We present a case of a 54 years old male who initially presented with one month history of worsening epigastric pain and vomiting. He was referred to our care after an ultrasound and CT abdomen showing dilated common bile duct up to 13mm with no obvious intraductal obstruction. An incidental type 1 duplicated IVC was demonstrated on the CT abdomen (Figure and 2).\nNo intra-abdominal mass or lymphadenopathy were detected. Notably, he is a known BRCA2 mutation carrier. Both, his mother and sister had BRCA2-positive breast cancer. One of his great uncles also had male breast cancer. The patient was clinically jaundiced on presentation, with a bilirubin of 106. His other liver function tests were ALT at 465, GGT at 1032 and at ALP 271. His tumour markers CA-125 and CA-199 were 12 and 94 respectively.\nThe patient was subsequently found to be hypotensive and tachycardic with a new drop in haemoglobin from 100 to 72 during his stay. An urgent gastroscopy then revealed a 10mm punched-out ulcer with adherent clot at the ampulla. The lesion was partially obstructed and no active bleeding was seen. Histology on biopsy showed moderately differentiated adenocarcinoma. CT angiography was then performed. No active extravasation was seen and the gastroduodenal artery was empirically embolised with microcoils. An apparent cavitation at the medial aspect of the second part of duodenum was now identified on the CT imaging (Figure ). No metastasis was seen on staging CT imaging.\nA whipple procedure was performed. The duplicated right IVC was visualised intraoperatively with mobilisation of the uncinate process but appeared relatively normal. The left sided IVC was not encountered. No major complications were reported during his inpatient stay. Patient was discharged home and subsequently commenced on adjuvant therapy.
A 54-year-old male patient with long standing history of type II DM, dyslipidemia and hypertension, with medical therapy of bisoprolol 10 mg daily, valsartan 160 mg daily, HCTZ 25 mg daily, atorvastatin 20 mg nocturnally, insulin and metformin was admitted to a peripheral hospital with bronchopneumonia requiring high dependency unit admission. This was complicated by a transient ischemic attack. Brain computed tomography (CT) was normal. On the second day of admission, he had a significant episode of chest pain. Electrocardiogram (ECG) showed transient ST-segment elevation with spontaneous resolution in the inferior lead. There was mild troponin leak. He was later referred to our center for further workup. His physical exam revealed oxygen saturation at 98% on room air, pulse 70 bpm, BP both upper limb 155/65 mm Hg, and BP lower limb 105/45 mm Hg. There was a brachio-femoral delay. Apex was mildly displaced; he had S1+ S2+ S4 and a systolic murmur at the tip of left scapula; no clicks were appreciated on auscultation.\nECG showed sinus rhythm and left ventricular hypertrophy (LVH) with strain pattern. A 24-h Holter came back with normal sinus rhythm, no atrial fibrillation, no heart blocks or arrhythmia. Transthoracic echocardiogram revealed concentric LVH, borderline left ventricular function of 45-50%, mild to moderate aortic regurgitation, bicuspid aortic valve and a coarctation of the aorta with a 70 mm Hg gradient across it. Brain MRI demonstrated lacunar infarcts and no AV-malformations. Both carotid arteries were free of atherosclerosis on Doppler. Coronary CT angiogram not only demonstrated the tight coarctation but also showed a rare anomaly of a PLSVC draining into the left atrium (). Anomalous pulmonary drainage and pulmonary arteriovenous malformation were excluded. The approach to management of this patient was discussed in a heart team meeting. It was decided to proceed percutaneously.\nThe patient was brought to the catheterization laboratory. Coronary angiography showed normal coronaries. He did have a significant coarctation with a pressure gradient of 40 mm Hg. Angiographic confirmation of the PLSVC draining into the left superior pulmonary vein was confirmed. A 40 mm CP stent mounted on a 20 × 45 mm BIB balloon was deployed successfully (), guided by fluoroscopy and overdrive pacing. There was complete abolition of the gradient. At a later date, the patient was brought for PLSVC exclusion therapy. Selective angiography of the PLSVC was performed to delineate vessel course and venous drainage (). Using a marker pigtail measurement of the vessel was obtained. The PLSVC measured 9 mm proximally, 10.5 mm at its mid-point and 8 mm near the entrance to the left upper pulmonary vein. The PLSVC was then temporarily occluded with an 8 mm peripheral balloon to make sure that the patient would tolerate closure of the vessel. There was no significant change in the patient’s hemodynamic measurements, and the decision was made to proceed with transcatheter occlusion of the PLSVC which was achieved using a 12 mm Amplatzer vascular plug II (AGA Medical Corporation, Golden Valley, MN) ().