medical patients (who made up almost 80% of those in the SMART trial) and those with sepsis may benefit. The critical care community has again outdone itself by performing large, well-designed trials to address important questions. Despite not having a definitive answer on crystalloid resuscitation, we know a lot more than we did when I was a medical student.

Dr. Holley is associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He reported receiving research grant from: Fisher-Paykel and receiving income from the American College of Chest Physicians. A version of this article first appeared on Medscape.com.

Hemodynamic instability is rewarded with a sojourn in the intensive care unit (ICU). When the intensivists see it, they’re going to throw fluids at it. Most likely a crystalloid of some type. This has been true for decades, centuries even. When I was a medical student, which was decades but not centuries ago, I used crystalloids every day on the surgical wards, in the operating room, in the emergency department, or on the medicine wards. Medicine docs preferred normal saline (NS) and surgeons used lactated Ringer’s solution (LR). I never gave this a second thought.

During medical school, I was drawn to internal medicine by the heavy emphasis on evidence-based medicine in the field. Prior to 2015 though, there wasn’t much data to support using one crystalloid formulation over another. Pre-2010, we had an American Thoracic Society (ATS) consensus statement on using crystalloid vs. colloid, making recommendations largely drawn from the SAFE trial. The ATS statement also suggested starches may be harmful, a view that was confirmed in a series of articles published in 2012 and 2013. There was less discussion about what type of crystalloid was best.

In 2014, I finally read a paper that compared crystalloid formulations. It was a network meta-analysis, which is “statistician speak” for combining disparate trials to make indirect comparisons. In the absence of large, randomized trials, this approach was a welcome addition to the data we had at the time. The authors concluded that “balanced” (typically LR or Plasma-Lyte) are superior to “unbalanced” (another term for NS) crystalloids. Balanced fluids typically have acetate or lactate and have a higher pH and lower chloride than NS. I found the signal for balanced fluids interesting at the time but promptly forgot about it.

Since 2015, the critical care community has rallied to produce a bevy of large trials comparing balanced vs. unbalanced crystalloids. The first was the SPLIT trial, which showed equivalence. Then came the SMART trial in 2018, which showed balanced fluids were better. Of note, another trial with an identical design (SALT-ED) was published in the same issue of The New England Journal of Medicine as SMART. SALT-ED enrolled patients in the emergency department, not the ICU, but also found benefit to using balanced fluids, albeit not for their primary outcome. I admit, after SMART and SALT-ED were published, I made the switch to LR. A secondary analysis of patients with sepsis pushed me further toward LR, while others withheld judgment.

Then we saw publication of the BaSICs trial, another large, randomized study evaluating crystalloid composition. I was hoping this one might put the issue to rest. That nephrologist who perseverated on every patient’s chloride during morning report would be vindicated. NS would prove to be too unbalanced and would finally be retired. No such luck. This is critical care medicine, where the initial signal is rarely confirmed in the follow-up trials. BaSICs found no difference between crystalloids for most important outcomes. The study did find balanced fluids may worsen outcomes for patients with head injuries.

Finally, there’s the PLUS trial, a large, multicenter randomized controlled trial comparing Plasma-Lyte vs. NS in the ICU. I could make the argument that this trial was the best of the bunch, and it was negative. The researchers did an excellent job of showing that serum pH and chloride levels did vary by fluid composition, but despite this, mortality and renal outcomes did not differ. Case closed? Crystalloid composition doesn’t matter, right?

An editorial that accompanies the BaSICs trial does an outstanding job of reviewing SPLIT, SMART, and BaSICs. The authors discuss design and population differences that may have led to differing results, and there are many. They conclude for most patients in the ICU, there’s no compelling reason to choose one crystalloid over another. Perhaps they’re right.

An updated meta-analysis that included all the studies I’ve mentioned concluded there was an 89% probability that balanced fluid reduces mortality for ICU patients. How could the meta-analysis authors reach this conclusion given all the negative trials? It has to do with their statistical methods – they performed both standard, frequentist (if statistical significance isn’t reached the study, is considered negative) and Bayesian analyses (posterior probability of benefit is calculated, regardless of P value). The frequentist approach was negative, but the posterior probability for benefit remained high.

Personally, I see no reason not to favor LR when resuscitating ICU patients without head injuries. In particular, it seems that medical patients (who made up almost 80% of those in the SMART trial) and those with sepsis may benefit. The critical care community has again outdone itself by performing large, well-designed trials to address important questions. Despite not having a definitive answer on crystalloid resuscitation, we know a lot more than we did when I was a medical student.

Dr. Holley is associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He reported receiving research grant from: Fisher-Paykel and receiving income from the American College of Chest Physicians. A version of this article first appeared on Medscape.com.

Hemodynamic instability is rewarded with a sojourn in the intensive care unit (ICU). When the intensivists see it, they’re going to throw fluids at it. Most likely a crystalloid of some type. This has been true for decades, centuries even. When I was a medical student, which was decades but not centuries ago, I used crystalloids every day on the surgical wards, in the operating room, in the emergency department, or on the medicine wards. Medicine docs preferred normal saline (NS) and surgeons used lactated Ringer’s solution (LR). I never gave this a second thought.

During medical school, I was drawn to internal medicine by the heavy emphasis on evidence-based medicine in the field. Prior to 2015 though, there wasn’t much data to support using one crystalloid formulation over another. Pre-2010, we had an American Thoracic Society (ATS) consensus statement on using crystalloid vs. colloid, making recommendations largely drawn from the SAFE trial. The ATS statement also suggested starches may be harmful, a view that was confirmed in a series of articles published in 2012 and 2013. There was less discussion about what type of crystalloid was best.

In 2014, I finally read a paper that compared crystalloid formulations. It was a network meta-analysis, which is “statistician speak” for combining disparate trials to make indirect comparisons. In the absence of large, randomized trials, this approach was a welcome addition to the data we had at the time. The authors concluded that “balanced” (typically LR or Plasma-Lyte) are superior to “unbalanced” (another term for NS) crystalloids. Balanced fluids typically have acetate or lactate and have a higher pH and lower chloride than NS. I found the signal for balanced fluids interesting at the time but promptly forgot about it.

Since 2015, the critical care community has rallied to produce a bevy of large trials comparing balanced vs. unbalanced crystalloids. The first was the SPLIT trial, which showed equivalence. Then came the SMART trial in 2018, which showed balanced fluids were better. Of note, another trial with an identical design (SALT-ED) was published in the same issue of The New England Journal of Medicine as SMART. SALT-ED enrolled patients in the emergency department, not the ICU, but also found benefit to using balanced fluids, albeit not for their primary outcome. I admit, after SMART and SALT-ED were published, I made the switch to LR. A secondary analysis of patients with sepsis pushed me further toward LR, while others withheld judgment.

Then we saw publication of the BaSICs trial, another large, randomized study evaluating crystalloid composition. I was hoping this one might put the issue to rest. That nephrologist who perseverated on every patient’s chloride during morning report would be vindicated. NS would prove to be too unbalanced and would finally be retired. No such luck. This is critical care medicine, where the initial signal is rarely confirmed in the follow-up trials. BaSICs found no difference between crystalloids for most important outcomes. The study did find balanced fluids may worsen outcomes for patients with head injuries.

Finally, there’s the PLUS trial, a large, multicenter randomized controlled trial comparing Plasma-Lyte vs. NS in the ICU. I could make the argument that this trial was the best of the bunch, and it was negative. The researchers did an excellent job of showing that serum pH and chloride levels did vary by fluid composition, but despite this, mortality and renal outcomes did not differ. Case closed? Crystalloid composition doesn’t matter, right?

