Asymptomatic bacteriuria as a warning sign of purulent pericardial effusion in a patient with systemic lupus erythematosus: a case report

Abstract

Background

Purulent pericardial effusions are rare, comprising less than 1% of pericardial disease. Patients with systemic lupus erythematosus are particularly vulnerable owing to immunosuppression, and distinguishing infectious from autoimmune causes of pericardial effusion can be challenging. This distinction is critical, as treating a flare with immunosuppression can worsen an occult infection. We describe a unique case of a patient with systemic lupus erythematosus who developed purulent pericardial effusion secondary to methicillin-sensitive Staphylococcus aureus, and we highlight asymptomatic bacteriuria as a potential early indicator of this process. To our knowledge, this is the first reported case of purulent pericardial effusion preceded by methicillin-sensitive Staphylococcus aureus bacteriuria in a patient with systemic lupus erythematosus.

Case presentation

A 45-year-old African-American woman with systemic lupus erythematosus presented with joint pain, pleuritic chest pain, and malaise. She was initially treated for a presumed systemic lupus erythematosus flare. She was also found to have a small–moderate pericardial effusion and asymptomatic methicillin-sensitive Staphylococcus aureus bacteriuria. Days later, she developed acute encephalopathy, respiratory distress, and hemodynamic instability. Blood cultures grew methicillin-sensitive Staphylococcus aureus, transthoracic echocardiogram revealed mitral valve vegetations consistent with infective endocarditis, and brain imaging showed septic emboli. Despite appropriate antibiotics, the patient’s pericardial effusion enlarged and required pericardiocentesis, yielding purulent fluid which grew methicillin-sensitive Staphylococcus aureus. The effusion recurred, eventually prompting pericardial window surgery. Postoperatively, the patient’s mental and functional status continued to improve, and she was discharged to a long-term care facility. Repeat transthoracic echocardiogram 6 weeks after discharge showed a small pericardial effusion and a normal ejection fraction.

Conclusion

This case highlights an atypical presentation of purulent pericardial effusion due to methicillin-sensitive Staphylococcus aureus in a patient with systemic lupus erythematosus. Purulent pericardial effusions can present with nonspecific symptoms, and the diagnosis may be obscured in critically ill patients with multiple active processes contributing to a shock state. As methicillin-sensitive Staphylococcus aureus is an uncommon bacteria to be found in the urine, it may be a warning sign of disseminated infection in immunocompromised patients and should prompt further work-up. In addition, point-of-care ultrasound can serve as a valuable tool in identifying tamponade physiology and prompting timely intervention. Clinicians should be alert to the possibility of purulent pericardial effusion in immunocompromised patients with methicillin-sensitive Staphylococcus aureus bacteremia.

Background

Since the advent of antibiotics, purulent pericardial effusions are rare clinical presentations, accounting for less than 1% of overall pericardial disease [1]. The most common bacterial causes of purulent effusion are Streptococcus pneumoniae, S. aureus, and Mycobacterium tuberculosis [2]. Purulent effusions often develop insidiously with nonspecific symptoms such as fever and tachycardia, and they carry a mortality rate of nearly 100% if not treated [3]. The major complications associated with purulent pericardial effusions are cardiac tamponade, constrictive pericarditis, and death [3].

Patients with systemic lupus erythematosus (SLE) are at theoretically greater risk of purulent pericarditis owing to their immunosuppressed state. Only a handful of cases of purulent pericardial effusion in patients with SLE have been described in literature [4–6]. Given the immunocompromised status of patients with SLE and the higher overall prevalence of pericarditis in this population, it may be challenging to distinguish infectious from autoimmune etiologies of pericardial effusion [7]. This distinction is critical, as immunosuppressive therapy intended for an autoimmune flare can dangerously accelerate an underlying infection.

We present a rare case of purulent pericardial effusion secondary to methicillin-sensitive S. aureus (MSSA) in a patient with SLE that highlights asymptomatic bacteriuria as a potential early indicator of this occult infectious process. To our knowledge, this is the first reported case of MSSA bacteriuria preceding MSSA bacteremia, infective endocarditis, and purulent pericardial effusion in a patient with SLE.

