The most common atrial septal defect occurs in the central part of the atrial septum in the region of fossa ovalis called secundum ASD [1]. Most patients with ASD are asymptomatic and may remain undiagnosed until later in life. In adults worsening of the clinical condition has been attributed to various factors such as an increased LV end-diastolic pressure and reduced LV compliance, RV failure, atrial arrhythmia, and elevated pulmonary artery pressure [1].
Secundum ASDs can be closed surgically or with percutaneous devices. The first device closure of secundum ASD was done by Mills and King in 1976 [6]. Percutaneous ASD closure has become a popular procedure in defects with suitable size and septal rims. Common complications associated with transcatheter ASD closure include residual shunts, embolization, device-related thrombosis, erosion and perforation of the heart, infective endocarditis, and sudden death [7].
Post ASD closure pericardial effusion occurs with a reported incidence of 0.5–1.5 % secondary to cardiac perforation, device erosion, or reactive PE. Pre-existing PE could be due to different causes include uremic, autoimmune, hypothyroidism, Viral, bacterial, fungal or parasitic infections. In a retrospective study (n = 40), Spodick et al. found 13 of their 40 patients (32.5%); > 21 years of age with isolated secundum ASDs have circumferential PE preoperatively [8].
Our first patient had mild pre-existing PE secondary to uremia that aggravated after device implantation. The first modality for determining the etiology of the worsening of PE is Spiral Cardiac CT Angiography (CTA) which in this patient confirmed the disastrous complication, it means cardiac erosion; so, immediate surgical management of the patient was performed.
The second patient had mild to moderate pre-existing PE with no response to anti-inflammatory agents during 2- to 3-month follow-up that seems to be due to ASD itself. With mild to moderate pre-existing PE, Reddy et al. speculated that, if septal defects were left untreated, the effusion may accumulate over time because of chronic volume overload, which may lead to more PE [9]. The amount of PE in this patient also increased significantly after two ASD device implantations that necessitate pericardiocentesis. Cardiac CTA revealed no evidence of cardiac perforation, device erosion, or cardiac hematoma. Reactive PE was assumed as an etiologic factor that worsened the patient’s pre-existing PE.
The third patient had mild to moderate PE due to unknown etiology that after device implantation increased to moderate PE without evidence of cardiac perforation, erosion, or hematoma, so we managed her conservatively. Fortunately, she was asymptomatic and the PE decreased significantly within 3-month follow-up.
Generally speaking, several reasons should be considered in patients who develop pericardial effusion after TCC of ASDs; the most and catastrophic cause is cardiac erosion which frequently happens at the left atrium roof or aortic side. So, the immediate diagnostic modality which could rule out is cardiac CTA; if no evidence of cardiac erosion was found, looking for hematoma around the pulmonary vein or left atrium appendage which commonly occurs by wire manipulation which leads to perforation should be appraised. In fact, the diagnosis of cardiac erosion was confirmed by detection of hemopericardium based on the density and Hounsfield CT number of the pericardial fluid and retroaortic hematoma in the first patient. Echocardiography may not be enough to rule out cardiac erosion. CTA can reveal information about structures that are difficult to visualize with TEE such as erosion of an ASD closure device into adjacent structures and performing cardiac CTA and looking for the evidence of cardiac erosion are essential [10].
The uncommon cause of PE, post TCC of ASD is case reports of seroritis (pleuro-pericarditis) which the underlying stimulus is not clear, but one hypothesis is the reaction to Nickle and the materials of the device; it seems to respond well to anti-inflammatory agents with low recurrence rate. In some patients, the underlying advanced RV failure leads to persistent PE even after ASD closure who have a very poor prognosis. In fact, this group of patients with advanced right ventricular failure which is somewhat irreversible develop pericardial effusion after ASD closure due to RV failure and require treatment for right ventricular failure and they have increased risk for atrial and ventricular arrhythmia. finally, in some cases, no reasonable source of PE could be found and extensive work-up for acute, sub-acute, and chronic pericarditis should be performed.
