1/5. Hypotensive hemorrhagic necrosis in basal ganglia and brainstem.Hypotensive hemorrhagic necrosis of the basal ganglia and brainstem has only occasionally been described. Three such cases are reported. Cardiac arrest had occurred in all cases, and it took at least 1 hour to restore adequate circulation. The patients remained comatose for 2 days to 2 weeks until death. Persistent hypotension causing ischemia in the distribution of deep perforating arteries is considered to have been the key underlying mechanism. hemorrhage is thought to have been caused by extravasation of red blood cells through damaged blood vessels.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
2/5. Reperfusion pulmonary edema after pulmonary endarterectomy.pulmonary artery thromboendarterectomy is a potentially curative procedure in chronic, major vessel thromboembolic pulmonary hypertension. However, persistent pulmonary hypertension and unrelenting reperfusion edema have serious complications, often requiring prolonged mechanical ventilation. A 50-year-old man who was diagnosed with a thromboembolism in both pulmonary arteries underwent a bilateral pulmonary endarterectomy. He received O2-isoflurane-fentanyl anesthesia. When the lungs were reperfused with CPB weaning, massive hemorrhage occurred in the left lung. After the operation, the patient was taken to the intensive care unit. Mechanical ventilation was performed immediately and then both inhaled NO and i.v. furosemide therapies were administered. The patient was discharged from ICU 15 days postoperation.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
3/5. Hyperperfusion syndrome after carotid endarterectomy: a transcranial Doppler evaluation.Transcranial Doppler ultrasonography was used to evaluate 2 patients who developed hyperperfusion syndromes after carotid endarterectomy. During the initial postoperative period, each patient had symptoms that were associated with elevated flow velocities in the ipsilateral cerebral vasculature. In addition, vascular resistance of these vessels was found to be abnormally low, as reflected by the Gosling pulsatility index. As the patients' symptoms improved, flow velocities decreased to normal levels and pulsatilities were noted to increase proportionately.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
4/5. Fatal ischaemic brain oedema after early thrombolysis with tissue plasminogen activator in acute stroke.Two patients with acute major, disabling cerebral infarction with presumed middle cerebral artery occlusion were treated with the clot specific thrombolytic agent tissue plasminogen activator roughly three and a half hours after the onset of symptoms. Both patients had a normal computed tomography (CT) scan before treatment. No appreciable systemic bleeding complications occurred, apart from bruising. One patient had bleeding into the subarachnoid space from a microscopic angioma, which was found at necropsy. Haematological monitoring of the two patients showed pronounced fibrinogenolysis and alpha 2 antiplasmin consumption in one. One patient showed transient improvement during the infusion. In both cases extensive infarction, partly haemorrhagic in one, with massive concomitant oedema was found on repeated CT. Both patients deteriorated and eventually died as a consequence of transtentorial herniation. In the one patient who came to necropsy a moderate, probably pre-existing smooth stenosis of the ipsilateral carotid artery was found, all cerebral vessels being patent. It is concluded that thrombolytic treatment with a clot specific agent such as tissue plasminogen activator started three to four hours after a major ischaemic stroke may be hazardous, not because of haemorrhagic transformation of the original ischaemia but because early reperfusion may promote massive, potentially fatal cerebral oedema.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |
5/5. life-threatening reperfusion injury in skeletal muscle: a simple technique to control critical hyperkalemia.A 55-year-old male suffering from acute abdominal aortic occlusion due to iatrogenic aortic dissection was urgently admitted to hospital. An axillo-bifemoral bypass was constructed 6 hours from the onset of dissection. Before and after revascularization, blood samples were repeatedly obtained from a systemic artery and femoral vein. The arterial potassium concentration gradually increased, reaching 7.3 mM/L. oliguria and arrhythmias occurred, and the left lower limb became rigid 3 hours after reperfusion. The femoral artery and vein were clamped and within 30 minutes, the arterial potassium concentration fell to 4.8 mM/L. The urine output increased. The left lower limb was amputated, and the patient survived. Immediately following revascularization, hyperkalemia may occur. Clamping of the afferent and efferent vessels is recommended as a simple and practical technique to quickly control life-threatening hyperkalemia.- - - - - - - - - - ranking = 1keywords = vessel (Clic here for more details about this article) |