Letter to the Editor. Ketamine sedation for the suppression of spreading depolarizations

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Correspondence Jed A. Hartings: jed.hartings@uc.edu.

INCLUDE WHEN CITING Published online August 3, 2018; DOI: 10.3171/2018.6.JNS18235.

Disclosures The authors report no conflicts of interest.

© AANS, except where prohibited by US copyright law.

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    Ketamine bolus suppresses SDs in a case of severe brain trauma. A 49-year-old man fell 30 feet from a ladder. Upon arrival to our Level I trauma center, he was withdrawing his upper extremities. Head CT scan (left) showed a large subdural hematoma, and the patient was taken emergently to the operating room for hemicraniectomy and hematoma evacuation. A subdural electrode strip was placed on the left inferior frontal gyrus, ICP and tissue oxygen (PtiO2) probes were placed through a bolt in the contralateral hemisphere, and scalp electroencephalography (EEG) monitoring was performed. In the 1st day of postoperative neurointensive care, ICP became progressively refractory to standard treatment, while SDs occurred continuously at electrodes 4–6 of the subdural strip. In order to maximize sedation while preserving arterial pressure, a 1.5-mg/kg intravenous bolus of racemic ketamine was given. The traces (right) show a 9-hour period around this time. Upper trace: Recordings from electrode 5 of the subdural strip show SDs evidenced by the negative deflections (asterisks) in the direct-current electrocorticography (ECoG) study and simultaneous depressions of spontaneous ECoG activity (0.5–50 Hz; second trace). Center trace: EEG study from the C3–P3 channel shows amplitude fluctuations reflecting the depression periods of SD. Similar fluctuations were present in other ipsilateral EEG channels. Note that both ECoG and EEG studies show a dramatic recovery of spontaneous brain activity after ketamine administration, which persists continuously for 2 hours until SDs resume. ICP increased progressively from 55 to 75 mm Hg over the period shown, and mean arterial pressure was maintained at 100–110 mm Hg. Due to the patient’s poor neurological examination results and lack of improvement, the family elected to withdraw care, and the patient died the next day.

References

  • 1

    Carlson APAbbas MAlunday RLQeadan FShuttleworth CW: Spreading depolarization in acute brain injury inhibited by ketamine: a prospective, randomized multiple crossover trial. J Neurosurg [epub ahead of print May 25 2018; DOI: 10.3171/2017.12.JNS171665]

    • PubMed
    • Search Google Scholar
    • Export Citation
  • 2

    Chang LCRaty SROrtiz JBailard NSMathew SJ: The emerging use of ketamine for anesthesia and sedation in traumatic brain injuries. CNS Neurosci Ther 19:3903952013

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 3

    Dreier JPFabricius MAyata CSakowitz OWShuttleworth CWDohmen C: Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: review and recommendations of the COSBID research group. J Cereb Blood Flow Metab 37:159516252017

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 4

    Dreier JPMajor SPannek HWWoitzik JScheel MWiesenthal D: Spreading convulsions, spreading depolarization and epileptogenesis in human cerebral cortex. Brain 135:2592752012

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 5

    Hartings JA: Spreading depolarization monitoring in neurocritical care of acute brain injury. Curr Opin Crit Care 23:941022017

  • 6

    Hartings JAShuttleworth CWKirov SAAyata CHinzman JMForeman B: The continuum of spreading depolarizations in acute cortical lesion development: Examining Leao’s legacy. J Cereb Blood Flow Metab 37:157115942017

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation
  • 7

    Hartings JAStrong AJOkonkwo DOBullock MR: Spreading depolarisations and traumatic brain injury: time course and mechanisms—authors’ reply. Lancet Neurol 11:3893902012

    • Crossref
    • Search Google Scholar
    • Export Citation
  • 8

    Hertle DNDreier JPWoitzik JHartings JABullock ROkonkwo DO: Effect of analgesics and sedatives on the occurrence of spreading depolarizations accompanying acute brain injury. Brain 135:239023982012

    • Crossref
    • PubMed
    • Search Google Scholar
    • Export Citation

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