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[18], to our knowledge there are only 2 reported cases of SSS secondary to a dialysis AVF in the absence of subclavian stenosis [19, 20]. Boettinger et al. reported a case of 59-year-old man with chronic renal failure presenting with acute left homonymous hemianopsia as a result of a SSS due to an AVF [19]. In another case reported by Schenk III, a 28-year-old dialysis-dependent man presented with symptoms of vertebrobasilar insufficiency secondary to a brachiocephalic AVF. There was reversal of symptoms S6 Kinase and reestablishment of antegrade flow in the VA after surgical reduction of flow through the AVF by a banding technique [20]. 4. Conclusion Although subclavian steal phenomenon is a benign vascular this website condition, subclavian steal syndrome is clinically significant and may result in symptoms of vertebrobasilar insufficiency and ipsilateral hand ischemia. Atherosclerosis is the most common etiology; however, other rare causes must be considered including high-flow dialysis AVFs. Recognition of this rare iatrogenic cause of SSS is important as it can lead to permanent neurological injury but is promptly reversed by decreasing AVF flow. Conflict of Interests No competing interests are declared.""A 75-year-old male patient with progressive shortness of breath and known history of chronic mitral valve regurgitation following mitral valve repair 19 years ago was admitted to hospital with an episode of dyspnea and syncope. Further investigation revealed severe mitral and tricuspid regurgitation. His past medical history included hypertension, hypercholesterolemia, and chronic atrial fibrillation treated Lapatinib cell line with warfarin. He was also on prednisolone 7.5?mg for follow-up of pituitary macroadenoma resected 15 years ago. He did not have a history of any hypercoagulable disorders including protein S/C deficiency. He underwent a right minithoracotomy redo mechanical mitral valve replacement and tricuspid valve repair. His course in the Intensive Care Unit was initially uncomplicated, and he was extubated on postoperative day (POD) 1. Warfarin (5?mg) and dalteparin (17000 units) were commenced on POD 1 and his INR reached 2.1 on POD 4. Prednisolone (7.5?mg) was restarted on POD 1. Starting on POD 4, there was progressive worsening of respiratory parameters, and prednisolone was increased to 50?mg for 4 days. On POD 5, he began to develop toe and finger cyanosis which eventually progressed to necrosis on POD 6 (Figure 1). His preoperative platelet count was 148,000/��L and it decreased to 76,000/��L on POD 1. A further drop occurred on POD 6 and the nadir of the platelet count was 34,000/��L on POD 7 (Figure 2). An enzyme-linked immunosorbent assay (ELISA) for HIT was done and reported as positive, with an optical density equal to 1.09?U (normal
