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Year : 2009  |  Volume : 55  |  Issue : 4  |  Page : 317-318

Cardiac failure causing jaundice in a child

Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Mumbai, India

Date of Web Publication14-Jan-2010

Correspondence Address:
S A Zaki
Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Mumbai
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0022-3859.58948

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How to cite this article:
Zaki S A. Cardiac failure causing jaundice in a child. J Postgrad Med 2009;55:317-8

How to cite this URL:
Zaki S A. Cardiac failure causing jaundice in a child. J Postgrad Med [serial online] 2009 [cited 2023 Feb 3];55:317-8. Available from:


Jaundice as a presenting feature of congestive cardiac failure is rare in children. [1] It tends to be mild when present and a key feature in the history is breathlessness.

A four-year-old male child was admitted with complaints of fever, breathlessness, and abdominal pain for four days. These were associated with yellowish discoloration of eyes. There was no history of cough but history of past recurrent lower respiratory tract infections was present. The child was admitted on three previous occasions in another hospital, but was not investigated for recurrent respiratory infections. Birth and family history were non-contributory.

On admission the child was afebrile, with a heart rate of 160/ min, respiratory rate of 56/min and blood pressure of 100/70 mmHg. Pallor and icterus were present. Jugular venous pressure was elevated. Respiratory system examination revealed bilateral diffuse crepitations and rhonchi. Tender hepatomegaly and positive hepatojugular reflux were noted. On cardiovascular system examination, the first heart sound was soft while the second heart sound was loud with wide and variable split. A pansystolic murmur was heard in the fourth intercostal space in the left lateral sternal border. Investigations revealed a hemoglobin concentration of 11.8 gm/dL, total leukocyte count of 12600/mL and platelet count of 179000/mL. The total serum bilirubin was 4 mg/dL with a conjugated fraction of 3 mg/dL. The serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and serum alkaline phosphatase levels were 387 U/L, 222.06 U/L, and 698 U/L respectively.The serial measurements of liver enzymes are shown in [Table 1]. Serum electrolyte and blood sugar levels and renal function tests were normal. Serological tests for Hepatitis A, B and C were negative. Chest radiograph showed cardiomegaly and diffuse bilateral infiltrates in the lungs. Two-dimensional echocardiography and color Doppler examinations revealed a 6-mm muscular ventricular septal defect with severe pulmonary hypertension.

Child was treated with restricted intravenous fluids, intravenous cefotaxime and amikacin, furesemide and digitalis. The icterus gradually disappeared on the sixth day and the liver function tests also returned to normal by the ninth day of admission. The child was discharged on the 12 th day on anti-cardiac failure drugs and is awaiting corrective cardiac surgery.

Two mechanisms are described for explaining liver dysfunction associated with severe congestive heart failure: Passive congestion and acute hepatocellular necrosis caused by impaired perfusion, which is also known as ischemic hepatitis. [2] Ischemic hepatitis or shock liver is defined as an extensive hepatocellular necrosis associated with a decrease in hepatic perfusion due to systemic hypotension. Serum aminotransferase levels (ALT and AST) increase rapidly after an ischemic episode and peak within one to three days. After recovery, aminotransferases return to near normal levels in 7-10 days of the initial insult. Histologically, it is characterized by centrolobular necrosis without inflammation. [3] Some patients might also present in hepatic encephalopathy. However, in most cases ischemic hepatitis is comparatively benign and self-limited. Jaundice due to the passive liver congestion is seen in low-output cardiac failure. Some studies have described a raised alkaline phosphatase in these circumstances. The phenomenon has been linked to the severity of tricuspid regurgitation. Suggested mechanisms for the jaundice of low-output heart failure are decreased hepatic blood flow, increased hepatic venous pressure and decreased arterial oxygen saturation. In addition, work in animals raises the possibility of endotoxin-mediated damage of hepatocytes, as one of the cause for jaundice in heart failure. [4]

In conclusion, a combination of jaundice, hepatomegaly and breathlessness in a child should prompt a careful cardiological examination, including assessment of the jugular venous pressure, electrocardiogram, chest radiograph and echocardiogram to exclude a cardiac cause.

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1.Lowe MD, Harcombe AA, Grace AA, Petch MC. Restrictive-constrictive heart failure masquerading as liver disease. BMJ 1999;318:585-6.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Giallourakis CC, Rosenberg PM, Friedman LS. The liver in heart failure. Clin Liver Dis 2002;6:947-67.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Squella F, Zapata R. Ischemic hepatitis. Case report. Rev Med Chil 2003;131:659-64.  Back to cited text no. 3      
4.Cogger VC, Fraser R, Le Couteur DG. Liver dysfunction and heart failure. Am J Cardiol 2003;91:1399.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  


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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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