Residency · Residency · Anesthesiology
Anesthesia for Craniotomy and Supratentorial Tumor Surgery
Preoperative Assessment
Neurologic Evaluation
The preoperative evaluation begins with documenting baseline neurologic status and deficits in motor, sensory, speech, and cognitive function. Tumor characteristics should be reviewed: location, size, and degree of mass effect (including midline shift and hydrocephalus). Symptoms of elevated ICP, such as headache, nausea and vomiting, papilledema, and altered consciousness, must be assessed. The patient's seizure history and anticonvulsant medications should be reviewed, including drug levels and potential interactions. Current steroid use (dexamethasone for peritumoral edema) should be noted.
Imaging Review
MRI defines tumor location relative to eloquent cortex, the degree of mass effect, and any midline shift. CT assessment reveals hydrocephalus, calcification, and hemorrhage. Cerebral angiography or MRA may be needed if a vascular tumor (meningioma or AVM) is suspected.
Key Considerations
Enzyme-inducing anticonvulsants such as phenytoin, carbamazepine, and phenobarbital increase hepatic metabolism of opioids, muscle relaxants (vecuronium and rocuronium), and many other drugs, necessitating dose adjustments. Levetiracetam (Keppra) does not induce significant enzyme activity and is increasingly preferred. Patients on dexamethasone should have their glucose control assessed for steroid-induced hyperglycemia. If mannitol has been used chronically, electrolytes and renal function should be checked.
Anesthetic Goals
Primary Objectives
The primary anesthetic objectives for craniotomy include maintaining hemodynamic stability and adequate CPP, minimizing brain swelling to provide a relaxed brain for surgical exposure, providing a smooth emergence with rapid neurologic assessment capability, and avoiding factors that increase ICP (hypercarbia, coughing, straining, and venous congestion).
Target Parameters
MAP should be maintained within 20% of the patient's baseline, individualized for chronic hypertension. CPP should exceed 60-70 mmHg. PaCO2 should be targeted at 30-35 mmHg for mild hyperventilation to promote brain relaxation. Glucose should be kept below 180 mg/dL, as hyperglycemia worsens neurologic outcomes. Temperature should be maintained at normothermia, avoiding hyperthermia.
Anesthetic Technique
Induction
Propofol (1.5-2.5 mg/kg) is the preferred induction agent because it decreases CMRO2, CBF, and ICP while providing a smooth induction. Fentanyl or remifentanil is added to blunt the hemodynamic response to laryngoscopy. Intravenous lidocaine (1.5 mg/kg) suppresses the cough reflex and attenuates ICP spikes during intubation. Rocuronium (0.6-1.2 mg/kg) provides neuromuscular blockade, with higher doses for rapid-sequence intubation when ICP is elevated. Succinylcholine is avoided if possible due to transient ICP increases, though the clinical significance of this effect is debated.
Maintenance
TIVA is preferred, using propofol (75-150 mcg/kg/min) combined with remifentanil (0.05-0.2 mcg/kg/min). This combination preserves autoregulation and flow-metabolism coupling, does not increase ICP, and is required when intraoperative neuromonitoring (MEPs and SSEPs) is planned. A low-dose volatile agent (below 1 MAC sevoflurane or desflurane) is acceptable when there are no ICP concerns and neuromonitoring is not being used. Nitrous oxide should be added cautiously, as it increases CMRO2 and CBF and should be avoided when there is a risk of pneumocephalus. Neuromuscular blockade is maintained during positioning but may need to be allowed to recover if MEPs are being monitored. Ventilation targets mild hyperventilation (PaCO2 30-35 mmHg).
