Reproduced from Newfield P, Cottrell JE, ed. Handbook of Neuroanesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:21, with permission.

  i) Normal ICP is <10 mm Hg.

  ii) When growth of an intracranial lesion is slow, ICP will remain stable for a while because of shunting of cerebrospinal fluid (CSF) into spinal reservoirs and blood into the central vascular system.

  iii) When an increase in volume can no longer be accommodated, a small change in volume can cause a large and rapid increase in ICP, which can quickly lead to herniation and death.

    b) Cerebral perfusion pressure (CPP) and cerebral blood flow (CBF)

  i) CPP is the net perfusion pressure causing blood to flow to the brain (CBF). This can be expressed as: CPP = MAP (mean arterial pressure) – ICP (or central venous pressure (CVP), whichever is greater)

  ii) Autoregulation of CBF (Fig. 139-2A)

(1) Autoregulation is the ability of the cerebral vasculature to maintain relatively constant CBF despite large changes in blood pressure.

(2) Effected via dilation or constriction of the cerebral blood vessels, with some matching (or “coupling”) of flow to metabolism of glucose and cerebral metabolism of oxygen (CMRO₂)

(3) Range for autoregulation

   (a) Historically thought to be between 50 and 150 mm Hg.

   (b) Recent expert opinion is that the MAP for the lower limit of autoregulation (LLA) may be ≥70 mm Hg.

(4) Once the limits of autoregulation are exceeded, flow is dependent on perfusion pressure.

   (a) Areas of the brain that are chronically underperfused may be maximally vasodilated and blood flow will be dependent on MAP.

   (b) Acceptable intra-and postoperative BP must be individualized for each patient based on usual BP readings (1).

(5) Cerebral autoregulation is impaired by the following

   (a) Vascular disease

   (b) Anesthesia

   (c) Tumors

   (d) Disruption in the blood-brain barrier (BBB)

   (e) Medications

   (f) Cerebral Edema

   (g) Trauma

A: The traditional view of CBF autoregulation between MAP 50 to 150 mm Hg. The LLA is more likely ≥70 mm Hg. B: Linear relationship between partial pressure of arterial carbon dioxide (PaCO₂) and CBF for PaCO₂ = 20 to 80 mm Hg. C: PaO₂ and CBF. D: ICP and CBF. Adapted from: Newfield P, Cottrell JE, ed. Handbook of Neuroanesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:113.

  iii) CBF is directly proportional to PaCO₂ between 20 and 80 mm Hg, and tightly coupled regionally (Fig. 139-2B).

(1) Blood vessels in ischemic regions do not react normally to changes in CO₂ levels.

(2) Hypoventilation with hypercarbia may result in a steal phenomenon with increased CBF to normal areas.

(3) Hyperventilation may result in an inverse steal effect with improved CBF to damaged brain areas.

  iv) CBF is inversely affected by PaO₂ (Fig. 139-2C)

  v) CaO₂ and viscosity changes caused by changes in hematocrit will also affect CBF (2).

    c) Cerebral metabolism of oxygen (CMRO₂)

  i) The cerebral metabolic rate for oxygen (CMRO₂) is the brain’s oxygen consumption requirement to maintain normal function and viability.

  ii) Normal coupling between CMRO₂ and CBF is maintained under anesthesia.

  iii) A decrease in CMRO₂ is the basis for most current neuroprotection therapies.

(1) Burst suppression can decrease CMRO₂ by up to 60% from baseline, which is the maximum achievable as the remaining 40% is used for cellular maintenance. Sodium thiopental (STP) has been used for burst suppression in the past, but because it will not be available in the foreseeable future, propofol is the current preferred agent.

(2) Lowering the patient’s temperature will decrease CMRO₂ by 5% to 7% per°C (3).

    d) Blood-brain barrier (BBB)

  i) A barrier between the vascular system and brain tissue that protects the CNS.

  ii) Tight junctions in capillary endothelial cells prevent passage of large, water-soluble, or charged substances between the blood and brain cells.

  iii) Can be disrupted by hypertension (HTN), tumors, drugs, traumatic brain injury (TBI), and disease (e.g., encephalopathies, meningitis, multiple sclerosis)

    e) Cerebral edema

  i) Vasogenic edema

(1) Results from disruption of the BBB that causes protein leakage into extracellular areas

(2) Seen with tumors

(3) Responds to steroids and diuretics

  ii) Cytotoxic edema

(1) BBB is not disrupted, so there is no protein leak.

