P
ericardial effusion in children is caused by
bacterial and viral infections, connective tissue disease, metabolic
disorders and malignancies[1]. Echocardiography is an accurate and
sensitive, bedside, non-invasive diagnostic tool [1,2]. Pericardial
drainage can be achieved either by percutaneous catheter drainage or by
surgery [3]. We report our experience with large pericardial effusions.
Methods
Records of children admitted in pediatric department
of Dr Ram Manohar Lohia Hospital, New Delhi, with significant
pericardial effusion from January 2010 to March 2013 were
retrospectively analyzed. Clinical findings and investigations,
including electrocardiogram, chest X-ray and echocardiography
findings were recorded. Cardiac tamponade was diagnosed by either : (a)
paradoxical pulse of more than 12mm Hg, (b) poor peripheral
perfusion and peripheral pulses with heart rate greater than 95th
percentile for age, or c) systolic blood pressure <5
th
percentile for age with increase of systolic pressures and decrease of
heart rate after pericardiocentesis [4].
Echocardiography was performed using Phillips 11HDXE
machine. ‘Significant pericardial effusion’ was defined as echo-free
space more than 1cm in front of the right/left ventricle, and
pericardial tamponade was confirmed in the presence of right ventricular
diastolic collapse [5].
Two-dimensional echocardiography guided pericardial
puncture was performed in patients with tamponade. A 7 F cordis
introducer sheath (Johnson and Johnson) was placed in the pericardial
space over a soft tipped 0.038 Terumo (Terumo; Tokyo, Japan) guidewire.
A multiholed soft 7 F pigtail catheter was advanced into the pericardial
sac and the pericardial fluid was suctioned from the catheter tip into a
reservoir. The catheter and sheaths were removed when echo showed almost
complete emptying of the pericardial fluid with drainage volume
decreased to less than 100 mL per day for more than 48 hrs. Surgical
intervention was considered in thick organized pus not amenable to
catheter drainage. Pericardial fluid was sent for Gram staining, Ziehl-
Neelson (Z-N) staining, cytology, biochemistry, culture and sensitivity.
Outcome was measured as hospital stay, mortality, constrictive
pericarditis and recurrence. A descriptive analysis was done.
Results
Twenty-five children (16 boys and 9 girls) were
diagnosed to be having significant pericardial effusion during study
period. Mean age was 8.1 years (range 2-17 yr). All children had
tachycardia and tachypnea; fever, cough and chest pain was present in
23, 9 and 5 subjects, respectively. Jugular venous pressure was raised
in nine children: two had pedal edema and nine had hepatomegaly. Distant
heart sounds could be appreciated in 12 children; only one had
pericardial rub. Chest roentgenography revealed cardiomegaly in 19 (76%)
and bronchopneumonia in two children. Electrocardiography showed sinus
tachycardia and low-voltage QRS complex in all the study subjects, and
ST segment changes in 3 cases.
Echocardiography guided pericardiocentesis was done
in 22 patients but pigtail catheter was placed only in nine.
Three children with failed pericardiocentesis
required surgical drainage. There were no pericardiocentesis-related
complications. Aspirate was exudative (pericardial fluid: serum protein
ratio >0.5) in all the cases. Pericardiocentesis was not done in three
children; one had echocardiographic evidence of myocarditis (dilated
left ventricular cavity, global hypokinesia and ejection fraction of
48%) and the other two had disseminated tuberculosis. Thirteen effusions
were considered tubercular based on clinical findings, positive Mantoux
test , ADA, PCR or ZN stain. Six (23%) had pyogenic pericardial
effusion; culture was positive in 4 cases [Staphylococcus aureus :
2 (blood) and 1(pus aspirated from thigh pyomyositis);
Pseudomonas aeruginosa: 1 (pericardial fluid)]. No organism could be
isolated in two cases with bronchopneumonia. Three had viral etiology;
coxackie virus serology was positive in one. Two were labeled probable
viral etiology after excluding other causes.
Two patients were labeled as having idiopathic
recurrent pericardial effusion. One was a three-year-old boy with atrial
septal defect and the other was a 12-year-girl, admitted 4 times with
recurrent pericardial effusions, and died later with septic shock. One
child had pericardial effusion associated with acute lymphoblastic
leukemia; pericardial fluid cytology was positive for malignant cells.
Of the 9 children with tamponade, 3 were tubercular,
4 pyogenic, and 2 had idiopathic recurrent pericardial effusion.
Appropriate treatment was administered in patients with tubercular and
pyogenic effusions along with supportive treatment of congestive heart
failure. Follow-up of these patients showed complete resolution of
effusion in all except the one with recurrent pericardial effusion. None
of them developed constrictive pericarditis over a median period of
follow-up of 18 months (range: 2 to 28 months).
Discussion
Tuberculosis (52%) was the most common etiological
diagnosis in our series of pericardial effusion followed by bacterial
(23%), viral (12%), recurrent idiopathic (8%) and malignant. All cases
had congestive heart failure while 9 had cardiac tamponade. ECHO-guided
percutaneous catheter drainage and pigtail catheter insertion was an
effective and safe procedure for decompressing tamponade.
The study is limited by the fact that it reflects the
profile in a tertiary care referral center and hence the results can not
be generalized. Moreover diagnostic work-up for all viruses, and
detailed immunological work-up was not done. Most children had received
pre-referral antibiotics, possibly affecting bacteriological results.
Idiopathic effusions account for 20% to 40% of the
cases in adults whereas they are rare in children [4-6]. With the advent
of antibiotic therapy, there is decline in bacterial etiology and most
frequent causes are presumed to be viruses in developed, and
tuberculosis in developing countries [5,7]. Mok, et al. [8] and
Roodpeyma, et al. [9] did not find any case of tubercular
effusion in children. Guven, et al. [5] from Turkey reported
tubercular etiology in 30% of their cases whereas we found it to be the
most important etiology.
