Title : Pericardial decompression syndrome post pericardiocentesis in a case of miliary and disseminated tuberculosis in a young male presenting with cardiac temponade
Abstract:
Background: Pericardial effusion and cardiac tamponade encompass a clinical spectrum with diverse presentations. While significant pericardial effusions warrant clinical attention, emergent drainage is primarily indicated for patients exhibiting hemodynamic compromise. Cardiac tamponade with circulatory collapse necessitates immediate intervention via pericardiocentesis or surgical pericardiotomy^1. Historically, the lethality of pericardial effusions has been acknowledged for centuries. In 1653, Riolanus proposed sternal trephination for fluid relief. The first successful pericardial aspiration was performed by Franz Schuh in 1840 using a blind left parasternal approach. Subsequently, in 1911, Marfan introduced the subxiphoid technique, which remained standard despite associated risks until the late 20th century [^2]. The advent of echocardiography-guided pericardiocentesis in the 1970s significantly enhanced procedural safety and efficacy [^3]. Despite advancements, pericardiocentesis can occasionally lead to rare complications such as transient acute left ventricular dysfunction (ALVD), the pathophysiology of which remains under investigation.
Case Presentation: A 32-year-old male with a history of disseminated tuberculosis and early-onset Parkinsonism presented with progressive dyspnoea and hypotension. Clinical examination and echocardiography confirmed a large pericardial effusion with signs of tamponade, including right atrial and right ventricular diastolic collapse. LVEF on presentation was normal. Emergency pericardiocentesis under fluoroscopic and echocardiographic guidance, we evacuated around 800 mL of straw coloured fluid. Post-procedure, the patient developed acute hypotension and respiratory distress. Repeat echocardiography revealed global hypokinesia of LV with a significantly reduced left ventricular ejection fraction (LVEF) of approximately 25%, contrasting with normal pre-procedure ventricular function. There were no segmental wall motion abnormalities, Troponin levels were within normal limits, patient had no chest pain and there were no ECG changes suggestive of Acute coronary syndrome; no arrhythmic events were noted. Supportive management, including inotropic support and careful fluid management, was initiated. Over 72 hours, the patient exhibited progressive hemodynamic improvement. A follow-up echocardiogram at one week demonstrated normalization of left ventricular function (LVEF: 60%).
Discussion: Acute left ventricular dysfunction following pericardiocentesis is an uncommon but recognized complication. The proposed mechanisms include:
- Interventricular Volume Imbalance: In cardiac tamponade, elevated pericardial pressure restricts right ventricular filling. Rapid decompression via pericardiocentesis abruptly increases right ventricular preload, potentially overloading the left ventricle and leading to elevated end-diastolic pressure and wall stress, culminating in transient LV dysfunction^4.
- Myocardial Stunning: The sudden removal of pericardial pressure may result in acute ventricular wall stretch and increased transmural pressures, impairing myocardial energetics and leading to reversible contractile dysfunction akin to stress cardiomyopathy^5.
- Autonomic Imbalance: Acute withdrawal of sympathetic stimulation post-pericardiocentesis may precipitate myocardial dysfunction through autonomic dysregulation[^6].
Recognition of this phenomenon is crucial, especially during large-volume pericardial fluid evacuation. Management is primarily supportive, with most patients experiencing full recovery, as illustrated in this case.
Conclusion: This case underscores the importance of awareness regarding transient left ventricular dysfunction as a potential complication following pericardiocentesis. Prompt recognition and supportive management are essential to ensure favourable outcomes.