(2) Not improved with steroid use

  iii) Ischemic edema

(1) Blend of vasogenic and cytotoxic

(2) May have a delayed onset

2) Neuroanesthesia considerations

    a) Preoperative assessment and planning

  i) Recommend discussion with surgeon to assess neurosurgical issues impacting planned anesthetic.

(1) Films should be reviewed for signs of increased ICP or compression or invasion of other structures. Examples include:

   (a) Compression of brain stem by tumor (e.g., large acoustic neuroma) or vascular malformation.

   (b) Large pituitary tumor invading the cavernous sinus, with proximity to the carotid artery (Fig. 139-3)

Reproduced from Newfield P, Cottrell JE, ed. Handbook of Neuroanesthesia. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007:188, with permission.

(2) Underlying structures that may be entered with the chosen surgical approach, especially venous sinuses.

(3) Positioning for best surgical exposure should be discussed with the surgeon.

  ii) Blood should be available in the OR for neurovascular surgeries and others where rapid and extensive blood loss may be likely.

  iii) Preoperative airway management planning is an important aspect of neuroanesthesia.

(1) Difficult airway issues are common in neurosurgical patients, due to concerns such as spinal pathology, presence of a halo fixation device, facial trauma, congenital deformities.

(2) A wide variety of airway devices should be available.

(3) Proceed with rapid sequence induction and intubation if full stomach is expected.

(4) Minimal or no preoperative sedation is best for a patient with increased ICP due to possibility of inducing hypoventilation and intracranial HTN.

  iv) Preoperative discussion with patient.

(1) Prepare patient for frequent serial neurologic exams after the surgery until postoperative stability is assured.

(2) Instruct pituitary surgery patients that if nasal packing is placed at the conclusion of surgery, they must breathe through the mouth.

    b) Intraoperative considerations

  i) Monitoring: In addition to standard ASA monitors, special monitors may be considered for neurosurgical procedures.

(1) Intravascular monitors

   (a) Arterial line monitors are useful for continuous monitoring of blood pressure and to obtain arterial blood for analysis.

     (i) Helpful when large changes in arterial blood pressure are expected and/or undesirable

     (ii) An arterial line may be placed preinduction for patients in whom aggressive BP control is necessary (e.g., ruptured aneurysm).

     (iii) Insert an arterial line for all craniotomies, or if indicated for medical condition of patient.

   (b) Central venous access is useful for monitoring central venous pressures and infusing medications quickly to the central circulation.

     (i) A central venous pressure (CVP) catheter is placed for larger craniotomies, or may be inserted to improve ease of care in ICU postoperatively.

     (ii) Pulmonary artery catheter is used occasionally in patients receiving therapy for vasospasm (to monitor for adverse cardiac effects of hypervolemic hemodilution therapy used in vasospasm), in some sitting craniotomies, or if medically indicated based on patient status.

(2) Neurologic monitors

   (a) The use of BIS monitoring to prevent awareness is controversial. The BIS is not reliable for detection of ischemia in carotid endarterectomy (CEA) (4,5).

   (b) Neurophysiologic monitoring

     (i) Used to ensure the patient’s neurologic status does not change during positioning or surgical approach to the lesion, or if the lesion is in an eloquent brain area

     (ii) If the somatosensory evoked potentials (SSEPs) decrease within a short time after positioning, check the extremity involved for pressure issues.

     (iii) If SSEPs change after a clamp is applied to a vessel, the clamp must be released and the BP may be increased to high normal levels.

     (iv) Increased doses of anesthetic agents will decrease all SSEPs equally; causes should be sought for unilateral changes in SSEPs.

(3) Neuroimaging navigation system (aka wand guidance)

   (a) Correlates the topographic anatomy of the patient’s head to the preoperative MRI or CT scan

   (b) Used to optimize surgical approach and help the surgeon avoid critical structures

   (c) Once frame is attached to the head holder and calibrated, the frame and the system should not be moved. ICP if monitor or CSF drain is already in situ

(4) A urinary catheter is placed for any case longer than 2 to 3 hours, and in all patients with spinal cord injury.

   (a) Positioning

     (i) General considerations (6)

   (a) Surgical approach will be chosen by the surgeon to maximize view while minimizing retraction of brain tissue.