Brain Relaxation Techniques
A systematic approach to brain relaxation includes mild hyperventilation (PaCO2 30-35 mmHg), osmotherapy with mannitol (0.5-1 g/kg IV) or hypertonic saline (3%, 150-250 mL), head elevation to 15-30 degrees, ensuring venous drainage (head midline, no tight tape on the neck), CSF drainage via lumbar drain or ventriculostomy, TIVA (avoiding volatile agents above 1 MAC), adequate anesthetic depth to prevent coughing and straining, and dexamethasone if not already administered.
| Brain Relaxation Technique | Mechanism | Dose / Parameter | Onset | Caution |
|---|---|---|---|---|
| Hyperventilation | ↓ PaCO2 → cerebral vasoconstriction | PaCO2 30–35 mmHg | Seconds | Risk of cerebral ischemia if prolonged |
| Mannitol | Osmotic diuresis; reduces brain water | 0.5–1 g/kg IV | 15–30 min | Rebound edema; keep osmolality <320 |
| Hypertonic saline (3%) | Osmotic; expands intravascular volume | 150–250 mL IV | 15–20 min | Hypernatremia; central pontine myelinolysis |
| Head elevation | Promotes venous drainage | 15–30 degrees | Immediate | May reduce MAP if hypovolemic |
| TIVA (propofol/remifentanil) | ↓ CMRO2 and CBF | Standard infusion rates | Minutes | Hypotension at high doses |
| CSF drainage | Directly reduces intracranial volume | Lumbar drain or ventriculostomy | Immediate | Risk of herniation if supratentorial mass |
<image>Operating room setup for supratentorial craniotomy showing the patient in Mayfield pin head-holder with the head elevated 15-30 degrees. The illustration labels key elements: arterial line and CVP monitoring, TIVA infusion pumps (propofol and remifentanil), neuromonitoring electrodes, Foley catheter, warming blanket, and the anesthesiologist's view of the monitors including processed EEG, end-tidal CO2, and arterial waveform. An inset shows the brain relaxation checklist with the techniques listed.</image>
Positioning
Supine with Head Turned
This is the most common position for frontal, temporal, and parietal lesions. Pin fixation with a Mayfield head-holder produces a sympathetic response that should be anticipated and treated with additional opioid, propofol bolus, or local anesthetic infiltration at the pin sites.
Lateral/Park Bench
This position is used for temporal and posterior parietal lesions. Proper padding is essential, including an axillary roll and protection of all pressure points.
Sitting Position (Rare for Supratentorial)
The sitting position carries risks of venous air embolism and hemodynamic instability. Precordial Doppler monitoring is required if this position is used.
General Positioning Concerns
The eyes must be taped and protected to prevent corneal injury and ischemic optic neuropathy. The endotracheal tube should be secured with tape rather than ties that could compress the jugular veins. Arms must be padded and positioned to prevent nerve injury.
Intraoperative Seizures
Recognition
Seizures may present as focal or generalized tonic-clonic activity. Intraoperative electrocorticography (ECoG) may detect seizures during awake craniotomy. Under general anesthesia, seizures may manifest as sudden cardiovascular changes, pupillary changes, or unexplained tachycardia.
Management
If the cortex is exposed, irrigating with cold saline can terminate seizure activity. Pharmacologic management includes propofol bolus (0.5-1 mg/kg) or midazolam (2-4 mg IV). For refractory seizures, thiopental, phenytoin (15-20 mg/kg IV loading dose), or levetiracetam (1-2 g IV) may be needed. Throughout seizure management, oxygenation and ventilation must be maintained and the patient protected from injury.
Awake Craniotomy
Indications
Awake craniotomy is indicated for tumor resection near eloquent cortex, including the motor strip and speech areas (Broca's and Wernicke's). The goal is to maximize tumor resection while preserving neurologic function through real-time intraoperative testing.
Technique: Asleep-Awake-Asleep
In Phase 1 (Asleep), general anesthesia is provided for the craniotomy opening, typically using an LMA or ETT with propofol and remifentanil. In Phase 2 (Awake), the patient is awakened for cortical mapping and tumor resection with ongoing neurologic testing of speech and motor function. In Phase 3 (Asleep), general anesthesia is resumed for closure. An alternative technique uses monitored anesthesia care throughout, with dexmedetomidine and remifentanil sedation combined with scalp nerve blocks.
Sedation Agents for Awake Phase
Dexmedetomidine provides cooperative sedation without respiratory depression, making it ideal for awake cortical mapping. Remifentanil is an ultra-short-acting opioid providing the analgesic component during the awake phase. Propofol TCI can be carefully titrated to achieve a drowsy but arousable state. Benzodiazepines should be avoided because they interfere with cortical mapping and produce prolonged sedation.
