A 40-year-old man with a history of tuberculosis developed massive hemoptysis. Embolization of a bronchial artery branch did not resolve the bleeding. Selective angiography eventually revealed three pseudoaneurysms arising from an apical segmental branch of the right pulmonary artery, two of which were successfully embolized with coils. The patient's hemoptysis resolved within 48 hours. Although most patients with hemoptysis and active tuberculosis bleed from the bronchial circulation, the pulmonary arterial circulation should be immediately evaluated if the bronchial angiogram is normal. Coil embolization is a safe and effective means of treating these pseudoaneurysms.
SUMMARY Giant fusiform basilar aneurysms (dolicho-ectatic basilar anomalies) are rare and have not previously been reported to cause embolic infarction in territory distal to the aneurysm. They most commonly present as posterior fossa mass lesions with brainstem compression and cranial neuropathies. Originally considered atherosclerotic in etiology, recent authors feel that they may represent a unique arteriopathy characterized by loss of elastin in the vessel wall. We report a case which presented solely as an occipital lobe infarction. To our knowledge, this is the first case in which a fusiform basilar aneurysm presented with an embolic infarction as its only manifestation. Stroke, Vol 13, No 5, 1982 GIANT FUSIFORM BASILAR ANEURYSMS (doli cho-ectatic basilar anomalies') are aneurysmal dilations of the basilar artery and usually present clinically as posterior fossa mass lesions ( 5 Emboli arising from in tracerebral aneurysms are unusual 22 -23 and to our knowledge have not been reported originating from a fusiform basilar aneurysm. We report a case which presented solely as an embolic occipital lobe in farction.Case Report A 59-year-old man with mild hypertension and Type IV hyperlipidemia experienced abrupt onset of right periorbital headache accompanied by loss of vision in the left visual field. He had no previous history of transient ischemic attacks (TIAs) or stroke. Several weeks prior to the event, he noted frequent right peri orbital headachees lasting 45-60 minutes without neurologic symptoms. Nine years previously he under went surgery for repair of an abdominal aortic aneu rysm. His risk factors included a 20 year history of mild hypertension (highest recorded pressure 140/100 mg Hg), smoking, hypertriglyceridemia, and moder ate obesity. His general physical examination was normal ex cept for early retinal vessel sclerosis. Blood pressure was 130/84 mm Hg. There were no carotid bruits. Neurologic examination demonstrated a left superior _, quadrantanopsia, but was otherwise unremarkable.The following studies were normal: serum electro lytes, complete blood count, syphilis serology, urinal ysis, coagulation profile, echocardiogram, and lumbar puncture. Serum triglycerides were 261 mg/dl (nor mal, 30-150 mg/dl). The electrocardiogram demon strated borderline nonspecific ST-T wave changes and rare multifocal premature ventricular contractions.A computed tomographic (CT) scan of the head demonstrated a nonhemorrhagic right occipital lobe infarction ( fig. 1), and a large eccentrically positioned basilar artery, with calcification in its walls, extending well above the posterior clinoids ( fig. 2a). The contrast enhanced ( fig. 2b) and reformatted coronal ( fig. 3) images revealed the presence of incomplete thrombo sis in the aneurysm which measured up to 2 cm in diameter. Pancerebral angiography ( fig. 4) confirmed the diagnosis of a partially thrombosed giant fusiform basilar aneurysm and showed the lesion to be continu ous with an ectatic and elongated dominant right verte bral artery. In additio...
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