   (b) The patient must be protected during what could unexpectedly become a very lengthy case.

   (c) If table rotation is planned, the patient may be taped to the table across the chest and thighs.

   (d) The position should be as anatomically correct as possible.

   (e) All pressure points should be well padded.

   (f) Ensure there are no restrictive elements on the patient (armbands, rings, and so on).

   (g) Patient access will be limited once the case has started.

     (i) The table will frequently be turned 90 to 180 degrees placing the anesthesiologist at the side or foot of the bed.

     (ii) Secure all lines and tubes completely before draping.

     (iii) The ETT must be well secured to the patient.

(2) Head positioning

   (a) Application of the head holder (“pins”)

     (i) Can cause intense adrenergic stimulation, bradycardia, or even asystole (more likely in children or patients with high vagal tone).

     (ii) Pretreat the patient with narcotic, propofol, esmolol, and/or an increase in gas concentration.

     (iii) Pins may also be used in short cases if wand guidance is planned (e.g., VP shunts, brain biopsy).

     (iv) The horseshoe head holder is not used in cases expected to last longer than 2 hours, due to potential effects of pressure on the scalp.

   (b) Limiting rotation of the head to 45 degrees or less is preferred. If more rotation is required, the shoulder opposite from the direction of the head turn can be “bumped up” with a sandbag, and the table can be rotated after the patient is secured to it.

   (c) Disastrous consequences have been reported from overextension or overflexion of the head and/or neck with resultant inadequate arterial flow to the brain stem and spinal cord. Avoid venous outflow obstruction as well.

(3) Prone position

   (a) For high posterior cervical and occipital surgeries, the head will usually be in pins with arms tucked at the sides.

   (b) In cases where the head is quite flexed, a soft bite block or an oral airway will ensure that the patient does not bite the tongue or occlude the ETT.

     (i) Chin position should be checked and padded as needed; at least two fingerbreadths thyromental distance should be maintained.

     (ii) If peak inspiratory pressures increase after positioning, check for ETT obstruction; surgeon to reposition the head as necessary.

(4) Sitting position

   (a) Used infrequently

   (b) Patients with carotid stenosis may have insufficient CBF in the sitting position

   (c) The arterial pressure transducer should be placed at the level of the Circle of Willis (ear level), as it is possible to for CPP to be undesirably low if BP is adjusted based on the pressure transduced at heart level (every 1″ is ~ 2 mm difference) (1).

  iii) Induction and maintenance

(1) Choice of anesthesia

   (a) GA is used for most intracranial (IC) cases; no difference in outcome has been shown between use of volatile agents vs. total intravenous anesthetic (TIVA) in intracranial cases.

   (b) Awake craniotomies are used for seizure focus resection (lesion in eloquent area), thermal rhizotomy, and deep brain–stimulating electrode (DBS) placement where the patient will be awake intermittently to facilitate placement of the probe.

(2) Anesthetic agents and other medications

   (a) Induction agents

     (i) Intravenous

             1. Propofol (1 to 2 mg/kg) and sodium thiopental (STP, 3 to 5 mg/kg) are acceptable induction agents as both decrease CBF (via vasoconstriction) and ICP and preserve autoregulation.

             2. Etomidate (0.1 to 0.4 mg/kg) decreases CBF and CMRO₂ and may be a reasonable induction agent for patients with unstable cardiovascular status.

             3. Ketamine, long thought to increase ICP, is still generally not used in IC surgery but may be acceptable under certain conditions (7).

     (ii) Inhalation agents are rarely used for induction due to potential increase in CBF and ICP

     (iii) Neuromuscular blockade (NMB)

             1. Usually accomplished with an intubating dose of rocuronium (0.5 to 0.6 mg/kg), vecuronium (0.1 to 0.2 mg/kg), or cisatracurium (0.15 to 0.20 mg/kg).

             2. Succinylcholine may transiently increase ICP; it is contraindicated in some chronic neuromuscular and CNS diseases and in trauma with crush injury which has occurred more than 24 hours earlier.

             3. For most neurosurgeries, repeat dosing of NMB is not necessary after intubation as long as anesthetic depth is maintained; they especially should not be redosed in cases where EMGs or motor evoked potentials (MEPs) are monitored.

