Eur J Cardiothorac Surg 2003;24:1043-1045
© 2003 Elsevier Science NL
Boxer’s pericardium
A. Ooia*,
A.C. Doudsb,
E.B. Kumarb,
S.A.M. Nashefa
a Department of Cardiothoracic Surgery, Papworth Hospital, Cambridge, UK
b Department of Medicine and Cardiology, QE Hospital, Norfolk, UK
Received 15 July 2003;
accepted 22 August 2003.
* Corresponding author. 64, Andes Close, Ocean Village, Southampton SO14 3HS, UK. Tel.: +44-2380-339-054; fax: +44-2380-339-054
e-mail: adrianooisw{at}yahoo.co.uk
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Abstract
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A 65-year-old retired professional boxer presented with progressively worsening shortness of breath, peripheral oedema and mild abdominal swelling over a period of 6 months. His only past medical history was hypertension. Subsequent investigations revealed chylous ascites, pericardial constriction and bilateral chylothorax. He had uneventful pericardectomy, and post-operatively the chylothorax resolved only after administration of octreotide for 10 days. The histopathological features of fibrosis, haemosiderin deposition in the pericardium and abundant haemosiderin-laden macrophages are consistent with chronic resolving haemopericardium. These findings suggested that the cause of pericardial constriction was repeated chest trauma from boxing.
Key Words: Pericardial constriction • Boxing • Chylothorax • Octreotide
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1. Introduction
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The two unusual features in this case are the chylous effusion in the context of pericardial constriction and the link with boxing. Chylothorax and chylous ascites are rare but recognised complications of pericardial constriction, and are usually reversed after relief of constriction. When this fails to resolve spontaneously, the administration of octreotide should be considered, as there is growing evidence of its success in treating a number of conditions with persistent chylous effusion. Second, haemopericardium and trauma are also extremely rare causes of chronic pericardial constriction, but an association with boxing has never been previously described.
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2. Case report
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A 65-year-old retired professional boxer presented with progressively worsening shortness of breath, peripheral oedema and mild abdominal swelling over 6 months. His only past medical history was hypertension. On examination, he had raised jugular venous pulse and ascites. Routine blood tests were normal, and no autoantibodies were detected. Electrocardiography (ECG) showed widespread T-wave inversion. Chest radiology was normal and echocardiography showed good bilateral ventricular function. Abdominal tap revealed chylous ascites and liver biopsy was normal.
In view of his cardiac symptoms and ECG changes, cardiac catheterisation was performed, which showed normal coronary arteries with good left ventricular systolic function. There was no gradient across the aortic valve. Simultaneous bi-ventricular pressure tracings indicated high end-diastolic pressures which were virtually identical at 25 mmHg, suggestive of pericardial constriction (Fig. 1)
. Computed tomography showed thickening of the pericardium, chylous effusion in the posterior mediastinum and bilateral chylothorax (Fig. 2)
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Fig. 1. Simultaneous ECG and bi-ventricular pressure tracings (RV, right ventricle; LV, left ventricle).
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Fig. 2. CT scan showing pericardial thickening and chylous effusion (RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle).
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He was referred for surgical treatment and urgent pericardectomy was performed via median sternotomy. At operation, the heart was dissected entirely free of its adherence to the pericardium and the anterior pericardium was resected to about 1 cm from each phrenic nerve. Resected tissue was sent for histopathological and microbiological analysis. At the end of the procedure, mean central venous pressure dropped from 21 to 14 mmHg. Post-operatively he had a persistent bilateral chylothorax, which resolved after administration of octreotide 150 mcg s.c. b.d. for 10 days.
Microbiology cultures including tuberculosis were negative. Histopathology showed fibrosis, haemosiderin deposition in the pericardium and abundant haemosiderin-laden macrophages consistent with chronic resolving haemopericardium. These findings suggest that the cause of pericardial constriction was repeated chest trauma, probably from boxing.
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3. Discussion
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The two unusual features in this case are the chylous effusion in the context of pericardial constriction and the link with boxing. Chylothorax and chylous ascites are rare but recognised complications of pericardial constriction. The reduced venous return in the superior vena cava directly interferes with lymphatic duct circulation. The resultant lymphatic congestion and dilatation causes chylous effusion in the chest and abdomen. The process is usually reversed after relief of pericardial constriction. However, when this fails to resolve spontaneously, the administration of octreotide should be considered, as there is growing evidence of its success in treating a number of conditions with persistent chylous effusion [1–3].
In many patients, the cause of constrictive pericarditis is unknown. The condition can follow infective pericarditis, especially tuberculosis. Any infectious and inflammatory process may initiate dense pericardial scarring. Haemopericardium resulting from a penetrating injury is a rare cause of chronic pericardial constriction [4] and blunt trauma to the chest can precipitate chronic scarring although the time interval between injury and pericardial disease may be considerable [5]. Pericardial constriction has been reported after cardiac surgery, but the incidence is probably lower than 1%. It also has been noted in patients with post-pericardiotomy syndrome, previous mediastinal irradiation and significant post-operative haemopericardium. Similarly, constrictive pericarditis may occur after Dressler's syndrome following myocardial infarction.
To our knowledge, pericardial constriction due to boxing has never been previously described. Boxers are subjected to repeated blunt chest trauma and hence may suffer repeated haemopericardium. This may resolve with ensuing scarring and eventually progress to pericardial constriction. Interestingly, during his boxing days all boxers wore gloves no heavier than 8 ounces, which would suggest that the trauma inflicted was likely to be more pronounced than it would be today. In this case study, the patient has no other established risk factors of pericardial constriction apart from his boxing activity. Furthermore, with the evidence of histopathology consistent with chronic resolving haemopericardium, we would like to conclude that the only cause of his pericardial constriction was due to repeated chest trauma from boxing.
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Acknowledgments
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Many thanks to Mr A.T. Goodwin (Cardiothoracic Senior Registrar, Papworth Hospital) for contributing to the writing of this paper.
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References
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- Kelly R.F., Shumway S.J. Conservative management of post-operative chylothorax using somatostatin. Ann Thorac Surg 2000;69:1944-1945.[Abstract/Free Full Text]
- Rimensberger P.C., Muller-Schenker B., Kalangos A., Beghetti M. Treatment of a persistent post-operative chylothorax with somatostatin. Ann Thorac Surg 1998;66:253-254.[Abstract/Free Full Text]
- Markham K.M., Glover J.L., Welsh R.J., Lucas R.J., Bendick P.J. Octreotide in the treatment of thoracic duct injuries. Am Surg 2000(12):1165-1167.
- McKusick V.A., Kay J.H., Isaac J.P. Constrictive pericarditis following traumatic haemopericardium. Ann Surg 1955;142:97.[Medline]
- Schneider S., Rivier J.L. Hemopericarde traumatique et pericarde calleux. Rev Med Suisse Romande 1960;80:171.[Medline]
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Abstract
1. Introduction
