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Research paper
Bedside cerebral microdialysis monitoring of delayed cerebral hypoperfusion in comatose patients with poor grade aneurysmal subarachnoid haemorrhage
  1. Camille Patet1,
  2. Hervé Quintard1,2,
  3. Jean-Baptiste Zerlauth3,
  4. Thomas Maibach4,
  5. Laurent Carteron1,
  6. Tamarah Suys1,
  7. Pierre Bouzat5,6,
  8. David Bervini7,
  9. Marc Levivier7,
  10. Roy T Daniel7,
  11. Philippe Eckert1,
  12. Reto Meuli3,
  13. Mauro Oddo1
  1. 1Neuroscience Critical Care Research Group, Departments of Intensive Care Medicine, Centre Hospitalier Universitaire Vaudois (CHUV)—Lausanne University Hospital, Lausanne, Switzerland
  2. 2Department of Anesthesia and Critical Care, University Hospital, Nice, France
  3. 3Department of Radiology, Centre Hospitalier Universitaire Vaudois (CHUV)—Lausanne University Hospital, Lausanne, Switzerland
  4. 4University of Lausanne, Lausanne, Switzerland
  5. 5Department of Anesthesia and Critical Care, University Hospital, Grenoble, France
  6. 6Neuroscience Institute, Grenoble, France
  7. 7Division of Neurosurgery, Clinical Neurosciences, Centre Hospitalier Universitaire Vaudois (CHUV)—Lausanne University Hospital, Lausanne, Switzerland
  1. Correspondence to Dr Mauro Oddo, Department of Intensive Care Medicine, Rue du Bugnon 46—CHUV, Lausanne University Hospital, Lausanne CH1011, Switzerland;mauro.oddo{at}chuv.ch

Abstract

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.

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Footnotes

  • Contributors CP collected the data, performed data analysis and drafted the manuscript; HQ, J-BZ, TM, LC and TS helped with data collection; PB, DB, ML, RTD, PE and RM revised the manuscript and provided important intellectual contribution; MO conceived the study design, supervised data collection and analysis, and revised the manuscript. All authors have read and approved the content of the present manuscript.

  • Funding Supported by research grants from the Swiss National Science Foundation (grant number 32003B_155957) and the Novartis Foundation for Biomedical Research (both to MO).

  • Competing interests None declared.

  • Ethics approval The Ethical Committee of the University of Lausanne.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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