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COUNTERPOINT: Does Spontaneous Bacterial Empyema Occur? NoDoes Spontaneous Bacterial Empyema Occur? No 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):1208-1210. doi:10.1378/chest.15-0094
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Spontaneous bacterial empyema (SBEM) has been defined as a transudative pleural effusion with either a polymorphonuclear count that is > 500 cells/μL or a positive pleural fluid culture in patients without any radiographic evidence of pneumonia.1 It is reported to have an incidence of up to 15% in patients with cirrhosis and to have a mortality rate of up to 20%.2,3 This condition almost always is seen in patients with preexisting liver cirrhosis and secondary ascites. We believe that this condition is poorly defined and named, in that it is not spontaneous to the pleural space and it does not necessarily meet classic criteria of an empyema.

Nearly all reported cases of SBEM in the literature involve patients with preexisting liver disease and ascites. In a study by Allam,4 patients with preexisting liver disease, as evidenced by low serum albumin, prolonged prothrombin time, and higher Child-Pugh scores, had a much higher risk of developing SBEM. In an analysis of 862 patients with cirrhosis with 17 clinical diagnoses of SBEM, 88% had preexisting ascites.5 Mansour et al6 found in their study of patients with SBEM and preexisting hepatic hydrothorax that pleural effusions were more often right-sided and were greater on the right side even in cases of bilateral pleural effusion. This parallels what is seen in patients with hepatic hydrothorax alone, where up to 85% are right-sided, likely secondary to a combination of gaps between diaphragm muscle fibers that develop with increasing intraabdominal pressure and negative intrapleural pressure in the thorax that promotes attraction of ascitic fluid.3 The observation that SBEM is almost always right-sided suggests that SBEM may actually start in the peritoneal space and then simply migrate via diaphragmatic defects in the pleural space, making it a secondary infection and not a spontaneous de novo infection of the pleural space.3,7

Patients with cirrhosis inherently have lower immune activity in their pleural and ascitic fluid. In an analysis of pleural fluid in patients with cirrhosis, Sese et al8 found that the differences in opsonic activity (measured by log-kill) and concentrations of C3, C4, C5, C3PA, and protein were statistically lower in the patients with cirrhosis than in patients with exudative effusions or effusions due to heart failure. More specifically, the patients with cirrhosis who developed SBEM had lower opsonic activity and complement levels than those who did not.8 They also found that in patients who developed both SBP and SBEM, these levels were lower in the ascitic fluid when compared with pleural fluid.8 Akalin et al9 found that patients with ascitic fluid from cirrhosis have significantly reduced opsonic and antimicrobial activity when compared with patients with ascites from other causes, such as malignancy. The observation that ascitic fluid in patients with cirrhosis who develop SBP and SBEM has significantly lower opsonic activity and complement levels compared with other conditions suggests very strongly that the problem starts within the abdomen and migrates to the pleural space.

Pleural fluid culture in SBEM often yields gram-negative infradiaphragmatic organisms such as Escherichia coli and Klebsiella pneumonia, suggesting a GI source of infection.7 In the study by Chen et al5 it was found that in 26 reported episodes of SBEM, 56% had a concomitant SBP. In another study by Xiol et al,1 it was found that of the cases with culture-positive SBEM, 75% of them had culture-positive ascitic fluid with the same organisms. E coli was the primary isolate in the ascitic and pleural fluids in these cases, again suggesting a migration of infected peritoneal fluid into the pleural space.1 Differences in positive cultures between SBEM and SBP may in part be explained by culture technique. Culture sensitivities vary based on inoculation technique; Xiol et al10 found that a modified culture technique (inoculate in blood culture) vs conventional (inoculate in sterile container) had more than twice the rate of positive cultures, which may lead to an underestimation of culture positivity. They found a 75% culture positivity rate using the modified culture vs 33% using the conventional method.10 This underestimation could explain how patients with SBP can have culture-negative hepatic hydrothorax or that patients with culture-positive SBEM may have culture-negative ascitic fluid. Had the pleural and ascitic fluid cultures both been completed using the modified technique, they may have yielded similar culture results. Rather than a spontaneous event in the pleural space, the microbiology of SBEM supports our idea that infected ascitic fluid from a preceding SBP transmigrates across the diaphragm to secondarily seed and infect the pleural space.

In 1995, Light11 proposed a new classification scheme for empyema to include biochemical properties of pH < 7.0 or glucose < 40 mg/dL, positive culture or gram stain, or frank pus. Spontaneous bacterial “empyema” criteria define the pleural fluid as having transudate properties and do not require any of the criteria for an empyema to make the diagnosis.1 Despite this, there are a number of cases of SBEM that actually meet exudative criteria. In an analysis of 11 cases of SBEM, Xiol et al1 found that all instances met transudative pleural fluid characteristics; however, transudate was defined as having to meet at least two of Light’s criteria. If traditional Light’s criteria were applied, 45% of the SBEM cases would have been exudates. The distinction between SBEM and traditional empyema is important, because the treatments are different. Empyemas usually require urgent tube thoracostomy, whereas SBEM is generally treated with antibiotics alone.7,10 The name spontaneous bacterial “empyema” is at best misleading, because it is a transudate by definition and does not have to meet any commonly accepted definition of an empyema.

