Craniotomy for Tumor Resection Under General Anesthesia

Key Points:

    • Have TIVA ready with Propofol and Narcotic (Remi vs. Sufenta)

    • Titrate paralytic to 2 twitches while in pins

    • Propofol boluses ready in case patient moves


    • The patient's head is placed in a Mayfield pin fixation system to prevent head movement and allow for image-guided stereotactic navigation

    • Patients are usually extubated at the end of the case to obtain a neurologic exam as soon as possible


    • Art line

    • Hot line

    • Plum pumps or syringe pumps for TIVA x 2

    • BIS monitor

    • iSTAT with cartridges

[Non-Standard] Medications:

    • Mannitol (100 gm bag)

    • Remifentanil (2 mg or 5 mg diluted to 50 mcg/mL)

    • Propofol vials x 4 (100 mL)

    • Albumin 5% (250 mL) x 2

    • Labetalol syringe (5 mg/mL)

    • Nicardipine box (for infusion)


    • Normovolemia

    • Normoglycemia

    • Normothermia

    • Maintain CPP

    • PaCO2 25-30 mmHg

    • Avoid hypoxemia

    • Decrease ICP – Head up 20-30˚, Mannitol, Steroids


    • Tests- CBC, CMP, Coags; other tests as indicated by H&P

        • Platelet count should be > 100,000 for nonurgent surgery

        • Type & cross should be completed if tumor invades the cranial sinuses

    • Premedication- avoid midazolam (especially in patients with ­ ICP)

        • Hypoventilation ­ CO2 which ­ ICP and may lower seizure threshold

    • Perform a good physical exam and document any deficits

        • Symptoms of ­ ICP (> 15 mmHg)- headache, N/V, drowsiness, papilledema, seizures, altered LOC

    • Check to see if the patient is on anti-convulsant meds because they alter drug metabolism


  • Anesthetic technique- GETA

  • Position

      • Supine, lateral, sitting or prone based on location of tumor

      • Supratentorial tumors: supine/lateral with patient facing anesthesia. Table turned 90 degrees

      • Posterior fossa: prone/sitting (likely prone at OUMC). Table turned 90-180 degrees

      • The patient's head will be secured a Mayfield-Kees skeletal fixation device by the neurosurgeons.

      • Will usually require a bolus of Propofol prior to securing the pins. Excessive flexion, extension, or rotation of the neck may impair cerebral venous drainage via compression of the internal jugular veins. Head up (20-30 degrees) position is favorable to promote venous drainage and decrease ICP

  • Incision- Linear (small tumors or posterior fossa) or curvilinear (large tumors)

  • Special instrumentation- operating microscope, image-guide navigation

  • Unique considerations- treat as if patient has ­ ICP

      • Maintain normovolemia - an increase in intracranial volume may ­­ ICP

      • Keep BP in normal range for the patient

      • PaCO2 = 25-30 mmHg to achieve less cerebral blood volume (providing better surgical access) + increased cerebral blood flow to ischemic areas

      • Avoid hypoxemia

      • Give Mannitol 0.5-1.0 g/kg over 20 minutes -- can decrease K+; replace as necessary. Careful in patients with CHF, pulmonary edema, or renal failure as the initial elevation in central circulatory volume can be detrimental prior to the diuretic phase

      • Steroids: Dexamethasone 4 mg IV if on chronic replacement; 10 mg IV if naive.

      • Head up 20-30 degrees to promote venous drainage

  • Surgical time- 4-6 hours

  • EBL- 50-500 mL

  • Blood and fluid requirements

      • IV: 16-18 ga x 2

      • NS @ 2-3 mL/kg/h+ 1/2 urine output. If volume is needed, use albumin (crystalloids worsen cerebral edema). If crystalloids are used, isotonic or slightly hypertonic solutions (0.9% sodium chloride) should be used over hypotonic solutions (i.e. lactated ringers) due to the risk of cerebral edema

  • Monitors: standard ASA + arterial line + BIS monitor + NMT monitor

  • Induction

      • Start TIVA (Propofol 100 mcg/kg/min + Remifentanil 0.3 mcg/kg/min) in the closest IV port. Remifentanil is dosed by LEAN body weight. Go to this website to calculate LBW:

      • Induce with Lidocaine + Propofol + Paralytic. Induction should be "slow and controlled" with constant attention on blood pressure. Bag mask ventilate until paralytic is in full effect (check via twitch monitor or by NMT monitor). Hypoventilation and hypercapnia should be avoided.

      • Intubate with minimal stimulation. Confirm bilateral breath sounds and +EtCO2 before working on lines.

  • Maintenance

      • Continue TIVA throughout the case. Some attendings may want 0.3-0.5 MAC of volatile anesthetics for assured amnesia.

