Canadian Journal of Cardiology 31 (2015) 691.e13e691.e14 www.onlinecjc.ca
Letters to the Editor Spontaneous Bacterial Peritonitis: An Unusual Life-Threatening Complication of Congestive Heart Failure To the Editor: Spontaneous bacterial peritonitis (SBP) typically arises on a background of ascites due to hepatic cirrhosis.1 We describe an unusual case of SBP in a man with cardiac ascites. A middle-aged man with a history of heavy smoking and alcohol consumption was unwell for a month, with fatigue, shortness of breath, lower limb edema, and abdominal swelling. He did not seek medical attention and was found dead in bed. Postmortem examination showed pitting edema of the lower limbs and genitalia. There was 5 L of cloudy ascitic fluid and diffuse peritoneal congestion (Fig. 1A), but no evidence of bowel perforation or ischemic injury. A swab from the small intestine serosa grew numerous viridans group streptococci. Microscopy of the parietal peritoneum (Fig. 1B) and intestine showed early acute peritonitis (24-48 hours) with numerous Gram-positive cocci (Fig. 1C). There was bilateral pleural effusion, emphysema, cardiomegaly (691 g) with biventricular dilation and hypertrophy and moderate coronary atherosclerosis. The liver was macroscopically unremarkable, but histologically showed congestive hepatopathy (Fig. 1, D and E) secondary to right-sided heart failure. There was mild nonspecific periportal fibrosis (Fig. 1D) but no cirrhosis or alcoholic hepatitis. These findings indicated congestive heart failure due to ischemic heart disease, cor pulmonale, and possibly alcoholic cardiomyopathy, with associated cardiac ascites, complicated by acute SBP, resulting in death. SBP is a well recognized complication of ascites due to advanced liver disease. It is typically caused by Gram-negative bacilli, but sometimes by Gram-positive cocci, including
viridans group streptococci. Early diagnostic paracentesis and antibiotic therapy is essential to reduce mortality.1 SBP related to cardiac ascites has only occasionally been reported, but has a very high mortality rate.2-4 The infrequency of SBP in congestive heart failure is probably due to preserved opsonic and bactericidal activity of the high protein level of ascitic fluid and integrity of the hepatic reticuloendothelial system, unlike in ascites due to advanced cirrhosis.1 Although unusual, the present case supports the importance of including SBP in the differential diagnosis of sepsis and/or diffuse abdominal pain, even in the absence of fever, in patients with cardiac ascites, with the goal of prompt life-saving management.2-4 John P. Rossiter, MB, BCh, PhD [email protected] Kristopher Cunningham, PhD, MD Paul N. Manley, MD Disclosures The authors have no conflicts of interest to disclose. References 1. Wiest R, Krag A, Gerbes A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut 2012;61:297-310. 2. Runyon BA. Spontaneous bacterial peritonitis associated with cardiac ascites. Am J Gastroenterol 1984;79:796. 3. Bulger K, Sugrue D, Crowe J. Spontaneous bacterial peritonitis in cardiac ascites: a case report. Ir J Med Sci 1987;156:333. 4. Higgins N, Burke JP, McCreery CJ. Acute peritonitis as the first presentation of valvular cardiomyopathy. Am J Emerg Med 2012;30:247. e5-6.
http://dx.doi.org/10.1016/j.cjca.2014.12.015 0828-282X/Ó 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
691.e14
Canadian Journal of Cardiology Volume 31 2015
Figure 1. (A) Dilated small intestine with serosal congestion; (B) parietal peritoneum with acute inflammation; (C) groups and chains of Grampositive cocci; (D) liver with sinusoidal congestion, mild periportal fibrosis (white asterisks) and prominent central vein (black asterisks), which at higher magnification (E) exhibits mild surrounding fibrosis, indicative of chronicity. (B) Hematoxylin phloxine saffron (HPS) stain; magnification, 500; (C) Gram stain; magnification, 2250; (D) HPS stain; magnification, 80; (E) HPS stain; magnification, 360.
