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1/14. Acute embolic carotid occlusion after cardiac catheterization: effect of local intra-arterial urokinase thrombolysis.

    A 64-year-old woman developed a severe embolic cerebral attack with total left hemiplegia approximately 30 hours after cardiac catheterization for mitral stenosis. She underwent intra-arterial thrombolysis of the right internal carotid artery four and one-half hours after the onset of neurologic deficit with subsequent recanalization of the occluded vessel and near complete neurologic recovery.
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2/14. Endovascular thrombolysis for symptomatic cerebral venous thrombosis.

    OBJECT: The authors sought to treat potentially catastrophic intracranial dural and deep cerebral venous thrombosis by using a multimodality endovascular approach. methods: Six patients aged 14 to 75 years presented with progressive symptoms of thrombotic intracranial venous occlusion. Five presented with neurological deficits, and one patient had a progressive and intractable headache. All six had known risk factors for venous thrombosis: inflammatory bowel disease (two patients), nephrotic syndrome (one), cancer (one), use of oral contraceptive pills (one), and puerperium (one). Four had combined dural and deep venous thrombosis, whereas clot formation was limited to the dural venous sinuses in two patients. All patients underwent diagnostic cerebral arteriograms followed by transvenous catheterization and selective sinus and deep venous microcatheterization. Urokinase was delivered at the proximal aspect of the thrombus in dosages of 200,000 to 1,000,000 IU. In two patients with thrombus refractory to pharmacological thrombolytic treatment, mechanical wire microsnare maceration of the thrombus resulted in sinus patency. Radiological studies obtained 24 hours after thrombolysis reconfirmed sinus/vein patency in all patients. All patients' symptoms and neurological deficits improved, and no procedural complications ensued. Follow-up periods ranged from 12 to 35 months, and all six patients remain free of any symptomatic venous reocclusion. Factors including patients' age, preexisting medical conditions, and duration of symptoms had no statistical bearing on the outcome. CONCLUSIONS: patients with both dural and deep cerebral venous thrombosis often have a variable clinical course and an unpredictable neurological outcome. With recent improvements in interventional techniques, endovascular therapy is warranted in symptomatic patients early in the disease course, prior to morbid and potentially fatal neurological deterioration.
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3/14. pseudotumor cerebri from cranial venous obstruction.

    Dural sinus hypertension from cerebral venous outflow impairment is a cause of pseudotumor cerebri. The authors documented six such patients: two with unilateral neck dissection, one with surgical ligation of the dominant sigmoid sinus, two with thrombosed central intravenous catheterization, and one with dural sinus thrombosis. The site of cerebral venous outflow obstruction was variable and identified in three patients with computed tomography, conventional magnetic resonance imaging, magnetic resonance angiography, and/or angiography. magnetic resonance angiography used in two patients characterized the venous flow pattern and identified the site of obstruction, confirming magnetic resonance angiography as an effective noninvasive blood flow technique in diagnosing and following these patients. Three patients were treated successfully with medical therapy and one patient with optic nerve fenestration. The two patients with thrombosed central venous catheters had serious systemic illnesses and suffered permanent visual loss.
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4/14. tissue plasminogen activator thrombolysis of a middle cerebral artery embolus in a patient with an arteriovenous malformation. Case report.

    A patient harboring a cerebral arteriovenous malformation (AVM) underwent angiography in an attempt to embolize the AVM. During catheterization (and prior to embolization) he became hemiplegic and aphasic. Angiography revealed a complete middle cerebral artery (MCA) occlusion by an embolus. The patient was treated with recombinant tissue plasminogen activator (t-PA), a thrombolytic agent. Restoration of MCA flow was achieved, and the patient recovered. Immediately after MCA embolus, t-PA infusion may lead to thrombolysis and neurological recovery. The decision-making process as well as the risks associated with the use of t-PA are discussed.
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5/14. Spontaneous calcific cerebral embolus from a calcific aortic stenosis in a middle cerebral artery infarct.

    Calcific emboli from a calcific aortic stenosis is an uncommon event, usually following local trauma, as from cardiac surgery or left heart catheterization or as a sequel to bacterial endocarditis. We report what we believe to be the first case of a spontaneous calcareous emboli demonstrated by cranial computed tomography. In this patient, systemic hypertension and mild aortic insufficiency may have caused increasing mechanical forces acting on the aortic cusps and may have precipitated embolism.
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6/14. Calcific cerebral emboli and aortic stenosis: detection of computed tomography.

    Embolism with brain infarction rarely complicates calcific aortic stenosis (CAS). We report a case with severe CAS where the patient experienced multiple embolic strokes immediately following retrograde heart catheterization. Calcific emboli in the cerebral arteries were demonstrated by computed tomography (CT).
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7/14. Displacement of preexisting thrombus by umbilical vein catheterization.

    Balloon atrial septostomy is recommended as a standard palliative procedure in neonates with congenital heart defects who are dependent on intracardiac shunting. We describe an unusual and unreported complication associated with "bedside" balloon atrial septostomy. The umbilical venous catheterization resulted in displacement of a thrombus from the ductus venosus or the hepatic vein. We recommend careful two-dimensional echocardiographic monitoring during such procedures.
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8/14. Paradoxical embolism. A diagnostic challenge and its detection during life.

    Two cases of paradoxical embolism, one with recurrent cerebral embolism and one with brachial and coronary embolism and both associated with pulmonary embolism, were diagnosed during life. Although there was neither pulmonary hypertension nor intracardiac shunt present at the time of cardiac catheterization in both cases, the presence of a patent foramen ovale with an interatrial right-to-left shunt was demonstrated by a simple ascorbate dilution technique following a valsalva maneuver. Each patient was treated by surgical interruption of the inferior vena cava and did well. Paradoxical embolism should be included in the differential diagnosis of arterial embolism for which there is no obvious source, especially when there is also evidence of venous thrombosis or pulmonary embolism.
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9/14. A case of cerebral air embolism predominant in the left cerebral hemisphere following subclavian catheterization.

    We report a case of cerebral air embolism caused by right subclavian vein catheterization. A large amount of air was seen only over the left cerebral hemisphere on computed tomographic (CT) scans. Although neurological deficit was observed bilaterally at the onset, the degree of ischemic brain damage was far greater in the left cerebral hemisphere than in the right. This unusual left-sided predominancy of cerebral air embolism was presumably due to the tortuosity of the ascending aorta.
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10/14. Computed tomography detection of a cerebral calcific embolus following coronary catheterization.

    A 77-year-old man underwent coronary artery angiography quite well. However, several attempts were required to pass the pigtail catheter across a calcified stenotic aortic valve. On return to the floor, motor aphasia and right hemiparesis developed and improved steadily within a few days. Computed tomography (CT) of the head revealed a calcific density in the left middle cerebral artery. The authors believe the calcific plaque originated from the calcified aorta and aortic valve. The patient was discharged within 48 hours with minimal neurological signs. Spontaneous calcified emboli to cranial vessels from calcific aortic stenosis or other sources are rare. CT detection of a calcific plaque in a cranial vessel following coronary vessel catheterization is well documented in this patient.
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