Amebic liver abscess (ALA) is a common infection of the liver in the tropical world.1 It is caused by the intestinal protozoan Entamoeba histolytica (EH) which inhabits the cecum and enter the liver through portal blood flow.  Beyond intestine, an ALA is the most common manifestation of invasive amebiasis. The majority of ALA patients have an uncomplicated clinical course which respond effectively to metronidazole (MTZ)-based anti-amebic therapy.2 only small subsets of such patients require image-guided percutaneous catheter drainage (PCD). Overall, 4% to 40% of ALA patients develop some form of complications. 2 The most frequent ALA complication is rupture into the thoracic or intraabdominal cavity leading to localised subcapsular collection, empyema, and diffuse peritonitis.3

A rupture of ALA into the adjacent hollow viscus, such as the stomach, duodenum and colon, is highly rare, despite their close proximity. The literature has only reported a few number of these ruptures that resulted in hepatic fistulas. 1,3 Furthermore, there have been a few reports of vascular complications linked to ALA. The vascular complications include thrombosis or compression of vessels such as the inferior vena cava (IVC), hepatic veins (HV) and portal vein (PV), as well as hepatic artery pseudoaneurysm (HAPA). 1,3 The natural history and management of such uncommon complications are not well defined in the literature. In this case series, we describe three interesting cases of ALA with rare complications - hepatogastric fistula, HAPA and IVC thrombosis.

Case 1

A 65-year-old man came in with a history of several episodes of haematemesis and malena. He had surgery for ALA with intraperitoneal rupture approximately one month before this presentation. Upon examination, the patient showed signs of paleness, fever, mild tachycardia, and tender hepatomegaly.  His blood hemoglobin level was found to be 4.4 g/dl, total leukocyte count (TLC) was 11,380/mm3, and platelet count was 210000/μL. His liver function test (LFT) showed that the following values: serum bilirubin 1.4 mg/dl, alanin transaminase (ALT): 34 IU/L, aspartate transaminase (AST) 102 IU/L, alkaline phosphatase (ALP) 980 U/L), and serum albumin 2.3 g/dl.  His kidney function test and coagulation profile were within normal limits. Abdominal ultrasound revealed multiple abscesses in the liver. His serum for amebic serology was found positive, and the pus from PCD of right lobe abscess looked like anchovy sauce, suggesting a diagnosis of ALA. On contrast enhanced CT scan, a fistulous communications was noted between the abscess in the left lateral segment of liver and gastric lumen along the lesser curvature. Additionally, there was a sizable haematoma close to the hepatogastric fistula site [Figure]. The presence of hepatogastric fistula was further confirmed on upper endoscopy [figure]. A conservative non-surgical treatment was adopted and he was managed with antibiotics including MTZ. While the abscess with the gastric fistula was treated conservatively to allow a spontaneous drainage into the stomach, the largest abscess in the right lobe was drained by PCD under ultrasound guidance. Over the course of a week, he showed good response to the treatment, with improvements noted in his clinical indicators and laboratory results.

Case 2

A 67-year-old man presented with upper abdominal pain for 15 days, along with fever for 10 days and shortness of breath for 4 days. Upon examination, he had tachycardia, tachypnoea, pedal edema and a tender hepatomegaly. Hematological investigations revealed hemoglobin level of 10.9 g/dL and TLC of 14800/mm3. LFT revealed a total bilirubin of 1.48 mg/dL, serum ALP of 576 IU/L, AST 60.5 IU/L and ALT 54.2 IU/L. An abdominal ultrasonography revealed a large abscess in the right lobe of the liver, along with signs of rupture and a pleural effusion on the right side. On contrast enhanced CT scan, large liver abscess was found to be ruptured into the right pleural cavity. In addition, there evidence of partial thrombosis of IVC adjacent to the abscess. The amebic serology test of the patients came out to be positive. The patient was started on intravenous MTZ and broad spectrum antibiotics. The liver abscesses were drained by inserting PCD under ultrasonic guidance, and the empyema was drained via intercosal chest tube drainage. The pus was sterile, thick, and brownish in colour. Anticoagulation medication was not administered due to the risk of bleeding complications. He started to improve symptomatically after day five. His dyspnoea and pedal oedema began to lessen, and an IVC colour Doppler examination revealed near complete recanalization.