   (b) Maintenance

     (i) Intravenous agents

             1. Dexmedetomidine, an α₂ agonist, can be useful in BP control and may decrease the dose of narcotics required.

             2. TIVA is popular for cases requiring MEP monitoring; the use of a volatile agent at ≤1 MAC with a small amount of narcotic will be as effective.

             3. Narcotics do not have clinically important direct effects on CMRO₂, CBF, or ICP

a. Fentanyl, sufentanil, alfentanil, remifentanil, morphine, meperidine and hydromorphone are all acceptable choices in neurosurgery.

b. Ventilation must be adequate to prevent hypercarbia.

     (ii) Inhalation agents

             1. Volatile agents

a. At >1 MAC may increase CBF due to vasodilation.

b. Sevoflurane is least problematic in terms of effects on CBF; isoflurane would be the next best choice (5,8).

c. Desflurane may increase CBF and cause loss of autoregulation, and can also increase ICP through increased CSF production.

             2. Nitrous oxide (N₂O)

a. Use of N₂O in intracranial neurosurgery is controversial.

b. N₂O has been shown to increase CPP (9).

c. However, a recent study shows no difference in outcomes with use of N₂O in aneurysm surgery in patients with subarachnoid hemorrhage (SAH) (10).

d. The increase in CBF from N₂O can usually be overcome by hyperventilation.

e. N₂O will interfere with MEPs and should not be used in cases when they are monitored.

f. N₂O will increase volume of an intracranial air space and if used it may be desirable to turn off near the end of the case before the dura is closed.

g. Endotracheal tube cuff pressures may increase during a long case if N₂O is used.

   (c) Adjuvant agents include

     (i) Mannitol 0.25 to 1 mg/kg

     (ii) Dexamethasone 4 to 10 mg

     (iii) Vasoactive agents

             1. Phenylephrine increases MAP and may cause reflex decrease in HR; it is often used during neuroradiologic procedures, and during STP administration.

             2. Currently, β-adrenergic antagonists or nicardipine are the most frequently used agents to decrease MAP intra-or postoperatively for neurosurgical patients.

             3. Sodium nitroprusside causes vasodilation and impairs autoregulation.

             4. Adenosine is occasionally used in aneurysm surgeries to facilitate clip placement in technically challenging cases by causing short-duration hypotension and possibly asystole. If use is planned, consider application of defibrillator leads to the patient before draping. A 2010 report recommends a dose of 0.3 to 0.4 mg/kg ideal body weight to achieve 45 seconds of profound hypotension.

     (iv) Antibiotics

     (v) Anticonvulsants (phenytoin or fosphenytoin)

     (vi) Desmopressin, vasopressin

     (vii) Hypertonic saline (HS) may rarely be necessary for severe hyponatremia (e.g., SIADH) or cerebral edema.

  iv) Fluid and electrolyte management

(1) Goal is euvolemia (normal CVP), while maintaining normal glucose and electrolyte levels.

(2) Management of intraoperative glucose levels

   (a) Avoid dextrose-containing fluids

     (i) Hyperglycemia worsens outcome in both global and focal ischemia (11,12).

     (ii) Aneurysm patients with SAH who underwent clipping with blood glucose levels >152 mg/dL were more likely to experience postoperative deficits in gross neurologic function (13).

   (b) Current practice is to treat glucose levels >150 to 200; best intraoperative control may be obtained with use of insulin infusion protocols.

  v) Cerebral protection

(1) Neuroprotection entails the use of certain pharmacologic agents or hypothermia to protect the CNS from injury during periods of low blood flow, via decrease in CMRO₂.

(2) The maximum achievable decrease in CMRO₂ has occurred when burst suppression is seen on EEG; however, an isoelectric EEG may not be required for cerebral protection (14).

(3) During a focal ischemic event, STP and propofol may be used to decrease CMRO₂ and afford a measure of neuroprotection; these drugs have not been proven to be effective in global ischemia at clinically useful doses.

(4) Other agents may also decrease CMRO₂ but should not be assumed to be neuroprotective.

(5) Volatile inhalation agents will also decrease cerebral metabolism until the EEG becomes isoelectric, but the dose required to do so (>1.5 to 2 MAC) may increase CBF.

(6) Moderate hypothermia has also been shown to be neuroprotective, at least in global ischemia (15).

   (a) If used during neurovascular cases, the patient may be rewarmed once the lesion has been treated.

