Acute heart failure due to invasive pneumococcal disease and purulent pericarditis: A case report

Gregorio Tersalvi; Manuela Averaimo; Dario Winterton; Francesca Scopigni

doi:10.4103/hm.hm_26_21

CASE REPORT

Year : 2021 | Volume : 5 | Issue : 2 | Page : 58-60

Acute heart failure due to invasive pneumococcal disease and purulent pericarditis: A case report

Gregorio Tersalvi¹, Manuela Averaimo¹, Dario Winterton², Francesca Scopigni¹
¹ Division of Cardiology, Cardiocentro Ticino Institute, Ente Ospedaliero Cantonale, Lugano, Switzerland
² Department of Health Sciences, University of Milano-Bicocca, Monza, Italy

Date of Submission	29-Apr-2021
Date of Acceptance	10-May-2021
Date of Web Publication	29-Jun-2021

Correspondence Address:
Dr. Gregorio Tersalvi
Division of Cardiology, Cardiocentro Ticino Institute, Via Tesserete 48, Lugano 6900
Switzerland

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/hm.hm_26_21

Abstract

This report describes a 61-year-old female with no previous cardiovascular history presented with acute heart failure. Clinical, laboratory, and imaging findings suggested the diagnosis of pneumococcal invasive disease with concomitant purulent pericarditis. Prompt pharmacological and operatory treatment with both pericardiocentesis and further fenestration brought to a complete recovery.

Keywords: Acute heart failure, invasive pneumococcal disease, pneumococcal cardiomyopathy, pneumococcal pericarditis, purulent pericarditis, Streptococcus pneumoniae

How to cite this article:
Tersalvi G, Averaimo M, Winterton D, Scopigni F. Acute heart failure due to invasive pneumococcal disease and purulent pericarditis: A case report. Heart Mind 2021;5:58-60

How to cite this URL:
Tersalvi G, Averaimo M, Winterton D, Scopigni F. Acute heart failure due to invasive pneumococcal disease and purulent pericarditis: A case report. Heart Mind [serial online] 2021 [cited 2022 Oct 2];5:58-60. Available from: http://www.heartmindjournal.org/text.asp?2021/5/2/58/319651

Introduction

Adverse cardiac events of community-acquired pneumonia are a contributing factor to mortality during hospitalization for pneumonia and thereafter,^[1] especially if the pathogen is Streptococcus pneumoniae.^[2] There are several mechanisms that concur to cardiac dysfunction in invasive pneumococcal disease (IPD): Cell-wall-mediated inhibition of cardiomyocyte contractility, pneumococcal invasion forming myocardial microlesions, and dysregulation of calcium entry in the cardiac cell by bacterial pneumolysin-formed pores.^[3],[4]

Due to the widespread use of antibiotics, purulent pericarditis in immunocompetent subjects is nowadays a very rare complication of pneumonia. In a Spanish retrospective review between 1972 and 1991, only 33 cases of purulent pericarditis were observed among an inpatient population of 593,600, and only in 11 cases pneumonia was identified as the infection source.^[5] The mechanism by which patients with pneumococcal pneumonia develop purulent pericarditis is, in most cases, a hematogenous spread.^[6]

When left untreated, purulent pericarditis is inevitably fatal.^[7] The mortality rate remains high at up to 40% even with treatment, generally due to cardiac tamponade, constriction, and septic shock.^[5]

We report a case of an adult female patient with IPD secondary to pneumonia, developing in acute heart failure (AHF) with reduced ejection fraction complicated by purulent pericarditis.

Case Report

A 61-year-old female presented with increasing dyspnea in the previous weeks, up to New York Heart Association (NYHA) IV at the time of presentation, a 4 kg weight gain, leg swelling, and fatigue. She denied anginal symptoms, except for a single episode of chest pain after lifting a heavy object 4 days before, reproducible with palpation, and self-treated with proton pump inhibitor.

The patient had a history of obesity, arterial hypertension, and type II diabetes under treatment for 17 years.

On clinical examination, her Glasgow coma scale was 14, blood pressure 100/70 mmHg, tachyarrhythmic, tachypnoic, with cold extremities, massive bilateral peripheral edema from ankles to knees, distended jugular veins, and bibasilar crackles. The palpation of the abdomen revealed a positive Murphy sign. Electrocardiogram showed atrial fibrillation with rapid ventricular response, with average heart rate of 140 bpm [Figure 1].

Figure 1: Twelve-lead electrocardiogram on admission showing atrial fibrillation with rapid ventricular response, left anterior hemiblock, flattened T waves in DI and aVL

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Due to concern for acute cholecystitis, empiric broad-spectrum antibiotics with cefepime and metronidazole were initiated, and an abdominal computed tomography was performed, excluding cholecystitis but showing a left lower lobe consolidation with a large pleural effusion.

Laboratory findings were remarkable for a white blood cell count of 11,700/mL with 88.6% neutrophils, C reactive protein 332 mg/L, procalcitonin 3.77 μg/L, elevation of liver enzymes, renal insufficiency with creatinine 138 μmol/L, hyperglycemia (37.8 mmol/L), and a NT-ProBNP of 13.547 ng/L.