An editorial that accompanies the BaSICs trial does an outstanding job of reviewing SPLIT, SMART, and BaSICs. The authors discuss design and population differences that may have led to differing results, and there are many. They conclude for most patients in the ICU, there’s no compelling reason to choose one crystalloid over another. Perhaps they’re right.

An updated meta-analysis that included all the studies I’ve mentioned concluded there was an 89% probability that balanced fluid reduces mortality for ICU patients. How could the meta-analysis authors reach this conclusion given all the negative trials? It has to do with their statistical methods – they performed both standard, frequentist (if statistical significance isn’t reached the study, is considered negative) and Bayesian analyses (posterior probability of benefit is calculated, regardless of P value). The frequentist approach was negative, but the posterior probability for benefit remained high.

Personally, I see no reason not to favor LR when resuscitating ICU patients without head injuries. In particular, it seems that medical patients (who made up almost 80% of those in the SMART trial) and those with sepsis may benefit. The critical care community has again outdone itself by performing large, well-designed trials to address important questions. Despite not having a definitive answer on crystalloid resuscitation, we know a lot more than we did when I was a medical student.

Dr. Holley is associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He reported receiving research grant from: Fisher-Paykel and receiving income from the American College of Chest Physicians. A version of this article first appeared on Medscape.com.

All else being equal, I’d prefer to do nothing. Whether this is nihilism, laziness, or experience is a matter of debate. The American College of Chest Physicians (CHEST) Guidelines on therapy for venous thromboembolism (VTE) opened a door for withholding treatment for isolated subsegmental pulmonary embolism (ISSPE) in 2016 and kept it open in 2021. I was happy to walk through it and withhold therapy if it wasn’t indicated.

ISSPE is truly a conundrum. With advances in technology, the distal vessels in the lung became visible on commercial CT a little more than 10 years ago. The subsegmental branches are located after the fourth bifurcation of the pulmonary arterial system, and the new technology offered resolution adequate to identify clot in these vessels. But the new technology told us nothing about how to manage clot isolated to the subsegmental vasculature.

Autopsy data say clot in these vessels is common, even in patients who were never diagnosed with VTE while they were alive. To some degree then, the pulmonary arterial system is thought to serve as a filter to prevent clot from crossing to the systemic circulation and causing stroke. This led some to speculate that the subsegmental pulmonary arteries are supposed to contain clot and that we simply couldn’t see it before now. If this theory is correct, the practice of providing anticoagulation for ISSPE could increase bleeding without reducing the risk for VTE recurrence.

Management studies generally supported this concept. In 2007, a trial that was published in JAMA randomized patients to two different diagnostic strategies: ventilation-perfusion (VQ) and CT. CT detected more clot than VQ did, so more anticoagulation was given in the CT arm. Yet, the VTE rate during follow-up was not significantly different between arms. The implication? Some of the clots detected by CT were of lesser clinical significance and didn’t need to be treated.

Meta-analytic data from management trials also suggested that some pulmonary emboli (PE) need not be treated. Data also show when compared with patients who have more proximal PE, those with ISSPE have lower pretest probability for VTE, are less symptomatic, and have a lower burden of coexistent lower extremity thrombosis (deep vein thrombosis [DVT]).

In response to this data, the CHEST Guidelines began cautiously providing the option for withholding therapy in patients who were diagnosed with ISSPE in 2016. Their recommendations stated that patients should be stratified for recurrence risk and have lower extremity ultrasonography performed to rule out DVT. A patient with ISSPE, a low recurrence risk, and a negative ultrasound can have anticoagulation withheld. This made perfect sense to me based on what I thought I knew at the time.

Recently published data cast doubt on my nihilism. The first prospective study designed specifically to assess the safety of withholding therapy for ISSPE suggests that this practice could be dangerous. How did this happen? The trial was very well done, and the authors enrolled the right population. All of the patients had ISSPE, low recurrence risk, and negative lower extremity ultrasound. The authors were anticipating a 1% VTE rate at 90 days based on prior data but instead found a rate of 3.1% (1.6%-6.1%). They point out that this rate is not different from those seen in patients with more proximal PE who are treated with anticoagulation. However, they acknowledge that it is higher than what’s considered acceptable and warrants therapeutic anticoagulation.

So what should we do now? We treat ISSPE, that’s what. All the arguments for withholding therapy remain valid, the recurrence rate is reasonably low, and none of the recurrent VTEs in the new study were fatal. There’s still no doubt that some patients with PE won’t benefit from anticoagulation. Unfortunately, we currently lack the tools to identify them. The risk-benefit ratio for recurrence versus bleeding will be tighter with ISSPE, particularly when there’s only one clot. Unless the bleeding risk is elevated though, the ratio still favors treatment.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center.

A version of this article first appeared on Medscape.com.

All else being equal, I’d prefer to do nothing. Whether this is nihilism, laziness, or experience is a matter of debate. The American College of Chest Physicians (CHEST) Guidelines on therapy for venous thromboembolism (VTE) opened a door for withholding treatment for isolated subsegmental pulmonary embolism (ISSPE) in 2016 and kept it open in 2021. I was happy to walk through it and withhold therapy if it wasn’t indicated.

ISSPE is truly a conundrum. With advances in technology, the distal vessels in the lung became visible on commercial CT a little more than 10 years ago. The subsegmental branches are located after the fourth bifurcation of the pulmonary arterial system, and the new technology offered resolution adequate to identify clot in these vessels. But the new technology told us nothing about how to manage clot isolated to the subsegmental vasculature.

Autopsy data say clot in these vessels is common, even in patients who were never diagnosed with VTE while they were alive. To some degree then, the pulmonary arterial system is thought to serve as a filter to prevent clot from crossing to the systemic circulation and causing stroke. This led some to speculate that the subsegmental pulmonary arteries are supposed to contain clot and that we simply couldn’t see it before now. If this theory is correct, the practice of providing anticoagulation for ISSPE could increase bleeding without reducing the risk for VTE recurrence.

Management studies generally supported this concept. In 2007, a trial that was published in JAMA randomized patients to two different diagnostic strategies: ventilation-perfusion (VQ) and CT. CT detected more clot than VQ did, so more anticoagulation was given in the CT arm. Yet, the VTE rate during follow-up was not significantly different between arms. The implication? Some of the clots detected by CT were of lesser clinical significance and didn’t need to be treated.

Meta-analytic data from management trials also suggested that some pulmonary emboli (PE) need not be treated. Data also show when compared with patients who have more proximal PE, those with ISSPE have lower pretest probability for VTE, are less symptomatic, and have a lower burden of coexistent lower extremity thrombosis (deep vein thrombosis [DVT]).

In response to this data, the CHEST Guidelines began cautiously providing the option for withholding therapy in patients who were diagnosed with ISSPE in 2016. Their recommendations stated that patients should be stratified for recurrence risk and have lower extremity ultrasonography performed to rule out DVT. A patient with ISSPE, a low recurrence risk, and a negative ultrasound can have anticoagulation withheld. This made perfect sense to me based on what I thought I knew at the time.

Recently published data cast doubt on my nihilism. The first prospective study designed specifically to assess the safety of withholding therapy for ISSPE suggests that this practice could be dangerous. How did this happen? The trial was very well done, and the authors enrolled the right population. All of the patients had ISSPE, low recurrence risk, and negative lower extremity ultrasound. The authors were anticipating a 1% VTE rate at 90 days based on prior data but instead found a rate of 3.1% (1.6%-6.1%). They point out that this rate is not different from those seen in patients with more proximal PE who are treated with anticoagulation. However, they acknowledge that it is higher than what’s considered acceptable and warrants therapeutic anticoagulation.