   (b) Though hypothermia decreases CMRO₂, a recent large prospective study showed that mild intraoperative hypothermia (33°C) did not improve outcome during hospitalization or at 3 months in good-grade (WFNS score I, II, or III) SAH patients (16,17).

(7) Intraoperatively, begin STP or propofol administration once the risk of an ischemic event is present.

   (a) During aneurysm surgery, this is usually when the aneurysm is visualized but before the surgeon is closely dissecting. If an aneurysm has ruptured preoperatively, a neuroprotective agent may be started on induction.

   (b) Arteriovenous malformations (AVMs) and cavernous malformations are often larger and more complicated lesions, requiring higher total dose.

   (c) Doses of STP over 6 to 10 mg/kg (depending on age, condition, and tolerance) decrease the probability of successful extubation at the end of the case. The relatively short action of propofol means that most patients can be extubated if indicated.

   (d) Once the lesion has been resected or treated, burst suppression can be discontinued if ICP is not grossly elevated.

  vi) ICP management

(1) Can be critical in the perioperative period

(2) Treatment of increased ICP

   (a) Raise head of bed

   (b) Hyperventilation (may sometimes need very high minute ventilation)

   (c) Mannitol; rarely, 3% saline.

   (d) Neuroprotective agents

   (e) Drainage of small amount of CSF if drain is in situ.

  vii) High venous pressures:

(1) May cause excessive intraoperative venous bleeding and obscure surgical field

(2) Treatment

   (a) Ensure no venous compression or restriction of venous drainage in the neck.

   (b) Raise head of bed up to 30 degrees

   (c) Change respiratory parameters (decrease tidal volume, increase respiratory rate).

   (d) Low-dose venodilators (NTG, morphine) can be administered if increased CBF is not a concern, or if deliberate hypotension may be useful.

   (e) Redose neuromuscular blocking agents.

    c) Emergence

  i) Wakeup must be smooth to avoid increase in ICP or CBF.

  ii) Extubation

(1) Most desirable would be to have patient awake at end of case

(2) Extubation under deep anesthesia, when appropriate, may help prevent coughing.

(3) If the ability to maintain an airway could be compromised, it may be prudent to keep the patient intubated until awake.

   (a) Use of larger doses of neuroprotective agents

   (b) Posterior fossa surgeries where CNs 9, 10, and 12 might be injured or edematous

   (c) Cases in which brain stem swelling might be expected (tumor, hemorrhage)

   (d) Lengthy prone cases where dependent edema of the airway is possible

  iii) Watch for BP spikes during emergence and extubation. Treat promptly.

  iv) If a postoperative MRI is planned, remove all metal from the patient (SaO₂ probe, esophageal stethoscope, wires from neurophysiologic monitoring), and replace EMG-wired ETT with plain ETT if patient is to remain intubated.

    d) Postoperative care

  i) Frequent serial neurologic exams should be performed; any postoperative decrement in the exam should prompt immediate investigation as to cause.

  ii) Continue meticulous BP control (systolic < 160) so that recently coagulated blood vessels on and within the brain do not bleed. Keep BP even lower (<120) in AVM patients.

  iii) Nausea and vomiting are especially common after posterior fossa cases; consider prophylactic therapy with antiemetics before emergence.

  iv) Intubated patients may be returned directly to the ICU.

  v) Carry vasoactive agents and/or sedation (propofol) during transport in case of hypo-or hypertension.

  vi) Postoperative neurologic assessment

(1) Assess level of consciousness and mental status.

(2) Check pupillary response.

(3) Perform basic cranial nerve function.

   (a) Eyes follow finger

   (b) Smile

   (c) Gag

   (d) Tongue function

(4) Flexion/extension of all four extremities.

    e) Potential complications

  i) Vasospasm

(1) Usually treated medically with “triple H” therapy (hypertension, hypervolemia, and hemodilution), although a recent study shows that autoregulation may be impaired with hypervolemic hemodilution (18).

(2) Other options include direct intra-arterial administration of calcium channel blockers (injected by the surgeon, or via radiologic catheter), bathing the artery in papaverine solution, or angioplasty.

  ii) Bleeding

(1) Because the posterior fossa is a small space, even a small amount of bleeding can cause serious problems, including compression and herniation.

