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Subcapsular Hepatic Fluid Collection Caused by Cardiac Dysfunction
ELECTRONIC IMAGE OF THE MONTH Subcapsular Hepatic Fluid Collection Caused by Cardiac Dysfunction Alex S. Peters,* Michael B. McCabe,‡ and Neeral L. Shah‡ *School of Medicine, University of Virginia, Charlottesville, Virginia; and ‡Division of Gastroenterology and Hepatology, University of Virginia, Charlottesville, Virginia
60-year-old man with a complex cardiac history including multivessel coronary artery disease and constrictive pericarditis with preserved right ventricle (RV) and left ventricle function demonstrated on right heart catheterization was admitted with decompensated heart failure. He subsequently underwent 2-vessel coronary artery bypass graft (left internal mammary artery to left anterior descending artery, and saphenous vein graft to obtuse marginal) and pericardiectomy. Postoperative course was complicated by cardiogenic shock and new RV dysfunction. Hepatology was consulted on postoperative Day 13 for progressively worsening hepatitis alanine aminotransferase/aspartate aminotransferase of 345/366 from prior baseline of 35/42 on admission. Workup of the acute hepatitis
A
demonstrated a new large subcapsular fluid collection on computed tomography (Figures A and B) and ultrasound (Figure C). The patient was sent for ultrasound-guided paracentesis and 3.8 L of fluid were removed, appearing grossly consistent with ascites. Unfortunately, laboratory studies of this fluid were not performed by the proceduralist, as recommended. Of note, the patient had a similar-appearing fluid collection that was drained 2 months prior with studies demonstrating serum ascites albumin gradient of 0.9 and total protein of 3.9, consistent with cardiogenic ascites. Remarkably enzymes normalized after his paracentesis. Repeat ultrasound 1 week later showed no evidence of reaccumulation of the subcapsular fluid Clinical Gastroenterology and Hepatology 2016;-:-–-
ELECTRONIC IMAGE OF THE MONTH, continued collection (Figure D). Notably, repeat transthoracic echocardiogram showed improvement in RV function. This patient’s presentation with ascites and mildly elevated transaminases in the setting of heart failure is consistent with congestive hepatopathy. Congestive hepatopathy has replaced the term cardiac cirrhosis and is a consequence of right-sided heart failure. Etiologic conditions include constrictive pericarditis, pulmonary arterial hypertension, mitral stenosis, tricuspid regurgitation, cor pulmonale, ischemic cardiomyopathy, and as a postoperative complication of the Fontan procedure.1 Signs on physical examination include jaundice, dependent edema, ascites, hepatomegaly with hepatojugular reflex, and pulsatile liver.2 There is usually only mild elevation of liver function tests up to 2–3 times the upper normal reference level.1 This case is interesting and unusual in that the patient accumulated a large volume (w4 L) of ascites within the capsule of his liver. Ascites tends to accumulate outside of the capsule and we were unable to find any reports of similar subcapsular accumulation on searching the literature. Large subcapsular fluid collections are most commonly hematomas related to trauma or malignancy, and less commonly represent abscess, bilioma, or contiguous spread from another intraabdominal process.3
e2
Presumably prior insidious development of ascites was secondary to this patient’s well established constrictive pericarditis. Although the patient had pericardiectomy to correct this at the time of his coronary artery bypass graft, recurrent rapid accumulation of ascites this admission and subsequent acute hepatitis was attributed to his new RV failure in the postoperative setting. Clinicians should be aware that in rare circumstances ascites can accumulate as a subcapsular fluid accumulation and not as free fluid within the peritoneum.
References 1.
Fouad YM, Yehia R. Hepto-cardiac disorders. World J Hepatol 2014;6:41–54.
2.
Moller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J 2013;34:2804–2811.
3.
Chen CJ, Chang WH, Shih SC, et al. Clinical presentation and outcome of hepatic subcapsular fluid collection. Taiwan Yi Xue Hui Za Zhi 2009;108:61–68.