So what should we do now? We treat ISSPE, that’s what. All the arguments for withholding therapy remain valid, the recurrence rate is reasonably low, and none of the recurrent VTEs in the new study were fatal. There’s still no doubt that some patients with PE won’t benefit from anticoagulation. Unfortunately, we currently lack the tools to identify them. The risk-benefit ratio for recurrence versus bleeding will be tighter with ISSPE, particularly when there’s only one clot. Unless the bleeding risk is elevated though, the ratio still favors treatment.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center.

A version of this article first appeared on Medscape.com.

All else being equal, I’d prefer to do nothing. Whether this is nihilism, laziness, or experience is a matter of debate. The American College of Chest Physicians (CHEST) Guidelines on therapy for venous thromboembolism (VTE) opened a door for withholding treatment for isolated subsegmental pulmonary embolism (ISSPE) in 2016 and kept it open in 2021. I was happy to walk through it and withhold therapy if it wasn’t indicated.

ISSPE is truly a conundrum. With advances in technology, the distal vessels in the lung became visible on commercial CT a little more than 10 years ago. The subsegmental branches are located after the fourth bifurcation of the pulmonary arterial system, and the new technology offered resolution adequate to identify clot in these vessels. But the new technology told us nothing about how to manage clot isolated to the subsegmental vasculature.

Autopsy data say clot in these vessels is common, even in patients who were never diagnosed with VTE while they were alive. To some degree then, the pulmonary arterial system is thought to serve as a filter to prevent clot from crossing to the systemic circulation and causing stroke. This led some to speculate that the subsegmental pulmonary arteries are supposed to contain clot and that we simply couldn’t see it before now. If this theory is correct, the practice of providing anticoagulation for ISSPE could increase bleeding without reducing the risk for VTE recurrence.

Management studies generally supported this concept. In 2007, a trial that was published in JAMA randomized patients to two different diagnostic strategies: ventilation-perfusion (VQ) and CT. CT detected more clot than VQ did, so more anticoagulation was given in the CT arm. Yet, the VTE rate during follow-up was not significantly different between arms. The implication? Some of the clots detected by CT were of lesser clinical significance and didn’t need to be treated.

Meta-analytic data from management trials also suggested that some pulmonary emboli (PE) need not be treated. Data also show when compared with patients who have more proximal PE, those with ISSPE have lower pretest probability for VTE, are less symptomatic, and have a lower burden of coexistent lower extremity thrombosis (deep vein thrombosis [DVT]).

In response to this data, the CHEST Guidelines began cautiously providing the option for withholding therapy in patients who were diagnosed with ISSPE in 2016. Their recommendations stated that patients should be stratified for recurrence risk and have lower extremity ultrasonography performed to rule out DVT. A patient with ISSPE, a low recurrence risk, and a negative ultrasound can have anticoagulation withheld. This made perfect sense to me based on what I thought I knew at the time.

Recently published data cast doubt on my nihilism. The first prospective study designed specifically to assess the safety of withholding therapy for ISSPE suggests that this practice could be dangerous. How did this happen? The trial was very well done, and the authors enrolled the right population. All of the patients had ISSPE, low recurrence risk, and negative lower extremity ultrasound. The authors were anticipating a 1% VTE rate at 90 days based on prior data but instead found a rate of 3.1% (1.6%-6.1%). They point out that this rate is not different from those seen in patients with more proximal PE who are treated with anticoagulation. However, they acknowledge that it is higher than what’s considered acceptable and warrants therapeutic anticoagulation.

So what should we do now? We treat ISSPE, that’s what. All the arguments for withholding therapy remain valid, the recurrence rate is reasonably low, and none of the recurrent VTEs in the new study were fatal. There’s still no doubt that some patients with PE won’t benefit from anticoagulation. Unfortunately, we currently lack the tools to identify them. The risk-benefit ratio for recurrence versus bleeding will be tighter with ISSPE, particularly when there’s only one clot. Unless the bleeding risk is elevated though, the ratio still favors treatment.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center.

A version of this article first appeared on Medscape.com.

Nothing about sarcoidosis is easy. First identified in 1877, it is quite common. In the United States, lifetime risk is 2.4% and 0.85% for African American persons and White persons, respectively. Still, it remains an enigma. Despite study of its genetics and immunopathology, we don’t know its cause. Diagnosis is challenging because noncaseating granulomas, the tissue finding associated with sarcoidosis, aren’t specific for the disease. With the exception of Löfgren syndrome, a well-described sarcoid presentation that portends an excellent prognosis, initial signs and symptoms are variable and disease course is unpredictable. Alas, because sarcoid affects the lungs in more than 90% of patients, the general pulmonologist is left carrying the bag as the “sarcoidologist.”

The inherent heterogeneity of sarcoid makes it challenging to study. In the modern era of evidence-based medicine, it’s hard to say much about it with certainty. The American Thoracic Society (ATS) is one of just a few, premier organizations that creates respiratory medicine guidelines. In 1999, they published a sarcoid consensus statement with the European Respiratory Society (ERS), another outstanding and influential respiratory medicine organization, and the World Association of Sarcoidosis and other Granulomatous Disorders (WASOG). For the past 20 years, I’ve been referring trainees to this document for guidance on managing their patients with sarcoid.

Twenty years later, sarcoid remains frustrating and mysterious, but much has changed. Our methods for evaluating evidence and creating guidelines are now based on the GRADE criteria. Now that we have easy access to advanced technologies such as endobronchial ultrasound, obtaining tissue for diagnosis is easier. Our study of sarcoid itself has advanced, with large cohorts providing data on phenotyping, new immunosuppressants being used for treatment, and an improved understanding of cardiac sarcoidosis. In short, we’re in need of a sarcoidosis guideline for the 21st century.

Within in the past 18 months, the ATS and ERS have delivered updated guidelines for diagnosis and treatment. Despite the advancements cited above, sarcoid remains difficult to study. So predictably, neither document issues earth-shattering conclusions. Truth be told, well-done guidelines rarely do. They do provide several important updates that physicians managing patients with sarcoid should note.

The guideline on diagnosis provides recommendations for routine monitoring after diagnosis. Many practicing clinicians took from the 1999 ATS/ERS/WASOG consensus statement that all patients with sarcoid needed to be seen annually. At pulmonary clinics where I’ve worked, we’ve defaulted to annual follow-up for everyone, usually with chest radiography, lab testing, electrocardiography, and referral to ophthalmology. Because a majority of patients with sarcoid will remain asymptomatic or experience spontaneous remission, this practice never really seemed cost-effective or clinically efficient. The new guidelines are far more proscriptive on what monitoring is required and grade requirements at specific levels of certainty and often advise symptom-based assessments in lieu of reflexive annual testing.

The ERS guideline on treatment provides a thoughtful discussion of corticosteroid indications and dosing, broken down by underlying disease severity (assessed by lung function abnormalities and imaging). It also recognizes that two of the most common sarcoid symptoms are fatigue and dyspnea, which are both inherently nonspecific. In practice, proving these symptoms are directly attributable to sarcoid is challenging. The treatment guideline allows for flexibility in these cases, with shared decision-making and trials of low-dose steroids recommended. This seems an excellent hedge against overtreatment with immunosuppressive medications that have harmful side effects.

The ATS and ERS guidelines are not without controversy. Their approach to cardiac sarcoid differs slightly from that recommended by a commonly cited Heart Rhythm Society consensus statement, and despite discussing treatment options, the section on fatigue is quite limited. These two facts and other limitations largely reflect differing interpretations of the limited data; they do not detract from the overall importance of the ATS and ERS guidelines. Sarcoid remains an enigma, but little by little the outstanding academic physicians at the ATS and ERS are providing clarity.

