By Matthew E. Fink, MD
Professor and Chairman, Department of Neurology, Weill Cornell Medical College, and Neurologist-in-Chief, New York Presbyterian Hospital
Smoking is a Risk Factor for Perimesencephalic Subarachnoid Hemorrhage
SOURCE: Mensing LA, et al. Risk factors in patients with perimesencephalic subarachnoid hemorrhage. Eur J Neurol 2014;21:816-819.
Smoking and hypertension are well-documented risk factors for aneurysmal subarachnoid hemorrhage (aSAH), while excessive alcohol consumption is less well documented. The cause of benign perimesencephalic subarachnoid hemorrhage (PMH) is unknown, and this study was undertaken to elucidate the risk factors for PMH.
Seventy-nine patients with PMH, admitted to the University Medical Center Utrecht, were studied and compared to 574 control patients admitted from general medical practices. All participants filled out questionnaires regarding smoking habits, history of hypertension, and alcohol consumption, and odds ratios (ORs) were calculated to assess the association of risk factors and PMH. Adjusted ORs for the occurrence of PMH were 1.7 (95% confidence interval [CI], 1.0-2.8) for smoking cigarettes, cigars, pipes, or any combination of these; 1.1 (95% CI, 0.6-2.0) for hypertension; and 1.1 (95% CI, 0.5-2.1) for excessive alcohol consumption. Similar to aSAH, smoking is a risk factor for PMH, but hypertension and excessive alcohol consumption were not, suggesting a different pathophysiology for PMH compared to aSAH.
Early Intensive Hemodynamic Management May be Beneficial in Poor-Grade
Patients with Aneurysmal Subarachnoid Hemorrhage
SOURCE: Mutoh T, et al. Early intensive versus minimally invasive approach to postoperative hemodynamic management after subarachnoid hemorrhage. Stroke 2014;45:1280-1284.
After aneurysmal subarachnoid hemorrhage (aSAH), and following obliteration of the offending aneurysm, one of the main remaining causes of severe disability and death is delayed cerebral ischemia (DCI). The pathogenesis of cerebral ischemia in this setting is multifactorial and includes vasospasm, microcirculatory dysfunction, microembolism, and cortical spreading depolarization. Systemic hemodynamic insufficiency and low intravascular volume seem to contribute to the development of DCI. Controversy has existed for decades regarding the benefits and risks of invasive hemodynamic monitoring for administration of hemodynamic therapies, and proof of its benefit is lacking from randomized trials. Mutoh et al now present new evidence in a randomized, clinical trial of invasive monitoring and early goal-directed fluid therapy (EGDT) vs standard hemodynamic therapy.
One hundred sixty patients with aSAH, who had their aneurysm obliterated with surgery or endovascular coiling, were randomized to receive early (within 24 hours) EGDT guided by cardiac output monitoring with a transpulmonary thermodilution catheter method (PiCCO) or standard therapy guided by measurements of fluid balance or central venous pressure during hemodynamic therapy in patients with clinical and radiographic indications of DCI. The groups were then compared for the frequency of DCI and outcomes were measured by modified-Rankin score at 3 months.
For all clinical grades combined, there were no significant differences in the rates of DCI between the two groups (33% intensive vs 42% standard; P = 0.33) or in the modified-Rankin score at 3 months (67% intensive vs 57% standard; P = 0.22). However, in patients with poor clinical grade, those who received early intensive therapy had a significantly lower rate of DCI compared to those who received standard therapy (5% vs 14%; P = 0.036), a higher modified-Rankin score at three months (52% vs 36%; P = 0.026), and a shorter length of stay in the intensive care unit (14 days vs 17 days; P = 0.043). Poor grade patients fared better with intensive fluid therapy and monitoring compared to standard therapy.
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