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  3. Bedside cerebral microdialysis monitoring of delayed cerebral hypoperfusion in comatose patients with poor grade aneurysmal subarachnoid haemorrhage.
 

Bedside cerebral microdialysis monitoring of delayed cerebral hypoperfusion in comatose patients with poor grade aneurysmal subarachnoid haemorrhage.

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BORIS DOI
10.7892/boris.92280
Date of Publication
December 7, 2016
Publication Type
Article
Division/Institute

Universitätsklinik fü...

Contributor
Patet, Camille
Quintard, Hervé
Zerlauth, Jean-Baptiste
Maibach, Thomas
Carteron, Laurent
Suys, Tamarah
Bouzat, Pierre
Bervini, David
Universitätsklinik für Neurochirurgie
Levivier, Marc
Daniel, Roy T
Eckert, Philippe
Meuli, Reto
Oddo, Mauro
Subject(s)

600 - Technology::610...

Series
Journal of neurology, neurosurgery and psychiatry
ISSN or ISBN (if monograph)
0022-3050
Publisher
BMJ Publishing Group
Language
en
Publisher DOI
10.1136/jnnp-2016-313766
PubMed ID
27927702
Description
BACKGROUND

Delayed cerebral ischaemia (DCI) is frequent after poor grade aneurysmal subarachnoid haemorrhage (SAH). Owing to the limited accuracy of clinical examination, DCI diagnosis is often based on multimodal monitoring. We examined the value of cerebral microdialysis (CMD) in this setting.

METHODS

20 comatose SAH participants underwent CMD monitoring-for hourly sampling of cerebral extracellular lactate/pyruvate ratio (LPR) and glucose-and brain perfusion CT (PCT). Patients were categorised as DCI when PCT (8±3 days after SAH) showed cerebral hypoperfusion, defined as cerebral blood flow <32.5 mL/100 g/min with a mean transit time >5.7 s. Clinicians were blinded to CMD data; for the purpose of the study, only patients who developed cerebral hypoperfusion in anterior and/or middle cerebral arteries were analysed.

RESULTS

DCI (n=9/20 patients) was associated with higher CMD LPR (51±36 vs 31±10 in patients without DCI, p=0.0007) and lower CMD glucose (0.64±0.34 vs 1.22±1.05, p=0.0005). In patients with DCI, CMD changes over the 18 hours preceding PCT diagnosis revealed a pattern of CMD LPR increase (coefficient +2.96 (95% CI 0.13 to 5.79), p=0.04) with simultaneous CMD glucose decrease (coefficient -0.06 (95% CI -0.08 to -0.01), p=0.03, mixed-effects multilevel regression model). No significant CMD changes were noted in patients without DCI.

CONCLUSIONS

In comatose patients with SAH, delayed cerebral hypoperfusion correlates with a CMD pattern of lactate increase and simultaneous glucose decrease. CMD abnormalities became apparent in the hours preceding PCT, thereby suggesting that CMD monitoring may anticipate targeted therapeutic interventions.
Handle
https://boris-portal.unibe.ch/handle/20.500.12422/147554
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