Dr. Holley is an associate professor, department of medicine, Uniformed Services University (USU); program director, pulmonary and critical care medical fellowship, department of medicine, Walter Reed National Military Medical Center, Bethesda, Maryland. He has received a research grant from Fisher-Paykel and income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

Nothing about sarcoidosis is easy. First identified in 1877, it is quite common. In the United States, lifetime risk is 2.4% and 0.85% for African American persons and White persons, respectively. Still, it remains an enigma. Despite study of its genetics and immunopathology, we don’t know its cause. Diagnosis is challenging because noncaseating granulomas, the tissue finding associated with sarcoidosis, aren’t specific for the disease. With the exception of Löfgren syndrome, a well-described sarcoid presentation that portends an excellent prognosis, initial signs and symptoms are variable and disease course is unpredictable. Alas, because sarcoid affects the lungs in more than 90% of patients, the general pulmonologist is left carrying the bag as the “sarcoidologist.”

The inherent heterogeneity of sarcoid makes it challenging to study. In the modern era of evidence-based medicine, it’s hard to say much about it with certainty. The American Thoracic Society (ATS) is one of just a few, premier organizations that creates respiratory medicine guidelines. In 1999, they published a sarcoid consensus statement with the European Respiratory Society (ERS), another outstanding and influential respiratory medicine organization, and the World Association of Sarcoidosis and other Granulomatous Disorders (WASOG). For the past 20 years, I’ve been referring trainees to this document for guidance on managing their patients with sarcoid.

Twenty years later, sarcoid remains frustrating and mysterious, but much has changed. Our methods for evaluating evidence and creating guidelines are now based on the GRADE criteria. Now that we have easy access to advanced technologies such as endobronchial ultrasound, obtaining tissue for diagnosis is easier. Our study of sarcoid itself has advanced, with large cohorts providing data on phenotyping, new immunosuppressants being used for treatment, and an improved understanding of cardiac sarcoidosis. In short, we’re in need of a sarcoidosis guideline for the 21st century.

Within in the past 18 months, the ATS and ERS have delivered updated guidelines for diagnosis and treatment. Despite the advancements cited above, sarcoid remains difficult to study. So predictably, neither document issues earth-shattering conclusions. Truth be told, well-done guidelines rarely do. They do provide several important updates that physicians managing patients with sarcoid should note.

The guideline on diagnosis provides recommendations for routine monitoring after diagnosis. Many practicing clinicians took from the 1999 ATS/ERS/WASOG consensus statement that all patients with sarcoid needed to be seen annually. At pulmonary clinics where I’ve worked, we’ve defaulted to annual follow-up for everyone, usually with chest radiography, lab testing, electrocardiography, and referral to ophthalmology. Because a majority of patients with sarcoid will remain asymptomatic or experience spontaneous remission, this practice never really seemed cost-effective or clinically efficient. The new guidelines are far more proscriptive on what monitoring is required and grade requirements at specific levels of certainty and often advise symptom-based assessments in lieu of reflexive annual testing.

The ERS guideline on treatment provides a thoughtful discussion of corticosteroid indications and dosing, broken down by underlying disease severity (assessed by lung function abnormalities and imaging). It also recognizes that two of the most common sarcoid symptoms are fatigue and dyspnea, which are both inherently nonspecific. In practice, proving these symptoms are directly attributable to sarcoid is challenging. The treatment guideline allows for flexibility in these cases, with shared decision-making and trials of low-dose steroids recommended. This seems an excellent hedge against overtreatment with immunosuppressive medications that have harmful side effects.

The ATS and ERS guidelines are not without controversy. Their approach to cardiac sarcoid differs slightly from that recommended by a commonly cited Heart Rhythm Society consensus statement, and despite discussing treatment options, the section on fatigue is quite limited. These two facts and other limitations largely reflect differing interpretations of the limited data; they do not detract from the overall importance of the ATS and ERS guidelines. Sarcoid remains an enigma, but little by little the outstanding academic physicians at the ATS and ERS are providing clarity.

Dr. Holley is an associate professor, department of medicine, Uniformed Services University (USU); program director, pulmonary and critical care medical fellowship, department of medicine, Walter Reed National Military Medical Center, Bethesda, Maryland. He has received a research grant from Fisher-Paykel and income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

Nothing about sarcoidosis is easy. First identified in 1877, it is quite common. In the United States, lifetime risk is 2.4% and 0.85% for African American persons and White persons, respectively. Still, it remains an enigma. Despite study of its genetics and immunopathology, we don’t know its cause. Diagnosis is challenging because noncaseating granulomas, the tissue finding associated with sarcoidosis, aren’t specific for the disease. With the exception of Löfgren syndrome, a well-described sarcoid presentation that portends an excellent prognosis, initial signs and symptoms are variable and disease course is unpredictable. Alas, because sarcoid affects the lungs in more than 90% of patients, the general pulmonologist is left carrying the bag as the “sarcoidologist.”

The inherent heterogeneity of sarcoid makes it challenging to study. In the modern era of evidence-based medicine, it’s hard to say much about it with certainty. The American Thoracic Society (ATS) is one of just a few, premier organizations that creates respiratory medicine guidelines. In 1999, they published a sarcoid consensus statement with the European Respiratory Society (ERS), another outstanding and influential respiratory medicine organization, and the World Association of Sarcoidosis and other Granulomatous Disorders (WASOG). For the past 20 years, I’ve been referring trainees to this document for guidance on managing their patients with sarcoid.

Twenty years later, sarcoid remains frustrating and mysterious, but much has changed. Our methods for evaluating evidence and creating guidelines are now based on the GRADE criteria. Now that we have easy access to advanced technologies such as endobronchial ultrasound, obtaining tissue for diagnosis is easier. Our study of sarcoid itself has advanced, with large cohorts providing data on phenotyping, new immunosuppressants being used for treatment, and an improved understanding of cardiac sarcoidosis. In short, we’re in need of a sarcoidosis guideline for the 21st century.

Within in the past 18 months, the ATS and ERS have delivered updated guidelines for diagnosis and treatment. Despite the advancements cited above, sarcoid remains difficult to study. So predictably, neither document issues earth-shattering conclusions. Truth be told, well-done guidelines rarely do. They do provide several important updates that physicians managing patients with sarcoid should note.

The guideline on diagnosis provides recommendations for routine monitoring after diagnosis. Many practicing clinicians took from the 1999 ATS/ERS/WASOG consensus statement that all patients with sarcoid needed to be seen annually. At pulmonary clinics where I’ve worked, we’ve defaulted to annual follow-up for everyone, usually with chest radiography, lab testing, electrocardiography, and referral to ophthalmology. Because a majority of patients with sarcoid will remain asymptomatic or experience spontaneous remission, this practice never really seemed cost-effective or clinically efficient. The new guidelines are far more proscriptive on what monitoring is required and grade requirements at specific levels of certainty and often advise symptom-based assessments in lieu of reflexive annual testing.

The ERS guideline on treatment provides a thoughtful discussion of corticosteroid indications and dosing, broken down by underlying disease severity (assessed by lung function abnormalities and imaging). It also recognizes that two of the most common sarcoid symptoms are fatigue and dyspnea, which are both inherently nonspecific. In practice, proving these symptoms are directly attributable to sarcoid is challenging. The treatment guideline allows for flexibility in these cases, with shared decision-making and trials of low-dose steroids recommended. This seems an excellent hedge against overtreatment with immunosuppressive medications that have harmful side effects.

The ATS and ERS guidelines are not without controversy. Their approach to cardiac sarcoid differs slightly from that recommended by a commonly cited Heart Rhythm Society consensus statement, and despite discussing treatment options, the section on fatigue is quite limited. These two facts and other limitations largely reflect differing interpretations of the limited data; they do not detract from the overall importance of the ATS and ERS guidelines. Sarcoid remains an enigma, but little by little the outstanding academic physicians at the ATS and ERS are providing clarity.

