Recurrent bilateral pleural effusion in a patient with rheumatic heart disease: A case report

Mahalakshmi*

Physician Assistant, Kauvery Hospital, Cantonment, Trichy, Tamil Nadu

*Correspondence

Abstract

Recurrent pleural effusion is a frequent clinical entity with a wide differential diagnosis. We report a case of a 42-year-old female with known rheumatic heart disease who presented with recurrent, alternating pleural effusions associated with pericardial effusion, pulmonary arterial hypertension, and elevated inflammatory markers. Despite initial improvement following intercostal drainage, the patient developed contralateral pleural effusion on readmission. Extensive evaluation ruled out pulmonary thromboembolism, tuberculosis, and malignancy. Imaging raised the possibility of drug-induced pulmonary toxicity. This case highlights the diagnostic challenges of recurrent pleural effusion in patients with underlying cardiac disease and emphasizes the importance of a multidisciplinary approach.

Key words: Recurrent pleural effusion; Rheumatic heart disease; Pulmonary thromboembolism

Introduction

Pleural effusion commonly arises from cardiac failure, infections, malignancy, or systemic inflammatory conditions. In patients with rheumatic heart disease (RHD), pleural effusion is often secondary to elevated pulmonary pressures or heart failure. However, recurrent and shifting pleural effusions require thorough evaluation to identify less common causes. This report describes a complex case of recurrent pleural effusion in a patient with RHD.

Case Presentation

A 42-year-old female was admitted with recurrent episodes of breathlessness.

Initial Presentation (December 2024)

Chief Complaints

  • Breathing difficulty
  • Cough with expectoration
  • Loose stools
  • Voice change
  • History of fever one week prior to admission
  • There was no history of vomiting or nausea. Urine output was adequate.

Past Medical History

  • Rheumatic heart disease on oral anticoagulation (Acitrom 1 mg)
  • Valvular lesions: Mild mitral stenosis, moderate aortic regurgitation, mild tricuspid regurgitation, mild pulmonary arterial hypertension
  • Status post percutaneous transvenous mitral commissurotomy (PTMC) in 2024
  • Status post electrophysiological study with radiofrequency ablation (EPS + RFA) on 08/01/2024
Clinical Examination
Conscious, oriented, afebrile
Pulse rate79/min ,
Blood pressure100/70 mmHg
Systemic examination
Cardiovascular systemS1, S2 present
Respiratory systemBilateral air entry present
AbdomenSoft, non-tender
Central nervous systemNo focal neurological deficit

Investigations

CT Chest (Plain)

  • Massive left pleural effusion with collapse–consolidation of the left lung parenchyma
  • Collapsed left lung parenchyma appeared diffusely hyperdense, suggestive of pulmonary ossification
  • Cardiomegaly with pulmonary arterial hypertension and pericardial effusion
  • Congested right lung fields with atelectatic changes

Ultrasonography of Abdomen

  • Bulky uterus with fibroids
  • Bilateral mild pleural effusion
  • Minimal ascites

Chest X-ray

Findings consistent with left-sided massive pleural effusion

Management

Pulmonology opinion was obtained, and intercostal drainage (ICD) tube insertion was performed on 29/12/2024. Obstetrics and gynecology consultation for uterine fibroids advised conservative management. The ICD was later removed after clinical improvement.

Laboratory Investigations (28/12/2024)
Hemoglobin10 g/dL
PCV30.4%
RBC count3.73 million/mm³
WBC count8610/mm³
PlateletsWithin normal limits
ESR120 mm/hr
CRP177.67 mg/L
Serum sodium134 mEq/L
Serum potassium3.0 mEq/L
Renal function testsNormal
Thyroid profileTSH 100 µIU/mL (markedly elevated)
Liver function testsMild elevation of liver enzymes, hypoalbuminemia (2.81 g/dL)

Discharged on antibiotics, anticoagulation, antiarrhythmics, thyroid hormone eplacement, and supportive therapy.

Readmission (February 2025)

Presenting Complaints (07/02/2025)

  • Breathlessness
  • Chest pain, aggravated on inspiration
  • Decreased appetite
  • Involuntary movements of the right upper limb
  • Dyspnea on exertion
  • Cough
  • There was no fever, vomiting, or loose stools.

On Examination

Conscious, oriented, afebrile

Pulse rate78/min
Blood pressure100/60 mmHg
Cardiovascular systemS1, S2 present
Respiratory systemBilateral air entry present
AbdomenSoft

Investigations

CT Pulmonary Angiography (09/02/2025)

  • Cardiomegaly with dilated pulmonary artery
  • Congested lung fields
  • Moderate Pericardial Effusion
  • Gross right pleural effusion with collapse–consolidation of the right lower lobe
  • Minimal left pleural effusion with collapse of the left lower lobe and atelectatic changes with hyperattenuation
  • Findings suggestive of possible amiodarone-induced pulmonary toxicity
  • Focal lesion in the inferior pole of the spleen, likely infarct
  • No evidence of pulmonary thromboembolism

Pleural Fluid Analysis (08/02/2025)

Therapeutic and diagnostic pleural tapping600 mL drained
Pleural fluid protein5.3 g/dL
LDH276 IU/L
Sugar89 mg/dL
AFBNegative
GeneXpertNegative
Gram stain and cultureNo growth
CytologyNegative for malignant cells

Additional Laboratory Findings (07/02/2025)

Hemoglobin9.6 g/dL
ESR98 mm/hr
NT-proBNP564 pg/mL
Thyroid profileImproving TSH (9.56 µIU/mL)
Renal function testsNormal

Imaging

Chest X-ray showed moderate right pleural effusion with minimal left pleural effusion.

Fig (1): Chest Xray PA View (06/02/2025)

Management and Outcome

Pulmonology consultation was obtained, and pleural drainage was performed. Supportive and symptomatic management was continued. The patient showed clinical improvement following intervention.

Discussion

This patient with rheumatic heart disease presented with recurrent, alternating pleural effusions associated with pericardial effusion, pulmonary hypertension, and elevated inflammatory markers. Cardiac etiology alone did not fully explain the recurrent nature and laterality shift of the effusion. Extensive evaluation excluded tuberculosis, malignancy, and pulmonary embolism. Imaging findings raised the possibility of drug-induced pulmonary toxicity, which has been reported with antiarrhythmic agents such as amiodarone. Hypothyroidism and hypoalbuminemia may have further contributed to serosal effusions.

Conclusion

Recurrent pleural effusion in patients with rheumatic heart disease requires comprehensive evaluation beyond cardiac causes. Drug toxicity, systemic inflammation, and endocrine abnormalities should be considered. Multidisciplinary management is essential for accurate diagnosis and optimal outcome.

 

 

 

 

Kauvery Hospital