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Point and Counterpoint |

Rebuttal From Dr Nguyen et alRebuttal From Dr Nguyen et al FREE TO VIEW

Thien A. Nguyen, MD; Cesar Liendo, MD, FCCP; Michael W. Owens, MD
Author and Funding Information

From the Department of Pulmonary/Critical Care and Sleep Medicine, Louisiana State University, Health Sciences Center Shreveport.

CORRESPONDENCE TO: Michael W. Owens, MD, Louisiana State University, Health Sciences Center Shreveport, Department of Pulmonary/Critical Care and Sleep Medicine, 1501 Kings Highway, Shreveport, LA 71103; e-mail: Michael.Owens@va.gov


FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;147(5):1211-1212. doi:10.1378/chest.15-0095
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As stated previously, we believe spontaneous bacterial empyema (SBEM) is neither a spontaneous entity nor an empyema by classic definition. This condition is most often seen in patients with preexisting liver disease and ascites. We believe that it most often originates in the peritoneal space, where infection of ascitic fluid with infradiaphragmatic organisms leads to migration across the diaphragm to secondarily seed the pleural space. Dr Lai and colleagues1 have suggested that SBEM occurs without preexisting spontaneous bacterial peritonitis (SBP), that reduced opsonic activity of pleural fluid predisposes to the development of spontaneous infection, and that there are selected case reports of patients without cirrhosis with SBEM.

Dr Lai and colleagues1 quote the article by Xiol et al2 stating that none of their cases had SBP. However, Xiol et al2 found positive pleural fluid cultures in six of the cases, and, of these, 66% had identical organisms in the ascitic fluid cultures.2 The main organisms isolated from culture were gram-negative infradiaphragmatic organisms, again suggesting migration of infected peritoneal fluid into the pleural space. The article by Xiol et al2 strongly suggests that SBEM most often starts in the peritoneal space and therefore is not spontaneous to the pleural space.

Although Dr Lai and colleagues1 correctly point out that Sese et al3 found reduced activity of complement levels and opsonic activity in pleural fluid, they failed to mention that the ascitic fluid in these patients had values that were even lower than what was observed in the pleural fluid.3 This once again supports our contention that in most patients the process actually starts in the peritoneal space and then migrates into the pleural space.

There are a limited number of case reports of SBEM in conditions without preexisting liver disease. To date, there has only been one case reported of SBEM in a patient with pleural effusion from congestive heart failure.4 However, this patient’s bilateral pleural effusions had fluid characteristics (pH < 7.1 and glucose < 40 mg/dL), classifying the condition more as a true empyema and not a case of SBEM.4 Chen et al5 reported a case of a patient with nephrotic syndrome on pulse-dose steroids who developed bilateral pleural effusions; the left effusion revealed transudate and culture grew Aeromonas hydrophila, and the right effusion was exudative and culture grew Escherichia coli, requiring tube thoracostomy for drainage. Both of these pathogens are traditionally found in the gut, and complement deficiencies associated with nephrotic syndrome likely predisposed this patient to secondary pleural seeding. These isolated cases do not support the diagnosis of SBEM, in that they are exudative and likely were true empyemas related to a subdiaphragmatic process.

Although we concede that there exists a clinical entity that occurs in some patients with cirrhosis that leads to development of pleural space infection, we believe that it most often starts with SBP and moves into the pleural space, making it not spontaneous to the pleural space. We also believe that this condition does not meet the classic criteria for an empyema, which could lead to a delay in diagnosis and inappropriate treatment.

References

Lai YK, Eiger G, Fischer RA. Point: does spontaneous bacterial empyema occur? Yes. Chest. 2015;147(5):1207-1208.
 
Xiol X, Castellote J, Baliellas C, et al. Spontaneous bacterial empyema in cirrhotic patients: analysis of eleven cases. Hepatology. 1990;11(3):365-370. [CrossRef] [PubMed]
 
Sese E, Xiol X, Castellote J, Rodríguez-Fariñas E, Tremosa G. Low complement levels and opsonic activity in hepatic hydrothorax: its relationship with spontaneous bacterial empyema. J Clin Gastroenterol. 2003;36(1):75-77. [CrossRef] [PubMed]
 
Nguyen H, Gupta S, Eiger G. Spontaneous bacterial empyema in a noncirrhotic patient: an unusual scenario. Am J Med Sci. 2011;342(6):521-523. [CrossRef] [PubMed]
 
Chen WC, Huang JW, Chen KY, Hsueh PR, Yang PC. Spontaneous bilateral bacterial empyema in a patient with nephrotic syndrome. J Infect. 2006;53(3):e131-e134. [CrossRef] [PubMed]
 

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References

Lai YK, Eiger G, Fischer RA. Point: does spontaneous bacterial empyema occur? Yes. Chest. 2015;147(5):1207-1208.
 
Xiol X, Castellote J, Baliellas C, et al. Spontaneous bacterial empyema in cirrhotic patients: analysis of eleven cases. Hepatology. 1990;11(3):365-370. [CrossRef] [PubMed]
 
Sese E, Xiol X, Castellote J, Rodríguez-Fariñas E, Tremosa G. Low complement levels and opsonic activity in hepatic hydrothorax: its relationship with spontaneous bacterial empyema. J Clin Gastroenterol. 2003;36(1):75-77. [CrossRef] [PubMed]
 
Nguyen H, Gupta S, Eiger G. Spontaneous bacterial empyema in a noncirrhotic patient: an unusual scenario. Am J Med Sci. 2011;342(6):521-523. [CrossRef] [PubMed]
 
Chen WC, Huang JW, Chen KY, Hsueh PR, Yang PC. Spontaneous bilateral bacterial empyema in a patient with nephrotic syndrome. J Infect. 2006;53(3):e131-e134. [CrossRef] [PubMed]
 
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