Dr. Holley is an associate professor, department of medicine, Uniformed Services University (USU); program director, pulmonary and critical care medical fellowship, department of medicine, Walter Reed National Military Medical Center, Bethesda, Maryland. He has received a research grant from Fisher-Paykel and income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

CT scans are used to diagnose, track, and screen for a variety of diseases. Even before the National Lung Screening Trial research team proved that an annual CT scan could reduce lung cancer mortality, physicians were ordering 62 million scans per year. At the same time, advances in technology have improved power and resolution. The CT scan has changed the way that health care is practiced, and that change has created challenges and opportunities. We’re now experiencing a modern pandemic of incidental findings. It falls to the clinician to decide when the dreaded “incidentaloma” is clinically relevant.

Pulmonologists are adept at managing pulmonary nodules found on scans performed for other reasons. Multiple risk-stratification models exist and guidelines provide algorithms that are easy to follow. Radiologists generally reference these guidelines in their reports and instruct the clinician on how to proceed. A less common but still prevalent incidental finding in the pulmonary parenchyma is an interstitial lung abnormality (ILA).

What is an ILA and how is it defined? Well, it’s tricky. A position paper from the Fleischner Society outlines specific radiographic findings that are consistent with an ILA: honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone. To be called an ILA, the patient in whom these abnormalities are present must not yet be diagnosed with a clinical interstitial lung disease (ILD). In one sense, then, an ILA can be considered a subclinical ILD. Detecting fibrosing ILDs before they progress is of vital importance because lung function lost cannot be restored. ILAs detected on CT scan are associated with increased morbidity and mortality, and 50% will progress radiographically over a period of 5 years. Case closed then, right? ILAs represent subclinical ILD and they should be treated as such. Let’s throw antifibrotics at them and preserve lung function!

Not so fast. ILAs are identified in 2%-10% of adults and 7%-9% of patients with higher smoking rates and cardiovascular risk factors. They’re observed in up to 10% of CTs done for lung cancer screening. Their prevalence is far greater than that of all ILDs combined, so most will not progress to clinically important ILD. Furthermore, the elevated mortality rates may not be directly attributable to the ILAs, and some of the excess morbidity is of questionable clinical significance. The million-dollar question: How do we identify which ILAs are important?

A new paper published online in the CHEST journal tackled this difficult question. The authors designed an iterative survey which they provided to pulmonologists and thoracic radiologists with expertise in ILD. The survey assessed the experts’ views on how to diagnose and manage ILAs. They included a total of 44 experts, and greater than 75% agreement on a particular response constituted a consensus. Consensus was reached on proper annotation on reports and referral to pulmonologists for lung testing.

The short version: ILAs should be annotated on radiology reports and in most cases should trigger referral to a pulmonologist. In underresourced areas with few specialists, there are probably scenarios where high-resolution CT or lung function testing could be recommended without referral. In my opinion, though, you’re going to need a good pulmonologist to sort these out and avoid unnecessary testing, treatment, and anxiety. Recognition of ILAs is an important step forward in identifying ILD early; let’s just be careful not to diagnose disease when it doesn’t exist.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed receiving a research grant from Fisher-Paykel and income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

CT scans are used to diagnose, track, and screen for a variety of diseases. Even before the National Lung Screening Trial research team proved that an annual CT scan could reduce lung cancer mortality, physicians were ordering 62 million scans per year. At the same time, advances in technology have improved power and resolution. The CT scan has changed the way that health care is practiced, and that change has created challenges and opportunities. We’re now experiencing a modern pandemic of incidental findings. It falls to the clinician to decide when the dreaded “incidentaloma” is clinically relevant.

Pulmonologists are adept at managing pulmonary nodules found on scans performed for other reasons. Multiple risk-stratification models exist and guidelines provide algorithms that are easy to follow. Radiologists generally reference these guidelines in their reports and instruct the clinician on how to proceed. A less common but still prevalent incidental finding in the pulmonary parenchyma is an interstitial lung abnormality (ILA).

What is an ILA and how is it defined? Well, it’s tricky. A position paper from the Fleischner Society outlines specific radiographic findings that are consistent with an ILA: honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone. To be called an ILA, the patient in whom these abnormalities are present must not yet be diagnosed with a clinical interstitial lung disease (ILD). In one sense, then, an ILA can be considered a subclinical ILD. Detecting fibrosing ILDs before they progress is of vital importance because lung function lost cannot be restored. ILAs detected on CT scan are associated with increased morbidity and mortality, and 50% will progress radiographically over a period of 5 years. Case closed then, right? ILAs represent subclinical ILD and they should be treated as such. Let’s throw antifibrotics at them and preserve lung function!

Not so fast. ILAs are identified in 2%-10% of adults and 7%-9% of patients with higher smoking rates and cardiovascular risk factors. They’re observed in up to 10% of CTs done for lung cancer screening. Their prevalence is far greater than that of all ILDs combined, so most will not progress to clinically important ILD. Furthermore, the elevated mortality rates may not be directly attributable to the ILAs, and some of the excess morbidity is of questionable clinical significance. The million-dollar question: How do we identify which ILAs are important?

A new paper published online in the CHEST journal tackled this difficult question. The authors designed an iterative survey which they provided to pulmonologists and thoracic radiologists with expertise in ILD. The survey assessed the experts’ views on how to diagnose and manage ILAs. They included a total of 44 experts, and greater than 75% agreement on a particular response constituted a consensus. Consensus was reached on proper annotation on reports and referral to pulmonologists for lung testing.

The short version: ILAs should be annotated on radiology reports and in most cases should trigger referral to a pulmonologist. In underresourced areas with few specialists, there are probably scenarios where high-resolution CT or lung function testing could be recommended without referral. In my opinion, though, you’re going to need a good pulmonologist to sort these out and avoid unnecessary testing, treatment, and anxiety. Recognition of ILAs is an important step forward in identifying ILD early; let’s just be careful not to diagnose disease when it doesn’t exist.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed receiving a research grant from Fisher-Paykel and income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

CT scans are used to diagnose, track, and screen for a variety of diseases. Even before the National Lung Screening Trial research team proved that an annual CT scan could reduce lung cancer mortality, physicians were ordering 62 million scans per year. At the same time, advances in technology have improved power and resolution. The CT scan has changed the way that health care is practiced, and that change has created challenges and opportunities. We’re now experiencing a modern pandemic of incidental findings. It falls to the clinician to decide when the dreaded “incidentaloma” is clinically relevant.

Pulmonologists are adept at managing pulmonary nodules found on scans performed for other reasons. Multiple risk-stratification models exist and guidelines provide algorithms that are easy to follow. Radiologists generally reference these guidelines in their reports and instruct the clinician on how to proceed. A less common but still prevalent incidental finding in the pulmonary parenchyma is an interstitial lung abnormality (ILA).

What is an ILA and how is it defined? Well, it’s tricky. A position paper from the Fleischner Society outlines specific radiographic findings that are consistent with an ILA: honeycombing, traction bronchiectasis, parenchymal distortions, and reticular abnormalities that take up more than 5% of a particular lung zone. To be called an ILA, the patient in whom these abnormalities are present must not yet be diagnosed with a clinical interstitial lung disease (ILD). In one sense, then, an ILA can be considered a subclinical ILD. Detecting fibrosing ILDs before they progress is of vital importance because lung function lost cannot be restored. ILAs detected on CT scan are associated with increased morbidity and mortality, and 50% will progress radiographically over a period of 5 years. Case closed then, right? ILAs represent subclinical ILD and they should be treated as such. Let’s throw antifibrotics at them and preserve lung function!

Not so fast. ILAs are identified in 2%-10% of adults and 7%-9% of patients with higher smoking rates and cardiovascular risk factors. They’re observed in up to 10% of CTs done for lung cancer screening. Their prevalence is far greater than that of all ILDs combined, so most will not progress to clinically important ILD. Furthermore, the elevated mortality rates may not be directly attributable to the ILAs, and some of the excess morbidity is of questionable clinical significance. The million-dollar question: How do we identify which ILAs are important?