      • During the procedure, titrate the twitches/NMT monitor to 2 twitches or less while the patient's head is in pins. Have Propofol boluses ready in case the patient were to move during the procedure

      • Positive end-expiratory pressure (PEEP) should be avoided unless needed to improve oxygenation. PEEP increases intrathoracic pressures and may impede cerebral venous drainage.

  • Emergence

      • Continue the Propofol infusion until the bone flap is secured (always have boluses ready if needed). Stop the remifentanil infusion and reverse the paralytic once the patient is out of pins. May need to work in long acting narcotics as remifentanil can cause a reflexive hyperalgesia

      • Extubate patient when they are spontaneously breathing and start to open their eyes. Do not want the patient coughing on the endotracheal tube because of the risk of increased ICP.

      • Careful control of blood pressure may require the use of labetalol, esmolol, nicardipine, or cleviprex

      • Once procedure is completed, transport the patient to PACU with monitoring and oxygen

  • Complications

      • Neurological deficits -- Quadriplegia from excessive flexion of the head is rare. Make sure the chin does not touch the patient's chest.

      • Tension pneumocephalus -- may delay emergence or cause postop neurologic deficits. CT scan may be necessary for diagnosis

      • Hemorrhage

      • Edema and ­ ICP

      • Venous air embolism (VAE) -- especially in sitting position. 30-75% but usually hemodynamically insignificant. 8-15% cause significant hemodynamic change à arrhythmias, decreased cardiac output, severe pulmonary hypertension, intrapulmonary shunting, hypoxemia, and decreased EtCO2

Dr. Smith's Requests:


    • Table in position prior to start (likely 90 degrees from anesthesia machine)

    • Use a prone pillow for the patient's pillow prior to placing in pins

    • Every line draped over the patient so that lines are organized lengthwise along patient. Be cognizant of the EKG lead placement so that you do not have to relocate them after turning lateral recumbent

    • RN will start working on Foley catheter while you put in lines

    • If there is time, do the arterial line in holding using an ultrasound and local anesthetic to minimize time in the OR

    • Attach 2nd IV to IV extension line and have available but do not hook up to fluids.

    • Place Bispectral (BIS) monitor on patient's forehead after pins are placed.

    • Throughout the case, continue the Propofol gtt at 100 mcg/kg/min unless warranted to increase by the BIS monitor/vital signs (never decrease). Titrate the remifentanil to keep blood pressure within targeted range.

    • Does not like volatile anesthetics during craniotomies

Review Notes

Relevant neuroanatomy

  • Brain tumors are classified by their location (supratentorial vs. infratentorial or intraaxial vs. extra axial)

      • Supratentorium contains paired cerebral hemispheres and the diencephalon that is composed of the thalamus and hypothalamus. Each cerebral hemisphere is divided into 4 lobes: frontal, temporal, parietal, and occipital. Examples: gliomas, astrocytomas, oligodendrogliomas, meningiomas, metastases (lung, breast, kidney)

      • Infratentorium contains the brainstem and the cerebellum. Most common in kids. Examples: medulloblastoma, pilocytic astrocytoma, ependymoma, and brainstem glioma

      • Intra-axial tumors are lesions that are within the brain parenchyma. Examples: astrocytoma, glioblastoma, metastatic tumors, hemangioblastoma, medulloblastoma, PNET

      • Extra-axial tumors are outside the brain. Examples: meningioma, acoustic neuroma, craniopharyngioma

Relevant neurophysiology

  • Cerebral metabolic rate of oxygen consumption (CMRO2) is normally 3-3.8 mL/100g/min (~20% of totally body oxygen consumption) and brain glucose consumption is 5 mg/100g/min (~25% of total body glucose consumption)

  • Normal cerebral blood flow (CBF) is 50 mL/100g/min or 75 mL/min (~15% of cardiac output). CBF is regulated by "flow-metabolism coupling" such that CBF matches changes in CMRO2 very quickly

  • Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) minus either intracranial pressure (ICP) or central venous pressure (CVP) whichever is higher

  • Cerebral autoregulation of blood flow is thought to remain intact between a MAP of about 60-160 mmHg and functions by altering the cerebral vascular resistance (CVR). Dynamic autoregulation in CVR is the "rapid phase" that is demonstrated by the pulsatility changes in systolic blood pressure, whereas static autoregulation is demonstrated by the changes in MAP over longer time periods. Outside the autoregulation limits, CBF is pressure-dependent. Below the lower limit of autoregulation maximal cerebral vasodilation occurs and cerebral ischemia can result. Above the upper limit of autoregulation, maximal cerebral vasoconstriction occurs which leads to an increase in CPP causing a disruption of the blood-brain barrier, cerebral edema or cerebral hemorrhage.

