Cases reported "Hyperemia"

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1/6. Occlusive hyperemia: a radiosurgical phenomenon?

    OBJECTIVE: Causes of neurological deficits after arteriovenous malformation (AVM) radiosurgery, including hemorrhage, radiation injury, and delayed cyst formation, are described. CONCEPT: Occlusive hyperemia has been described as a reason for neurological deterioration after AVM resection. thrombosis of draining veins or dural sinuses is thought to cause postoperative bleeding or neurological deficits secondary to venous hypertension. In a similar manner, local hemodynamic changes can occur in the brain adjacent to an AVM after radiosurgery if venous outflow is obstructed. Two patients are presented whose cases demonstrate this phenomenon. CONCLUSION: patients can experience clinical worsening after AVM radiosurgery from premature thrombosis of draining veins. Local hemodynamic changes could explain why imaging changes thought to be radiation related occur more frequently after radiosurgery of AVMs than of tumors.
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ranking = 1
keywords = venous outflow, outflow
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2/6. The relationship between occlusive hyperemia and complications associated with the radiosurgical treatment of arteriovenous malformations: report of two cases.

    OBJECTIVE AND IMPORTANCE: It has been suggested that impaired venous drainage of normal brain after surgical removal of an arteriovenous malformation (AVM) may cause perinidal edema and hemorrhage. The term occlusive hyperemia has been proposed for this phenomenon. There is evidence that occlusive hyperemia also may occur after radiosurgical treatment of AVMs. The purpose of this article is to lend further support to the concept that venous occlusion may be responsible for some complications observed after AVM radiosurgery. CLINICAL PRESENTATION: We report two patients with unusual radiosurgery-associated complications, and we examine the evidence for venous occlusion as the mechanism underlying the observed clinical sequelae in each patient. INTERVENTION: Patient 1 had a large parietal venous infarct remote from her frontal AVM site 11 months after radiosurgery. At that time, the AVM was confirmed by angiography to have been obliterated. During the next 4 years, the patient experienced persistent posterior hemispheric edema with recurrent focal hemorrhages until the patient's death from massive swelling and uncal herniation. During this period, radiographic studies, including repeat angiography, demonstrated sequential cortical venous occlusions and findings most consistent with venous insufficiency. Postmortem examination revealed no evidence of radionecrosis. Patient 2 exhibited a biphasic pattern of neurological deterioration at 3 and 6 years after radiosurgery. Associated with this unusual phenomenon, there was radiographic evidence of venous outflow obstruction of her thalamic AVM with prominent perinidal edema and progressive occlusion of the nidus. CONCLUSION: We conclude that occlusive hyperemia is responsible for some cases of neurological deterioration after AVM radiosurgery, especially in a setting for which the time course or other clinical features are not as might be expected from a radiobiological perspective. The two patients we describe in this report suggest that manifestations may vary.
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ranking = 1.0009009475067
keywords = venous outflow, outflow, obstruction
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3/6. Ureteral stent encrustation.

    Palliative ureteral stent placement is effective in relieving obstructive renal impairment, especially that precedent to malignant spreading, and can take the place of surgical intervention. Furthermore, cutaneous antegrade and/or endoscopic retrograde stenting can be indicated for other pyelo-ureteric operations and prevent their complications, but is has its consequences: We experienced three cases in which stenting had to be repeated because of its obstruction. The stent catheter blockage is discussed.
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ranking = 0.0009009475067405
keywords = obstruction
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4/6. thallium-201 uptake in variant angina: probable demonstration of myocardial reactive hyperemia in man.

    Myocardial thallium scintigraphy was performed in four subjects with variant angina and in one subject with isolated, fixed coronary obstruction. Three subjects with variant angina had short episodes of ischemic ST-segment elevation that lasted 20--100 seconds. thallium scintigrams demonstrated excess uptake in regions judged to be ischemic by angiographic and electrocardiographic criteria. Two subjects, one with variant angina and the other with a fixed coronary lesion, had prolonged episodes of ischemia that lasted 390--900 seconds. Both had reduced thallium uptake in the ischemic regions. We conclude that myocardial reactive hyperemia is the cause of excess thallium uptake in patients with variant angina who have short episodes of myocardial ischemia.
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ranking = 0.0009009475067405
keywords = obstruction
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5/6. pulmonary edema following relief of acute upper airway obstruction.

    Five children, aged one to five years, with severe upper airway obstruction, three of whom had epiglottitis and two of whom had laryngotracheobronchitis, developed acute pulmonary edema after the obstruction had been relieved by placement of an artificial airway. Although major physiologic changes, such as hypoxemia and massive sympathetic discharge, play a significant role in the development of acute pulmonary edema, we have postulated a possible etiological cause for the development of pulmonary edema in these children which involves a series of physiologic events. The generation of very high transpulmonary pressure gradients during inspiration is opposed by a decreased venous return due to the obstruction during exhalation. Airway pressures then fall abruptly with the insertion of the artifial airway, resulting in a sudden increase in venous return to the central circulation and marked increase in the intravascular hydrostatic pressures. The final result of this series of events is the development of pulmonary hyperemia and edema. The prevention of this situation must begin the moment the airway is inserted and involves the application of moderate amounts of continuous positive pressure to the airway, thus allowing time for circulatory adaption to take place.
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ranking = 0.0063066325471835
keywords = obstruction
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6/6. Occlusive hyperemia: a theory for the hemodynamic complications following resection of intracerebral arteriovenous malformations.

    An alternative theory is proposed to explain the brain edema and hemorrhage that may occur after resection of high-flow intracerebral arteriovenous malformations (AVM's). This theory, termed "occlusive hyperemia," is based on a retrospective analysis of operative dictations along with postoperative imaging studies (191 angiograms and 273 computerized tomography scans) in 295 cases of intracerebral AVM's operated on at the Mayo Clinic between 1970 and 1990. In this series, 34 cases (12%) of postoperative deterioration were documented, of which 15 were due to incomplete resection of the AVM. Of the remaining 19 cases, six had brain edema alone and 13 had hemorrhage with edema, despite complete excision of the AVM. In these 19 cases, the AVM's were greater than 6 cm in diameter in 10 patients, between 3 and 6 cm in six, and less than 3 cm in three. Obstruction of the venous drainage system was observed in 14 (74%) of the 19 cases. Ten of these 14 were due to obstruction of the primary venous drainage of the brain parenchyma immediately surrounding the lesions, while four were due to obstruction of other venous structures. In no case was a rapid circulation identified on postoperative angiograms. The flow pattern was slow or stagnant in former AVM feeders and their parenchymal branches. It is proposed that postoperative intracranial hemorrhage and/or brain edema in AVM patients may be due to: 1) obstruction of the venous outflow system of brain adjacent to the AVM, with subsequent passive hyperemia and engorgement; and 2) stagnant arterial flow in former AVM feeders and their parenchymal branches, with subsequent worsening of the existing hypoperfusion, ischemia, and hemorrhage or edema into these areas. Supportive hemodynamic evidence for this theory was derived from the literature.
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ranking = 1.0027028425202
keywords = venous outflow, outflow, obstruction
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