Bilateral Asymmetrical Pleural Effusion Due to Congestive Heart Failure





History of Present Illness


An 80-year-old man presented to a cardiologist because he had worsening dyspnea and asthenia. Chest radiography showed right pleural effusion ( Fig. 18.1 ). The cardiologist prescribed increased dosage of a loop diuretic (furosemide), an angiotensin-converting enzyme (ACE) inhibitor (enalapril), and an aldosterone receptor blocker (spironolactone). However, the patient became increasingly fatigued and confused. Arterial hypotension developed, and urine output decreased. Chest radiography showed an increase in the right pleural effusion, and blood tests revealed prerenal acute kidney injury. The patient was therefore admitted to the geriatric department.




Fig. 18.1


Posteroanterior chest radiograph showing right pleural effusion.


Past Medical History


The patient was a retired office clerk, a former smoker (about 10 cigarettes a day for 25 years; he had quit 40 years before the current presentation). He had coronary artery disease (CAD), with residual diffuse myocardial hypokinesia and reduced left ventricular ejection fraction (LVEF: 25%). Two years earlier, a dual-chamber implantable cardioverter defibrillator (DR-ICD) was implanted. Three months before his current presentation, the patient had undergone right thoracentesis, and 1500 mL of transudative pleural fluid had been extracted. The patient also suffered from high blood pressure, type 2 diabetes mellitus, hypercholesterolemia, bilateral hearing loss, gallbladder stones, and central sleep apnea syndrome. He habitually used a bilevel positive airway pressure (BiPAP) device and oxygen therapy during the night. His home pharmacological therapy included acetylsalicylic acid 100 mg per day, omeprazole 20 mg per day, furosemide 125 mg two times daily, allopurinol 300 mg per day, metformin 500 mg two times daily, ursodeoxycholic acid 300 mg two times daily, enalapril 20 mg per day, and spironolactone 25 mg two times daily.


Physical Examination and Early Clinical Findings


At admission, the patient was afebrile, pale, confused, and complaining of breathlessness with minimal activity. Oxygen saturation (Sp O 2 ) measured with pulse oximetry was 88% on room air. Arterial blood gas (ABG) analysis showed significant hypoxemia, with partial pressure of oxygen (Pa O 2 ) of 53 mm Hg. Heart rate was 88 beats/min, respiratory rate was 20 breaths/min, and blood pressure was 90/50 mm Hg. On chest examination, breath sounds were absent in the lower right hemithorax, with dullness on percussion and decreased fremitus. Small symmetrical lower limb edema was also evident.


Blood tests showed high levels of serum creatinine (2.6 mg/dL), urea (102 mg/dL), and potassium (6.1 mEq/L). Total white blood cells (WBC) count was normal (7,220 cells/mm 3 ) as were the inflammatory markers (C-reactive protein [CRP] < 10 mg/L). Hemoglobin was 11.2 g/dL, and platelet count was 120,000 cells/μL. Serum protein electrophoresis revealed only a slight reduction in total proteins (5.6 g/dL) and albumin (3.3 g/dL). Electrocardiography (ECG) showed sinus tachycardia, previously known left bundle branch block, left ventricular hypertrophy, prolonged corrected QT interval (QTc 490 ms).


Clinical Course


The patient received 40% oxygen via a Venturi mask, intravenous dopamine at intermediate rates of infusion (5 μg/kg/min), and oral sodium polystyrene sulfonate (15 mg every 6 hours). Enalapril and spironolactone were stopped. Administration of furosemide was changed to the intravenous route. Thoracic ultrasonography ( Fig. 18.2 ) revealed a large area of right pleural effusion, with a flattened diaphragm, that was appreciable through four intercostal spaces and a small area of pleural effusion on the left. Additional signs of fluid overload were noted: both lungs showed vertical pulmonary artifacts (B-lines), and the inferior vena cava had increased in size and decreased in respiratory variability.




Fig. 18.2


Chest ultrasonography (convex probe) scans demonstrating large right pleural effusion (A); vertical pulmonary artefacts (B-lines) (B); and increased size of inferior vena cava (C).


Chest computed tomography (CT) confirmed these findings and demonstrated absence of significant pulmonary parenchymal lesions, except for pulmonary atelectasis adjacent to the pleural effusion ( Fig. 18.3 ).




Fig. 18.3


Axial chest computed tomography (CT) scan showing bilateral asymmetrical pleural effusion.


In a few days, diuresis became adequate, and kidney function improved. However, the pleural effusion persisted, and the patient still needed supplemental oxygen at rest and had shortness of breath even on slight exertion.




Discussion Topic





Right therapeutic thoracentesis was performed, and a large amount of fluid (1700 mL) was drained. The patient had no cough during the procedure and obtained subjective relief of dyspnea soon after. Pleural fluid analysis showed that it was still a transudate, with protein at 2.7 g/dL and lactate dehydrogenase (LDH) at 105 units/L. The search for malignant tumor cells on cytological examination yielded negative results. In the following days, oxygen saturation (Sp O 2 ) increased to 92% at rest in room air. The patient was discharged, without a requirement for oxygen use during daylight hours.


Follow-Up and Outcomes


Four weeks after discharge, the patient was evaluated in the outpatient clinic. He was still fatigued and dyspneic with minimal effort. Blood pressure was low (100/60 mm Hg), but diuresis was sufficient, and serum creatinine was normal. Thoracic ultrasonography showed recurrence of the right pleural effusion, again appreciable through four intercostal spaces.



Jun 19, 2021 | Posted by in RESPIRATORY | Comments Off on Bilateral Asymmetrical Pleural Effusion Due to Congestive Heart Failure
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