  • Physiologic parameters affecting CBF:

      • CPP as discussed above

      • Arterial carbon dioxide tension (PaCO2) -- CBF is linearly associated with PaCO2 between 20 and 80 mmHg. A change in PaCO2 of 1 mmHg correlates to a change in CBF of 1-2 mL/100g/min. However, a PaCO2 below 20 mmHg causes maximal cerebral vasoconstriction leading to tissue hypoxia and a reflex vasodilation

      • Temperature -- 6-7% decrease in CBF per 1 degree decrease in core temperature

      • IV anesthetics (propofol, etomidate, benzos, and thiopental) decrease CBF and decreased CMRO2. Ketamine increases CBF and CMRO2 and should be avoided. Volatile anesthetics (isoflurane, sevoflurane, and desflurane) are direct cerebral vasodilators and can disrupt the flow-metabolism coupling between CBF and CMRO2 which can lead to a dose-dependent increase in CBF.

  • Intracranial Pressure

        • Normal ICP is 7-15 mmHg. Poor neurologic outcome is associated with prolonged ICP above 20-25 mmHg.

        • The Monro-Kellie doctrine states that "an increase in the volume of one intracranial compartment will lead to a rise in ICP unless it is matched by an equal reduction in the volume of another compartment."

        • The intracranial elastance curve has 3 sections: 1. At low volumes, ICP remains low and relatively constant. 2. When the "elbow" of curve is reached (when compensatory measures are exhausted), small changes in volume lead to moderate changes in pressure. 3. When the critical intracranial volume is reached, the pressure increases exponentially.

        • The most common contributing factor to increased ICP is cerebral edema. Cytotoxic edema is increased intracellular water in the setting of cerebral ischemia. Interstitial edema is caused by increased extracellular fluid in the setting of an intact BBB (i.e. hydrocephalus). Vasogenic edema occurs when there is loss of BBB integrity leading to extracellular water. Vasogenic edema occurs surrounding tumors, abscesses, or contusions. Dexamethasone is only effective at decreasing vasogenic edema by upregulating the expression of proteins for the integrity of the tight junctions between endothelial cells in the brain.

Clinical manifestations of brain tumors:

      • Headache

      • Seizures

      • Focal deficits - weakness, sensory loss, aphasia, visual dysfunction

      • Cognitive dysfunction - mood and memory changes

      • Increased ICP à Cushing's triad (hypertension, bradycardia, and irregular respiration)

Anesthetic management for cerebral tumor resection

      • Goals: hemodynamic stability, sufficient cerebral perfusion pressure (CPP), and avoidance of agents that increase intracranial pressure (ICP)

      • Petersen et al compared 3 anesthetic groups: propofol-fentanyl, isoflurane-fentanyl, and sevoflurane-fentanyl

      • Found that subdural ICP is lower, the degree of cerebral swelling is less pronounced, and CPP is higher in patients anesthetized with propofol compared with isoflurane or sevoflurane


    • Jaffe, R.A., Schmiesing, C.A., & Golianu, B. (2014). Anesthesiologist’s Manual of Surgical Procedures (5th ed.). Philadelphia, PA: Wolters Kluwer.

    • Barash, P. G., Cullen, B. F., Stoelting, R. K., Cahalan, M. K., Stock, M. C., Ortega, R., . . . Holt, N. F. (2017). Clinical Anesthesia (8th ed., 1003-1028). Philadelphia, PA: Wolters Kluwer.

    • Petersen, K. D., Landsfeldt, U., Cold, G. E., Petersen, C. B., Mau, S., Hauerberg, J., . . . Olsen, K. S. (2003). Intracranial Pressure and Cerebral Hemodynamic in Patients with Cerebral Tumors. Anesthesiology, 98(2), 329-336. doi:10.1097/00000542-200302000-00010

    • Holmström, A., & Åkeson, J. (2004). Desflurane Increases Intracranial Pressure More and Sevoflurane Less Than Isoflurane in Pigs Subjected to Intracranial Hypertension. Journal of Neurosurgical Anesthesiology,16(2), 136-143. doi:10.1097/00008506-200404000-00005

    • Fraga, M., Rama-Maceiras, P., Rodiño, S., Aymerich, H., Pose, P., & Belda, J. (2003). The Effects of Isoflurane and Desflurane on Intracranial Pressure, Cerebral Perfusion Pressure, and Cerebral Arteriovenous Oxygen Content Difference in Normocapnic Patients with Supratentorial Brain Tumors. Anesthesiology, 98(5), 1085-1090. doi:10.1097/00000542-200305000-00010

Last Reviewed: 11/04/2018