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All intermediate-risk pulmonary embolism is not the same, Victor F. Tapson, MD, declared at HM20 Virtual, hosted by the Society of Hospital Medicine.
This additional classification is worthwhile because it has important treatment implications.
Patients with intermediate- to low-risk PE, along with those who have truly low-risk PE, require anticoagulation only. In contrast, patients with intermediate- to high-risk PE are at increased risk of decompensation. They have a much higher in-hospital mortality than those with intermediate- to low-risk PE. So hospitalists may want to consult their hospitals’ PE response team (PERT), if there is one, or whoever on staff is involved in helping make decisions about the appropriateness of more aggressive interventions, such as catheter-directed thrombolysis or catheter-directed clot extraction, said Dr. Tapson, director of the venous thromboembolism and pulmonary vascular disease research program at Cedars-Sinai Medical Center in Los Angeles.
“We don’t have evidence of any real proven mortality difference yet in the intermediate-high risk PE group by being more aggressive. I think if the right patients were studied we could see a mortality difference. But one thing I’ve noted is that by being more aggressive – in a cautious manner, in selected patients – we clearly shorten the hospital stay by doing catheter-directed therapy in some of these folks. It saves money,” he observed.
Once the diagnosis of PE is confirmed, the first priority is to get anticoagulation started in all patients with an acceptable bleeding risk, since there is convincing evidence that anticoagulation reduces mortality in PE. The 2019 European Society of Cardiology guidelines recommend a direct-acting oral anticoagulant over warfarin on the basis of persuasive evidence of lower risk of major bleeding coupled with equal or better effectiveness in preventing recurrent PE.
Dr. Tapson said it’s worthwhile for hospitalists to take a close look at these European guidelines (Eur Respir J. 2019 Oct 9. doi: 10.1183/13993003.01647-2019).
“I think our Europeans friends did a really nice job with those guidelines. They’re great guidelines, better than many of the others out there. I think they’re very, very usable,” he said. “I took part in the ACCP [American College of Chest Physicians] guidelines for years. I think they’re very rigorous in terms of the evidence base, but because they’re so rigorous there’s just tons of 2C recommendations, which are basically suggestions. The ESC guidelines are more robust.”
Risk stratification
Once anticoagulation is on board, the next task is risk stratification to determine the need for more aggressive therapy. A high-risk PE is best defined hemodynamically as one causing a systolic blood pressure below 90 mm Hg for at least 15 minutes. The term “high risk” is increasingly replacing “massive” PE, because the size of the clot doesn’t necessarily correlate with its hemodynamic impact.
An intermediate-risk PE is marked by a simplified Pulmonary Embolism Severity Index (sPESI) score of 1 or more, right ventricular dysfunction on echocardiography or CT angiography, or an elevated cardiac troponin level.
The sPESI is a validated, user-friendly tool that grants 1 point each for age over 80, background cardiopulmonary disease, a systolic blood pressure below 100 mm Hg, cancer, a heart rate of 110 bpm or more, and an oxygen saturation level below 90%.
“All you really need to know about a patient’s sPESI score is: Is it more than zero?” he explained.
Indeed, patients with an sPESI score of 0 have a 30-day mortality of 1%. With a score of 1 or more, however, that risk jumps to 10.9%.
No scoring system is 100% accurate, though, and Dr. Tapson emphasized that clinician gestalt plays an important role in PE risk stratification. In terms of clinical indicators of risk, he pays special attention to heart rate.
“I think if I had to pick the one thing that drives my decision the most about whether someone needs more aggressive therapy than anticoagulation, it’s probably heart rate,” he said. “If the heart rate is 70, the patient is probably very stable. Of course, that might not hold up in a patient with conduction problems or who is on a beta blocker, but in general if I see someone who looks good, has a relatively small PE, and a low heart rate, it makes me feel much better. If the heart rate is 130 or 120, I’m much more concerned.”
Both the European guidelines and the PERT Consortium guidelines on the diagnosis, treatment, and follow-up of acute PE (Clin Appl Thromb Hemost. 2019 Jun 17. doi: 10.1177/1076029619853037), which Dr. Tapson coauthored, recommend substratifying intermediate-risk PE into intermediate to low or intermediate to high risk. It’s a straightforward matter: If a patient has either right ventricular dysfunction on imaging or an elevated cardiac troponin, that’s an intermediate- to low-risk PE warranting anticoagulation only. On the other hand, if both right ventricular dysfunction and an elevated troponin are present, the patient has an intermediate- to high-risk PE. Since this distinction translates to a difference in outcome, a consultation with PERT or an experienced PE interventionalist is in order for the intermediate- to high-risk PE, he said.
Dr. Tapson reported receiving research funding from Bayer, Bristol-Myers Squibb, Janssen, BiO2, EKOS/BTG, and Daiichi. He is also a consultant to Janssen and BiO2, and on speakers’ bureaus for EKOS/BTG and Janssen.
