Internal medicine
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Bow hunter's stroke is a rare cause of vertebrobasilar infarction. There is no consensus regarding the optimal treatment. We herein report a case of bow hunter's stroke successfully treated by endovascular treatment. ⋯ Dynamic angiography revealed thrombus formation and hypoperfusion of the right vertebral artery upon head rotation to the left. Endovascular parent artery occlusion of the right vertebral artery was performed, and there was no recurrence at follow-up MRI. Endovascular parent artery occlusion might be a useful treatment for bow hunter's stroke.
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Massive hemoptysis is a fatal complication associated with pulmonary tuberculosis (TB). It can lead to severe respiratory failure. Extracorporeal membrane oxygenation (ECMO) is a life-saving technology that is rarely indicated for bleeding disorders. ⋯ Transcatheter artery embolization was successfully performed with venovenous ECMO support. The hemostatic procedure allowed concomitant anticoagulant use, and neither bleeding nor thrombotic complications occurred throughout the clinical course. Administering the appropriate hemostatic procedure with subsequent management, including anticoagulant therapy, supported ECMO application in a case of bleeding.
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We encountered a 77-year-old Japanese man who presented with nephrotic-range proteinuria 20 days after receiving ramucirumab treatment for metastatic sigmoid colon cancer. A kidney biopsy showed two characteristic histological findings. The first finding was podocyte injury with cellular crescent-like formation, although focal segmental glomerulosclerosis (FSGS) (collapsing variant) according to the Columbia classification may have been a more appropriate name for this injury, as hypertrophy and hyperplasia of epithelial cells, presumably resulting from podocyte injury, were seen between Bowman's capsule and the glomerular basement membrane (GBM); these changes appeared to be due to the collapse of the GBM rather than to GBM destruction with fibrinoid necrosis. ⋯ Proteinuria and renal dysfunction subsided after discontinuation of ramucirumab. Bevacizumab has been reported to induce glomerular microangiopathy with endothelial damage and swelling six months after treatment, but in this case, ramucirumab may have induced focal segmental glomerulosclerosis (FSGS) collapsing variant and glomerular microangiopathy with endotheliopathy via mesangial damage within 1 month. We believe that the damage to the glomerular podocyte and endothelial cells via mesangial damage secondary to ramucirumab in our patient was a different type of glomerular microangiopathy than the endothelial cell damage with enlargement of the subendothelial space caused by bevacizumab.
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The pathophysiology of unilateral cortical fluid-attenuated inversion recovery (FLAIR)-hyperintense lesions in anti-myelin oligodendrocyte glycoprotein (MOG)-associated encephalitis with seizures (FLAMES) is unclear. A 26-year-old man was referred because of a seizure. FLAIR showed an increased signal intensity and swelling of the right frontal cortex. ⋯ Therefore, the patient was diagnosed with FLAMES. Myelin basic protein (MBP) was elevated in CSF. The high MBP value in the CSF in the present case suggested that demyelination as well as inflammation can occur in some FLAMES patients.
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Regarding extracorporeal membrane oxygenation (ECMO) support against hemorrhagic conditions, there seems to be a dilemma when deciding between maintaining the circuit patency by systemic anticoagulation and increasing the risk of bleeding. We herein report two cases of diffuse alveolar hemorrhage (DAH) caused by myeloperoxidase (MPO) anti-neutrophil cytoplasmic autoantibody-associated vasculitis (AAV) successfully treated with venovenous (VV)-ECMO support, both initially started without systemic anticoagulation. Under anticoagulation-free ECMO management, we should consider the shortcomings of frequent circuit exchange and hemorrhagic diathesis related to circuit-induced disseminated intravascular coagulation (DIC).