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Anaes TopicsNeuroanaesthesia

Anaes · Neuroanaesthesia

Neuroanaesthesia

Also known as Neuroanaesthesia · Intracranial pressure anaesthesia · Awake craniotomy · Venous air embolism sitting · SS_NS specialised study unit

Exam-pass neuroanaesthesia hub (SS_NS): Monroe-Kellie, CPP=MAP−ICP, agent effects on CBF/CMR, BTF TBI targets, VAE in sitting position, aneurysm rupture plan, awake craniotomy, and leaf links.

medium10 referencesUpdated 26 July 202610 min readVerification in progress

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Practise this topic8 MCQs with explanations

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ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • CPP = MAP − ICP. Hypotension below systolic 90 carried a 150 percent mortality increase in severe TBI — defend MAP/CPP early.
  • Sitting position + open venous sinuses = VAE risk. PFO is a strong relative/absolute contraindication without mitigation; detection hierarchy starts with TOE/Doppler.
  • Prophylactic hyperventilation is outdated for routine TBI — use temporary hyperventilation only for herniation bridge.
  • Volatile agents increase CBF dose-dependently; propofol reduces CBF and CMR — match agent to intracranial compliance.
  • Acute intraoperative brain swelling: deepen anaesthesia, optimise CO2/O2, head-up neutral neck, osmotherapy, surgical communication.
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Your progress

Saved on this device.

Practise this topic8 MCQs with explanations

Target exams

ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • CPP = MAP − ICP. Hypotension below systolic 90 carried a 150 percent mortality increase in severe TBI — defend MAP/CPP early.
  • Sitting position + open venous sinuses = VAE risk. PFO is a strong relative/absolute contraindication without mitigation; detection hierarchy starts with TOE/Doppler.
  • Prophylactic hyperventilation is outdated for routine TBI — use temporary hyperventilation only for herniation bridge.
  • Volatile agents increase CBF dose-dependently; propofol reduces CBF and CMR — match agent to intracranial compliance.
  • Acute intraoperative brain swelling: deepen anaesthesia, optimise CO2/O2, head-up neutral neck, osmotherapy, surgical communication.
The one-line answer

Neuroanaesthesia is cerebral perfusion pressure defence plus brain relaxation. Own the Monro-Kellie doctrine and the equation CPP = MAP minus ICP. Choose propofol-lean TIVA when intracranial compliance is poor, avoid hypoxia and hypotension as the twin secondary insults in TBI, run a venous-air-embolism drill for every sitting case, and never start an awake craniotomy without an emergency airway conversion plan.[6][7]

Meet the patient

A 24-year-old motorcyclist arrives in the emergency department with a GCS of 7 after a head-on collision. His pupils are asymmetric, his blood pressure is 88/50, and the CT shows an expanding extradural haematoma. He needs theatre now — and every minute of hypotension and hypoxia between here and the burr hole is brain tissue he will never get back.[6][3]

Neuroanaesthesia is governed by a single equation and two insults. The equation is CPP = MAP minus ICP — defend it with blood pressure, head-up positioning, and an anaesthetic that does not raise intracranial pressure. The insults are hypoxia and hypotension: in 717 severe-head-injury cases, hypotension (systolic below 90) was associated with a 150 percent increase in mortality, and both insults independently raised morbidity and mortality. Hold those two ideas and every decision below slots into place.[6][7]

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References10ShowHide
  1. [1]Hawryluk GWJ, Rubiano AM, Totten AM, et al. Guidelines for the Management of Severe Traumatic Brain Injury: 2020 Update of the Decompressive Craniectomy Recommendations Neurosurgery, 2020.PMID 32761068
  2. [2]Bou Sleiman V, Benson B, Gumbert S Anesthetic management of neurosurgical emergencies Curr Opin Anaesthesiol, 2025.PMID 40071979
  3. [3]Blacker SN, Burbridge M, Chowdhury T, et al. Intraoperative Anesthetic Care During Emergent/Urgent Craniotomy or Craniectomy for Intracranial Hypertension or Herniation: A Systematic Review J Neurosurg Anesthesiol, 2026.PMID 39793097
  4. [4]Haywood S, Pence R, Mudrakola V Ketamine Use in Acute Brain Injury: Debunking the Myth Emerg Med Clin North Am, 2026.PMID 42342307
  5. [5]Banik S, Rath GP, Lamsal R, Bithal PK Effect of dexmedetomidine on dynamic cerebral autoregulation and carbon dioxide reactivity during sevoflurane anesthesia in healthy patients Korean J Anesthesiol, 2020.PMID 32209963
  6. [6]Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery, 2017.PMID 27654000
  7. [7]Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma, 1993.PMID 8459458
  8. [8]Mirski MA, Lele AV, Fitzsimmons L, et al. Diagnosis and treatment of vascular air embolism. Anesthesiology, 2007.PMID 17197859
  9. [9]Goettel N, Bharadwaj S, Venkatraghavan L, et al. Dexmedetomidine vs propofol-remifentanil conscious sedation for awake craniotomy: a prospective randomized controlled trial. Br J Anaesth, 2016.PMID 27099154
  10. [10]Walker CT, Kim HJ, Park P, et al. Neuroanesthesia Guidelines for Optimizing Transcranial Motor Evoked Potential Neuromonitoring During Deformity and Complex Spinal Surgery: A Delphi Consensus Study. Spine, 2020.PMID 32539292

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