Purulent pericardial effusion is most often
associated with infection at another site, with hematogeneous or direct
spread to the pericardium [4,5]. The most common concomitant site
involved is usually the lung. However, in our series bronchopneumonia
was present in only two cases (33%) and no organism could be isolated.
S. aureus, H. influenzae, and S. pneumoniae are the usual
causative agents. We found S. aureus to be the most common agent
for purulent pericardial effusion [10,11]. Viruses commonly causing
acute pericarditis are Coxackie group B and Echovirus type 8 [9]. We
could detect antibodies to coxackie virus in only one case. It is
difficult to distinguish active viral pericarditis from idiopathic
pericarditis; many cases of community acquired idiopathic pericarditis
may be due to unrecognized viral infections [12]. Idiopathic effusions
constituted 8% of our patients, which is similar to that reported by
Zreik, et al. [4]. In adults it constitutes around 20 to 40% of
pericardial effusions. [5,6,13].
Etiology from developed countries is quite different
from the developing world where chest trauma, post-pericardiotomy
syndrome, infections, immunological and idiopathic pericarditis
predominate; tuberculosis was not reported in these series [4,8].
Immunological, traumatic and postsurgical pericardial effusions were not
found in our study.
Echocardiography-guided pericardiocentesis has a
well-established diagnostic and therapeutic role [14]. We also obtained
reassuring results without any significant procedural complications.
Constrictive pericarditis, a common complication of tubercular etiology,
can be prevented by early diagnosis and institution of anti-tubercular
treatment and steroids as in this study [8,15].
Acknowledgments: Dr NK Dubey, Head of the
Department, Pediatrics, PGIMER and Dr RML Hospital, for infrastructural
and administrative support, and Dr Sudha Chandelia for PICU support.
Contributors: DKY: conceived and designed the
study and revised the article critically for important intellectual
content. He will act as guarantor; NKB: helped in designing study,
collected data ,analysed it and drafted the paper; TA: collection and
analysis of data; SA: helped in data collection and statistical
analysis; VG: revised the article for important intellectual content.
The final manuscript was approved by all authors.
Funding: None; Competing interests: None
stated.
What This Study Adds?
•
Tuberculosis was the most common etiology for pericardial
effusion in this study.
• Pericardiocentesis and pigtail
catheter insertion were safe and effective procedures in
children.
|
References
1. Rheuban KS. Pericardial Diseases. In:
Allen HD, Gutgesell HP, editors. Moss and Adams’ Heart Disease in
Infants, Children, and Adolescents: Including the Fetus and Young
Adult. 7th ed. Philadelphia:Lippincott Williams & Wilkins;
2008.p.1290-9.
2. Levine MJ, Lorell BH, Diver DJ, Come
PC. Implications of echocardiographically assisted diagnosis of
pericardial tamponade in contemporary medical patients: detection
before hemodynamic embarrassment. J Am Coll Cardiol. 1991;17:59-65.
3. Ziskind AA, Palacios IF. Percutaneous balloon
pericardiotomy for patients with pericardial effusions and
tamponade. In: Topol EJ, editor. Textbook of Interventional
Cardiology. 3rd ed. Philadelphia: WB Saunders; 1999.
p.869-77.
4. Zreik H, Li J, Garson AT. Etiology and danger
of pericardial effusion in infants and children. Cardiol Young.
1996;6:162-5.
5. Guven H, Bakiler AR, Ulger Z, Iseri B, Kozan
M, Dorak C. Evaluation of children with a large pericardial effusion
and cardiac tamponade. Acta Cardiol. 2007;62:129-33.
6. Sagristà-Sauleda J, Mercé J, Permanyer-Miralda
G, Soler-Soler J. Clinical clues to the causes of large pericardial
effusions. Am J Med. 2000;109:95-101.
7. Gibbs CR, Watson RD, Singh SP, Lip GY.
Management of pericardial effusion by drainage: a survey of 10
years’ experience in a city centre general hospital serving a
multiracial population. Postgrad Med J. 2000;76:809-13.
8. Mok GC, Menahem S. Large pericardial effusions
of inflammatory origin in childhood. Cardiol Young. 2003;13:131-6.
9. Roodpeyma S, Sadeghian N. Acute pericarditis
in childhood: A 10-year experience. Pediatr Cardiol. 2000;21:363-7.
10. Corchran M, Poore P, Hadley GP, Tanner A.
Purulent pericarditis in Papua New Guinea: report of 12 cases and
review of the literature in a tropical environment. Trans R Soc Trop
Med Hygene. 1983;77:341-3.
11. Jaiyesimi F, Abioye AA, Antia AU. Infective
pericarditis in Nigerian children. Arch Dis Child. 1979;54:384-90.
12. Lorell BH. Pericardial Disease. In:
Braunwald E ,editors. Heart Disease. A Textbook of Cardiovascular
Medicine. 14th ed. Philadelphia:Saunders;1997.p.1505-34.
13. Eisenberg MJ, Oken K. Prognostic value of
echocardiography in hospitalized patients with pericardial effusion.
Am J Cardiol. 1994:70:934-93.
14. Mueller XM, Tevaearai HT, Hurni M, Ruchat P,
Fischer AP, Stumpe F, et al. Long-term results of surgical
subxiphoid pericardial drainage. Thorac Cardiovasc Surg. 1997;45:65-9.
15. Thebaud B, Sidi D, Kachaner J. Purulent pericarditis in children:
a 15 year experience. Arch Pediatr. 1996;3:1084-90.