Two patients presented with cerebral venous sinus thrombosis (CVST) associated with iron deficiency. A 14-year-old man had thrombosis extending from the end of the superior sagittal sinus to the left transverse sinus. Severe dehydration after competitive sport had induced CVST. The laboratory findings showed severe iron deficiency anemia which persisted for 1 year. A 47-year-old man had thrombosis in the entire superior sagittal sinus. Dehydration caused by poor nutrition had induced CVST. The laboratory findings showed transient iron deficiency in the acute phase. Both patients received conservative treatment for dehydration and iron supplementation. These two cases indicate that iron deficiency is a risk factor for CVST.
Serial cerebral blood flow (CBF) measurements were made with stable xenon-enhanced computed tomography in 20 patients with angiographically confirmed ruptured intracranial aneurysms, before and during induced hypertension with continuous infusion of dopamine. All patients showed angiographic vasospasm during their course. Twelve patients without symptomatic vasospasm (Group 1) had the lowest hemispheric CBF on the craniotomy side of 31.6 +/- 6.8 ml/100 gm/min on days 4-9 (control value, 40.1 +/- 2.0 ml/100 gm/min), while the other eight patients with symptomatic vasospasm (Group 2) had the lowest hemispheric CBF on the craniotomy side of 25.0 +/- 7.6 ml/100 gm/min on days 10-14. The critical hemispheric CBF inducing neurological deficits was about 20 ml/100 gm/min in Group 2. Dysautoregulation was usually present in Groups 1 and 2, but therapeutically induced hypertension could reverse the delayed neurological deficits, if begun early at the stage of delayed vasospasm.
The case of a 57-year-old woman with a 14-year history of progressive paraparesis is presented. Selective spinal angiography revealed a juvenile-type spinal arteriovenous malformation (AVM) with a typical large size and rapid flow. The AVM was located primarily in the retromedullary space at the cervicothoracic junction. The AVM was successfully obliterated by intraoperative embolization using isobutyl-2-cyanoacrylate and surgical excision.
Extravascular lung water (EVLW) was measured by the double-indicator dilution method in 25 patients with hemorrhagic cerebrovascular diseases. EVLW had a significantly positive correlation with both alveolar-arterial oxygen difference (AaDO2) and intrapulmonary shunt. The value of EVLW in the acute stage in 15 patients with increased AaDO2 more than 20 mm Hg was 7.8 +/- 2.2 ml/kg and that in the chronic stage 4 weeks after onset significantly decreased to 4.6 +/- 0.7 ml/kg (P less than 0.001). The value of EVLW in the acute stage in 10 patients with normal AaDO2 less than 20 mm Hg was 4.7 +/- 1.1 ml/kg and that in the chronic stage 4 weeks after onset was 4.5 +/- 0.2 ml/kg. There was no significant difference between them. Pulmonary arterial blood pressure, pulmonary capillary wedge pressure, central venous pressure, cardiac index, systemic vascular resistance index, and pulmonary vascular resistance index in the acute stage in the 25 patients were all within the normal range. Three patients with neurogenic pulmonary edema had markedly increased EVLW without abnormalities in pulmonary arterial blood pressure, pulmonary capillary wedge pressure, central venous pressure, cardiac index, systemic vascular resistance index, and pulmonary vascular resistance index. From these facts, the main cause of the increase in EVLW cannot be explained by left ventricular failure, but can be explained by high permeability pulmonary edema.
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