All intermediate-risk pulmonary embolism is not the same, Victor F. Tapson, MD, declared at HM20 Virtual, hosted by the Society of Hospital Medicine.
This additional classification is worthwhile because it has important treatment implications.
Patients with intermediate- to low-risk PE, along with those who have truly low-risk PE, require anticoagulation only. In contrast, patients with intermediate- to high-risk PE are at increased risk of decompensation. They have a much higher in-hospital mortality than those with intermediate- to low-risk PE. So hospitalists may want to consult their hospitals’ PE response team (PERT), if there is one, or whoever on staff is involved in helping make decisions about the appropriateness of more aggressive interventions, such as catheter-directed thrombolysis or catheter-directed clot extraction, said Dr. Tapson, director of the venous thromboembolism and pulmonary vascular disease research program at Cedars-Sinai Medical Center in Los Angeles.
“We don’t have evidence of any real proven mortality difference yet in the intermediate-high risk PE group by being more aggressive. I think if the right patients were studied we could see a mortality difference. But one thing I’ve noted is that by being more aggressive – in a cautious manner, in selected patients – we clearly shorten the hospital stay by doing catheter-directed therapy in some of these folks. It saves money,” he observed.
Once the diagnosis of PE is confirmed, the first priority is to get anticoagulation started in all patients with an acceptable bleeding risk, since there is convincing evidence that anticoagulation reduces mortality in PE. The 2019 European Society of Cardiology guidelines recommend a direct-acting oral anticoagulant over warfarin on the basis of persuasive evidence of lower risk of major bleeding coupled with equal or better effectiveness in preventing recurrent PE.
Dr. Tapson said it’s worthwhile for hospitalists to take a close look at these European guidelines (Eur Respir J. 2019 Oct 9. doi: 10.1183/13993003.01647-2019).
“I think our Europeans friends did a really nice job with those guidelines. They’re great guidelines, better than many of the others out there. I think they’re very, very usable,” he said. “I took part in the ACCP [American College of Chest Physicians] guidelines for years. I think they’re very rigorous in terms of the evidence base, but because they’re so rigorous there’s just tons of 2C recommendations, which are basically suggestions. The ESC guidelines are more robust.”
Risk stratification
Once anticoagulation is on board, the next task is risk stratification to determine the need for more aggressive therapy. A high-risk PE is best defined hemodynamically as one causing a systolic blood pressure below 90 mm Hg for at least 15 minutes. The term “high risk” is increasingly replacing “massive” PE, because the size of the clot doesn’t necessarily correlate with its hemodynamic impact.
An intermediate-risk PE is marked by a simplified Pulmonary Embolism Severity Index (sPESI) score of 1 or more, right ventricular dysfunction on echocardiography or CT angiography, or an elevated cardiac troponin level.
The sPESI is a validated, user-friendly tool that grants 1 point each for age over 80, background cardiopulmonary disease, a systolic blood pressure below 100 mm Hg, cancer, a heart rate of 110 bpm or more, and an oxygen saturation level below 90%.
“All you really need to know about a patient’s sPESI score is: Is it more than zero?” he explained.
Indeed, patients with an sPESI score of 0 have a 30-day mortality of 1%. With a score of 1 or more, however, that risk jumps to 10.9%.
No scoring system is 100% accurate, though, and Dr. Tapson emphasized that clinician gestalt plays an important role in PE risk stratification. In terms of clinical indicators of risk, he pays special attention to heart rate.
“I think if I had to pick the one thing that drives my decision the most about whether someone needs more aggressive therapy than anticoagulation, it’s probably heart rate,” he said. “If the heart rate is 70, the patient is probably very stable. Of course, that might not hold up in a patient with conduction problems or who is on a beta blocker, but in general if I see someone who looks good, has a relatively small PE, and a low heart rate, it makes me feel much better. If the heart rate is 130 or 120, I’m much more concerned.”
Both the European guidelines and the PERT Consortium guidelines on the diagnosis, treatment, and follow-up of acute PE (Clin Appl Thromb Hemost. 2019 Jun 17. doi: 10.1177/1076029619853037), which Dr. Tapson coauthored, recommend substratifying intermediate-risk PE into intermediate to low or intermediate to high risk. It’s a straightforward matter: If a patient has either right ventricular dysfunction on imaging or an elevated cardiac troponin, that’s an intermediate- to low-risk PE warranting anticoagulation only. On the other hand, if both right ventricular dysfunction and an elevated troponin are present, the patient has an intermediate- to high-risk PE. Since this distinction translates to a difference in outcome, a consultation with PERT or an experienced PE interventionalist is in order for the intermediate- to high-risk PE, he said.
Dr. Tapson reported receiving research funding from Bayer, Bristol-Myers Squibb, Janssen, BiO2, EKOS/BTG, and Daiichi. He is also a consultant to Janssen and BiO2, and on speakers’ bureaus for EKOS/BTG and Janssen.