(2) Watch for somnolence, decreased CN signs such as loss of gag reflex, altered respiratory patterns.

  iii) Venous air embolus (VAE)

(1) Sitting craniotomies and any other case where the operative site is higher than the right atrium carry a clinically significant risk of VAE.

(2) Watch for VAE particularly during turning of flap and bone work, when entry into venous sinuses is most likely.

(3) Preparation for cases with higher risk of occurrence

   (a) Evaluate patients for patent foramen ovale preoperatively.

   (b) Intraoperative monitoring should include precordial Doppler, as well as multiorifice CVC; TEE may be used if available.

   (c) Sensitivity for detection of VAE: transesophageal echo (TEE) > Doppler > PAP and ETCO₂> CVC > BP > ECG

   (d) It may be preferable to use air instead of N₂O.

(4) Signs and symptoms

   (a) Consider VAE if severe hypotension is accompanied by decrease in ETCO₂.

   (b) Pulmonary HTN and right-sided heart failure secondary to rapid entrainment of 100 to 300 cc of air may be lethal (19).

   (c) Right cardiac inflow/outflow obstruction may also be implicated in the mortality from VAE.

(5) Treatment

   (a) Immediate treatment of VAE

     (i) Notify surgeons.

     (ii) Call for help.

     (iii) Surgeons flood operative field with saline.

     (iv) Ensure 100% O₂ with controlled ventilation.

     (v) Attempt to aspirate air from CVC.

     (vi) Change position to have operative site lower than right atrium.

     (vii) Consider application of jugular venous compression.

     (viii) Support blood pressure.

     (ix) Prepare for cardiac arrest.

   (b) Rapid administration of fluids through the central line to increase CVP.

     (i) May help prevent further air entry and force the air into the pulmonary circulation where it can be absorbed (20).

     (ii) Must be weighed against the potential increased risk of paradoxical (arterial) air embolism and the possibility of worsening pulmonary HTN.

  iv) Syndrome of Inappropriate ADH (SIADH)

(1) Seen with many malignancies as well as intracranial processes.

(2) Be suspicious if urine output (UOP) is low relative to IV fluids given, Na + <124, serum Osm < 280, and high urine Osm.

(3) Treat with restriction of fluids, administration of furosemide, and possibly HS if severe.

  v) Diabetes insipidus

(1) Rarely seen intraoperatively but may develop during surgeries of the pituitary or hypothalamus.

(2) Large quantity of dilute urine (<200 mOsm, SG 1.001 to 1.005) with normal or elevated serum Osm and Na+.

(3) Treat with vigorous rehydration with 0.5 NS to match UOP, and 5 to 10 U vasopressin or 1 to 4 μg desmopressin IV.

  vi) Neurogenic pulmonary edema (NPE)

(1) May be due to massive sympathetic activation caused by acute spike in ICP

(2) Prevented by α blockade

(3) Frequently accompanied by pulmonary hemorrhage, probably due to increased pulmonary pressures during the sympathetic release

(4) Incidence of NPE is 50% in patients with severe TBI, and it may also be seen in subarachnoid and intraparenchymal hemorrhage (IPH), as well as status epilepticus.

(5) HPE develops rapidly within hours of initial injury, and often resolves just as quickly, though may have relapsing course.

(6) Treatment is symptomatic; use smaller tidal volumes with increased RR.

  vii) Eye injury

(1) Risk with any surgery on the head and neck

(2) Initial discussion of anesthetic risks may include the potential for postoperative ischemic optic neuropathy especially in patients who will be placed prone.

   (a) Risk may be highest in patients who have substantial blood loss and/or undergo prolonged procedures (>6.5 hours) (20).

   (b) Patients who are diabetic, obese, hypertensive, and smoke may have an incidence as high as 1:100 (21).

   (c) Avoid pressure on the globe, increased venous pressure (a slight head-up position may assist), and overhydration (22).

(3) Ophthalmic ointment may protect against corneal abrasions.

3) Intracranial procedures

    a) Intracranial neuroendovascular procedures

  i) Indications

(1) Diagnostic

   (a) Delineation of size and location of lesions to plan further therapy

(2) Therapeutic

   (a) Detection and treatment of vasospasm

     (i) Transluminal balloon angioplasty is the most effective treatment for vasospasm, whether it is the reason for the angiogram (e.g., post-SAH) or occurs unexpectedly during an angiogram.

