Articles: subarachnoid-hemorrhage.
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Subarachnoid haemorrhage (SAH) following cerebral aneurysm rupture or trauma can result in the induction of secondary ischaemic brain damage via a decrease in microvascular perfusion, a disruption of the blood-brain barrier and consequent vasogenic oedema, and the delayed spasm of the major cerebral arteries (i.e. vasospasm). It is increasingly apparent that oxygen radical-induced, iron-catalyzed lipid peroxidation (LP) within the subarachnoid blood and vascular wall plays a key role in the occurrence of these secondary events. ⋯ Much of its action is mediated by an effect on the vascular endothelium, although it also appears to exert some direct neuroprotection and to inhibit LP in the subarachnoid blood. These actions of tirilazad in experimental SAH are reviewed.
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Transcranial doppler (TCD) ultrasonography is often used to guide the management of patients with subarachnoid hemorrhage (SAH). However, the correlation between increased blood velocity as measured by TCD ultrasonography and angiographic vasospasm was established before the routine use of hypervolemia/hemodilution and administration of nimodipine and did not address blood flow. The relationship of blood velocity as measured by TCD ultrasonography and local cerebral blood flow (LCBF) in SAH managed with these modalities is unknown. ⋯ Furthermore, although focal neurological deficits corresponded with decreased contralateral LCBF in the MCA, increased velocity did not correlate with neurological findings. Therapeutic decisions based solely on blood velocity revealed by TCD ultrasonography might be inappropriate and potentially harmful. Xe/CT studies of LCBF are useful in guiding the management of SAH.
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Randomized Controlled Trial Comparative Study Clinical Trial
Hypermetabolism and increased peripheral release of amino acids after subarachnoidal hemorrhage and its operative treatment.
The metabolic response to surgery for acute subarachnoidal hemorrhage and its modification by amino acid infusions was studied. Thirty patients with acute subarachnoidal hemorrhage were randomly assigned to receive for 12 h either an infusion of glucose and a balanced amino acid solution (1.68 MJ = 400 kcal/d and 0.15 gN.kg-1.d-1; group AA) or a glucose and a solution containing 20% of total nitrogen as alanyl-glutamine (1.68 MJ = 400 kcal/d and 0.15 gN.kg-1.d-1; group ALAGLN). A separate control group received glucose alone (1.68 MJ = 400 kcal/d). ⋯ Also the release of alanine (ALAGLN: 35 +/- 24 mumol/min, AA: 34 +/- 24 mumol/min, and control: 30 +/- 18 mumol/min) and total amino acids (ALAGLN: 133 +/- 131 mumol/min, AA: 125 +/- 98 mumol/min, and control: 112 +/- 72 mumol/min) were similar in all groups. All groups were characterized by a pattern of preoperative hypermetabolism that persisted after the operation. The hypermetabolism was not related to increased peripheral oxygen consumption, since femoral oxygen consumption (VO2) represented only 3% of the whole body VO2-.
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Journal of neurosurgery · May 1996
Randomized Controlled Trial Multicenter Study Clinical TrialEffects of a hydroxyl radical scavenger on delayed ischemic neurological deficits following aneurysmal subarachnoid hemorrhage: results of a multicenter, placebo-controlled double-blind trial.
A water-soluble, novel synthetic compound, AVS ((+/-)-N, N'-propylenedinicotinamide; nicaraven) has no demonstrable vasoactive properties but scavenges hydroxyl radicals in aqueous environmental conditions at neutral pH. Based on the results of preceding experimental and clinical studies showing marked ameliorative effects of AVS on cerebral vasospasm and ischemic brain damage, a multicenter, placebo-controlled double-blind clinical trial was undertaken to verify its beneficial effects on delayed ischemic neurological deficits (DINDs) due to vasospasm and on the overall outcome of patients with subarachnoid hemorrhage (SAH). A total of 162 patients with SAH who had Glasgow Coma Scale scores between 7 and 15 on admission were enrolled in the trial. ⋯ The Glasgow Outcome Scale (GOS) score at 1 month was significantly improved by AVS (p < 0.05, U-test). At 3 months, the difference in the GOS scores between the groups became marginal on U-tests (p < 0.10), but the percentage of good outcome tended to increase, with a relative increase of 20.3% (AVS 76.3%, placebo 63.4%; p < 0.10, chi-square test), and the cumulative incidence of death was significantly reduced (p < 0.05, log-rank test). No significant adverse reaction attributable to treatment was observed. the usefulness of AVS in therapy for SAH is strongly indicated by the fact that the agent significantly ameliorated DINDs, leading to a marked improvement in the GOS scores at 1 month, as well as a reduction in the cumulative incidence of death by 3 months.
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We report two patients who had symptomatic cerebral vasospasm and cardiac failure after aneurysmal subarachnoid hemorrhage and who were treated successfully with intra-aortic balloon pump counterpulsation therapy. Both patients developed congestive heart failure and pulmonary edema while receiving postoperative hypertensive, hypervolemic, hemodilutional (Triple-H) therapy for symptomatic cerebral vasospasm. Both cases of cardiac failure were refractory to maximum pressor and inotropic infusions. ⋯ Both patients have had good long-term outcomes. These two cases illustrate the potential usefulness of the intra-aortic balloon pump as an adjunct to Triple-H therapy in patients with symptomatic cerebral vasospasm and cardiac failure. To our knowledge, this report documents the first clinical application of this adjunctive therapy for vasospasm after aneurysmal subarachnoid hemorrhage.