Open Journal of Pediatrics, 2011, 1, 87-89
doi:10.4236/ojped.2011.14020 Published Online December 2011 ( OJPed
Published Online December 2011 in SciRes.
Cardiac tamponade due to group a streptococcal pericarditis
in a 10-month-old boy and a review of the literature
Matthew C. Schwartz1*, Matthew J. Gillespie1, Paul Stephens Jr.1, Brian Fisher2
1Division of Cardiology, The Children’s Hospital of Philadelphia, Philadelph ia, USA;
2Division of Infectious Disease and Center for Clinical Epidemiology and Biostatistics, The Children’s Hospital of Philadelphia,
Philadelphia, USA.
Email: *
Received 18 September 2011; revised 27 October 2011; accepted 8 November 2011.
Group A streptococcus (GAS) is a rare cause of pu-
rulent pericarditis in pediatric patients as only 7
cases have been reported. We present a 10-month-old
boy who developed cardiac tamponade from GAS
and was successfully treated with subxiphoid tube
drainage and 4 weeks of antibiotics at the Children’s
Hospital of Philadelphia.
Keywords: Streptococcus; Pericarditis; Pericardiocente-
sis; Tamponade
Group A streptococcus (GAS) is a rare cause of bacterial
pericarditis in children with only 7 pediatric cases pre-
viously reported [1-5]. We describe a 10-month-old who
developed cardiac tamponade due to GAS pericarditis
and was successfully treated.
A 10-month-old boy presented to the Children’s Hospital
of Philadelphia (CHOP) Emergency Department (ED)
with 9 days of fever accompanied by a transient papular
rash, but no other localizing symptoms. He underwent
outpatient evaluation on day 6 and was diagnosed with
roseola. The patient’s fever continued prompting his
His birth and past medical histories were unremark-
able. He lived in Philadelphia and had no exposures or
travel. Several days into the child’s illness, his father
was diagnosed with GAS pharyngitis by rapid strepto-
coccal antigen test and was treated.
In the ED, he had a rectal temperature of 38.2˚C. The
remainder of his vital signs and physical exam were
normal except for mild bilateral anterior cervical lym-
phadenopathy. Initial laboratory testing showed a white
blood cell count of 20,500/uL (63% neutrophils, 26%
lymphocytes), a hemoglobin of 10.2 g/dL, a platelet
count of 57,400/u L, an erythrocyte sedimentation rate of
75 mm/hr, a C-reactive protein of 6.2 mg/dL, an albumin
of 3.7 g/dL, an aspartate aminotransferase of 109 U/L,
and an alanine aminotransferase <6 U/L. Urinalysis and
chest radiograph were normal. Urine and blood cultures
were sent as was a respiratory virus polymerase chain
reaction (PCR) panel on respiratory secretions.
The patient was admitted for evaluation. On hospital
day 1, the respiratory virus PCR panel returned negative
for adenovirus, respiratory syncytial virus, influenza A
and B, parainfluenza 1 - 3, metapneumovirus, and rhino-
virus. Serum was sent for adenovirus PCR, human her-
pes virus-6 (HHV6) PCR , cytomegalovi r us ( C M V) PCR,
and Ebstein Barr virus (EBV) serology. To consider oc-
cult osteomyelitis, a whole body magnetic resonance
imaging scan was obtained and was negative. In light of
possible Kawasaki Disease, an echocardiogram was
performed, revealing a small, 4 mm posterior pericardial
effusion, normal biventricular systolic function, and mild,
diffuse ectasia of the right coronary artery (proximal
right coronary artery z-score 2.62).
Due to fever, elevated inflammatory markers, an ele-
vated aspartate transferase, and ectasia of the right coro-
nary artery, incomplete Kawasaki Disease was suspected.
On hospital day 2, the patient was treated with intrave-
nous immunoglobulin and aspirin was started. From
hospital day 3 through 5, the patient’s fever continued
and his inflammatory markers increased. Serial blood
cultures remained negative and urine culture at the time
of admission was negative. The serum adenovirus PCR,
CMV PCR, and EBV serologies returned negative. The
patient’s HHV6 serum PCR returned as mildly positive
(1981 copies/mL). The Infectious Disease Service was
consulted and felt HHV6 not likely responsible for the
By hospital day 6, the patient remained febrile and
had increased work of breathing. Chest x-ray showed an
M. C. Schwartz et al. / Open Journal of Pediatrics 1 (2011) 87-89
enlarged cardiac silhouette and echocardiogram showed
a large circumferential pericardial effusion (1.2 cm) with
early signs of tamponade physiology including right
atrial collapse in late ventricular diastole (Figure 1). The
coronary arteries appeared normal with no evidence of
right coronary artery ectasia. An electrocardiogram
showed sinus tachycardia with no ST segment or PR
segment changes.
The patient was transferred to the Intensive Care Unit
and pericardiocentesis drained 65 cc of purulent fluid
and a drain left in place. The gram stain showed gram
positive cocci and empiric antibiotics were started. The
bacteria was subsequently identified as Group A beta
hemolytic streptococcus and the antibiotics changed to
intravenous penicillin G. The patient improved and the
pericardial drain was removed several days after peri-
cardiocentesis. The patient completed 14 days of intra-
venous antimicrobials following drainage and was dis-
charged home to complete another 14 days of oral peni-
cillin (total 4 week course).
Four months after discharge, the patient was well and
echocardiogram showed a normal pericardial sac.
