Articles: subarachnoid-hemorrhage.
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Journal of neurosurgery · Jan 1991
Reduced platelet aggregability and thromboxane release after rebleeding in patients with subarachnoid hemorrhage.
Serial blood samples were obtained from 80 patients with subarachnoid hemorrhage (SAH) to study adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release. The goal of the investigation was to detect whether reduced platelet function is involved in rebleeds. Seventeen patients (21%) suffered a rebleed, six of those experiencing their first rebleed within 24 hours after SAH. ⋯ Thromboxane release was lower in patients with rebleeds than in the others, both before and after rebleeding, although statistical significance was reached only in samples collected after rebleeds. Patients rebleeding within 24 hours after SAH had lower platelet aggregability (p = 0.037) than patients without a rebleed in the samples taken within 3 days after SAH. The results suggest that reduced platelet aggregability and thromboxane release are involved in rebleeds following primary SAH.
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Delayed cerebral ischemia is the major cause of death and disability in patients who initially survive an aneurysmal subarachnoid hemorrhage (SAH). In the present study, a protocol for prophylactic hypertensive hypervolemic hemodilution ("triple-H" therapy) was utilized in the treatment of SAH, and the response of cerebral blood flow (CBF) was evaluated. Serial CBF measurements, f1 and CBF15, were performed using the xenon-133 inhalation technique to maximize therapy. ⋯ Thirty-six of the 43 patients (84%) were discharged capable of an independent lifestyle. Triple-H therapy is a safe and effective modality for elevating and sustaining CBF after SAH. In combination with early aneurysm surgery, it can minimize delayed cerebral ischemia and lead to an improved overall outcome.
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Review Clinical Trial
Calcium antagonists in the management of patients with aneurysmal subarachnoid hemorrhage: a review.
Cerebral arterial vasospasm and infarction is the leading cause of death and disability among patients who reach a major medical center after aneurysmal subarachnoid hemorrhage (SAH). Recent evidence suggests that two calcium antagonists, nimodipine or nicardipine, may be useful in preventing this important complication of SAH. This paper reviews the current status of these two calcium antagonists in the management of SAH.
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Neurogenic pulmonary oedema followed a subarachnoid haemorrhage secondary to an arteriovenous malformation in an eight-year-old boy. Despite a complicated course, he made a full recovery. Neurogenic pulmonary oedema is rare in childhood. It is sudden in onset, and potentially fatal, but is amenable to prompt and vigorous treatment.
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In 13 patients who had ruptured intracranial aneurysms, serial transcranial Doppler (TCD) and cerebral blood flow (CBF) examinations were performed in order to evaluate the degree of cerebral vasospasm. All patients showed some extent of vasospasm on angiography, which was performed between Day 7 and 10. The flow velocities of either the middle cerebral arteries or the anterior cerebral arteries, measured by TCD, began to increase on post hemorrhage Day 5, and maximum flow velocities were recorded between Day 9 and 13, with normalization occurring within the following 2 weeks. ⋯ However, for judging when vessel narrowing was resolving, the usefulness of the TCD examinations were doubtful. This is because flow velocities measured by TCD are thought to be fairly much influenced by multiple factors such as the change of blood pressure, blood volume, which were caused by the active treatment for the vasospasm. Serial measurements of CBF were also made 2-7 times (mean 3.1 times) during the first two weeks following subarachnoid hemorrhage using the 133Xe intravenous injection method.(ABSTRACT TRUNCATED AT 250 WORDS)