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Michael N. Diringer

Researcher at Washington University in St. Louis

Publications -  15
Citations -  5622

Michael N. Diringer is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Intracerebral hemorrhage & Glasgow Coma Scale. The author has an hindex of 15, co-authored 15 publications receiving 5067 citations. Previous affiliations of Michael N. Diringer include Barnes-Jewish Hospital.

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Efficacy and Safety of Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage

TL;DR: Hemostatic therapy with rFVIIa reduced growth of the hematoma but did not improve survival or functional outcome after intracerebral hemorrhage.
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Critical Care Management of Patients Following Aneurysmal Subarachnoid Hemorrhage: Recommendations from the Neurocritical Care Society’s Multidisciplinary Consensus Conference

TL;DR: Recommendations were developed based on literature review using the GRADE system, discussion integrating the literature with the collective experience of the participants and critical review by an impartial jury and emphasis was placed on the principle that recommendations should be based not only on the quality of the data but also tradeoffs and translation into practice.
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Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage.

TL;DR: For patients with acute ICH, admission to a neuro vs. general ICU is associated with reduced mortality rate, and not being in a neuro ICU was associated with an increase in hospital mortality rate.
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Progression of Mass Effect After Intracerebral Hemorrhage

TL;DR: Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks,associated with increase in edema.
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Hypoperfusion without Ischemia Surrounding Acute Intracerebral Hemorrhage

TL;DR: CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia.