 Good evening, everyone, and I am Dr. Levline, Department of Radio Diagnosis from Pandit BD Sharma, PGMS Rottak, and I'm going to present on inferior venakava thrombosis, a rare vascular complication of liver abscess. Introduction, liver abscess is the most common extra intestinal manifestation of entomibia histolytica infestation. It arises from hematogenous spread of imbibic trophoside that enters liver through portal circulation after crossing the colonic mucosa. The most common complication includes rupture into the pleural cavity and peritoneal cavity. Rare complications include thrombosis or compression of vascular structures resulting in either hepatic vein outflow obstruction or inferior venakava obstruction due to mechanical compression of the vascular structures and localized inflammation. I'm going to present a case of 16-year-old boy presented with complaints of pain in epigastric region for seven days, which was insidious in onset, mild to moderate in intensity, progressive in nature, and radiating to back. He had a history of fever for seven days associated with chills and rigors, history of vomiting for one day containing gastric contents. His vitals were BP 120 by 88 and pulse was 90 per minute. Blood investigations were HP was 10 gram and TLC was 36,000, platelet was 60,000. Serum bilirubin was 1.3 total. Serum ALT was 141, serum criate was 0.7, INR was 1.45, and PT was 19.4 second. On imaging, chest x-ray showed non-homogeneous opacity in the right lower zone, silhouting the right hemidiaphragm with obliterated right claustrophantic angle. On abdominal x-ray, it was within normal limits. On ultrasound, free fluid noted in Pelvis and Morrison, right-sided Blural fusion was noted, which was mild. Liver showed a hyperecord lesion measuring nine into seven centimeter in right lobe subcapsular in location. On color Doppler, ecogenic thrombus noted in hepatic and infrahepatic inferior vena cava, partially occluding the lumen with no flow-on-color Doppler application. Another abnormality that was noted in the patient was reversal of SMV and SMA. On computed tomography, free fluid with CT value of 20 to 25 HU noted in perihepatic region, right paracolic gutter, Pelvis, and inter gut region. Mild right-sided Blural fusion was also noted. Liver showed a peripherally enhancing hypodense lesion in segment seven and eight measuring 10.8 into 10.6 into 8.8 centimeter with mild edema adjacent to it. The lesion is subcapsular and is well-delinated except at its supramedal aspect with suspicious rent into the plural cavity. The lesion seems to compress the IVC and its hepatic cores. A hypodensity is also noted extending into the IVC, which is the thrombus. Minimal pericolusistic fluid was also noted. As on ultrasound, there was a reversal of SMV and SMA. Small bowel loops are mostly noted on the right side and large bowel loops on the left side. Diagnosis was made as on ultrasound guidance. Brownish fluid was aspirated and pigtail catheter drainage of the abscess was performed. The pus was bacteriologically sterile. A repeat ultrasound examination after two weeks showed that the abscess had markedly reduced in size. As the patient presented with fever, vomiting, epigastric pain for seven days duration, along with ultrasound and CT scan evidence of liver abscess with a positive amoebic serology, drainage of ankovisos like material and response to therapy, a diagnosis of amoebic liver abscess was made. The differential with such focal lesions in the liver would include pyogenic liver abscess, metastasis, multifocal hepatocellular carcinoma, lymphoma, hemangiomas and hematomas. However, based on the typical ultrasound and CT scan findings, all possibilities except that of liver abscess were excluded. Discussion, MEBSs with protozoan entomibia histolitica is the leading parasitic cause of death worldwide after malaria and schistosomiasis. Amoebic liver abscess develops in less than 1% of patients infested with entomibia histolitica. The rate of various complications in amoebic liver abscess is 10.3. Vascular complications of hepatic abscess such as thromosis of portal vein, occlusion of hepatic vein or inferior vena cava thromosis are rare and have been previously described mostly in autopsies. However, few case reports reported this complication in a prospective manner. The exact pathophysiology of IVC thromosis occurrence in hepatic amoebic liver abscess is uncertain. Proposed mechanism include external mechanical compression, thrombotic state associated with inflammatory process of amoebiasis. The thrombotic events can be explained by the contiguity of the abscess containing trophozoids surrounding the dead hepatocytes and liquefied cellular debris with the venous structures. Prolonged endothelial cell activation by amoebic molecules will induce the local information. As IVC thrombosis is life-threatening, it requires high clinical suspicion followed by CCT in appropriate clinical setting. Vascular complications in liver abscess should be considered in patients with fever, tender liver or signs of portal hypertension. CCT is an excellent modality for diagnosis liver abscess as well as its complication. Ultrason may be helpful in detection and characterization of venous extension. On conclusion, we can conclude from this case that whenever a liver abscess is seen adjacent to a vascular channel or in the corded lobe, it is imperative for the radiologists to look for vascular complications because venous involvement may not be very symptomatic in some cases. Treatment of the abscess improves the recanalization of the thrombose vessel with anticoagulants. If the abscess is drained, then it improves the recanalization of the thrombose vessel even without anticoagulation. Hence early diagnosis and treatment will essentially reduce the mortality and morbidity with liver abscess. These are the references for the case study.