European Journal of Echocardiography 2006 7(6):460-462; doi:10.1016/j.euje.2005.07.010
Copyright © 2005, The European Society of Cardiology
Systemic lupus erythematosus: An unusual cause of cardiac tamponade in a young man
Serkan Topaloglua,*,
Dursun Arasa,
Kumral Erguna,
Hakan Altaya,
Omer Alyana and
Ahmet Akgulb
aTürkiye Yüksek Ihtisas Hospital, Department of Cardiology, Ankara, Turkey
bTürkiye Yüksek Ihtisas Hospital, Department of Cardiovascular Surgery, Ankara, Turkey
Received 14 March 2005; received in revised form 16 July 2005; accepted after revision 28 July 2005.
* Corresponding author. Türkiye Yüksek Ihtisas Hospital, Akp
nar mah. 23. cad. 10/22 Dikmen, Ankara, Turkey. Tel.: +903123061133; fax: +903123124120. topaloglus{at}yahoo.com
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Abstract
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Although pericarditis and pericardial effusion are common cardiac
complications of systemic lupus erythematosus (SLE), cardiac
tamponade is a very rare initial manifestation of this disease.
We describe a case of a young male patient in whom cardiac tamponade
secondary to a loculated pericardial effusion was the presenting
symptom of SLE.
Keywords: Cardiac tamponade; Systemic lupus erythematosus
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Introduction
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Systemic lupus erythematosus (SLE) is a connective tissue disorder
which often involves the heart, mostly the pericardium usually
manifests as diffuse pericardial effusion.
1 It is mostly of
a mild degree and more common in elderly.
2 Cardiac involvement
as the initial presentation of SLE has been reported in a few
patients and cardiac tamponade of the disease is rare as the
first manifestation.
3 SLE related cardiac tamponade has generally
a benign evolution with proper treatment.
4 Although pericardiocentesis
associated with anti-inflammatory drugs is the treatment of
choice, surgery is indicated in some cases. In this report,
we describe a young male in whom cardiac tamponade secondary
to localized pericardial effusion was surgically treated and
the diagnosis of SLE was established.
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Case report
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A 26-year-old male patient was admitted to another hospital
with a recent history of dyspnea, left shoulder pain, and lower
legs edema. A CT scan was performed and mild pericardial effusion
was found. His hemodynamic status deteriorated and he was transferred
to our hospital. At arrival he had mental confusion. His past
medical history was unremarkable except for smoking. The physical
examination showed an arterial pressure of 80/50mmHg, a pulse
rate of 125beats/min, a respiratory rate of 30/min and a body
temperature of 38°C with distended neck veins, mild hepatomegaly,
and decreased heart sounds. ECG revealed sinus tachycardia and
low voltage. Chest X-ray showed cardiomegaly with clear lungs.
Laboratory tests were normal except for moderate anemia. A 2-D
transthoracic echocardiogram (TTE) demonstrated near total collapse
of the right atrium (RA) and the right ventricle (RV) due to
compression by an adjacent cystic structure covered with a thick
membrane (
Fig. 1). When we examined the CT scan in the light
of these echocardiographic findings, we noticed that this large
cystic structure was misinterpreted as RV (
Fig. 2). Since the
patient was unstable, emergent surgery was planned. Surgical
exploration via a median sternotomy showed a loculated pericardial
effusion compressing the RV and the RA antero-laterally with
a thickened pericardium. The surgeon also noted the presence
of laciniae fibrosae which caused a septation and compartmentation
of the pericardium. After drainage of 800cc hemorrhagic fluid,
partial pericardiectomy was performed. Analysis of the fluid
revealed WBC count of 110/mm
3 (predominantly lymphocytes), protein
level of 5.2g/dl, LDH level of 628U/L, and ANA >1/2560 positive
with speckled cytoplasmic pattern. Pathologic examination of
the resected pericardium revealed prominent infiltration with
lymphocytes and plasma cells. Bacterial smears, cultures and
polymerase chain reaction to
Mycobacterium tuberculosis were
all negative with no malignant cell on cytologic examination.
Blood analysis with radioimmune assay was positive for anti-dsDNA
antibodies. Because the patient met the criteria adopted by
American Rheumatism Association,
5 the diagnosis of SLE was established
and steroid therapy was begun. Control TTE demonstrated that
the RV and the RA were free of compression. The patient had
an uneventful postoperative course and was discharged on 15th
postoperative day.
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Figure 1 2-D Transthoracic echocardiogram in apical 4-chamber view showing the near total collapse of the right atrium (RA) and the right ventricle (RV) caused by laterally located pericardial effusion. LA: Left atrium, LV: left ventricle.
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Discussion
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The cardiac manifestation of SLE includes pericarditis, myocarditis,
endocarditis and conduction system abnormalities. Although pericarditis
is common, cardiac tamponade, especially as an initial form
of presentation, is unusual. Pericardial involvement usually
manifests itself as diffuse pericardial effusion but the presence
of fibrous bands can cause loculated effusion. Although differential
diagnosis of SLE related pericardial effusion includes idiopathic,
viral, bacterial, tuberculous, uremic, postmyocardial infarction,
neoplastic, and traumatic pericardial effusions, in this case,
hydatid cyst had been considered first because of cystic appearance
of effusion and local reasons. Since SLE is more prevalent in
women and its cardiac manifestation usually occurs in later
years of life,
6 cardiac tamponade caused by SLE in a young male
is another striking finding in this patient.
Emergent surgery was needed in this patient before identification of the definite etiology. Because the surgeon had noticed an increased pericardial thickness during the surgery, he performed not only drainage of the fluid but also pericardiectomy at the same session. We think that this approach would be helpful to prevent future symptoms of constrictive pericarditis in addition to saving life. In the case of diffuse pericardial effusion, pericardiocentesis associated with steroid therapy is the treatment of choice.
In conclusion, SLE related loculated pericardial effusion should be kept in mind as a rare cause of cardiac tamponade even in patients without previous SLE diagnosis.
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References
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- Dubois E.L., Tuffanelli D.L. Clinical manifestations of systemic lupus erythematosus. Computer analysis of 520 cases. JAMA (1964) 190:104–111.[Abstract/Free Full Text]
- Gulati S., Kumar L. Cardiac tamponade as an initial manifestation of systemic lupus erythematosus in early childhood. Ann Rheum Dis (1992) 51:279–280.[Abstract/Free Full Text]
- Hetjmancik M.R., Wright J.C., Quint R., Jenning F.L. The cardiovascular manifestations of systemic lupus erythematosus. Am Heart J (1964) 68:119–130.[CrossRef][Web of Science][Medline]
- Castier M.B., Albeuquerque E.M.N., Menezes M.E.F.C.C., et al. Cardiac tamponade in systemic lupus erythematosus. Report of four cases. Arq Bras Cardiol (2000) 75:446–448.[Medline]
- Tan E.M., Cohen A.S., Fries J.F., et al. The 1982 revised criteria for the classification of systemic lupus erythematosus. Arthritis Rheum (1982) 25:1271–1277.[Web of Science][Medline]
- Baker S.B., Rovira J.R., Campion E.W., Milis J.A. Late onset systemic lupus erythematosus. Am J Med (1979) 66:727–732.[CrossRef][Web of Science][Medline]
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Abstract
Introduction