Case Report

Acta Cardiol Sin 2008;24:113-6

Indolent Purulent Pericarditis Due to Viridans

Streptococcus Infection Successfully Treated by
Pericardiocentesis and Penicillin G
Chung-Ming Tu,1 Shu-Meng Cheng,2 Shih-Ping Yang,2 Tsorng-Liu Hsieh3 and Shyi-Shiaw Jiau1

Although purulent pericarditis generally presents with acute cardiovascular decompensation and a sepsis-like
appearance, it can be indolent in rare settings, leading to a catastrophic outcome. We report a 77-year-old female
who presented with progressive dyspnea without fever. Massive pericardial effusion with cardiac tamponade was
detected by the transthoracic echocardiogram. The fluid culture yielded Viridans Streptococcus which was susceptible
to penicillin G. The patient dramatically improved after 14 days penicillin G treatment and did well during the 10
months follow-up. Purulent pericardial effusion should be kept in mind as a lethal cause of cardiac tamponade, even
in afebrile patients. Emergent pericardiocentesis followed by appropriate antibiotics treatment is essential to avoid
delayed diagnosis and improper management.

Key Words:

Cardiac tamponade Viridans Streptococcus Purulent pericarditis Gram stain

INTRODUCTION

tachypnea, cough, weakness, and tachycardia out of proportion to fever. Classic symptoms of pericarditis, including chest pain and pericardial friction rub, occur in
only about 50% of patients.2-4
The clinical course of purulent pericarditis is usually
fulminant, manifesting with shock syndrome due to cardiovascular collapse and/or septic phenomena. However,
it can also be insidious. Here, we describe an afebrile
woman presenting with indolent purulent pericarditis
due to Viridans Streptococcus infection, successfully
treated by both prompt pericardiocentesis and adequate
penicillin G treatment.

Purulent pericarditis, characterized by frank pus or

microscopically purulent effusion in the pericardial sac,
is usually a severely acute illness with still high mortality, especially if both diagnosis and treatment are delayed. 1,2,10 It is usually caused by Staphylococcus aureus, Streptococcus pneumoniae, or Streptococcus pyogenes.2,10 Predisposing factors include pneumonia, previous cardiac or thoracic surgery, immunosuppression, and
pre-existing aseptic pericarditis and infective organisms.3,8,10 Clinical findings include fever, chills, dyspnea,

CASE REPORT

Received: January 18, 2008 Accepted: March 26, 2008

1
Division of Cardiology, Department of Medicine, Song-Shan Armed
Forces General Hospital; 2Division of Cardiology, Department of
Medicine, Tri-Service General Hospital; 3Division of Infectious Diseases and Tropical Medicine, Department of Medicine, Song-Shan
Armed Forces General Hospital, Taipei, Taiwan.
Address correspondence and reprint requests to: Dr. Shyi-Shiaw Jiau,
Division of Cardiology, Department of Medicine, Song-Shan Armed
Forces General Hospital, No. 131, Jian-kang Rd., Song-Shan, Taipei
105, Taiwan. Tel: 886-2-2764-2151; Fax: 886-2-2756-8692; E-mail:
dodo.11@yahoo.com.tw

A 77-year-old female presented with a one-week history of progressive dyspnea. She was relatively well in
the past except for a 10-year history of hypertension under anti-hypertensive medications (losartan and nifedipine). She didnt take illicit drugs. Before hospitalization, no significant inflammatory symptoms such as fever and chills could be traced. Vital signs included a
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Chung-Ming Tu et al.

body temperature of 36.1 C, heart rate of 118 beats/

minute, respiration of 20 per minute and blood pressure
of 160/89 mmHg in supine position, and the oxygen
saturation was 92% when she was breathing ambient
air. Jugular venous pressure was about 12 cm of water.
Lung auscultation showed crackles over bilateral basal
lung fields. The patients heart sounds were distant but
regular, with no significant murmur. Dentition was poor,
but there was no abscesses nor gingival tenderness found
by a dentist. The remainder of the physical examination
was unremarkable.
Pertinent laboratory data showed a white cell count
of 7.6 103/mm3 with 60% segmented cells, 22% bands,
and 10% lymphocytes, hemoglobin of 12.4 g/dL, and a
platelet count of 250 103/mm3. The C-reactive protein
level was 12.2 mg/L. Arterial blood gas exam revealed

pH of 7.430, oxygen partial pressure of 68 mmHg, and

carbon dioxide partial pressure of 34 mmHg. Twelvelead electrocardiogram revealed sinus tachycardia with
rate of 118 beats/min, diffuse low voltage, and left axis
deviation (Figure 1). A chest radiograph showed cardiomegaly but no pulmonary infiltrates. Transthoracic
echocardiography revealed massive pericardial effusion
(2.0 cm) with early right ventricle diastolic collapse but
without evidence of oscillating vegetation or valve regurgitation, consistent with cardiac tamponade (Figure
2). Emergent pericardiocentesis was performed, releasing 675 ml of bloody fluid from the pericardial cavity.
Laboratory analysis of the pericardial fluid showed
280,000 nucleated cells/mm3 with 70% segmented cells,
10% bands, 15% lymphocytes, and 5% monocytes,
600,000 red blood cells/mm3, lactate dehydrogenase of

Figure 1. A 12-lead ECG showed diffuse low voltage.

Figure 2. Transthoracic echocardiography (A) Diastolic right ventricle free wall collapse (arrow) and large pericardial effusion in M-mode.
(B) Apical four-chamber view showed large pericardial effusion (*).

