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

Purulent pericarditis, characterized by frank pus or

microscopically purulent effusion in the pericardial sac,

is usually a severely acute illness with still high mortal-

ity, especially if both diagnosis and treatment are de-

layed.1,2,10 It is usually caused by Staphylococcus au-

reus, Streptococcus pneumoniae, or Streptococcus pyo-

genes.2,10 Predisposing factors include pneumonia, previ-

ous cardiac or thoracic surgery, immunosuppression, and

pre-existing aseptic pericarditis and infective organ-

isms.3,8,10 Clinical findings include fever, chills, dyspnea,

tachypnea, cough, weakness, and tachycardia out of pro-

portion to fever. Classic symptoms of pericarditis, in-

cluding 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 car-

diovascular 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.

CASE REPORT

A 77-year-old female presented with a one-week his-

tory of progressive dyspnea. She was relatively well in

the past except for a 10-year history of hypertension un-

der anti-hypertensive medications (losartan and nife-

dipine). She didn’t take illicit drugs. Before hospitaliza-

tion, no significant inflammatory symptoms such as fe-

ver and chills could be traced. Vital signs included a

113 Acta Cardiol Sin 2008;24:113�6

Case Report Acta Cardiol Sin 2008;24:113�6

Received: January 18, 2008 Accepted: March 26, 20081Division of Cardiology, Department of Medicine, Song-Shan Armed

Forces General Hospital; 2Division of Cardiology, Department of

Medicine, Tri-Service General Hospital; 3Division of Infectious Dis-

eases 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

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 patient’s 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. Twelve-

lead electrocardiogram revealed sinus tachycardia with

rate of 118 beats/min, diffuse low voltage, and left axis

deviation (Figure 1). A chest radiograph showed car-

diomegaly 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 re-

gurgitation, consistent with cardiac tamponade (Figure

2). Emergent pericardiocentesis was performed, releas-

ing 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

Acta Cardiol Sin 2008;24:113�6 114

Chung-Ming Tu et al.

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 (*).

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

dL, protein of 5.0 g/dL, and negative activity of ad-

enosine deaminase. The acid-fast stain was negative. A

rapid Gram stain of pericardial fluid revealed Gram-posi-

tive 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 tu-

mor 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’ intra-

venous penicillin G treatment. On hospital day 14, fol-

low-up transthoracic echocardiography revealed mini-

mal non-lobulated pericardial effusion. Oral amoxicillin

treatment was continued for another 4 weeks. The pa-

tient 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 in-

flammation, infection, immunologic disorder, neoplasm,

myxedema, renal insufficiency, pregnancy, aortic or car-

diac rupture, trauma, nephrotic syndrome, hepatic cir-

rhosis, 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, physi-

cians 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,

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 an-

other disorder. Viridans streptococcal infection is rarely

found in purulent pericarditis. Also, it is usually com-

bined with other organisms.1 The clinical course of viri-

dans streptococcal infection is usually sub-acute or chro-

nic, with low or absence of toxic sign.7 The common

sources of viridans streptococcal purulent pericarditis in-

clude mediastinitis from esophageal rupture, dental ca-

ries, and retropharyngeal abscess, infective endocar-

ditis, chest surgery, trauma, and pneumonia.8,10 The pos-

sible 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 anti-

biotics without pericardial drainage, the rapid unsu-

spected 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, in-

cluding antimicrobial agent selection, pericardial sur-

gery, and prognostic prediction. If the causative organ-

ism is Haemophilus influenza, early pericardiectomy is

recommended, since the exudates in the pericardial spa-

ce 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 drain-

age of pericardial fluid could be adequately performed

by closed pericardiocentesis to relieve the cardiac tam-

ponade at once and minimize the suffering of the patient.

In conclusion, purulent pericarditis is a potential le-

thal disease and should be considered as an indolent un-

derlying 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-

115 Acta Cardiol Sin 2008;24:113�6

Indolent Purulent Streptococcal Pericarditis

threatening condition associated with purulent pericar-

ditis and cardiac tamponade.

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