All intermediate-risk pulmonary embolism is not the same, Victor F. Tapson, MD, declared at HM20 Virtual, hosted by the Society of Hospital Medicine.
This additional classification is worthwhile because it has important treatment implications.
Patients with intermediate- to low-risk PE, along with those who have truly low-risk PE, require anticoagulation only. In contrast, patients with intermediate- to high-risk PE are at increased risk of decompensation. They have a much higher in-hospital mortality than those with intermediate- to low-risk PE. So hospitalists may want to consult their hospitals’ PE response team (PERT), if there is one, or whoever on staff is involved in helping make decisions about the appropriateness of more aggressive interventions, such as catheter-directed thrombolysis or catheter-directed clot extraction, said Dr. Tapson, director of the venous thromboembolism and pulmonary vascular disease research program at Cedars-Sinai Medical Center in Los Angeles.
“We don’t have evidence of any real proven mortality difference yet in the intermediate-high risk PE group by being more aggressive. I think if the right patients were studied we could see a mortality difference. But one thing I’ve noted is that by being more aggressive – in a cautious manner, in selected patients – we clearly shorten the hospital stay by doing catheter-directed therapy in some of these folks. It saves money,” he observed.
Once the diagnosis of PE is confirmed, the first priority is to get anticoagulation started in all patients with an acceptable bleeding risk, since there is convincing evidence that anticoagulation reduces mortality in PE. The 2019 European Society of Cardiology guidelines recommend a direct-acting oral anticoagulant over warfarin on the basis of persuasive evidence of lower risk of major bleeding coupled with equal or better effectiveness in preventing recurrent PE.
Dr. Tapson said it’s worthwhile for hospitalists to take a close look at these European guidelines (Eur Respir J. 2019 Oct 9. doi: 10.1183/13993003.01647-2019).
“I think our Europeans friends did a really nice job with those guidelines. They’re great guidelines, better than many of the others out there. I think they’re very, very usable,” he said. “I took part in the ACCP [American College of Chest Physicians] guidelines for years. I think they’re very rigorous in terms of the evidence base, but because they’re so rigorous there’s just tons of 2C recommendations, which are basically suggestions. The ESC guidelines are more robust.”
Risk stratification
Once anticoagulation is on board, the next task is risk stratification to determine the need for more aggressive therapy. A high-risk PE is best defined hemodynamically as one causing a systolic blood pressure below 90 mm Hg for at least 15 minutes. The term “high risk” is increasingly replacing “massive” PE, because the size of the clot doesn’t necessarily correlate with its hemodynamic impact.
An intermediate-risk PE is marked by a simplified Pulmonary Embolism Severity Index (sPESI) score of 1 or more, right ventricular dysfunction on echocardiography or CT angiography, or an elevated cardiac troponin level.
The sPESI is a validated, user-friendly tool that grants 1 point each for age over 80, background cardiopulmonary disease, a systolic blood pressure below 100 mm Hg, cancer, a heart rate of 110 bpm or more, and an oxygen saturation level below 90%.
“All you really need to know about a patient’s sPESI score is: Is it more than zero?” he explained.
Indeed, patients with an sPESI score of 0 have a 30-day mortality of 1%. With a score of 1 or more, however, that risk jumps to 10.9%.
No scoring system is 100% accurate, though, and Dr. Tapson emphasized that clinician gestalt plays an important role in PE risk stratification. In terms of clinical indicators of risk, he pays special attention to heart rate.
“I think if I had to pick the one thing that drives my decision the most about whether someone needs more aggressive therapy than anticoagulation, it’s probably heart rate,” he said. “If the heart rate is 70, the patient is probably very stable. Of course, that might not hold up in a patient with conduction problems or who is on a beta blocker, but in general if I see someone who looks good, has a relatively small PE, and a low heart rate, it makes me feel much better. If the heart rate is 130 or 120, I’m much more concerned.”
Both the European guidelines and the PERT Consortium guidelines on the diagnosis, treatment, and follow-up of acute PE (Clin Appl Thromb Hemost. 2019 Jun 17. doi: 10.1177/1076029619853037), which Dr. Tapson coauthored, recommend substratifying intermediate-risk PE into intermediate to low or intermediate to high risk. It’s a straightforward matter: If a patient has either right ventricular dysfunction on imaging or an elevated cardiac troponin, that’s an intermediate- to low-risk PE warranting anticoagulation only. On the other hand, if both right ventricular dysfunction and an elevated troponin are present, the patient has an intermediate- to high-risk PE. Since this distinction translates to a difference in outcome, a consultation with PERT or an experienced PE interventionalist is in order for the intermediate- to high-risk PE, he said.
Dr. Tapson reported receiving research funding from Bayer, Bristol-Myers Squibb, Janssen, BiO2, EKOS/BTG, and Daiichi. He is also a consultant to Janssen and BiO2, and on speakers’ bureaus for EKOS/BTG and Janssen.
FROM HM20 VIRTUAL