Bedside echocardiography showed a moderately dilated, stiff, and diffusely hypokinetic left ventricle with left ventricular ejection fraction (LVEF) 15%–20% and the presence of a pericardial effusion, yet not hemodynamically relevant. The blood cultures grew S. pneumoniae; therefore, the antibiotics were switched to only ceftriaxone.

After initial stabilization and electrical cardioversion which restored a normal sinus rhythm, a coronary angiogram was performed. This showed a significant stenosis on middle right coronary artery that we interpreted as a bystander finding that did not justify the severe LVEF reduction. To complete the diagnostic of AHF, we tested for autoimmunity, carbohydrate deficient transferrin, thyroid-stimulating hormone, virology including HIV, hepatitis B virus, and hepatitis C virus, and Chagas serology, all resulting negative, and we performed a cardiac magnetic resonance imaging that confirmed the echocardiographic findings of LVEF reduction and pericardial effusion (maximum 4 cm on the right atrium, maximum 2.6 cm ventricular, with thickening of the pericardium), but excluded myocardial fibrosis, necrosis, or criteria for myocardial inflammation [Figure 2].

Figure 2: Cine cardiac magnetic resonance imaging four-chamber view images at end-systole, showing massive pericardial effusion (maximum 4 cm on the right atrium, maximum 2,6 cm ventricular), with thickening of the pericardium (3–4 mm)

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Suspecting purulent pericarditis from the imaging and microbiological findings, we decided to perform pericardiocentesis and evacuated 750 ml of purulent white fluid [Figure 3], which tested positive on bacterial polymerase chain reaction and the pneumococcal antigen detection test. Cultures and a Ziehl–Nielsen stain were negative.

Figure 3: Purulent pericardial fluid with creamy appearance, obtained from pericardiocentesis

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Hence, we interpreted the results as consistent with parapneumonic pneumococcal pericarditis and continued intravenous ceftriaxone for a total of 6 weeks. Due to the persistence of pericardial effusion at echocardiography, a subxiphoid pericardial fenestration was executed, with evacuation of another 700 ml of pericardial purulent fluid.

In the following days, favored by antibiotic and diuretic therapy, we observed a progressive clinical and parametrical resolution of the inflammatory syndrome, and an improvement of dyspnea and fatigue, to such an extent that a complete autonomous active mobilization of the patient had been possible prior discharge. On echocardiographic control, the pericardial effusion appeared stable, partially reabsorbed, to a size of 8 mm in front of the right ventricle and 9 mm in front of the left ventricle. In addition, the left ventricle itself appeared no longer dilated (diastolic diameter = 50 mm).

Already 1 month after discharge, the patient reported a significant improvement in symptoms (NYHA I). Clinically, no signs of congestion were present. Echocardiography showed a LVEF of 30%. Successively, elective percutaneous coronary intervention of the affected coronary artery and up-titration of heart failure (HF) medication allowed further increase in LVEF at follow-up (43% at 6 months). No other rehospitalizations for HF were reported as yet.

Discussion

This case shows that patients with pneumococcal pneumonia and subsequent IPD are at risk of developing a complex clinical scenario of AHF, with multiple mechanisms that should always kept in mind. Primarily, the direct and indirect cardiotoxicity of S. pneumoniae that we mentioned before. Furthermore, acute purulent bacterial pericarditis, although rare, should always be excluded in patients presenting with pneumonia, pericardial effusion, and hemodynamic instability. Hence, early recognition and prompt intervention, with percutaneous and/or surgical approach, are mandatory for a successful outcome.

Our first approach to this patient was driven by the diagnostic workup of AHF according to European guidelines.^[8] We searched for common causes of AHF such as acute coronary syndrome, tachycardia-induced cardiomyopathy due to atrial fibrillation, and valvular disease and treated them accordingly. The absence of diffuse coronary artery disease or severe valve defects and the lack of clinical improvement after electrical cardioversion made us search for other causes of AHF. The presence of S. pneumoniae bacteremia suggested direct implication of the bacterium in the pathogenesis of left ventricular dysfunction. On top of the optimal therapy of AHF and atrial fibrillation, we started high-intensity statins both due to the coronary stenosis and for the possible cardioprotective effect in IPD.^[3],[4] The protective effect of statins against cardiac lesion formation during IPD is supported by a meta-analysis that showed that individuals on statin therapy who were hospitalized for pneumonia have significantly better posthospital discharge survival rates than controls.^[9]

The scenario of reduced LVEF and hemodynamic instability may be precipitated by concurrent purulent pericarditis, which can be overlooked and delayed, especially in complex clinical scenarios. Ultimately, the diagnosis of purulent pericarditis is established by obtaining pericardial fluid for culture and microscopy. According to European guidelines, drainage is crucial in purulent pericarditis. Purulent effusions are often heavily loculated and likely to rapidly reaccumulate. Subxiphoid pericardiostomy and rinsing of the pericardial cavity allow more complete drainage of the effusion, as loculations can be manually lysed.^[7]

Purulent pericarditis should be managed aggressively as in this case. Death is inevitable if untreated, whereas with comprehensive therapy up to 85% of cases have been reported to survive the episode and have a good long-term outcome.^[5],[10]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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