Pericarditis is uncommon in children. Of 20 cases re-
ported by Roodpeyma et al., 8 (40%) were bacterial, 6
(30%) associated with collagen vascular disease, 4 (20%)
were viral, and 2 (10%) due to mass invasion of the
pericardium [6]. Pericarditis can also be related to post-
pericardiotomy syndrome or can be idiopathic.
Clinical signs of purulent pericarditis include fever,
tachycardia, tachypnea, hepatomegaly, and decreased
Figure 1. Transthoracic apical four chamber view showing a
large, circumferential pericardial effusion with fibrinous
strands and diastolic right atrial collapse consistent with tam-
ponade physiology.
cardiac sounds. Patients rarely present with pericardial
friction rub because the pericardial space is distended
with pus. Electrocardiogram often shows decreased
voltages and diffuse ST elevation and chest x-ray usually
shows an enlarged cardiac shadow. All patients will have
significant pericardial fluid by echocardiography and
many children with bacterial pericarditis will present
with cardiac tamponade [2,7].
Our patient presented in a more indolent fashion with
long-standing fever. It is possible that the illness was two
separate infections such as a viral syndro me followed by
invasive GAS. GAS invasive disease occurring in the
setting of viral infection has been described although
association of GAS infection with HHV-6 has not been
reported [8,9]. The patient had a mildly positive serum
HHV-6 PCR on day 9 of his illness which raises the pos-
sibility of an initial HHV-6 infection, but is not conclu-
Purulent pericarditis co mmonly develops seco ndary to
a primary bacterial infection at an alternate location,
most commonly pneumonia [2,7]. Septic emboli or di-
rect spread from the lungs then acts to seed the pericar-
dium. In our patient, the pericardium likely was the pri-
mary site of invasive infection.
The most common cause of bacterial pericarditis in
children is Staphylococcus aureus [6,7]. Streptococcus
pneumonia e and Haemophilus influenzae are also some-
times isolated [2,7]. GAS, however, is a rare cause. Re-
view of the literature shows that only 7 cases have ever
been reported in pediatric patients (Ta b l e 1) [1-5]. One
case was not described in detail [2], but the ages of the
other 6 cases range from 13 months to 14 years with 3
males and 3 females. Our patient is the youngest patient
reported with this entity. Three patients had an identifi-
able source of GAS infection; 1 patient had pharyngitis
and cellulitis, 1 patient pharyngitis alone, and another
patient had pneumonia. All were treated with penicillin
or a penicillin derivative except one, whose antibiotic
regimen was not described. In the 2 reports that de-
scribed the entire course of antibiotics, both patients
received four weeks of therapy [1,5]. All underwent
pericardiocentesis with isolation of GAS from pericar-
dial fluid. Two patients also underwent surgical pericar-
dial intervention. One of the 6 patients died; a 2 year old
female was diagnosed with viral pharyngitis several days
before presenting in respiratory distress and deteriorating
shortly after admission despite pericardiocentesis [3]. Of
the 5 surviving patients, none developed constrictive
pericardial disease with limited follow-up.
Systemic antibiotics and pericardial drainage are both
needed to treat of purulent pericarditis. Antibiotics must
include an antistaphylococcal agent until the organism is
identified. There are no guidelines regarding length of
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Table 1. Previously reported cases of purulent pericarditis in children due to Group A Streptococcus.
Reference Year Treated Age SexAntibiotic Source Drainage Survival
Gersony, et al. 1967*
Vigneswaran, et al. 1985. Not documented 14 yo M Penicillin G ×10 days,
then oral Penicillin
V × 4 weeks
Cellulitis Pericardiocentesis,
Pericardial window Alive, f/u 8 weeks
Thebaud, et al. 1996. 1979 13 mo M Ampicillin,
Gentamicin No extracardiac
source Pericardiocentesis Not documented
Thebaud, et al. 1996. 1981 3 yo F Oxacillin,
Gentamicin No extracardiac
source Pericardiocentesis Not documented
Thebaud, et al. 1996. 1985 14 mo F Amoxicillin,
Neomycin Pneumonia Pericardiocentesis Not documented
Pruitt, et al. 1989. 1987 2 yo F Not
documented Pharyngitis Pericardiocentesis Died 4d after
et al. 2006. 2004 6 yo M Penicillin G × 4 weeksNo extracardiac
source Pericardiocentesis,
Pericardiectomy Alive, f/u 12
*Review does not incl ud e details of case.
antimicrobial therapy, but most patients are treated with
2 to 4 weeks of intravenous therapy [1,5,7]. Several op-
tions for pericardial drainage exist including subxiphoid
tube placement, pericardial window creation, partial
pericardiectomy, total pericardiectomy, and/or infusion
of thrombolytics into the pericardial space following
pericardiocentesis. Factors such as the consistency of the
fluid, the patient’s clinical status, and the cause of peri-
carditis influence which modality is chosen.
Even with therapy, the mortality in bacterial pericardi-
tis in children ranges from 5% to 12% [1,6,7]. Our pa-
tient was successfully treated with antibiotics and subxi-
phoid tube drainage without evidence of pericardial con-
striction 4 months after treatment completion.
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[3] Pruit, J.L. (1989) Group A streptococcal pericarditis in a
previously well child. Pediatric Infectious Disease Jour-
nal, 8, 338.
[4] Thebaud, B., Sidi, D. and Kachaner, J. (1996) Les peri-
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