The current definition of SBEM calls for having ruled out pneumonia as the cause of the effusion.1 The method of excluding preexisting pulmonary infection has been inconsistent in the SBEM literature, ranging from simple chest radiography (CXR), to ultrasonography, to CT scan.1,5 Previous studies that relied on CXR alone might have missed an underlying pneumonia. In a retrospective analysis of patients with the diagnosis of pneumonia, Hayden and Wrenn12 found that in patients with concurrent CXR and CT scan, the CXR was nondiagnostic or negative in 27% of cases. Chen et al5 used ultrasonography and found this modality more sensitive than CXR or CT scan in detecting pleural effusion. The lower sensitivity of CXR for ruling out pneumonia and CXR/CT scan for ruling out pleural effusion suggests that previous diagnoses of SBEM may not fit the defined diagnostic criteria, raising the possibility that a coexisting pneumonia was actually present with a secondary parapneumonic effusion.

The above studies critically outline the importance of establishing the correct diagnosis by excluding patients with a true empyema who require more aggressive treatment, accurately ruling out pneumonia, and using the proper methods to culture fluid. Because patients with hepatic hydrothorax do not always receive thoracentesis, and the symptoms can be vague, with fever being the predominant symptom and not dyspnea or chest pain, it is important that the physician have a high index of suspicion and be aware of the clinical presentation.4,5 We therefore propose that this disease state be referred to as secondary pleuritis of cirrhosis. This highlights our position that SBEM is neither a spontaneous event nor a classic empyema in all cases. By avoiding the confusion with the term “empyema,” this will allow clinicians to make a swift diagnosis and deliver the appropriate treatment.

References

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]
 
Garcia-Tsao G. Spontaneous bacterial peritonitis. Gastroenterol Clin North Am. 1992;21(1):257-275. [PubMed]
 
Lazaridis KN, Frank JW, Krowka MJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis, and management. Am J Med. 1999;107(3):262-267. [CrossRef] [PubMed]
 
Allam NA. Spontaneous bacterial empyema in liver cirrhosis: an underdiagnosed pleural complication. Saudi J Gastroenterol. 2008;14(1):43-45. [CrossRef] [PubMed]
 
Chen TA, Lo GH, Lai KH. Risk factors for spontaneous bacterial empyema in cirrhotic patients with hydrothorax. J Chin Med Assoc. 2003;66(10):579-586. [PubMed]
 
Mansour A, El-Rahman A, Besheer T. Prevalence and risk factors for spontaneous bacterial pleuritis in cirrhotic patients with hydrothorax. Egyptial Journal of Chest Diseases and Tuberculosis. 2013;62(3):435-438. [CrossRef]
 
Kim BN, Chung H, Shim TS. A case of spontaneous bacterial empyema and bacteremia caused byAeromonas hydrophilaEur J Clin Microbiol Infect Dis. 2001;20(3):214-215. [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]
 
Akalin HE, Laleli Y, Telatar H. Bactericidal and opsonic activity of ascitic fluid from cirrhotic and noncirrhotic patients. J Infect Dis. 1983;147(6):1011-1017. [CrossRef] [PubMed]
 
Xiol X, Castellví JM, Guardiola J, et al. Spontaneous bacterial empyema in cirrhotic patients: a prospective study. Hepatology. 1996;23(4):719-723. [CrossRef] [PubMed]
 
Light RW. A new classification of parapneumonic effusions and empyema. Chest. 1995;108(2):299-301. [CrossRef] [PubMed]
 
Hayden GE, Wrenn KW. Chest radiograph vs. computed tomography scan in the evaluation for pneumonia. J Emerg Med. 2009;36(3):266-270. [CrossRef] [PubMed]
 

Figures

Tables

References

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]
 
Garcia-Tsao G. Spontaneous bacterial peritonitis. Gastroenterol Clin North Am. 1992;21(1):257-275. [PubMed]
 
Lazaridis KN, Frank JW, Krowka MJ, Kamath PS. Hepatic hydrothorax: pathogenesis, diagnosis, and management. Am J Med. 1999;107(3):262-267. [CrossRef] [PubMed]
 
Allam NA. Spontaneous bacterial empyema in liver cirrhosis: an underdiagnosed pleural complication. Saudi J Gastroenterol. 2008;14(1):43-45. [CrossRef] [PubMed]
 
Chen TA, Lo GH, Lai KH. Risk factors for spontaneous bacterial empyema in cirrhotic patients with hydrothorax. J Chin Med Assoc. 2003;66(10):579-586. [PubMed]
 
Mansour A, El-Rahman A, Besheer T. Prevalence and risk factors for spontaneous bacterial pleuritis in cirrhotic patients with hydrothorax. Egyptial Journal of Chest Diseases and Tuberculosis. 2013;62(3):435-438. [CrossRef]
 
Kim BN, Chung H, Shim TS. A case of spontaneous bacterial empyema and bacteremia caused byAeromonas hydrophilaEur J Clin Microbiol Infect Dis. 2001;20(3):214-215. [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]
 
Akalin HE, Laleli Y, Telatar H. Bactericidal and opsonic activity of ascitic fluid from cirrhotic and noncirrhotic patients. J Infect Dis. 1983;147(6):1011-1017. [CrossRef] [PubMed]
 
Xiol X, Castellví JM, Guardiola J, et al. Spontaneous bacterial empyema in cirrhotic patients: a prospective study. Hepatology. 1996;23(4):719-723. [CrossRef] [PubMed]
 
Light RW. A new classification of parapneumonic effusions and empyema. Chest. 1995;108(2):299-301. [CrossRef] [PubMed]
 
Hayden GE, Wrenn KW. Chest radiograph vs. computed tomography scan in the evaluation for pneumonia. J Emerg Med. 2009;36(3):266-270. [CrossRef] [PubMed]
 
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