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An Exudative Pleural Effusion in Congestive Heart Failure: Time to Broaden the Differential
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A3200 - An Exudative Pleural Effusion in Congestive Heart Failure: Time to Broaden the Differential
Author Block: B. Seth1, S. Belok2, F. Schembri3; 1Internal Medicine, Boston University Medical Center, Boston, MA, United States, 2Pulmonary, Allergy, Sleep and Critical Care, Boston University Medical Center, Boston, MA, United States, 3Boston Univ Med Ctr, Boston, MA, United States.
Introduction
Classically, pleural effusions in patients with decompensated heart failure are transudative in nature. However, patients receiving diuretic therapy may have elevated pleural protein levels meeting criteria for an exudate. Differentiating heart-failure related exudative effusions from other pathological processes can prove challenging. We describe a patient presenting with decompensated heart failure and effusions, who was ultimately diagnosed with hydralazine-induced lupus serositis.
Case
A 66-year-old female with a history of hypertension, ischemic cardiomyopathy and chronic kidney disease presented with two days of worsening dyspnea, orthopnea, lower extremity edema, while compliant on her home diuretic and restricted salt regimen. Vitals signs on admission were HR 97, BP 128/70, Spo2 79%, RR 30. She was 10lbs above her dry weight and she had peripheral edema, elevated JVP and rales on auscultation. BNP was 3195pg/ml (normal 0-72.3pg/ml). Chest X-ray(CXR) demonstrated moderate bilateral pleural effusions. Echo revealed an ejection fraction of 35%, global hypokinesis and moderate pericardial effusion with no tamponade. Medications included aspirin, atorvastatin, amlodipine, isosorbide mononitrate, torsemide and hydralazine. She had been taking hydralazine for over three years.
Despite three days of adequate intravenous diuresis, the pleural effusions persisted and her oxygen requirement remained high. A thoracentesis was performed showing an exudative effusion by 2 of 3 Lights criteria: pleural fluid LDH(538U/L), pleural to serum LDH ratio of 1.4, pleural to serum protein of 0.4. Fluid RBC was 21K/UL with total nucleated cells of 3366/UL, 74% polymorphs. Given the elevated pleural fluid LDH, WBCs and her hydralazine use, additional autoimmune labs were obtained. Add-on pleural fluid ANA was positive at 1:320, serum ANA was 1:2560 and serum anti-histone Ab was elevated at 5.4U. This was consistent with hydralazine-induced lupus serositis. The hydralazine was subsequently held and a steroid taper was initiated. A follow-up CXR after 4 weeks showed resolution of her pleural effusions.
Discussion
Our case demonstrates a patient with a classic presentation of a heart failure exacerbation whose pleural effusions were refractory to adequate diuresis. She was found to have drug-induced lupus complicating her presentation. Drug-induced lupus occurs in 5-10% of patients on hydralazine, with average time to onset of 2 years since starting the offending medication. Although exudative effusions can at times be attributed to heart failure, particularly after diuresis, other etiologies should be considered in patients who fail to respond to therapy or have high inflammatory markers in the pleural fluid.
Author Block: B. Seth1, S. Belok2, F. Schembri3; 1Internal Medicine, Boston University Medical Center, Boston, MA, United States, 2Pulmonary, Allergy, Sleep and Critical Care, Boston University Medical Center, Boston, MA, United States, 3Boston Univ Med Ctr, Boston, MA, United States.
Introduction
Classically, pleural effusions in patients with decompensated heart failure are transudative in nature. However, patients receiving diuretic therapy may have elevated pleural protein levels meeting criteria for an exudate. Differentiating heart-failure related exudative effusions from other pathological processes can prove challenging. We describe a patient presenting with decompensated heart failure and effusions, who was ultimately diagnosed with hydralazine-induced lupus serositis.
Case
A 66-year-old female with a history of hypertension, ischemic cardiomyopathy and chronic kidney disease presented with two days of worsening dyspnea, orthopnea, lower extremity edema, while compliant on her home diuretic and restricted salt regimen. Vitals signs on admission were HR 97, BP 128/70, Spo2 79%, RR 30. She was 10lbs above her dry weight and she had peripheral edema, elevated JVP and rales on auscultation. BNP was 3195pg/ml (normal 0-72.3pg/ml). Chest X-ray(CXR) demonstrated moderate bilateral pleural effusions. Echo revealed an ejection fraction of 35%, global hypokinesis and moderate pericardial effusion with no tamponade. Medications included aspirin, atorvastatin, amlodipine, isosorbide mononitrate, torsemide and hydralazine. She had been taking hydralazine for over three years.
Despite three days of adequate intravenous diuresis, the pleural effusions persisted and her oxygen requirement remained high. A thoracentesis was performed showing an exudative effusion by 2 of 3 Lights criteria: pleural fluid LDH(538U/L), pleural to serum LDH ratio of 1.4, pleural to serum protein of 0.4. Fluid RBC was 21K/UL with total nucleated cells of 3366/UL, 74% polymorphs. Given the elevated pleural fluid LDH, WBCs and her hydralazine use, additional autoimmune labs were obtained. Add-on pleural fluid ANA was positive at 1:320, serum ANA was 1:2560 and serum anti-histone Ab was elevated at 5.4U. This was consistent with hydralazine-induced lupus serositis. The hydralazine was subsequently held and a steroid taper was initiated. A follow-up CXR after 4 weeks showed resolution of her pleural effusions.
Discussion
Our case demonstrates a patient with a classic presentation of a heart failure exacerbation whose pleural effusions were refractory to adequate diuresis. She was found to have drug-induced lupus complicating her presentation. Drug-induced lupus occurs in 5-10% of patients on hydralazine, with average time to onset of 2 years since starting the offending medication. Although exudative effusions can at times be attributed to heart failure, particularly after diuresis, other etiologies should be considered in patients who fail to respond to therapy or have high inflammatory markers in the pleural fluid.
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