Case report

A 68-year-old African-American woman presented to the emergency department for gradual worsening of dyspnea. The patient denied experiencing chest pain, diaphoresis, nausea, vomiting, or fever. She had been admitted three months earlier to another institution for alcoholic pancreatitis, at which time she suffered a non Q-wave myocardial infarction. She was also treated for methicillin-resistant Staphylococcus aureus (MRSA) line sepsis with intravenous vancomycin for 6 weeks. At the time of her current admission, she had been off antibiotics for approximately 3 weeks. On physical examination, she was afebrile, but was hypotensive with a blood pressure of 88/56 mmHg, mildly tachycardic, and tachypneic. Lungs were clear to auscultation, and no abnormal heart sounds, murmurs, or rub were heard. No jugular venous distention or peripheral edema was present. The EKG showed sinus rhythm with occasional premature ventricular contractions. Laboratory data were significant for a leukocytosis of 16.2×109/lwith 66% neutrophils and 7% bands.

Initial chest X-ray showed clear lungs with an enlarged cardiac silhouette and pericardial calcification. A transthoracic echocardiogram showed a complex mass-like structure, with an echogenic component as well as cystic, multi-septated areas. This was located anterior to and caused extrinsic compression on the right ventricle (Fig. 1). CT of the chest was performed next, although without intravenous contrast due to renal insufficiency. This showed a large, soft-tissue-density mass, which appeared to be located within the pericardial space. Calcifications along the posterior pericardium were also visualized. The anterior location and mass effect on the right ventricle were confirmed on the CT scan (Fig. 2a). The cystic component and septations seen on echocardiography were, however, not appreciated.

Fig. 1. a
figure 1

Parasternal short-axis view at the level of the aorta shows a heterogeneous anterior mass with cystic areas and septations. AO aorta, RVOT right ventricular outflow tract, M mass). b Apical four-chamber view shows extrinsic compression of the right ventricle by an echogenic mass. RV right ventricle, LV left ventricle, LA left atrium, RA right atrium, M mass

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Fig. 2. a
figure 2

Non-contrast CT scan shows an anterior pericardial soft-tissue-density mass (M) with areas of calcification (arrows). Note the impression upon the right ventricle. b, c Axial and coronal ECG-gated HASTE images clearly show the pericardium (arrows) and the presence of an intrapericardial mass (M). The mass is isointense to muscle. Area of signal void (arrowhead) within the mass represents the calcification seen on CT. d Axial T1-weighted postcontrast image shows the pericardial mass (M) to be predominantly nonenhancing, with enhancing septations (arrows), more consistent with a complex pericardial collection

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As it was unclear whether the findings on echocardiography and unenhanced CT constituted a neoplastic process, MRI of the heart was performed. MRI was also performed to determine the site of origin of the mass and confirm that it was confined to the pericardial space. T1-weighted HASTE images were obtained before and after the intravenous administration of gadolinium. Precontrast images showed a mass-like process within the anterior pericardial space that was isointense to muscle, with focal areas of signal dropout related to the pericardial calcifications. Following administration of gadolinium, only enhancement of multiple septations was observed, without enhancement of the remainder of the mass. The findings on MRI were consistent with a complex pericardial fluid collection, with infection or resolving hematoma being the most likely etiologies (Fig. 2b, c).

The patient then underwent surgery, where phlegmonous inflammation was found to be present over the anterior pericardium. At pericardiectomy approximately 300 ml purulent fluid was aspirated from the pericardial space (Fig. 3). Intraoperative transesophageal echocardiogram following aspiration showed relief of right ventricular compression. Pathologic examination of a section of pericardium demonstrated extensive granulation tissue and fibrosis with focal areas of acute inflammation. Culture of the pericardial collection grew MRSA. Intravenous vancomycin treatment was initiated and subsequent CT scans demonstrated no further pericardial collection. Her hospital course was, however, complicated by the development of venous thombosis in the right upper extremity and internal jugular vein following placement of a central catheter. Furthermore, the patient developed gastrointestinal bleeding secondary to the anticoagulation therapy. The patient was subsequently discharged to complete a 6-week course of intravenous vancomycin and has done well without reaccumulation of pericardial pus.

Fig. 3.
figure 3

Intraoperative image shows purulent fluid being suctioned from the pericardial space

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Discussion

Pericardial inflammation is most commonly a self-limited process caused by viral infection. However, bacterial and fungal infections as well as noninfectious causes of pericarditis are described in the literature [1]. The clinical presentation is variable depending on the etiology and acuity of symptoms. Cardiac tamponade may occur with a severe, acute pericarditis, while the chronic form results in a constrictive pericarditis. In general, patients present with dyspnea, malaise, and chest pain. Tachycardia, tachypnea, and occassionally a pericardial friction rub are present on examination.

Purulent bacterial pericarditis is an uncommon, yet potentially fatal condition, which can rarely present, as in our patient, as a complex pericardial mass [2, 3]. Pericardial involvement may be secondary to hematogenous spread, contiguous extension from adjacent structures, or a complication of cardiothoracic surgery. Common organisms include Staphylococcus, anaerobes and gram-negative bacilli. Immunocompromised patients, especially HIV-positive patients, are at increased risk for purulent pericarditis [1].

Pericardial involvement is most often diffuse and results in an effusion that is easily appreciated on imaging studies. Although echocardiography remains the primary modality for evaluation of pericardial processes, cross-sectional imaging has been utilized to further characterize pericardial lesions in difficult cases [4]. In our patient both echocardiography and unenhanced CT revealed a complex extracardiac mass compressing the right ventricle. Because of the questionable relationship of this mass with the pericardium, MRI was indicated. This confirmed that the process was confined to the pericardial space and revealed the multiseptated appearance of the lesion, better seen after gadolinium injection. When combined with the clinical information, the findings provided strong evidence for an infectious pericardial collection.

In the acute setting, purulent pericarditis requires image-guided drainage of the fluid to relieve hemodynamic compromise. In subacute or chronic cases, a surgical approach is preferred. The indolent presentation in our patient and the imaging findings were more consistent with a subacute process and prompted a median sternotomy and pericardiectomy.

Conclusion

Purulent pericarditis is an uncommon condition with a variable clinical presentation. It is, however, associated with a high mortality rate, making early diagnosis and treatment crucial. Prior septicemia, immunocompromise, percutaneous angioplasty, cardiothoracic surgery, and postpartum state[5, 6] have been reported as risk factors for the development of bacterial pericarditis. In such patients, a high index of suspicion must be maintained.

Presentation of purulent pericarditis as a mediastinal mass is extremely rare. As in our patient, CT and particularly MRI may localize the mass to the pericardial space and furthermore demonstrate its complex nature, thus raising the suspicion for an infectious pericardial collection and enabling prompt diagnosis and treatment.