Abstract
INTRODUCTION: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect multiple organ systems. Cardiac involvement is common but usually mild, with pericarditis being the most frequent manifestation. However, cardiac tamponade as an initial presentation is rare and potentially life-threatening. Early recognition and treatment are critical to prevent morbidity and mortality. We present a case of an 18-year-old female whose first manifestation of SLE was cardiac tamponade accompanied by lupus nephritis, highlighting the importance of considering autoimmune causes in young patients presenting with unexplained pericardial effusion. CASE DESCRIPTION: An 18-year-old female with no known history of chronic illness or medication use presented to the emergency department with a two month history of progressive fatigue, chest and epigastric pain, and exertional dyspnea. On initial evaluation, she was tachycardic and tachypneic with a blood pressure of 100/60 mmHg, heart rate of 128 bpm, respiratory rate of 26/min, and oxygen saturation of 92% on room air. Physical examination revealed muffled heart sounds and bilateral fine crackles at the lung bases. No jugular venous distension or peripheral edema was noted. ECG showed sinus tachycardia with low voltage in limb and precordial leads. Initial laboratory findings included anemia (Hb 9.2 g/dL), leukopenia (WBC 4.2 ×10(9)/L), elevated BUN (67 mg/dL), and normal creatinine (0.73 mg/dL). Troponin, BNP, and D-dimer were within normal limits. Urinalysis revealed proteinuria with 1 g/day, raising suspicion for renal involvement. Chest CT demonstrated a pericardial effusion up to 2 cm in thickness and bilateral pleural effusions up to 3 cm. Transthoracic echocardiography showed a 1 cm localised pericardial effusion in the posterolateral basal region of the right ventricle, with right ventricular diastolic collapse—findings consistent with early cardiac tamponade. She was admitted to the ICU and underwent urgent pericardiocentesis, with drainage of approximately 500 mL of serous fluid. Pericardial fluid was negative for malignant cells and acid-fast bacilli. Viral and bacterial serologies (HIV, hepatitis panel, syphilis) were negative. An autoimmune panel was ordered, with results detailed in Table 1. A kidney biopsy was also performed due to persistent proteinuria and confirmed a diagnosis of lupus nephritis. Based on the clinical picture and subsequent findings, she was diagnosed with systemic lupus erythematosus and started on prednisone, hydroxychloroquine, azathioprine, and colchicine. The patient showed clinical improvement and was discharged with close rheumatology follow-up. DISCUSSION: Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease that most commonly affects women of reproductive age. Although pericardial involvement is frequent in SLE, cardiac tamponade as an initial presentation is extremely rare, with a reported incidence of less than 2% among SLE patients. It typically indicates active disease and may coexist with pleural effusion, nephritis, or hematologic abnormalities. Our patient presented with signs and symptoms suggestive of pericardial tamponade—tachycardia, hypotension, dyspnoea, muffled heart sounds, and imaging-confirmed right ventricular collapse. She also demonstrated other typical features of SLE including anaemia, leukopenia, proteinuria, and serositis (pleural and pericardial effusions). Her kidney biopsy confirmed lupus nephritis, further supporting a diagnosis of active systemic disease. In young patients, especially females, a high index of suspicion is essential when multi-organ symptoms are present, even in the absence of a prior autoimmune diagnosis. Prompt recognition and management of cardiac tamponade is life-saving, while early initiation of immunosuppressive therapy may prevent long-term organ damage. This case emphasises the importance of a multidisciplinary approach, involving cardiology, nephrology, and rheumatology. Treatment with corticosteroids and immunosuppressants such as hydroxychloroquine, azathioprine, and colchicine resulted in marked clinical improvement in this patient. Ultimately, this case highlights that pericardial tamponade may be a sentinel and life-threatening manifestation of undiagnosed SLE. Timely diagnosis and intervention can significantly alter the disease course and prognosis in such patients. KEY LEARNING POINTS: This case highlights several important clinical lessons. Although pericardial involvement is relatively common in systemic lupus erythematosus (SLE), cardiac tamponade as an initial manifestation is exceptionally rare and life-threatening. In young females presenting with unexplained pericardial effusion, particularly when accompanied by systemic symptoms, clinicians should consider autoimmune aetiologies early in the diagnostic process. Multisystem findings such as serositis (pleural and pericardial effusions), hematologic abnormalities (anaemia, leukopenia), and proteinuria may offer vital diagnostic clues pointing toward SLE. Prompt recognition of cardiac tamponade and urgent pericardiocentesis are essential to prevent cardiovascular collapse. In this case, early ICU admission and drainage of 500 mL of pericardial fluid resulted in rapid hemodynamic stabilisation. The presence of proteinuria warranted further renal evaluation, and a kidney biopsy confirmed lupus nephritis, a common but serious manifestation that influences both prognosis and treatment. Early initiation of immunosuppressive therapy—including corticosteroids, hydroxychloroquine, azathioprine, and colchicine—led to significant clinical improvement. This case reinforces the need for a multidisciplinary approach involving cardiology, nephrology, rheumatology, and emergency medicine to ensure comprehensive care. Ultimately, it underscores the importance of maintaining a high index of suspicion for SLE in patients with multisystem involvement and pericardial effusion, even in the absence of a previous diagnosis, as early diagnosis and treatment can be life-saving and prevent irreversible organ damage.