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(Chest. 1999;116:1506-1507.)
© 1999 American College of Chest Physicians

Bloody Pericardial Effusion

Clinically Significant Without Intrinsic Diagnostic Specificity

David H. Spodick, MD, DSc, FCCP and Worcester, MA

Dr. Spodick is Professor of Medicine, University of Massachusetts Medical School; and is also affiliated with the Cardiovascular Division, Saint Vincent Hospital.

Correspondence to: David H. Spodick, MD, DSc, FCCP, Saint Vincent Hospital, 25 Winthrop St, Worcester, MA 01604

Bleeding in any tissue is always concerning and potentially serious, either as a marker of disease or of potential blood loss. Hemopericardium (Table 1 ) comprises sanguineous pericardial effusions (which do not clot), frank blood due to wounds, and rupture into the pericardium of cardiovascular structures. The latter usually overwhelms the fibrinolytic and anticlotting activities of the pericardial mesothelium1 and therefore usually clots. In cases of frank bleeding, the cause is frequently manifest or rapidly becomes so. Bloody pericardial effusion, on the other hand, is diagnostically more challenging because of the wide variety of conditions that simultaneously produce fluid (mostly exudates) and various degrees of bleeding into it, presumably from irritated capillaries. Contemporary experience indicates the very broad range of effusions, including common viral pericarditides, that may exhibit sanguineous pericardial effusion,2 in contrast to the time-dishonored teachings about the frequency of life-threatening underlying lesions, notably tuberculosis. With the exception of AIDS patients, tuberculosis has been disappearing, at least in the industrialized Western world. Of course, diagnostic specificity is heavily related to the prevalence of any disorder in a given population, and the skewed populations of referral centers and institutions, which have developed populations of particular kinds of patients, will reflect this.


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  		Table 1.. Hemopericardium*

 
In this issue of CHEST (see page 1564), Atar and colleagues render a signal service in their analysis of serosanguineous pericardial effusions in a hospital with a patient population paralleling that of most community hospitals that have catheterization laboratories and cardiopericardial surgery. They have amplified the value of their article by defining their terms and classifying the etiologies of bloody pericardial effusions (their Table 1 ); they specifically confined their study to nonclotting effusions, ie, excluding pure hemopericardium, in 150 patients, all with cardiac tamponade. Clearly their state-of-the-art and state-of-the-science presentation demonstrates the nonspecificity of merely finding a significant amount of blood in a pericardial effusion, with three fourths of their group classified among iatrogenic (due to invasive procedures), malignant, idiopathic, and complications of atherosclerotic heart disease. Their Table 3 lists and directly cites five "most referenced" United States textbooks (from 1994 to 1998 editions) that perpetuate the notion that tuberculosis is a common cause of bloody pericardial fluid. This should alert readers that textbooks frequently perpetuate the notions and ideas of previous editions, often because some contributing authors are less interested in making serious efforts to write precisely or to rewrite chapters than they are in doing original work. This is also a symptom of medicine’s glacial movement in fields like pericardiology, in which there are only a few dedicated specialists.

Atar and colleagues present a picture of symptoms, signs (including pulsus paradoxus), ECG abnormalities, and imaging abnormalities that reflect contemporary experience, as do their mortality statistics: patients with malignancy-related effusions died within months, excepting those with lymphomata, while patients with iatrogenic and idiopathic bloody effusions survived quite nicely. Moreover, the authors point out the overall poor results of effusion cytology studies and cultures (laboratory results changed the prepericardiocentesis diagnosis in only 3 of 96 patients). Indeed, only 12 patients had any positive findings in their pericardial fluid. Pericardial biopsy was performed at the discretion of the patient’s physician and is not reported. This is probably because there were either too few biopsies or those that were obtained were not helpful. This would reflect a common experience that the results of pericardial biopsies are either negative or nonspecific, probably because both normal and abnormal pericardial fluids exude via the visceral pericardium, containing combinations of substances from the cardiac interstitium and the visceral pericardial mesothelium. Yet, a biopsy of the visceral pericardium is almost never performed. A potentially productive investigation would be to perform a biopsy of the visceral pericardium at surgery or by pericardioscopy (taking care to avoid the coronary vessels) in patients for whom determining etiology could provide targets for specific therapy.

References

  1. Spodick, DH (1997) Microphysiology of the normal pericardium. The pericardium: a comprehensive textbook ,23-24 Marcel Dekker (New York, NY).
  2. Spodick, DH (1997) Hemopericardium. The pericardium: a comprehensive textbook ,82-84 Marcel Dekker (New York, NY).




This Article
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Citing Articles
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Right arrow Articles by Spodick, D. H.
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Right arrow Articles by Spodick, D. H.
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