A 75-year-old man had undergone pancreatoduodenectomy with modified-Child reconstruction for pancreatic cancer 3 years earlier and did not experience recurrence on follow-up. He was admitted to our hospital owing to fever and general fatigue. His vital signs on admission were as follows: consciousness, alert; heart rate, 69 beats/min; blood pressure, 77/48 mmHg; respiratory rate, 15 breaths/min; peripheral capillary oxygen saturation, 95 % on room air; and body temperature, 36.5 °C. On physical examination, his abdomen was soft and flat, and his skin turgor was poor. We detected elevated inflammatory levels and decreased renal function. Non-contrast computed tomography (CT) revealed an approximately 30-mm low-density area and an air density in segment 8 of the liver (Fig. ). Furthermore, there was an air density in the middle hepatic vein. We diagnosed PLA due to cholangitis in the middle hepatic vein and septic shock. We subsequently initiated conservative treatment using antibiotics (meropenem 1.5 g/d).\nThe patient had no medical history of any diseases, except pancreatic cancer. Laboratory results on admission were as follows: leukocyte count, 14.5 × 103/μL; hemoglobin level, 10.9 g/dL; platelet count, 23 × 103/μL; aspartate aminotransferase level, 68 IU/L; alanine aminotransferase level, 68 IU/L; alkaline phosphatase level, 747 IU/L; total protein level, 4.9 g/dL; total bilirubin level, 1.6 mg/dL; blood urea nitrogen level, 99 mg/dL; creatinine level, 2.71 mg/dL; amylase level, 43 IU/L; C-reactive protein level, 15.6 mg/dL; prothrombin percentage activity, 53 %; and activated partial thromboplastin time, 37.2 s.\nAfter being admitted to the hospital, the patient gradually recovered with antibiotic treatment. However, a contrast CT scan on hospital day 8 revealed a thrombus in the middle hepatic vein (Fig. ). Therefore, we started anticoagulant therapy using heparin (15,000 U/d) and continued meropenem 1.5 g/d treatment. A follow-up CT scan on hospital day 17 revealed that the abscess had reduced in size but that the thrombus had slightly enlarged. We thought that the abscess was being controlled by the antibiotics; therefore, we continued the same treatment approach. A follow-up CT scan on hospital day 25 showed that the abscess had reduced further. However, the thrombus had enlarged again and reached the IVC close to the right atrium (Fig. ). Considering the risk of pulmonary embolism, we planned a surgical intervention. A blood culture on admission was positive for Citrobacter freundii.\nThe patient underwent a thrombectomy using extracorporeal circulation. We made an incision in the right atrium and removed the thrombus through the orifice of the middle hepatic vein. The thrombus was yellow (Fig. a), and pathological observation showed that it consisted of fibrous material including many neutrophils and macrophages. Accordingly, we made a diagnosis of septic thrombosis. Intraoperative trans-esophageal echocardiography showed a thrombus in the right pulmonary artery. A preoperative CT scan showed no thrombus in the right pulmonary artery; therefore, we believed that the embolism might have occurred since the preoperative CT scan was performed. We made an incision in the artery and attempted to remove it using a Fogarty catheter. We then noted extensive bleeding from the right bronchus. We diagnosed a fistula of the right pulmonary artery and bronchus caused by catheter handling. To control the bleeding, the patient underwent a right lower lobectomy. We did not identify the pulmonary thrombus. Subsequently, we transferred the operating field to the abdomen. We dissected the middle hepatic vein using an automated suturing device to prevent the thrombus from extending into the IVC (Fig. b). The operation took 14 h and 5 min, while the total blood loss was 11,920 g.\nThe patient was discharged 10 weeks after surgery despite experiencing respiratory failure and undergoing tracheotomy. Before discharge, we confirmed the disappearance of the liver abscess on a CT scan. No atrophic changes were seen in the drainage area of the middle hepatic vein, but the density of the area was lower than that of the other owing to a change in venous drainage (Fig. ). At the present, 18 months after the surgery, the patient experienced no recurrence of either the liver abscess or thrombus.\nPLA reportedly occurs in 20–22 of every 100,000 hospitalized patients, and the mean age at the time of admission is reportedly 55.5–56.4 years [, , ]. PLA affects the sexes equally [, ], but one study reported that more men suffer from the disease than women (69.6 %) []. The infection route is classified as biliary, portal, hematogenous, direct extension, abdominal trauma, chronic granulomatous disease, or cryptogenic []. Fever, abdominal pain, and hepatomegaly comprise the PLA triad. PLA is treated with either broad-spectrum antibiotics and drainage or antibiotics alone [, ]. A number of complications have been reported in cases of PLA, such as abscess rupture and metastatic central nervous system infections [, ], but vascular complications such as IVC thrombosis are rare. A few cases have been reported for amebic liver abscess [–] compared to just one for PLA []. IVC thrombosis is a life-threatening complication because of the associated risk of pulmonary embolism.\nOur case involved a thrombus in the middle hepatic vein and the IVC complicating PLA after pancreatoduodenectomy with hepaticojejunostomy. Cholangitis reportedly occurs in 6.4 % of patients after hepaticojejunostomy []. In our case, blood culture on admission yielded C. freundii, an intestinal bacterial species. There was no evidence of abdominal trauma, intestinal infection, or chronic granulomatous disease. Therefore, the PLA seemed to occur through the biliary route.