Amebiasis is a common parasitic infection in the tropics. Though usually asymptomatic, invasive disease can lead to amoebic liver abscess. We report a case of pericardial rupture of amoebic liver abscess presenting with jaundice, dysphagia, and cardiac tamponade. Jaundice is a rare manifestation of amebic liver abscess. An emergency pericardiotomy was done to relive the cardiac tamponade, and liver abscess was drained through a diaphragmatic rent identified during surgery. This case highlights the catastrophic complications of untreated amebic liver abscess.
Keywords: Amoebic liver abscess, cardiac tamponade, hepatopericardial fistula
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Chandran SR, Balakrishnan RK, Chinnasamy B, Srinivasan GK. Amebic hepatopericardial fistula causing cardiac tamponade. Ann Trop Med Public Health 2012;5:387-9
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Chandran SR, Balakrishnan RK, Chinnasamy B, Srinivasan GK. Amebic hepatopericardial fistula causing cardiac tamponade. Ann Trop Med Public Health [serial online] 2012 [cited 2020 Aug 7];5:387-9. Available from: https://www.atmph.org/text.asp?2012/5/4/387/102079
Amebiasis caused by Entamoeba histolytica can cause invasive disease affecting 40 to 50 million people worldwide annually.  Most infections are asymptomatic, but amebic dysentery, amebic liver abscess, and rarely, other manifestations such as pulmonary, cardiac, or brain involvement can occur.  Amebic liver abscess is the most common extraintestinal manifestation of amebiasis. Ameba establishes hepatic infection by ascending the portal venous system.  If not detected early and treated, it can erode and rupture into almost all of the adjacent organs. Depending on the site of rupture, the presentation can vary from mild to catastrophic. Rupture into pericardium is a well-known and well-documented complication of amebic liver abscess. We report a unique case of pericardial rupture of amebic liver abscess who presented with jaundice, dysphagia, and cardiac tamponade who was managed by a pericardiotomy leading to drainage of both the pericardial and hepatic abscess solely through the pericardial route.
A 25-year-old man presented to our hospital with history of high grade intermittent fever of 4 months duration, progressive dysphagia for 15 days, and passing clay-colored stools for the last week. He developed sudden onset burning chest pain associated with breathlessness, which started on the day of admission. Examination revealed an ill-nourished man with tachycardia, tachypnea, profuse sweating, and a normal blood pressure. His jugular venous pressure was elevated and heart sounds muffled. Palpation of abdomen revealed soft tender hepatomegaly. Investigations revealed mild elevation of total bilirubin (2 mg%) with elevated alkaline phosphatase (238 IU/L) and neutrophilia. His chest X-ray (CXR) showed cardiomegaly, and electrocardiogram (ECG) showed tachycardia with low voltage complexes. The patient had an ECG and CXR taken 2 weeks back when he had presented to a local hospital with fever. The CXR taken 2 weeks back showed a normal cardiac shadow [Figure 1], and the ECG showed normal voltage complexes [Figure 2]. An abdominal ultra sonogram revealed hepatomegaly and large hypoechoic lesion in the left lobe of the liver measuring 13 × 11 × 10 cms. An emergency trans-thoracic echocardiogram revealed a large pericardial effusion measuring 11 mm anteriorly and 24 mm posteriorly causing cardiac tamponade. The hypoechoic lesion in the liver was found to communicate with pericardial space, and early tamponade was present. A trans-esophageal echocardiogram confirmed the findings.
|Figure 1: Figure showing the normal x ray before and cardiomegaly after pericardial rupture of liver abscess
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|Figure 2: Figure showing low voltage complexes after pericardial rupture of hepatic abscess and reappearance of normal voltage complexes after surgery
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In view of the cardiac tamponade and patient’s deteriorating hemodynamic status, an emergency pericardiotomy was planned. The pericardial fluid gushed out as a stream when the pericardiotomy was performed [Video 1]. A rent in the diaphragm was identified and widened. Around 2 liters of thick anchovy sauce pus was drained. Anterior pericardium was excised. Cavity was closed with drains in place. Post-operative echocardiogram revealed a normal cardiac function with minimal effusion. Abdominal ultrasonogram revealed a collapsed abscess site. Histopathological examination of the pericardium revealed areas of hemorrhage and necrosis, ovoid bodies in the necrotic tissue resembling ameba. Serological tests for amebiasis were positive. Patient was treated with parenteral metronidzole and broad spectrum antibiotics. He made an uneventful recovery and was discharged after 2 weeks.
