PMC5467283_01
ECG showed diffuse ST elevation and PR segment depression (except in leads aVR and V1), consistent with pericarditis.
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The 12-lead ECG demonstrated classic signs of pericarditis (Figure 1) and the chest radiograph revealed cardiomegaly with normal pulmonary vascularity (Figure 2(a)).
Evolution of the patient's chest radiographs. The prepericardiocentesis film (a) showed cardiomegaly secondary to the massive pericardial effusion. Five days after removal of fluid, new pockets of radiolucency were detected within the cardiac silhouette on both frontal (b) and lateral (c) projections, representing air within the pericardium (arrows pointing at outline of the sac).
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The 12-lead ECG demonstrated classic signs of pericarditis (Figure 1) and the chest radiograph revealed cardiomegaly with normal pulmonary vascularity (Figure 2(a)). A chest radiograph taken after five days showed new pockets of radiolucency within the cardiac silhouette (Figures 2(b) and 2(c)).
Echocardiographic apical four-chamber views demonstrating pneumopericardium. (a) There was a large (20 mm) circumferential layer (white arrows) within the pericardial space, with its heterogenous nature suggestive of possibly purulent pericardial fluid. Marked thickening of the pericardium (5 mm) can also be appreciated in this view (red arrow). (b) Slight angulation of the probe to focus on the anterior pericardial space (anterior to the right ventricle) revealed the presence of microbubbles (yellow arrow) representing air freely moving within the pericardial sac.
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Air microbubbles were visualized mainly in the anterior pericardial space (likely due to gravitational effects in the supine position), with a significant amount of reaccumulated pericardial fluid and frond-like structures (Figure 3). Even though diastolic collapse of the right-sided chambers was no longer observed, several indicators of constrictive physiology were demonstrated in this second study, such as marked thickening of the pericardium (Figure 3(a)), septal bounce due to interventricular independence (Figure 4), exaggerated respiratory variation in tricuspid and mitral inflow (Figure 5), and IVC plethora (Figure 6).
Echocardiographic parasternal short axis views at the level of the mid-left ventricle (LV). (a) The free wall of the right ventricle (RV) appears adherent to the adjacent pericardium (red arrows). There was note of septal bounce, leading to a D-shaped LV cavity during diastole. (b) M-mode of the same view confirmed the wavy motion (yellow arrows) of the interventricular septum representing septal bounce.
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Even though diastolic collapse of the right-sided chambers was no longer observed, several indicators of constrictive physiology were demonstrated in this second study, such as marked thickening of the pericardium (Figure 3(a)), septal bounce due to interventricular independence (Figure 4), exaggerated respiratory variation in tricuspid and mitral inflow (Figure 5), and IVC plethora (Figure 6).
Exaggerated respiratory variations in tricuspid and mitral valve inflow. During inspiration, there was a significant increase in velocity for the tricuspid valve (a), while the mitral valve exhibited decreased inflow velocity (b).
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Even though diastolic collapse of the right-sided chambers was no longer observed, several indicators of constrictive physiology were demonstrated in this second study, such as marked thickening of the pericardium (Figure 3(a)), septal bounce due to interventricular independence (Figure 4), exaggerated respiratory variation in tricuspid and mitral inflow (Figure 5), and IVC plethora (Figure 6).
The IVC was dilated (23 mm), with minimal decrease in diameter on inspiration (only 26%), indicative of IVC plethora.
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Even though diastolic collapse of the right-sided chambers was no longer observed, several indicators of constrictive physiology were demonstrated in this second study, such as marked thickening of the pericardium (Figure 3(a)), septal bounce due to interventricular independence (Figure 4), exaggerated respiratory variation in tricuspid and mitral inflow (Figure 5), and IVC plethora (Figure 6).
CT scan images. (a) Cross-sectional cut of the heart and pericardium revealed an air-fluid level within the pericardial sac (white arrows). (b) Cross-sectional cut of the liver showed multiple hypodense nonenhancing foci (yellow arrows).
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A CT scan with contrast confirmed the diagnosis of pneumopericardium, manifesting as a clearly visible air-fluid level (Figure 7(a)). The study also revealed a left-sided pleural effusion with consolidation and atelectasis of adjacent lung segments, enlarged and confluent para-aortic and pre- and postcarinal lymph nodes, and several hypodense nonenhancing foci throughout the liver (Figure 7(b)).
Intraoperative findings. (a) Pericardiectomy through median sternotomy was performed. (b) Stripped pericardium with measured thickness of 5-7 mm. (c) Caseous material extracted from the pericardial sac.
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Surgical treatment consisted of pericardiectomy through a median sternotomy (Figure 8(a)). Intraoperatively, the thickness of the stripped pericardium was measured to be 5-7 mm (normal: <2 mm) (Figure 8(b)). Caseous material was extracted from the pericardial sac (Figure 8(c)).