\nVirchow’s triad, which consists of abnormalities in blood composition, vessel wall components, and blood flow, is reportedly associated with thrombus formation []. Jun et al. [] reported that spontaneous rupture of PLA occurs in 3.8 % of cases. Liver cirrhosis, gas-forming abscess, abscess ≥ 6 cm in diameter, and other septic metastases have been reported as risk factors for rupture. In the present case, a gas-forming abscess was detected by CT upon admission; this abscess ruptured affecting the middle hepatic vein. Direct injury of the endothelial cells of the middle hepatic vein might explain the thrombus formation in this case. Bagri et al. [] reported that sepsis-induced endotheliitis seems to be the most important factor for thrombus formation. In the present case, we considered the endothelial condition (injury and inflammation) as the most important factor of thrombus formation as well as the dehydrated state of the patient on admission.\nThe optimal management of IVC thrombosis complicating PLA has not yet been established. Infection control and anticoagulation therapy might prevent thrombus occurrence or enlargement. However, a threatened pulmonary embolism such as right atrium thrombosis should be removed, regardless of whether the patient’s infection could be controlled. Bagri et al. [] successfully used surgical intervention and antibiotics to treat IVC thrombosis complicating PLA following aspiration. In our case, we considered using an indwelling IVC filter to prevent a pulmonary embolism. We attempted to indwell the filter at the heart side from the hepatic vein, but it was too difficult to perform for technical reasons. Therefore, we attempted anticoagulation therapy. Although we started anticoagulation therapy as soon as possible, the thrombus extended close to the right atrium. We consulted a cardiovascular surgeon for treating the thrombus and chose surgical intervention. Because the thrombus enlarged despite infection control, we believe that the surgical timing was appropriate. The patient underwent surgical thrombectomy with extracorporeal circulation. With regard to the thrombus of the right pulmonary artery that was found intraoperatively, there was a reflection. We could not identify it, and it was diagnosed only on intraoperative trans-esophageal echocardiography, so there was a possibility of no existing in fact. However, because it was diagnosed intraoperatively, we attempted to remove the thrombus using a Fogarty catheter. We ultimately treat the patient but encountered severe complications such as fistula of the right pulmonary artery and bronchus that induced extensive bleeding. As such, we should use a Fogarty catheter more carefully.\nIn the case of IVC thrombosis complicating an amebic liver abscess, one case was reportedly treated successfully with conservative therapy such as oral metronidazole, abscess aspiration, and anticoagulation [], whereas others were treated with surgical removal [–]. The effect of anticoagulation therapy is not yet clear for thrombi complicating PLA. The surgical stress induced by extracorporeal circulation is excessive, but a pulmonary embolism is life-threatening. Therefore, it is important to choose the most suitable surgical timing for IVC thrombosis complicating PLA.
A 24-year old man presented with pain in right upper abdomen with fever for five days. Physical examination revealed high grade fever and tachycardia. There was tenderness and guarding in right hypochondrium. There was bilateral pedal edema. Hematological investigations revealed a hemoglobin (Hb) level of 11.2 g/dL and white blood cell (WBC) count of 18,400/mm3 (normal range, 4,000-11,000/mm3). The biochemical investigations showed a blood urea nitrogen (BUN) of 34 mg/dL (normal range, 15-40 mg/dL), serum creatinine of 1.1 mg/dL (normal range, <1 mg/dL). Liver functions tests showed a total bilirubin of 1.5 mg/dL (normal range, <1 mg/dL), serum alkaline phosphatase (ALP) of 178 IU/L (normal range, 40-280 IU/L), aspartate aminotransferase (AST) 32 IU/L (normal range, <40 IU/L), alanine aminotransferase (ALT) 48 IU/L (normal range, <40 IU/L). Chest X-ray was normal. Ultrasound at admission showed a large (8.6×7.3×6.2 cm), volume 202 mL, heterogeneously hypoechoic lesion with internal echoes in the caudate lobe suggestive of liver abscess. On ultrasonography, the abscess was compressing the intra-hepatic IVC with abnormal color fill (slowed down) and flow pattern. Magnetic resonance imaging (MRI) with magnetic resonance cholangiopancreatography (MRCP) was performed which confirmed 6.9×6 cm abscess in the caudate lobe causing eccentric compression over the intrahepatic part of IVC (, ). There was a mass effect with compression of the main portal vein and the common hepatic duct just after the ductal confluence, however, the right and left hepatic ducts and intra-hepatic biliary radicals were not dilated. The patient tested positive for amoebic antibody by enzyme-linked immunosorbent assay (ELISA) test. The patient was started on broad spectrum antibiotics and metronidazole for two weeks. After initiating the treatment, there was a gradual amelioration in the fever and abdominal pain. Repeat ultrasound by the end of first week revealed a gradual reduction in the size of the abscess to 50% of its original size and the compression on IVC was also relieved as confirmed by doppler scan. The patient was asymptomatic. Follow-up investigations showed WBC of 8,800/mm3, and liver functions tests showed a total bilirubin of 0.5 mg/dL, serum ALP of 145 IU/L, AST 40 IU/L, ALT 45 IU/L. Patient was followed up for three months and repeat ultrasound done at the end of three months showed no residual abscess and IVC was normal in caliber, color fill and flow pattern.