Amebiasis is a common parasitic infection in the tropics. Mostly asymptomatic, it can lead to an invasive disease, which if left untreated, can lead to multiple complications.
Amebic liver abscess usually presents with chronic low grade fever, abdominal pain, and emaciation. Jaundice is an uncommon presenting manifestation occurring in less than a quarter of the patients.  Jaundice in patients with amebic liver abscess is caused by biliovascular fistula, resulting from hepatic necrosis leading to damage to bile ducts and hepatic veins  or due to pressure on the porta hepatis with stasis of the bile in the intra-hepatic biliary radicals. 
Liver involvement occurs following invasion of E histolytica into mesenteric venules. Amebae then enter the portal circulation and travel to the liver where they typically form large abscesses. The Gal/GalNAc lectin is an adhesion protein complex that sustains tissue invasion.  The abscess contains acellular proteinaceous debris, which is thought to be a consequence of induced apoptosis and is surrounded by a rim of amebic trophozoites invading the tissue.  If left untreated, it can be complicated by rupture into the thoracic structures like pleural or pericardial cavities and abdominal structures like stomach or peritoneal cavities.
A rare case of a 16-month-old child with pleural, pericardial, peritoneal, and gastric perforation of amebic liver has been reported.  2 large case series of hepatic amebic abscesses have been published. One spanning over 18 years by Carlos et al. examined 501 cases of amebic liver abscess. There were 326 cases of rupture through the diaphragm with 5 cases (0.01%) rupturing into the pericardium and 1 case rupturing into both pleural and pericardial cavities.  The second such study from China by Meng et al. reported 503 cases of amebic liver abscess over 21 years. 22% of the cases in this series developed complications due to perforation.  Perforation into pericardial cavity remained a very rare complication in both the studies. 11 cases of rupture into pericardium have been reported from Spain.  5 cases of amebic abscess rupturing into pericardium have been reported from India. , In total, around 27 cases of amebic liver abscess rupturing into pericardium have been reported worldwide.
Treatment of amebic liver abscess depends on the severity at presentation and on the associated complications. Most early, small, and uncomplicated abscesses can be treated by medical therapy alone. Drainage when required has been done in different ways according to the presentation of the patient. The most common being percutaneous aspiration; blind or ultrasound guided. Thoracic collection of abscess can be drained intra-abdominally when a diaphragmatic rent is identified as reported by Short et al.  Cases of pericardial rupture of an amebic liver abscess developing cardiac tamponade similar to this case and relieved by pericardiotomy have been reported. ,,, On the other hand, intra-pericardial ruptures have been managed only by percutaneous drainage when emergency intervention is not necessitated by development of cardiac tamponade; as reported from India. ,
Certain features make this case a unique one. Firstly, the patient presented with obstructive features due to liver abscess. He had dysphagia due to the left-sided abscess, compressing on lower esophagus. His evident icterus, elevated bilirubin, alkaline phosphatase, and history of passing clay-colored stools points to an obstructive component due to the abscess. Jaundice is a rare manifestation of hepatic amebic abscess. Secondly, the changes that occurred in the ECG and the CXR after the rupture of abscess could be documented since the patient had done the investigations 2 weeks prior to admission [Figure 1] and [Figure 2]. Thirdly, the way the hepatic abscess was drained was also unique. In this patient, during pericardiotomy, a diaphragmatic rent was identified; widening the rent resulted in gush of anchovy sauce pus. Around 2 liters of pus was drained, and the post-surgical ultrasound showed a collapsed abscess site. To the best of our knowledge, this is the first report of a hepatic abscess being drained solely through a pericardial approach.
Thus, this case highlights the rare and catastrophic complications of untreated hepatic amebiasis presenting with jaundice and cardiac tamponade; managed by pericardiotomy to drain both pericardial and hepatic pus collection.
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[Figure 1], [Figure 2]