Evidence map›Paper›PMID 27737684›Full record

ReviewCritical care (London, England)2016

Management of delayed cerebral ischemia after subarachnoid hemorrhage.

Charles L Francoeur, Stephan A Mayer

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Critical care (London, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04583163 (Inter- and Intra-Observer Variability in Transcranial Doppler), which is not on this map. Cited by 181 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
181citing papers in PubMed, 11 pooled it
17.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT04583163 terminatednot on this mapstarted 2020, after this paper: background citation

Inter- and Intra-Observer Variability in Transcranial Doppler (TCD) Technique in Neurocritical Care Patients

TypeobservationalSponsorHackensack Meridian HealthRan2020 to 2022Enrolled3ConditionsCerebral Aneurysm, Stroke, Vasospasm, Cerebral, Subarachnoid Hemorrhage, AneurysmalArmsTranscranial Doppler
3 · Its place in the literature

Who cites it

181 citing papers in PubMed, 11 syntheses or guidelines pooled it, 375 citations in OpenAlex.

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121 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Charles L FrancoeurCritical Care Division, Department of Anesthesiology and Critical Care, CHU de Québec-Université Laval, Québec, Canada.
Stephan A MayerDepartment of Neurology (Neurocritical Care), Mount Sinai, New York, NY, USA. stephan.mayer@mountsinai.org.
Mount Sinai Hospital · USUniversité Laval · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For patients who survive the initial bleeding event of a ruptured brain aneurysm, delayed cerebral ischemia (DCI) is one of the most important causes of mortality and poor neurological outcome. New insights in the last decade have led to an important paradigm shift in the understanding of DCI pathogenesis. Large-vessel cerebral vasospasm has been challenged as the sole causal mechanism; new hypotheses now focus on the early brain injury, microcirculatory dysfunction, impaired autoregulation, and spreading depolarization. Prevention of DCI primarily relies on nimodipine administration and optimization of blood volume and cardiac performance. Neurological monitoring is essential for early DCI detection and intervention. Serial clinical examination combined with intermittent transcranial Doppler ultrasonography and CT angiography (with or without perfusion) is the most commonly used monitoring paradigm, and usually suffices in good grade patients. By contrast, poor grade patients (WFNS grades 4 and 5) require more advanced monitoring because stupor and coma reduce sensitivity to the effects of ischemia. Greater reliance on CT perfusion imaging, continuous electroencephalography, and invasive brain multimodality monitoring are potential strategies to improve situational awareness as it relates to detecting DCI. Pharmacologically-induced hypertension combined with volume is the established first-line therapy for DCI; a good clinical response with reversal of the presenting deficit occurs in 70 % of patients. Medically refractory DCI, defined as failure to respond adequately to these measures, should trigger step-wise escalation of rescue therapy. Level 1 rescue therapy consists of cardiac output optimization, hemoglobin optimization, and endovascular intervention, including angioplasty and intra-arterial vasodilator infusion. In highly refractory cases, level 2 rescue therapies are also considered, none of which have been validated. This review provides an overview of current state-of-the-art care for DCI management.

Indexed as

Disease ManagementTime FactorsBrain IschemiaCalcium Channel BlockersHumansHyponatremiaHypotensionHypovolemiaMicrocirculationNimodipineSubarachnoid HemorrhageTomography, X-Ray ComputedUltrasonography, Doppler, TranscranialVasoconstrictor AgentsVasospasm, IntracranialCalcium Channel BlockersNimodipineVasoconstrictor AgentsDelayed cerebral ischemiaMultimodality monitoringSubarachnoid hemorrhageVasospasm

Identifiers

PMID27737684
PMCPMC5064957
OpenAlexW2510973590

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.