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A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O2 saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

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Past medical history: coronary artery disease, gastroesophageal reflux disease, and prostate cancer. Medications: fluticasone/salmeterol inhaler, albuterol inhaler, atorvastatin, and omeprazole. On exam: BP 120/70, pulse 110. Chest: wheezes bilaterally. Cardiac: normal S1 S2, no murmur. Extremities: no cyanosis or clubbing. Trace edema. Labs: hemoglobin 14, hematocrit 42, WBC 11,000. Chest x-ray: no infiltrates/hyperexpanded lungs/flat diaphragms. He receives oxygen and every-4-hours albuterol inhalers.

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.1 They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.2 A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.3 They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Douglas S. Paauw

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

 

 

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

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A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O2 saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock
Past medical history: coronary artery disease, gastroesophageal reflux disease, and prostate cancer. Medications: fluticasone/salmeterol inhaler, albuterol inhaler, atorvastatin, and omeprazole. On exam: BP 120/70, pulse 110. Chest: wheezes bilaterally. Cardiac: normal S1 S2, no murmur. Extremities: no cyanosis or clubbing. Trace edema. Labs: hemoglobin 14, hematocrit 42, WBC 11,000. Chest x-ray: no infiltrates/hyperexpanded lungs/flat diaphragms. He receives oxygen and every-4-hours albuterol inhalers.

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.1 They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.2 A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.3 They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Douglas S. Paauw

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

 

 

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

 

A 70-year-old man with chronic obstructive pulmonary disease (COPD) is admitted with increased shortness of breath. His O2 saturation levels are usually 90%, but they’re now running 84%-88%. He has had increasing symptoms for the past 3 days.

copyright designer491/Thinkstock
Past medical history: coronary artery disease, gastroesophageal reflux disease, and prostate cancer. Medications: fluticasone/salmeterol inhaler, albuterol inhaler, atorvastatin, and omeprazole. On exam: BP 120/70, pulse 110. Chest: wheezes bilaterally. Cardiac: normal S1 S2, no murmur. Extremities: no cyanosis or clubbing. Trace edema. Labs: hemoglobin 14, hematocrit 42, WBC 11,000. Chest x-ray: no infiltrates/hyperexpanded lungs/flat diaphragms. He receives oxygen and every-4-hours albuterol inhalers.

What would be your next step?

A) Begin a 5-day course of corticosteroids.

B) Begin a 14-day course of corticosteroids.

C) Begin azithromycin.

D) Start BiPAP.

E) Obtain D-dimer.

This is a situation we face frequently. COPD exacerbations are a clinical diagnosis that is often jumped to as the diagnosis in patients with COPD who have increasing dyspnea. This diagnosis is frequently correct – but not always.

Patients with COPD also may be at risk for or have heart failure, which can present with identical symptoms, including widespread wheezing. We are currently in a severe influenza epidemic, and influenza can mimic a COPD exacerbation or be the trigger.

About 20 years ago, I was out of the country when one of my patients with COPD was admitted to the hospital with a COPD exacerbation. I saw him in follow-up a week after his hospitalization. He was very dyspneic and had a room air oxygen saturation of 75%. He told me his dyspnea started a few days after he had injured his leg on a wood pile in his yard.

On exam, his right leg had 3+ edema; left leg, no edema. He reported to me that he was treated for 5 days with steroids and nebulizers, with minimal change in his dyspnea. I reviewed the chart, and five physicians had seen him while he was in the hospital. Starting with the emergency department, the diagnosis was COPD exacerbation, with no differential diagnosis in any note.

The patient had multiple pulmonary emboli, and he eventually improved with anticoagulation.

In 2009, Jacques Rizkallah, MD, and his colleagues published a systematic review and meta-analysis of articles looking at the prevalence of pulmonary emboli (PE) in patients diagnosed/treated for a COPD exacerbation.1 They found five articles comprising a total of 550 patients who met inclusion criteria. The prevalence was 19.9% (P = .014). The prevalence was much higher (24.7%) for hospitalized patients than it was for outpatients (3.3%). A very important finding in this study: There was no difference in symptoms between patients who did and did not have a pulmonary embolus.

Evrim Eylem Akpinar, MD, and colleagues studied all admissions for acute exacerbations of COPD at one hospital in Turkey over a 2-year period.2 A total of 172 patients admitted for COPD exacerbations were studied. The prevalence of pulmonary embolus was 29%.

In this study, patients who were obese or immobile were more likely to have pulmonary emboli. Pleuritic chest pain and lower-limb asymmetry were signs and symptoms more commonly found in patients who had PE. Obesity was the highest independent predictor (odds ratio, 4.97) for pulmonary embolus.

Floor Aleva, MD, and colleagues recently completed a systematic review and meta-analysis on prevalence and localization of pulmonary embolus in patients with acute exacerbations of COPD.3 They found similar numbers to the previous meta-analysis (16.1%) in a total of 880 patients. They also looked at location in the lungs of the emboli and found that two-thirds of the patients had pulmonary emboli in locations that had clear indication for anticoagulation treatment.

This is important, because criticisms of earlier studies were that clinically insignificant pulmonary emboli might be being found in the studies and that they had little to do with the patients’ symptoms.

In the case presented, I think that getting a D-dimer test would be the next best step. Acute exacerbation of COPD still is the most likely diagnosis, but PE is a plausible diagnosis that should be evaluated. If the D-dimer is normal, workup for PE would be complete. If elevated, then given the 20% prevalence of PE, a CT angiography would be warranted.

Key pearl: Among patients hospitalized for COPD exacerbations, 16%-24% have pulmonary embolism.

Dr. Douglas S. Paauw

Dr. Paauw is professor of medicine in the division of general internal medicine at the University of Washington, Seattle, and he serves as third-year medical student clerkship director at the University of Washington. Contact Dr. Paauw at dpaauw@uw.edu.

 

 

References

1. Chest. 2009 Mar;135(3):786-93.

2. J Bras Pneumol. 2014 Jan-Feb;40(1):38-45.

3. Chest. 2017 Mar;151(3):544-54.


 

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