Case 3

A 57-year-old gentleman presented with a 10-day history of upper abdominal pain and fever. He has been a regular user of local alcoholic beverage (toddy) for thirty years. On examination, he had a tender hepatomegaly. His haematological testing revealed a hemoglobin level of 10.9 g/dL and a TLC of 16130/mm3. LFT revealed a total bilirubin of 0.7 mg/dL, AST 35 IU/L, ALT 19 IU/L, and serum ALP of 206 U/L. Ultrasonography examination of the abdomen showed a large abscess in the right lobe of liver along with intraabdominal collection and pleural effusion. His serum tested positive for amebic serology. On subsequent contrast enhanced CT scan, there was an evidence of small right HAPA in addition to a large ruptured liver abscess (Figure). He had no evidence of bleeding from the HAPA, and his haemodynamic parameters, including haemoglobin levels, were stable. In view of small size of non-bleeding pseudoaneurysm. In consultation with an expert interventional radiologist and taking into account the small size non-bleeding pseudoaneurysm, an expectant management strategy was adopted.  He was managed with iv MTZ, broad spectrum antibiotics, and USG guided catheter drainage of the abscess. He recovered uneventfully and his subsequent imaging revealed disappearance of HAPA.

EH is a cytotoxic parasite which releases a variety of toxic chemicals leading to parenchymal destruction, abscess formation and occasional rupture of abscess into the adjacent organs. The rupture of ALA into a hollow viscus is distinctly rare. Fewer than 10 cases of hepatogastric fistula secondary to ALA has been reported to date. 1,3,4 While there isn't much consensus about the management of ALA that has ruptured into the stomach, it seems that this type of rupture may not be hazardous because it allows the contents to drain spontaneously without contaminating the peritoneal cavity. There have been prior reports of successful non-surgical management of ALA with a hepatogastric fistula, and the same also proved effective in our case.4

Vascular thrombosis in ALA patients appears to be caused by multiple reasons, such as direct vascular invasion by growing ALA, surrounding inflammation with endothelial damage, and compression of blood vessels causing interruption of blood flow. In autopsy series, IVC thrombosis has been found in 4% to 8% of ALA patients.5,6  IVC thrombosis can lead to pedal edema due to venous congestion and impaired venous return. The routine use of anticoagulants for ALA-induced vascular thrombosis  is controversial. The benefits of preventing thrombus propagation must be weighed against the risk of hemorrhagic complication, particularly after percutaneous intervention. There are reports suggesting that of appropriate treatment of ALA using antibiotics and PCD can lead to the resolution of IVC thrombosis without the need for anticoagulant treatment.7,8 In our case also, IVC thrombosis resolved without use of anticoagulant medication. Drainage of ALA is necessary, as necrotic material may impact antibiotic penetration and delay resolution of inflammation, which may impede re-canalization of thrombosed vessels.

There is no consensus about the management of non-bleeding small HAPA associated with ALA. HAPA can be treated with surgical excision, coil or glue embolisation, or expectant care under careful observation. Because surgical intervention poses a risk, the suggested procedure is percutaneous vascular embolisation. However, a number of cases indicate that HAPA can be resolved by treating ALA appropriately with PCD and antibiotics.9,10 In our case,  HAPA  was small and arose from the peripheral branch of the HA. Hence, we did not opt for vascular intervention. The HAPA resolved spontaneously following treatment of ALA with antibiotic and PCD.

In conclusion, patients with ALA may develop a number of uncommon complication. Many of such complications may appear serious that warrant aggressive management. The lack of precise guidelines further confuse the picture. It is important to understand that ALA complications such as vascular thrombosis, small HAPA and hollow-viscus perforation, have the potential to resolve spontaneously with the care of ALA alone. Consequently, employing an individualistic approach while taking the nature and severity of the complication into account can help avoid the need for unnecessary intervention.

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