Visceral Larva Migrans　refers to migration of second stage nematode larvae through human viscera most commonly the liver and lungs. This entity usually presents with fever, abdominal pain, hepatomegaly and respiratory symptoms. Here we describe hepatic visceral larva migrans causing hepatic artery pseudoaneurysm and presenting with upper gastro-intestinal bleeding and its management.

Parasitic infections of liver are commonly encountered in clinical practice and can have myriad presentations posing a clinical diagnostic challenge. Hepatic visceral larva migrans (VLM) is one such entity presenting with prolonged fever and liver involvement especially in areas endemic for the parasite. Hepatic artery pseudoaneurysm is a complication described mostly with traumatic liver injury and post-surgery [1]. We describe this complication secondary to hepatic VLM and its successful management.

A 12-year-old girl presented with high grade fever, jaundice and right upper abdominal pain with progressive abdominal distension associated with weight loss for four months and a history of recurrent black tarry stools requiring blood transfusions. She was resident of a rural area and her family of seven lived in an overcrowded house, belonged to lower socioeconomic status with poor hygiene practices, consumed vegetarian diet and had exposure to pet animals in neighborhood. On examination she was underweight (BMI 12.5 kg/m2), febrile and tachypneic, had severe pallor with pedal edema and no skin lesions. Systemic examination revealed firm tender hepatomegaly (liver span:17 cm) without ascites or splenomegaly and crepitations on right side of chest. Ophthalmoscopic examination was unremarkable. Investi-gations revealed anemia (hemoglobin 5.7g/dL), and leukocytosis (16×103/L) with eosinophilia (1.4×103/L). Liver function tests were alanine aminotransferase 23 U/L, aspartate aminotransferase 19 U/L, alkaline phosphatase 590 U/L, total bilirubin 1.5 mg/dL with direct fraction 1.2 mg/dL, serum albumin 1.9 g/dL with albumin:globulin ratio of 0.4. As the child was sick at arrival, she was started on broad spectrum antimicrobials and supportive treatment (blood transfusion and albumin). Ultrasonography showed hepatomegaly with diffuse hypoechoic cystic lesions in both lobes of the liver. MRI abdomen showed lesions in the liver appearing hypointense on T1-weighted and hyperintense on T2-weighted images (Fig.1a) with mildly dilated common bile duct and normal intrahepatic biliary radicles. Dual phase CT scan of abdomen revealed multiple discrete and confluent hypodense lesions in both lobes of liver along with a 1.5 cm pseudoaneurysm (arrow) arising from the posterior branch of the right hepatic artery (Fig.1b). Based on clinical and radiological findings, a differential diagnosis of visceral larva migrans, cat scratch disease, Fascioliasis, disseminated tuberculosis and invasive candi-diasis with underlying immunodeficiency along with pseudo-aneurysm with suspected hemobilia was kept. The patient underwent digital subtraction angiography (DSA) and successful embolization of the pseudoaneurysm with n-butyl cyanoacrylate glue. Subsequent investigations revealed normal stool examination and negative Toxocara IgG serology, Echinococcus IgG serology, procalcitonin, Mantoux test, gastric aspirate genexpert for Tuberculosis, and HIV serology. Bacterial and fungal blood culture was sterile and upper GI endoscopy was normal. Percutaneous liver biopsy demons-trated ill-defined eosinophilic granulomas suggesting parasitic infiltration. Special stains and tissue culture was negative for acid fast bacilli (AFB), Bartonella and fungal elements. Based on clinical, radiological and histopathological findings, diagnosis of visceral larva migrans was made and child was started on albendazole (10mg/kg/day), diethylcarbamazine (4mg/kg/day) and oral steroids (1mg/kg/day) in 3 cycles of 3 weeks each with gradual tapering of steroids over next one month. Follow up imaging at six months showed resolution of hepatic lesions.

Fig. 1 (a) Axial T2 weighted MR image shows multiple conglomerate heterogeneous lesions in both lobes of liver, (b) Coronal CT angiography image shows a pseudoaneurysm (arrow) arising from the posterior branch of right hepatic artery.

Visceral larva migrans (VLM) refers to migration of second stage nematode larvae through human viscera most commonly liver and lungs. The etiological agents include Toxocaracanis, Toxocaracati, Baylisascarisprocyonis, Cappilaria hepatica, and Ascarissuum [2]. Humans are accidental hosts and acquire infection by ingestion of food contaminated with infective eggs. The clinical manifestations are fever, hepatomegaly, weight loss and respiratory symptoms mimicking asthma. An IgG ELISA based on 30 kDa recombinant Toxocara excretory–secretory antigen has 92% sensitivity and 89% specificity [3]. Features suggestive of VLM on CT are presence of multiple confluent peripheral and periportal ill-defined hypodense, oval or elon-gated nodular lesions scattered throughout liver parenchyma with peripheral rim enhancement and MRI shows T2 hyperintense/T1 hypointense lesions with restriction on diffusion weighted sequences [4]. Confirmation is by histo-pathological examination which shows presence of eosino-philic granuloma, palisading histiocytes and very rarely larva may be visualized. The slow migration of larva through the tissue incites a host inflammatory response along with eosinophilic infiltration and destruction of liver parenchyma. The cytotoxic eosinophil derived proteins may damage the endothelium causing vascular complications [5]. Hepatic artery pseudoaneurysm, a rare complication has not been previously described with VLM. Pseudoaneurysm develops due to the erosion of the eosinophilic abscesses into the hepatic artery. Rupture of the aneurysm results in hemobilia and the patients may present with hematemesis or melena or both. In cases of rupture of the aneurysm, early intervention by angio-embolisation of feeding artery should be considered. The embolizing agents used include coils, n-butyl cyanoacrylate glue and thrombin [1]. Medical therapy includes diethyl-carbamazine, mebendazole or albendazole for 2-3 weeks. Steroids are indicated in cases of ocular and neurological toxo-cariasis and in acute inflammatory manifestations of VLM [6].

We conclude that hepatic VLM can be a rare cause of hepatic artery pseudoaneurysm resulting in upper gastro-intestinal bleeding. Early recognition and comprehensive management is of utmost importance.

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4. Laroia ST, Rastogi A, Bihari C, Bhadoria AS, Sarin SK. Hepatic visceral larva migrans, a resilient entity on imaging: Experience from a tertiary liver center. Trop Parasitol. 2016;6:56-68.

5. Young JD, Peterson CG, Venge P, Cohn ZA. Mechanisms of membrane damage mediated by human eosinophilic cationic protein. Nature. 1986;321:613-6.