Letters to the Editor Spontaneous Bacterial Peritonitis: An Unusual Life-Threatening Complication of Congestive Heart Failure To the Editor: Spontaneous bacterial peritonitis (SBP) typically arises on a background of ascites due to hepatic cirrhosis.1 We describe an unusual case of SBP in a man with cardiac ascites. A middle-aged man with a history of heavy smoking and alcohol consumption was unwell for a month, with fatigue, shortness of breath, lower limb edema, and abdominal swelling. He did not seek medical attention and was found dead in bed. Postmortem examination showed pitting edema of the lower limbs and genitalia. There was 5 L of cloudy ascitic fluid and diffuse peritoneal congestion (Fig. 1A), but no evidence of bowel perforation or ischemic injury. A swab from the small intestine serosa grew numerous viridans group streptococci. Microscopy of the parietal peritoneum (Fig. 1B) and intestine showed early acute peritonitis (24-48 hours) with numerous Gram-positive cocci (Fig. 1C). There was bilateral pleural effusion, emphysema, cardiomegaly (691 g) with biventricular dilation and hypertrophy and moderate coronary atherosclerosis. The liver was macroscopically unremarkable, but histologically showed congestive hepatopathy (Fig. 1, D and E) secondary to right-sided heart failure. There was mild nonspecific periportal fibrosis (Fig. 1D) but no cirrhosis or alcoholic hepatitis. These findings indicated congestive heart failure due to ischemic heart disease, cor pulmonale, and possibly alcoholic cardiomyopathy, with associated cardiac ascites, complicated by acute SBP, resulting in death. SBP is a well recognized complication of ascites due to advanced liver disease. It is typically caused by Gram-negative bacilli, but sometimes by Gram-positive cocci, including
viridans group streptococci. Early diagnostic paracentesis and antibiotic therapy is essential to reduce mortality.1 SBP related to cardiac ascites has only occasionally been reported, but has a very high mortality rate.2-4 The infrequency of SBP in congestive heart failure is probably due to preserved opsonic and bactericidal activity of the high protein level of ascitic fluid and integrity of the hepatic reticuloendothelial system, unlike in ascites due to advanced cirrhosis.1 Although unusual, the present case supports the importance of including SBP in the differential diagnosis of sepsis and/or diffuse abdominal pain, even in the absence of fever, in patients with cardiac ascites, with the goal of prompt life-saving management.2-4 John P. Rossiter, MB, BCh, PhD [email protected] Kristopher Cunningham, PhD, MD Paul N. Manley, MD Disclosures The authors have no conflicts of interest to disclose. References 1. Wiest R, Krag A, Gerbes A. Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut 2012;61:297-310. 2. Runyon BA. Spontaneous bacterial peritonitis associated with cardiac ascites. Am J Gastroenterol 1984;79:796. 3. Bulger K, Sugrue D, Crowe J. Spontaneous bacterial peritonitis in cardiac ascites: a case report. Ir J Med Sci 1987;156:333. 4. Higgins N, Burke JP, McCreery CJ. Acute peritonitis as the first presentation of valvular cardiomyopathy. Am J Emerg Med 2012;30:247. e5-6.
http://dx.doi.org/10.1016/j.cjca.2014.12.015 0828-282X/Ó 2015 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
691.e14
Canadian Journal of Cardiology Volume 31 2015
Figure 1. (A) Dilated small intestine with serosal congestion; (B) parietal peritoneum with acute inflammation; (C) groups and chains of Grampositive cocci; (D) liver with sinusoidal congestion, mild periportal fibrosis (white asterisks) and prominent central vein (black asterisks), which at higher magnification (E) exhibits mild surrounding fibrosis, indicative of chronicity. (B) Hematoxylin phloxine saffron (HPS) stain; magnification, 500; (C) Gram stain; magnification, 2250; (D) HPS stain; magnification, 80; (E) HPS stain; magnification, 360.
