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.
系统性红斑狼疮(SLE)是一种多系统自身免疫性疾病;心脏受累是一种公认的并发症,心包积液是最常见的表现之一。在此,我们报告一例已知患有SLE的患者出现大量心包积液,但无血流动力学不稳定情况,强调了自身免疫性疾病中心包顺应性和生理适应性的概念。我们报告一例33岁女性,已知有SLE病史,在三周内出现逐渐加重的胸膜炎性胸痛。她血流动力学稳定,心音遥远,无颈静脉扩张。她初次就诊时怀疑有肺栓塞,遂进行了胸部CT血管造影,结果显示了其症状的真正原因:大量心包积液。实验室检查显示炎症标志物升高,抗双链DNA、核糖核蛋白和史密斯抗体呈阳性。心电图显示低电压,但无电交替现象。超声心动图显示射血分数为65%,无右心室舒张期塌陷或心包填塞的证据,但有高达2.7厘米的大量心包积液。该患者在重症监护病房接受监测,接受了皮质类固醇、秋水仙碱和羟氯喹治疗,并进行了心包穿刺引流,引流出超过1100毫升的浆液性液体。她的症状得到缓解,对液体的分析显示没有感染或恶性病因的证据。心包顺应性是指心包对液体蓄积作出伸展反应的能力。SLE中的慢性炎症变化通常通过纤维化和心包增厚降低心包顺应性;积液缓慢增加可能反常地允许大量积液形成而不出现血流动力学损害。该病例表明,随着时间的推移逐渐蓄积可能使心包得以适应,延迟或防止血流动力学损害。这强调了积液量、蓄积速度和心包顺应性之间的相互作用。重要的是要考虑自身免疫性疾病中缓慢增长的积液可能表现不同,需要仔细监测和制定治疗计划。尽管进行了免疫抑制治疗仍持续存在积液,这突出表明需要更好地理解和制定针对这种复杂表现的治疗策略。