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Published on: November 26, 2018
Cardiac Adaptation in Lupus: A Case of Massive Pericardial Effusion With Preserved Hemodynamics
Zaineb Khawar1, Maria B Herrera-Gonzalez1, Mariam Mirza2
1Internal Medicine, Saint Michael's Medical Center, Newark, USA.
Insights
Systemic lupus erythematosus (SLE) can cause large pericardial effusions without hemodynamic compromise due to increased pericardial compliance. This case highlights physiological adaptation in autoimmune disease, emphasizing slow fluid accumulation.
Area of Science:
- Cardiology
- Rheumatology
- Internal Medicine
Background:
- Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease.
- Cardiac involvement, particularly pericardial effusion, is a frequent complication of SLE.
Observation:
- A 33-year-old female with known SLE presented with chest pain due to a massive pericardial effusion.
- Despite the large effusion (2.7 cm), she was hemodynamically stable, showing no signs of tamponade.
- Laboratory results revealed elevated inflammatory markers and positive SLE-specific antibodies.
Findings:
- Echocardiography confirmed a large pericardial effusion with preserved ejection fraction and no signs of right ventricular collapse.
- Pericardial compliance, the ability of the pericardium to stretch, is crucial in managing large effusions.
- Chronic inflammation in SLE can reduce pericardial compliance, yet slow fluid accumulation may allow adaptation, preventing hemodynamic instability.
Implications:
- This case underscores the importance of considering pericardial compliance and the rate of effusion accumulation in SLE patients.
- Understanding these factors is vital for accurate diagnosis, monitoring, and treatment planning of cardiac manifestations in autoimmune diseases.
- Persistent effusions despite treatment highlight the need for further research into managing this complex SLE complication.
Abstract:
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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