Case presentation

A 45-year-old African-American woman with systemic lupus erythematosus (SLE) complicated by lupus nephritis presented to our hospital with joint pain, pleuritic chest pain, and malaise. Initial laboratory studies revealed leukocytosis (24.0 × 10³/µL), thrombocytopenia (85 × 10³/µL), elevated creatinine (4.05 mg/dL; baseline ~2.0 mg/dL), and elevated inflammatory markers (erythrocyte sedimentation rate 100 mm/hour, C-reactive protein 186 mg/L). Anti-dsDNA was noted to be 172 IU/mL. She had been hospitalized 2 weeks prior for an SLE flare after months of medication nonadherence (anti-dsDNA at that time was > 300 IU/ml), and was discharged on hydroxychloroquine 200 mg twice daily and prednisone 40 mg daily with a steroid taper plan. Upon this admission, she endorsed taking these medications as prescribed. Given her initial presentation of generalized malaise and pain, along with her elevated inflammatory markers, she was initially treated for a presumed SLE flare and was started on prednisone 40 mg and continued on hydroxychloroquine. Transthoracic echocardiogram (TTE) on admission revealed an ejection fraction (EF) of 57.2% and a small–moderate pericardial effusion attributed to the SLE flare (Fig. 1). Urine cultures grew MSSA; however, since she was asymptomatic, she was not treated for a urinary tract infection. The patient continued to endorse body aches, chest pain, and shortness of breath. She reported that her joint and chest pain felt worse than her prior SLE flares. Her kidney function continued to deteriorate further, and she was started on hemodialysis.

Fig. 1.

Transthoracic echocardiogram obtained on admission showing small–moderate pericardial effusion

A few days later, the patient developed acute encephalopathy, hypotension, tachycardia, and respiratory distress. Though she had previously been on room air, she was newly tachypneic to 40 breaths per minute and required 13 L of supplemental oxygen via high-flow nasal cannula to maintain an oxygen saturation of 90%. Blood cultures were collected and were positive for MSSA. Repeat TTE showed new mitral valve vegetations, a reduced EF of 35.8%, and a slightly larger and now loculated pericardial effusion. Of note, there was no evidence of hemodynamic compromise at this time. The patient was started on broad spectrum antibiotics with vancomycin and cefepime for treatment of bacterial endocarditis. Owing to persistent tachypnea and altered mental status, she was intubated and mechanically ventilated. Computed tomography (CT) scan of the head revealed mild cortical and subarachnoid hemorrhages, consistent with septic emboli. Broad spectrum antibiotics were eventually narrowed to intravenous oxacillin for treatment of bacterial endocarditis. The patient’s prednisone dose was reduced to 20 mg to balance immunosuppression for her SLE with infection control. Valve replacement surgery was deferred owing to ongoing encephalopathy and poor surgical candidacy in the setting of septic emboli. The patient also intermittently had episodes of atrial fibrillation and supraventricular tachycardia, requiring increasing doses of metoprolol.

Several days later, on a routine bedside ultrasound, the patient was incidentally found to have an enlarged pericardial effusion. Formal TTE showed significant enlargement of the pericardial effusion with right ventricular and right atrial collapse (Fig. 2). Evidence of early tamponade physiology prompted emergent pericardiocentesis with drain placement, which yielded 1 L of turbid fluid that was cultured and confirmed to be growing MSSA. The patient continued to have ~100 cc purulent drain output for several days. Repeat TTE showed recurrent enlarged pericardial effusion. She subsequently underwent subxiphoid pericardial window surgery with washout, yielding purulent fluid. Chest and mediastinal tubes were placed for concurrent large pleural effusion.

Fig. 2.

Transthoracic echocardiogram obtained prior to emergent pericardiocentesis, showing large pericardial effusion measuring 3.9 cm in its greatest dimension and containing echodense material

The patient’s clinical status improved postoperatively after pericardial window surgery. Her mental status returned to her baseline, and she was successfully extubated. She was discharged to a long-term acute care facility with plans to continue intravenous oxacillin for a total of 6 weeks and follow-up for repeat TTE. Chest and mediastinal tubes and pericardial drain were removed prior to discharge. At follow-up with cardiac surgery 10 days post-discharge, she was participating in physical therapy, asymptomatic, and reported feeling well. Repeat TTE 6 weeks post-discharge showed a small pericardial effusion (significantly improved from the effusion seen on imaging prior to surgery), a normal (53.6%) EF, and a persistent echodensity on the mitral valve. One month later, she underwent mechanical mitral valve replacement. She was discharged home and was doing well at her 3-week follow-up visit.

Discussion and conclusion

This case illustrates an unusual presentation of purulent pericardial effusion in a patient with SLE. The patient was found to have asymptomatic MSSA bacteriuria, followed later by MSSA bacteremia and purulent pericardial effusion requiring drainage.