A new paper published online in the CHEST journal tackled this difficult question. The authors designed an iterative survey which they provided to pulmonologists and thoracic radiologists with expertise in ILD. The survey assessed the experts’ views on how to diagnose and manage ILAs. They included a total of 44 experts, and greater than 75% agreement on a particular response constituted a consensus. Consensus was reached on proper annotation on reports and referral to pulmonologists for lung testing.

The short version: ILAs should be annotated on radiology reports and in most cases should trigger referral to a pulmonologist. In underresourced areas with few specialists, there are probably scenarios where high-resolution CT or lung function testing could be recommended without referral. In my opinion, though, you’re going to need a good pulmonologist to sort these out and avoid unnecessary testing, treatment, and anxiety. Recognition of ILAs is an important step forward in identifying ILD early; let’s just be careful not to diagnose disease when it doesn’t exist.

Aaron B. Holley, MD, is an associate professor of medicine at Uniformed Services University and program director of pulmonary and critical care medicine at Walter Reed National Military Medical Center. He covers a wide range of topics in pulmonary, critical care, and sleep medicine. He disclosed receiving a research grant from Fisher-Paykel and income from the American College of Chest Physicians.

A version of this article first appeared on Medscape.com.

In past posts for this news organization, I’ve railed against the cost of inappropriate prescriptions for oxygen. A recent review recommended against prescribing oxygen for patients with isolated exertional or nocturnal desaturations, and recently published randomized trials found no demonstrable benefit to oxygen use in the absence of resting hypoxemia. My oxygen ire was previously directed at inappropriate screening for nocturnal or exertional hypoxemia in outpatients with chronic obstructive pulmonary disorder (COPD), a common practice in clinics where I’ve worked. However, oxygen prescriptions at hospital discharge are a far more pernicious cause of wasted resources.

Prescriptions at hospital discharge, sometimes referred to as short-term oxygen therapy (STOT), account for a large proportion of total oxygen use. Past data have shown that the term “STOT” is a misnomer, as most patients provided with oxygen at discharge are never reevaluated and become long-term oxygen users. The high cost of durable medical equipment related to oxygen delivery prompted the American Thoracic Society and American College of Chest Physicians to recommend postdischarge reassessment of oxygen needs in their Choosing Wisely campaign for adult pulmonary medicine.

A recent study published in the Annals of the American Thoracic Society (Ann ATS) highlights the benefits available if we decide to “choose wisely.” The authors studied patients covered by Veterans Affairs and discharged on STOT between 2006 and 2011. Only 43.6% (287/659) had complete reassessment (oxygen testing at rest and with ambulation) within 90 days. Of those, 124 (43.2%) were eligible for discontinuation via Centers for Medicare & Medicaid Services guidelines. A total of 70.7% (466/659) were tested at rest, and only 15.7% (73/466) had resting hypoxemia. If one accepts the results of the recently published Long-Term Oxygen Treatment Trial, this means that 84.3% (393/466) would be eligible for oxygen discontinuation.

The Ann ATS study provides a blueprint for how we might improve these dismal numbers. There were five separate sites reviewed in their paper. At one site, reassessment occurred in 78.5% of STOT patients and 100% had oxygen discontinued when appropriate. What was their secret? An automatic alert system and a dedicated clinic, coordinator, and respiratory therapist. Also, among the 124 patients who had a full reassessment and no longer qualified for oxygen, 86.3% had it discontinued.

There are countless reasons why STOT is common, but discontinuation is not. Most COPD exacerbations are managed by nonpulmonologists on general medicine wards prior to discharge. In my experience, these physicians are reluctant to release a patient with exertional hypoxia without STOT. They also assume that the pulmonary clinic will do its job during the obligatory outpatient follow-up appointment they schedule with us. At the follow-up, the patient and physician are reluctant to stop therapy because of psychological dependence and therapeutic overconfidence, respectively.

In summary, STOT following hospitalization comprises the majority of all oxygen prescriptions. Historically, the United States provides far more oxygen than other developed countries, and only CMS reimbursement changes have bent the “overprescription” curve. The Ann ATS study shows that a well-designed program at the hospital level can put oxygen decisions back in the hands of providers.

Let’s “choose wisely” and follow what works, or we’ll have only ourselves to blame when reimbursement decisions are taken out of our hands.

A version of this article first appeared on Medscape.com.

In past posts for this news organization, I’ve railed against the cost of inappropriate prescriptions for oxygen. A recent review recommended against prescribing oxygen for patients with isolated exertional or nocturnal desaturations, and recently published randomized trials found no demonstrable benefit to oxygen use in the absence of resting hypoxemia. My oxygen ire was previously directed at inappropriate screening for nocturnal or exertional hypoxemia in outpatients with chronic obstructive pulmonary disorder (COPD), a common practice in clinics where I’ve worked. However, oxygen prescriptions at hospital discharge are a far more pernicious cause of wasted resources.

Prescriptions at hospital discharge, sometimes referred to as short-term oxygen therapy (STOT), account for a large proportion of total oxygen use. Past data have shown that the term “STOT” is a misnomer, as most patients provided with oxygen at discharge are never reevaluated and become long-term oxygen users. The high cost of durable medical equipment related to oxygen delivery prompted the American Thoracic Society and American College of Chest Physicians to recommend postdischarge reassessment of oxygen needs in their Choosing Wisely campaign for adult pulmonary medicine.

A recent study published in the Annals of the American Thoracic Society (Ann ATS) highlights the benefits available if we decide to “choose wisely.” The authors studied patients covered by Veterans Affairs and discharged on STOT between 2006 and 2011. Only 43.6% (287/659) had complete reassessment (oxygen testing at rest and with ambulation) within 90 days. Of those, 124 (43.2%) were eligible for discontinuation via Centers for Medicare & Medicaid Services guidelines. A total of 70.7% (466/659) were tested at rest, and only 15.7% (73/466) had resting hypoxemia. If one accepts the results of the recently published Long-Term Oxygen Treatment Trial, this means that 84.3% (393/466) would be eligible for oxygen discontinuation.

The Ann ATS study provides a blueprint for how we might improve these dismal numbers. There were five separate sites reviewed in their paper. At one site, reassessment occurred in 78.5% of STOT patients and 100% had oxygen discontinued when appropriate. What was their secret? An automatic alert system and a dedicated clinic, coordinator, and respiratory therapist. Also, among the 124 patients who had a full reassessment and no longer qualified for oxygen, 86.3% had it discontinued.

There are countless reasons why STOT is common, but discontinuation is not. Most COPD exacerbations are managed by nonpulmonologists on general medicine wards prior to discharge. In my experience, these physicians are reluctant to release a patient with exertional hypoxia without STOT. They also assume that the pulmonary clinic will do its job during the obligatory outpatient follow-up appointment they schedule with us. At the follow-up, the patient and physician are reluctant to stop therapy because of psychological dependence and therapeutic overconfidence, respectively.

In summary, STOT following hospitalization comprises the majority of all oxygen prescriptions. Historically, the United States provides far more oxygen than other developed countries, and only CMS reimbursement changes have bent the “overprescription” curve. The Ann ATS study shows that a well-designed program at the hospital level can put oxygen decisions back in the hands of providers.

Let’s “choose wisely” and follow what works, or we’ll have only ourselves to blame when reimbursement decisions are taken out of our hands.

A version of this article first appeared on Medscape.com.