Conflicts of interest The authors disclose no conflicts. © 2016 by the AGA Institute 1542-3565/$36.00 http://dx.doi.org/10.1016/j.cgh.2016.11.009
60-year-old man with a complex cardiac history including multivessel coronary artery disease and constrictive pericarditis with preserved right ventricle (RV) and left ventricle function demonstrated on right heart catheterization was admitted with decompensated heart failure. He subsequently underwent 2-vessel coronary artery bypass graft (left internal mammary artery to left anterior descending artery, and saphenous vein graft to obtuse marginal) and pericardiectomy. Postoperative course was complicated by cardiogenic shock and new RV dysfunction. Hepatology was consulted on postoperative Day 13 for progressively worsening hepatitis alanine aminotransferase/aspartate aminotransferase of 345/366 from prior baseline of 35/42 on admission. Workup of the acute hepatitis
A
demonstrated a new large subcapsular fluid collection on computed tomography (Figures A and B) and ultrasound (Figure C). The patient was sent for ultrasound-guided paracentesis and 3.8 L of fluid were removed, appearing grossly consistent with ascites. Unfortunately, laboratory studies of this fluid were not performed by the proceduralist, as recommended. Of note, the patient had a similar-appearing fluid collection that was drained 2 months prior with studies demonstrating serum ascites albumin gradient of 0.9 and total protein of 3.9, consistent with cardiogenic ascites. Remarkably enzymes normalized after his paracentesis. Repeat ultrasound 1 week later showed no evidence of reaccumulation of the subcapsular fluid Clinical Gastroenterology and Hepatology 2016;-:-–-
ELECTRONIC IMAGE OF THE MONTH, continued collection (Figure D). Notably, repeat transthoracic echocardiogram showed improvement in RV function. This patient’s presentation with ascites and mildly elevated transaminases in the setting of heart failure is consistent with congestive hepatopathy. Congestive hepatopathy has replaced the term cardiac cirrhosis and is a consequence of right-sided heart failure. Etiologic conditions include constrictive pericarditis, pulmonary arterial hypertension, mitral stenosis, tricuspid regurgitation, cor pulmonale, ischemic cardiomyopathy, and as a postoperative complication of the Fontan procedure.1 Signs on physical examination include jaundice, dependent edema, ascites, hepatomegaly with hepatojugular reflex, and pulsatile liver.2 There is usually only mild elevation of liver function tests up to 2–3 times the upper normal reference level.1 This case is interesting and unusual in that the patient accumulated a large volume (w4 L) of ascites within the capsule of his liver. Ascites tends to accumulate outside of the capsule and we were unable to find any reports of similar subcapsular accumulation on searching the literature. Large subcapsular fluid collections are most commonly hematomas related to trauma or malignancy, and less commonly represent abscess, bilioma, or contiguous spread from another intraabdominal process.3
e2
Presumably prior insidious development of ascites was secondary to this patient’s well established constrictive pericarditis. Although the patient had pericardiectomy to correct this at the time of his coronary artery bypass graft, recurrent rapid accumulation of ascites this admission and subsequent acute hepatitis was attributed to his new RV failure in the postoperative setting. Clinicians should be aware that in rare circumstances ascites can accumulate as a subcapsular fluid accumulation and not as free fluid within the peritoneum.
References 1.
Fouad YM, Yehia R. Hepto-cardiac disorders. World J Hepatol 2014;6:41–54.
2.
Moller S, Bernardi M. Interactions of the heart and the liver. Eur Heart J 2013;34:2804–2811.
3.
Chen CJ, Chang WH, Shih SC, et al. Clinical presentation and outcome of hepatic subcapsular fluid collection. Taiwan Yi Xue Hui Za Zhi 2009;108:61–68.
Conflicts of interest The authors disclose no conflicts. © 2016 by the AGA Institute 1542-3565/$36.00 http://dx.doi.org/10.1016/j.cgh.2016.11.009