MSSA pericardial effusion in SLE is rarely described in literature. Knodell and Manders described a septic patient with SLE who developed an MSSA effusion late in hospitalization despite negative blood cultures and initially normal imaging [4]. Fu reported a case of acute tamponade due to MSSA in a patient with SLE [5]. Anis et al. described a patient with SLE who, most similar to ours, presented with pleuritic chest pain followed by MSSA bacteremia and purulent pericardial effusion [6]. However, none of these cases report preceding MSSA bacteriuria.

MSSA bacteriuria has been infrequently reported as a presenting symptom of MSSA pericardial effusion, but, to our knowledge, it has not been described in a patient with SLE [8]. It is unclear whether, in this case, MSSA bacteriuria represented distant hematogenous spread of pre-existing MSSA bacteremia, or if the infection spread in the reverse direction from the urinary tract to the bloodstream. Seeding of the pericardium likely occurred via hematogenous dissemination. The evolution of the effusion from a small, simple collection on admission to a large, loculated, purulent fluid suggests a two-step process. It is plausible that an initially sterile lupus effusion was secondarily seeded during the patient’s bacteremia, with her immunosuppressed state then accelerating bacterial proliferation and organization. Prior lupus pericarditis episodes may also have caused chronic scarring and inflammation, predisposing the pericardium to bacterial seeding.

In this case, diagnostic delay was influenced by several factors. Since the patient had been admitted just weeks before with symptoms of SLE flare in the setting of medication nonadherence, she was presumed to be having another flare. When urine cultures grew MSSA, her lack of urinary symptoms caused a 1-day delay in antibiotic initiation. No blood cultures were collected at that time either. In retrospect, her renal dysfunction and generalized body aches may have obscured the presence of an infection. As S. aureus is an uncommon urinary isolate, its presence should prompt further work-up for disseminated infection [9].

Moreover, though the pericardial effusion was present from the time she was admitted, the patient later developed infective endocarditis and a subarachnoid hemorrhage that diverted attention from the growing effusion. The patient’s intermittent tachyarrhythmia may have been a clue to her worsening effusion, as atrial fibrillation has been associated with purulent pericardial effusion [10]. A week elapsed between the TTE that confirmed her diagnosis of endocarditis and a repeat TTE that demonstrated significant enlargement of her pericardial effusion, leading to emergent pericardiocentesis. Notably, point-of-care ultrasound (POCUS) was instrumental in identifying the enlarging effusion, which was then confirmed with TTE.

Purulent pericardial effusion requires immediate treatment with broad-spectrum intravenous antimicrobials, which can then be narrowed on the basis of sensitivities [1]. The duration of therapy is not standardized, but it is typically 4–6 weeks. Drainage via pericardiocentesis or surgical intervention is often required to resolve the effusion. Minimally invasive surgical options include subxiphoid pericardial window and video-assisted thoracoscopic surgery (VATS). The former may carry a lower complication rate, while the latter may be associated with a reduced risk of recurrence [11]. Adding further complexity to this patient’s medical management was her immunocompromised status and ongoing treatment with steroids. There are no established guidelines for management of immunosuppressants while treating purulent pericarditis in patients with SLE, although it seems reasonable to reduce immunosuppression in the setting of disseminated infection. In this case, the patient’s initial 40 mg dose of prednisone was reduced to 20 mg.

Purulent pericardial effusion is a rare and potentially fatal condition with a highly variable presentation. It may present acutely with tamponade or insidiously with nonspecific symptoms after weeks in the hospital, and it is not always associated with bacteremia. This case highlights a rare series of events in which MSSA bacteriuria preceded disseminated infection and purulent pericardial effusion in a patient with SLE. Clinicians should maintain a heightened suspicion for this disease process in immunocompromised patients and utilize POCUS as a valuable and readily available diagnostic tool. Seemingly benign but unusual signs—such as MSSA bacteriuria—may forebode serious systemic infection.

Abbreviations

EF

Ejection fraction

MSSA

Methicillin-sensitive S. aureus

POCUS

Point-of-care ultrasound

SLE

Systemic lupus erythematosus

TTE

Transthoracic echocardiogram

VATS

Video-assisted thoracoscopic surgery

Author contributions

BR, HK, and NS contributed to patient care. NS performed patient chart review and drafted the original manuscript. BR, HK, and NS revised the manuscript. HK obtained consent from the patient. BR served as senior author. All authors read and approved the final manuscript.

Funding

This study did not receive funding.

Availability of data and materials

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Declarations

Ethics approval and consent to participate

Ethics approval was not required for this case report. Individual consent was obtained from the patient’s next-of-kin, as described below.

Consent for publication

Written informed consent was obtained from the patient’s next-of-kin for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.