Acta Cardiol Sin 2008;24:113-6

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Indolent Purulent Streptococcal Pericarditis

and made when pus is drained from the pericardial space

or when bacteria is cultured from the pericardial fluid.
But purulent pericarditis always coexists with another disorder. Viridans streptococcal infection is rarely
found in purulent pericarditis. Also, it is usually combined with other organisms.1 The clinical course of viridans streptococcal infection is usually sub-acute or chronic, with low or absence of toxic sign. 7 The common
sources of viridans streptococcal purulent pericarditis include mediastinitis from esophageal rupture, dental caries, and retropharyngeal abscess, infective endocarditis, chest surgery, trauma, and pneumonia.8,10 The possible source in our case might be related to dental caries
according to the history, chest radiograph, transthoracic
echocardiographic findings, and intact skin.
Pericardiocentesis and drainage of the pus, as well
as antibiotic treatment, are mandatory for patients with
purulent pericarditis.2,4 In patients treated only with antibiotics without pericardial drainage, the rapid unsuspected development of a large pericardial effusion
may result in sudden cardiovascular collapse and death
due to cardiac tamponade. 9,11 However, if the clinical
course is indolent, bedside Gram stain and acid-fast stain
can provide information for clinical decision-making, including antimicrobial agent selection, pericardial surgery, and prognostic prediction. If the causative organism is Haemophilus influenza, early pericardiectomy is
recommended, since the exudates in the pericardial space are described as having the density of scrambled
eggs and can hardly be drained with a catheter.12 Also,
the risk and difficulty of closed pericardiocentesis are
higher in lobulated effusion. The open approach should
be mandatory for safety and adequate management. In
our case, no significant lobulated pericardial effusion
and no significant strand bands were noted. Then drainage of pericardial fluid could be adequately performed
by closed pericardiocentesis to relieve the cardiac tamponade at once and minimize the suffering of the patient.
In conclusion, purulent pericarditis is a potential lethal disease and should be considered as an indolent underlying disease of cardiac tamponade. A stat Gram stain
as well as other pericardial effusion analysis should be
performed in every patient with cardiac tamponade.
Prompt percutaneous catheter drainage of pericardial
fluid along with appropriate antibiotic therapy according
to bedside Gram stain can rapidly terminate the life-

3200 U/L, triglycerides of 20 mg/dL, glucose of 10 mg/

dL, protein of 5.0 g/dL, and negative activity of adenosine deaminase. The acid-fast stain was negative. A
rapid Gram stain of pericardial fluid revealed Gram-positive cocci in chain. Antibiotic treatment with intravenous
3 million U of penicillin G every 4 hours was initiated.
Further laboratory studies including thyroid function
test, a polymerase chain reaction for tuberculous bacilli
in pericardial effusion, autoimmune disease test, and tumor markers were all within normal limits. Three days
later, culture from the pericardial fluid yielded Viridans
streptococcus which was susceptible to penicillin G. We
also followed transthoracic echocardiography every day,
which revealed only minimal non-lobulated pericardial
effusion. All culture reports, including blood culture,
sputum culture, and urine culture, showed no bacteria
growth. The patient recovered well after 14 days intravenous penicillin G treatment. On hospital day 14, follow-up transthoracic echocardiography revealed minimal non-lobulated pericardial effusion. Oral amoxicillin
treatment was continued for another 4 weeks. The patient did well during the next 10 months follow-up.

DISCUSSION
Cardiac tamponade is a medical emergency, which
should be diagnosed carefully and treated thoroughly.
Common etiologies of cardiac tamponade include inflammation, infection, immunologic disorder, neoplasm,
myxedema, renal insufficiency, pregnancy, aortic or cardiac rupture, trauma, nephrotic syndrome, hepatic cirrhosis, and chronic heart failure.5 Despite the indolent
disease course in our patient, the positive culture result
from the pericardial effusion and dramatic improvement
after both antibiotics treatment and adequate drainage
confirmed the diagnosis of purulent pericarditis with
cardiac tamponade.
Purulent pericarditis is typically an acute and often
catastrophic illness.6 Both early detection and effective
management of purulent pericarditis require much effort
and skill to achieve correct diagnosis. Therefore, physicians should be very alert to the type of disease setting.
Fast diagnosis is often by the aid of echocardiography,
computed tomography (CT), and/or physical findings
such as pulsus paradoxus or diminished heart sounds,
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Chung-Ming Tu et al.

6. Sagrista-Sauleda J, Barrabes JA, Permanyer-Miralda G, SolerSoler J. Purulent pericarditis: review of 20 years experience in a
general hospital. J Am Coll Cardiol 1993;22:1661-5.
7. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N
Engl J Med 2001;345:1318-30.
8. Rubin RH, Moellering RC Jr. Clinical microbiologic and therapeutic aspects of purulent pericarditis. American Journal of Medicine 1975;59:68-78.
9. Little WC, Freeman GL. Pericardial disease. Circulation 2006;
113:1622-32.
10. Klacsmann PG, Bulkley BH, Hutchins GM. The changed spectrum of purulent pericarditis. American Journal of Medicine
1977;63:666-73.
11. Imazio M, Trinchero R. Triage and management of acute pericarditis. International Journal of Cardiology 2007;118:286-94.
12. Morgan RJ, Stephenson LW, Edmunds H. Surgical treatment of
purulent pericarditis in children. J Thorac Cardiovasc Surg 1983;
85:527-31.

threatening condition associated with purulent pericarditis and cardiac tamponade.

REFERENCES
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