Purulent Pericarditis Complicated With Cardiac Tamponade, Multiorgan Failure, and Constrictive Pericarditis

Figures

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  Figure 1. Key Diagnostics and Timeline of Critical Events of the Case (A) Electrocardiogram at initial presentation showing sinus tachycardia of 110 beats/min, normal heart axis, low QRS voltages, RBBB, and diffuse ST-segment elevation without reciprocal ST-segment depressions. (B) Emergency TTE with classic signs of tamponade at presentation. Top left: Subcostal view with a large circumferential PEff of end-diastolic 2.5 cm (arrows) with inflow obstruction and diastolic right ventricular collapse (∗), with no masses, no vegetations, or hemopericardium. Top right: Apical 4-chamber view of a swinging heart with a markedly thickened pericardium (>3 mm) with debris and some fibrin strains (arrows). Bottom left: Apical 4-chamber view with mitral valve inflow variance of 47%. Bottom right: Subcostal view with IVC plethora of 2.7 cm and hepatic vein dilatation. (C) Timeline of key diagnostics and critical events with anti-inflammatory and antimicrobial therapies. Fulminant purulent pericarditis due to Streptococcus pneumoniae in a patient with 2 episodes of cardiac tamponade relieved by repeat pericardiocentesis, who was admitted to the ICU for multiorgan failure. He was hemodynamically…

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  Figure 2. Emergency Pericardiocentesis on Day 2 With Specimen of Serosanguinous Pericardial Effusion Specimen of the emergency pericardiocentesis on day 2 after a total of 340 mL exudative serosanguinolent fluid was obtained. PEff culture was positive for Streptococcus pneumoniae. PEff = pericardial effusion.

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  Figure 3. TTE on Day 19 With Classic Signs of Subacute Constrictive Pericarditis (A) Apical 4-chamber view with normal biventricular function and paradoxically early diastolic bulging of the intraventricular septum toward the left ventricle (ie, septal bounce; arrows), with respirophasic intraventricular shuddering (∗) and no valvular disease, vegetations, or thrombi. (B) Four-chamber view using pulsed-wave Doppler with peak early diastolic E-wave during inspiration and expiration, defining a mitral valve inflow variation of 47%. (C) Four-chamber view with annulus reversus using tissue Doppler imaging, with a medial e′ of 14.3 cm/s and a lateral e′ of 9.4 cm/s. (D) Inferior vena cava plethora of 2.7 cm with no collapse on sniff. IVC = inferior vena cava.

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  Figure 4. Multimodality Imaging of Purulent Pericarditis (A) FDG PET/CT on day 27 and (B and C) CMR after pericardiectomy on day 256. (A) Left: Axial contrast-enhanced computed tomography of the thorax demonstrating a large, protein-enriched (∼40 Hounsfield units) circumferential PEff (∗) with an enhanced, thickened, and fibrotic pericardium (solid arrows) and a pericardial calcification (dashed arrow). Bilateral pleural effusion was present, but no masses and no signs of coronary artery disease were found. Middle: Intense FDG uptake across the entire pericardium, consistent with a “ring-of-fire” pattern (arrows), that highlights enhanced metabolic activity due to severe infection in the pericardial space. Right: Attenuation-corrected axial FDG PET/CT image confirming the “ring-of-fire” pattern (arrows) at the pericardium, with no FDG uptake elsewhere (not shown). Hence, empyema, deep-seated abscess, or infection elsewhere were ruled out. (B) Left: Horizontal long-axis 4-chamber view of T1-weighted bright blood gradient-spin echo image demonstrating normal biventricular function and dimension, no atrial enlargement, and a relaxation pattern consistent of a right bundle branch block but no…

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  Figure 5. Histopathological Examination of the Surgically Removed Pericardium (A) Histopathological examination of the excised pericardium demonstrates marked fibrous thickening with architectural distortion of the mesothelial lining by dense inflammatory infiltrates, predominantly neutrophilic. Note the transition from fibrous tissue to focal fibrin-rich areas (∗). These findings are consistent with acute and chronic fibrosing pericarditis. (B) At higher magnification, extensive fibrous pericardium with abundant necrotic debris and dense aggregates of neutrophilic granulocytes, indicating intense active inflammation on a background of chronic fibrotic pericardial disease.