Khawar Zaineb, Herrera-Gonzalez Maria B, Mirza Mariam, Mirza Noreen, Suleiman Addi
Internal Medicine, Saint Michael's Medical Center, Newark, USA.
Medical Education, Saint Michael's Medical Center, Newark, USA.
Cureus. 2025 Jul 31;17(7):e89152. doi: 10.7759/cureus.89152. eCollection 2025 Jul.
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease; cardiac involvement is a recognized complication, with pericardial effusion being one of the most frequent manifestations. Here, we present a patient with massive pericardial effusion in a known SLE patient without hemodynamic instability, highlighting concepts of pericardial compliance and physiological adaptation in autoimmune disease. We present a case of a 33-year-old female with a known history of SLE who presented with progressively worsening pleuritic chest pain over three weeks. She was hemodynamically stable, with distant heart sounds and no jugular venous distension. Her initial encounter was suspicious of pulmonary embolism, and a CT angiography of the chest was performed, which revealed the true culprit of her symptoms: a large pericardial effusion. Laboratory workup showed elevated inflammatory markers and positive anti-dsNDA, RNP, and Smith antibodies. Electrocardiogram demonstrated a low voltage, but no presence of electrical alternans. Echocardiogram revealed an ejection fraction of 65%, no evidence of right ventricular diastolic collapse or tamponade, but a large pericardial effusion up to 2.7 cm. The patient was monitored in the intensive care unit, treated with corticosteroids, colchicine, and hydroxychloroquine, and underwent pericardiocentesis with drainage of over 1,100 cc of serous fluid. Her symptoms resolved, and analysis of the fluid showed no evidence of infectious or malignant etiology. Pericardial compliance refers to the pericardium's ability to stretch in response to fluid accumulation. Chronic inflammatory changes in SLE typically reduce pericardial compliance through fibrosis and pericardial thickening; a slow rate of accumulation may paradoxically permit large effusions to develop without hemodynamic compromise. This case suggests that gradual accumulation over time may allow the pericardium to adapt, delaying or preventing hemodynamic compromise. This emphasizes the interplay between effusion volume, rate of accumulation, and pericardial compliance. It is important to consider how slowly growing effusions in autoimmune diseases can behave differently and require careful monitoring and treatment planning. Persistent effusions despite immunosuppressive therapy underscore the need for better understanding and treatment strategies for this complex manifestation.
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