Complications
Intraoperative seizures occur in 5-20% of cases during cortical stimulation. Airway obstruction is a risk since there is no secured airway during the awake phase. Nausea, vomiting, patient anxiety, and inability to cooperate are additional concerns.
<image>Three-phase illustration of the asleep-awake-asleep craniotomy technique. Phase 1 shows the patient under general anesthesia with LMA, craniotomy being performed. Phase 2 shows the patient awake, talking to the neuropsychologist, performing hand motor tasks and picture naming while the neurosurgeon performs cortical stimulation mapping with numbered tags on the exposed brain surface. Phase 3 shows the patient re-anesthetized for closure. Drug infusion timelines for propofol, remifentanil, and dexmedetomidine are shown below each phase.</image>
Emergence and Extubation
Goals
The goals at emergence are a smooth, rapid awakening that permits immediate neurologic examination while avoiding coughing, straining, and hypertension (which risk intracranial hemorrhage). The patient should ideally be following commands within minutes of surgery completion.
Strategies
Continuing a low-rate remifentanil infusion through emergence blunts the cough response. Lidocaine 1 mg/kg IV before extubation further suppresses coughing. Nausea and vomiting-provoking reversal agents should be avoided when possible. Emergence hypertension is treated with labetalol or esmolol. Deep extubation is generally not recommended because the risk of airway loss is unacceptable in a patient with a head dressing and potential airway edema.
Delayed Emergence
Delayed emergence may result from residual anesthetic effects, hypothermia, metabolic derangements (hypoglycemia or hyponatremia), postoperative hemorrhage, cerebral edema, pneumocephalus, or new neurologic deficit from surgical injury. A CT scan should be obtained if emergence is significantly delayed or unexpected.
Postoperative Considerations
Monitoring
Patients require ICU or step-down unit admission with frequent neurologic checks (every 1-2 hours for 24 hours). Blood pressure management requires avoiding both hypertension (hemorrhage risk) and hypotension (ischemia risk). Seizure prophylaxis is continued perioperatively. Pain management uses acetaminophen and carefully titrated opioids, with caution to avoid over-sedation that could mask neurologic changes.
Complications
The most feared postoperative complication is intracranial hemorrhage, which presents as sudden neurologic decline. Cerebral edema peaks at 48-72 hours postoperatively. Other complications include seizures, CSF leak, cranial nerve deficits, and tension pneumocephalus (especially after posterior fossa surgery in the sitting position or after dural closure when N2O was used).
Clinical Pearls
TIVA with propofol and remifentanil is the gold standard anesthetic for most craniotomies, particularly when neuromonitoring is needed. Brain relaxation requires a systematic approach: head position, PaCO2, osmotherapy, and venous drainage should all be addressed before requesting surgical CSF drainage. Enzyme-inducing anticonvulsant effects are clinically significant; patients on phenytoin or carbamazepine may require higher doses of muscle relaxants and opioids. During awake craniotomy, dexmedetomidine provides cooperative sedation without respiratory depression, making it ideal for the awake mapping phase. Postoperative hypertension should be treated promptly because the risk of intracranial hemorrhage is highest in the first 6 hours after craniotomy. Nitrous oxide should never be used after dural closure in neurosurgery due to the risk of tension pneumocephalus.
References
- Dinsmore J. Anaesthesia for elective neurosurgery. British Journal of Anaesthesia. 2007;99(1):68-74.
- Pasternak JJ, Lanier WL. Neuroanesthesiology update. Journal of Neurosurgical Anesthesiology. 2018;30(2):106-145.
- Hervey-Jumper SL, Li J, Lau D, et al. Awake craniotomy to maximize glioma resection: methods and technical nuances over a 27-year period. Journal of Neurosurgery. 2015;123(2):325-339.
- Cottrell JE, Patel P, eds. Cottrell and Patel's Neuroanesthesia. 6th ed. Elsevier; 2017.