In past posts for this news organization, I’ve railed against the cost of inappropriate prescriptions for oxygen. A recent review recommended against prescribing oxygen for patients with isolated exertional or nocturnal desaturations, and recently published randomized trials found no demonstrable benefit to oxygen use in the absence of resting hypoxemia. My oxygen ire was previously directed at inappropriate screening for nocturnal or exertional hypoxemia in outpatients with chronic obstructive pulmonary disorder (COPD), a common practice in clinics where I’ve worked. However, oxygen prescriptions at hospital discharge are a far more pernicious cause of wasted resources.

Prescriptions at hospital discharge, sometimes referred to as short-term oxygen therapy (STOT), account for a large proportion of total oxygen use. Past data have shown that the term “STOT” is a misnomer, as most patients provided with oxygen at discharge are never reevaluated and become long-term oxygen users. The high cost of durable medical equipment related to oxygen delivery prompted the American Thoracic Society and American College of Chest Physicians to recommend postdischarge reassessment of oxygen needs in their Choosing Wisely campaign for adult pulmonary medicine.

A recent study published in the Annals of the American Thoracic Society (Ann ATS) highlights the benefits available if we decide to “choose wisely.” The authors studied patients covered by Veterans Affairs and discharged on STOT between 2006 and 2011. Only 43.6% (287/659) had complete reassessment (oxygen testing at rest and with ambulation) within 90 days. Of those, 124 (43.2%) were eligible for discontinuation via Centers for Medicare & Medicaid Services guidelines. A total of 70.7% (466/659) were tested at rest, and only 15.7% (73/466) had resting hypoxemia. If one accepts the results of the recently published Long-Term Oxygen Treatment Trial, this means that 84.3% (393/466) would be eligible for oxygen discontinuation.

The Ann ATS study provides a blueprint for how we might improve these dismal numbers. There were five separate sites reviewed in their paper. At one site, reassessment occurred in 78.5% of STOT patients and 100% had oxygen discontinued when appropriate. What was their secret? An automatic alert system and a dedicated clinic, coordinator, and respiratory therapist. Also, among the 124 patients who had a full reassessment and no longer qualified for oxygen, 86.3% had it discontinued.

There are countless reasons why STOT is common, but discontinuation is not. Most COPD exacerbations are managed by nonpulmonologists on general medicine wards prior to discharge. In my experience, these physicians are reluctant to release a patient with exertional hypoxia without STOT. They also assume that the pulmonary clinic will do its job during the obligatory outpatient follow-up appointment they schedule with us. At the follow-up, the patient and physician are reluctant to stop therapy because of psychological dependence and therapeutic overconfidence, respectively.

In summary, STOT following hospitalization comprises the majority of all oxygen prescriptions. Historically, the United States provides far more oxygen than other developed countries, and only CMS reimbursement changes have bent the “overprescription” curve. The Ann ATS study shows that a well-designed program at the hospital level can put oxygen decisions back in the hands of providers.

Let’s “choose wisely” and follow what works, or we’ll have only ourselves to blame when reimbursement decisions are taken out of our hands.

A version of this article first appeared on Medscape.com.

The COVID-19 pandemic has stressed all aspects of the world’s health care systems. The sheer volume of pandemic-related research produced over the past year has been challenging to process. This is as it should be, given its unprecedented spread and related morbidity and mortality. However, such rapid production and application leaves little time for proper vetting. Large numbers of providers adopted suggested, but largely unproven, practices that deviated from pre–COVID-19 guidelines. These “early adopters” theorized that COVID-19–related disease processes were different, necessitating a modification to existing practices.

While many unproven approaches were suggested and implemented, I’ll focus on two approaches. First, throughout the pandemic, many have argued that COVID-19 causes a novel acute respiratory distress syndrome (ARDS) phenotype. Early on, a group of prominent Italian ARDS researchers made a compelling case for physiological differences, concluding that early intubation was required to avoid large transpulmonary pressure swings. The logic was that COVID-19 causes significant gas-exchange abnormality without the typical effect on elastance. The resulting increase in respiratory drive would generate vigorous inspiratory effort, overstretch a relatively compliant lung, and lead to further injury.

Other equally prominent researchers countered this argument. Martin Tobin drew on physiology, while Arthur Slutsky and Niall Ferguson used emerging data to make their case. Tobin and colleagues cautioned against early intubation for anyone who could be maintained using noninvasive support. In August 2020 (well into the pandemic and after more data were available), Slutsky and colleagues argued that ARDS caused by COVID-19 wasn’t much different from lung injury due to other causes.

Two more recent studies published online recently are relevant to the debate over COVID-19 ARDS. One was a prospective study and the other a retrospective study; both had comparison groups, and both came to the same conclusions. Overall, COVID-19 ARDS isn’t much different from ARDS due to other causes. These studies were comprehensive in their comparisons and measures of outcomes, but they were both rather small and included patients from one and two hospitals, respectively. The discussions of both provide a nice review of the existing literature on COVID-19 ARDS.

A second controversial, but unproven, COVID-19 practice is aggressive anticoagulation. Early reports of a high prevalence of venous thromboembolism (VTE) in patients with COVID-19 pushed many to recommend empirically increasing prophylaxis. Most of the data guiding this approach were from retrospective, observational studies that suffered from selection bias. Early on, many of the studies were from China, where baseline VTE prophylaxis rates were low. Despite these limitations, many physicians acted on the basis of these data. An arbitrarily defined “intermediate” or treatment dose for prophylaxis was used, with some measuring D-dimer to guide their approach. An evidence-based argument against this practice, published in the New England Journal of Medicine, failed to sway readers. (Look at the poll at the end of the article and you’ll see how readers answered.)

Two articles recently published online in CHEST attempted to bring clarity to the debate over COVID-19 and VTE prophylaxis. The first study evaluated critically ill patients in France, and researchers found that higher doses of anticoagulation reduced thrombotic complications without an associated increase in bleeding events. The study is well done but certainly has its flaws. It is observational and retrospective, and it essentially uses a before-after comparison technique. Such an approach is particularly prone to bias during COVID-19, given that practice patterns change quickly.

The second paper is a systematic review looking at VTE and bleeding rates among patients hospitalized with COVID-19. The authors found high rates of VTE (17.0% overall), with screening, admission to the ICU, and the prospective study design all being associated with increased rates. Of importance, unlike the retrospective trial cited in the previous paragraph, the authors of the systematic review found treatment-dose anticoagulation was associated with higher bleeding rates.

I admit, the title of this piece is a bit of a misnomer. The “late adopters” would truly have their revenge if deviation from guidelines for COVID-19–related ARDS and VTE prophylaxis proves to be harmful. It’s not clear that’s the case, and at least for VTE prophylaxis, results from several randomized, controlled trials (REMAP-CAP, ATTACC, and ACTIV-4a) will be released soon. These are sure to provide more definitive answers. If nothing else, the COVID-19–related ARDS and VTE data reinforce how difficult it is to obtain high-quality data that yield clear results. Until something more definitive is published and released, I will remain a “late adopter.” Standard non–COVID-19 guidelines for ARDS and VTE prophylaxis are good enough for me.

Dr. Holley is program director of the Pulmonary and Critical Care Medical Fellowship at Walter Reed National Military Medical Center, Bethesda, Md.

A version of this article first appeared on Medscape.com.

The COVID-19 pandemic has stressed all aspects of the world’s health care systems. The sheer volume of pandemic-related research produced over the past year has been challenging to process. This is as it should be, given its unprecedented spread and related morbidity and mortality. However, such rapid production and application leaves little time for proper vetting. Large numbers of providers adopted suggested, but largely unproven, practices that deviated from pre–COVID-19 guidelines. These “early adopters” theorized that COVID-19–related disease processes were different, necessitating a modification to existing practices.

While many unproven approaches were suggested and implemented, I’ll focus on two approaches. First, throughout the pandemic, many have argued that COVID-19 causes a novel acute respiratory distress syndrome (ARDS) phenotype. Early on, a group of prominent Italian ARDS researchers made a compelling case for physiological differences, concluding that early intubation was required to avoid large transpulmonary pressure swings. The logic was that COVID-19 causes significant gas-exchange abnormality without the typical effect on elastance. The resulting increase in respiratory drive would generate vigorous inspiratory effort, overstretch a relatively compliant lung, and lead to further injury.

Other equally prominent researchers countered this argument. Martin Tobin drew on physiology, while Arthur Slutsky and Niall Ferguson used emerging data to make their case. Tobin and colleagues cautioned against early intubation for anyone who could be maintained using noninvasive support. In August 2020 (well into the pandemic and after more data were available), Slutsky and colleagues argued that ARDS caused by COVID-19 wasn’t much different from lung injury due to other causes.

Two more recent studies published online recently are relevant to the debate over COVID-19 ARDS. One was a prospective study and the other a retrospective study; both had comparison groups, and both came to the same conclusions. Overall, COVID-19 ARDS isn’t much different from ARDS due to other causes. These studies were comprehensive in their comparisons and measures of outcomes, but they were both rather small and included patients from one and two hospitals, respectively. The discussions of both provide a nice review of the existing literature on COVID-19 ARDS.

A second controversial, but unproven, COVID-19 practice is aggressive anticoagulation. Early reports of a high prevalence of venous thromboembolism (VTE) in patients with COVID-19 pushed many to recommend empirically increasing prophylaxis. Most of the data guiding this approach were from retrospective, observational studies that suffered from selection bias. Early on, many of the studies were from China, where baseline VTE prophylaxis rates were low. Despite these limitations, many physicians acted on the basis of these data. An arbitrarily defined “intermediate” or treatment dose for prophylaxis was used, with some measuring D-dimer to guide their approach. An evidence-based argument against this practice, published in the New England Journal of Medicine, failed to sway readers. (Look at the poll at the end of the article and you’ll see how readers answered.)

Two articles recently published online in CHEST attempted to bring clarity to the debate over COVID-19 and VTE prophylaxis. The first study evaluated critically ill patients in France, and researchers found that higher doses of anticoagulation reduced thrombotic complications without an associated increase in bleeding events. The study is well done but certainly has its flaws. It is observational and retrospective, and it essentially uses a before-after comparison technique. Such an approach is particularly prone to bias during COVID-19, given that practice patterns change quickly.

The second paper is a systematic review looking at VTE and bleeding rates among patients hospitalized with COVID-19. The authors found high rates of VTE (17.0% overall), with screening, admission to the ICU, and the prospective study design all being associated with increased rates. Of importance, unlike the retrospective trial cited in the previous paragraph, the authors of the systematic review found treatment-dose anticoagulation was associated with higher bleeding rates.

I admit, the title of this piece is a bit of a misnomer. The “late adopters” would truly have their revenge if deviation from guidelines for COVID-19–related ARDS and VTE prophylaxis proves to be harmful. It’s not clear that’s the case, and at least for VTE prophylaxis, results from several randomized, controlled trials (REMAP-CAP, ATTACC, and ACTIV-4a) will be released soon. These are sure to provide more definitive answers. If nothing else, the COVID-19–related ARDS and VTE data reinforce how difficult it is to obtain high-quality data that yield clear results. Until something more definitive is published and released, I will remain a “late adopter.” Standard non–COVID-19 guidelines for ARDS and VTE prophylaxis are good enough for me.

Dr. Holley is program director of the Pulmonary and Critical Care Medical Fellowship at Walter Reed National Military Medical Center, Bethesda, Md.

A version of this article first appeared on Medscape.com.

The COVID-19 pandemic has stressed all aspects of the world’s health care systems. The sheer volume of pandemic-related research produced over the past year has been challenging to process. This is as it should be, given its unprecedented spread and related morbidity and mortality. However, such rapid production and application leaves little time for proper vetting. Large numbers of providers adopted suggested, but largely unproven, practices that deviated from pre–COVID-19 guidelines. These “early adopters” theorized that COVID-19–related disease processes were different, necessitating a modification to existing practices.

While many unproven approaches were suggested and implemented, I’ll focus on two approaches. First, throughout the pandemic, many have argued that COVID-19 causes a novel acute respiratory distress syndrome (ARDS) phenotype. Early on, a group of prominent Italian ARDS researchers made a compelling case for physiological differences, concluding that early intubation was required to avoid large transpulmonary pressure swings. The logic was that COVID-19 causes significant gas-exchange abnormality without the typical effect on elastance. The resulting increase in respiratory drive would generate vigorous inspiratory effort, overstretch a relatively compliant lung, and lead to further injury.

Other equally prominent researchers countered this argument. Martin Tobin drew on physiology, while Arthur Slutsky and Niall Ferguson used emerging data to make their case. Tobin and colleagues cautioned against early intubation for anyone who could be maintained using noninvasive support. In August 2020 (well into the pandemic and after more data were available), Slutsky and colleagues argued that ARDS caused by COVID-19 wasn’t much different from lung injury due to other causes.

Two more recent studies published online recently are relevant to the debate over COVID-19 ARDS. One was a prospective study and the other a retrospective study; both had comparison groups, and both came to the same conclusions. Overall, COVID-19 ARDS isn’t much different from ARDS due to other causes. These studies were comprehensive in their comparisons and measures of outcomes, but they were both rather small and included patients from one and two hospitals, respectively. The discussions of both provide a nice review of the existing literature on COVID-19 ARDS.

A second controversial, but unproven, COVID-19 practice is aggressive anticoagulation. Early reports of a high prevalence of venous thromboembolism (VTE) in patients with COVID-19 pushed many to recommend empirically increasing prophylaxis. Most of the data guiding this approach were from retrospective, observational studies that suffered from selection bias. Early on, many of the studies were from China, where baseline VTE prophylaxis rates were low. Despite these limitations, many physicians acted on the basis of these data. An arbitrarily defined “intermediate” or treatment dose for prophylaxis was used, with some measuring D-dimer to guide their approach. An evidence-based argument against this practice, published in the New England Journal of Medicine, failed to sway readers. (Look at the poll at the end of the article and you’ll see how readers answered.)

Two articles recently published online in CHEST attempted to bring clarity to the debate over COVID-19 and VTE prophylaxis. The first study evaluated critically ill patients in France, and researchers found that higher doses of anticoagulation reduced thrombotic complications without an associated increase in bleeding events. The study is well done but certainly has its flaws. It is observational and retrospective, and it essentially uses a before-after comparison technique. Such an approach is particularly prone to bias during COVID-19, given that practice patterns change quickly.

The second paper is a systematic review looking at VTE and bleeding rates among patients hospitalized with COVID-19. The authors found high rates of VTE (17.0% overall), with screening, admission to the ICU, and the prospective study design all being associated with increased rates. Of importance, unlike the retrospective trial cited in the previous paragraph, the authors of the systematic review found treatment-dose anticoagulation was associated with higher bleeding rates.

I admit, the title of this piece is a bit of a misnomer. The “late adopters” would truly have their revenge if deviation from guidelines for COVID-19–related ARDS and VTE prophylaxis proves to be harmful. It’s not clear that’s the case, and at least for VTE prophylaxis, results from several randomized, controlled trials (REMAP-CAP, ATTACC, and ACTIV-4a) will be released soon. These are sure to provide more definitive answers. If nothing else, the COVID-19–related ARDS and VTE data reinforce how difficult it is to obtain high-quality data that yield clear results. Until something more definitive is published and released, I will remain a “late adopter.” Standard non–COVID-19 guidelines for ARDS and VTE prophylaxis are good enough for me.

Dr. Holley is program director of the Pulmonary and Critical Care Medical Fellowship at Walter Reed National Military Medical Center, Bethesda, Md.

A version of this article first appeared on Medscape.com.