     (ii) Treatment occasionally includes intra-arterial injection of vasodilators (papaverine or calcium channel blockers).

   (b) Coiling and embolization procedures

     (i) May be definitive therapy for vascular lesions such as arteriovenous malformation (AVM) or aneurysm.

     (ii) Often used as a staging procedure to decrease size, minimize blood loss and possibility of rupture during a planned resection to follow

   (c) Placement of stents for stenotic lesions, across ruptured vessels, or to direct flow away from a lesion

  ii) General considerations

(1) Patient immobility is critical.

(2) Minimal blood loss is expected.

(3) Monitor I/O: Patients may receive several liters of heparinized flush solution.

(4) An arterial line is needed if treatment is planned.

(5) Do not hyperventilate as this may predispose to vasospasm.

(6) Vasopressor and vasodilator therapy should be immediately available.

(7) Give heparin (70 U/kg) to maintain ACT > 250 if treatment of a lesion is planned; check ACT every hour and redose with partial heparin dose as needed.

(8) It is desirable to have a rapid but smooth awakening at the end of these procedures.

(9) Postoperative pain is minimal.

  iii) Procedures

(1) Diagnostic angiograms

   (a) Consider placing an arterial line and a foley catheter prior to beginning the procedure if treatment of lesion might become possible or necessary.

   (b) Have vasopressor ready to administer, as extremely rapid systemic vasodilatory effect may be seen with intra-arterial vasodilator injection by surgeons.

(2) Aneurysm coiling

   (a) The catheter travels from the femoral artery to the intracranial circulation.

   (b) A pusher wire is threaded through the catheter and numerous platinum coils inserted into the aneurysm where they remain after being disengaged.

(3) Arteriovenous malformations and dural AV fistulas

   (a) Feeding arteries of large vascular malformations and tumors may be embolized preoperatively to decrease bleeding during subsequent resection.

   (b) Neuroembolic agents include particulates and polymer glues, and the newer nonpolymerizing liquid agents.

  iv) Potential complications

(1) Vasospasm

(2) Vessel perforation or rupture with hemorrhage

   (a) Decrease BP and reverse heparin immediately.

   (b) Emergency craniotomy may be required if a stent cannot be placed.

(3) Vessel occlusion

   (a) Treatment is to increase BP to high normal.

(4) Contrast-induced nephropathy

   (a) N-acetylcysteine, 600 to 1200 mg before and after the procedure may be effective in reducing the incidence in patients at risk (23).

    b) Carotid endarterectomy

  i) Indications

(1) CEA is performed to remove a stenotic plaque from the carotid artery and improve blood flow to the brain.

  ii) Surgical Procedure

(1) After the carotid artery is exposed, vessel loops are passed around the carotid divisions (common, external or ECA, internal or ICA).

(2) The common carotid artery is clamped below the lesion; next the ECA and ICA are clamped.

(3) Before clamping the ICA, the surgeon may elect to measure perfusion pressure (“stump pressure”) transmitted to the ICA via the Circle of Willis (Fig. 139-4).

   (a) Needle placed into the ICA after clamping the ECA and common carotid

   (b) A (saline-flushed) sterile high-pressure line is attached to the needle, and the distal end passed to the anesthesiologist to be attached to a stopcock in the arterial line monitoring system.

   (c) If the pressure is <20 to 40 mm Hg (actual number is controversial) or if other monitors (e.g., EEG) indicate ischemia when the ICA clamp is applied, the surgeon may elect to insert a shunt from the common carotid to the ICA to ensure perfusion pressures are adequate.

(4) The common carotid artery is opened, and plaque is stripped off the endothelium at the bifurcation of the common carotid artery into the external and internal branches.

(5) The arterotomy is partially sutured, backflow is allowed in order to flush the artery of air and particulate matter, and the final sutures placed.

(6) The external and internal carotids are unclamped, then the common carotid; the incision is closed.

  iii) Preoperative considerations

(1) Studies support early operation in symptomatic patients, but probably not for asymptomatic patients (5,24).

(2) Preoperative BP should be optimized, as preoperative systolic BP > 180 may be associated with postoperative CVA or death, although no study has yet shown a decrease in operative risk if the BP is controlled preoperatively (25).

(3) It is probably appropriate to proceed in patients with severe bilateral stenosis or frequent symptoms (TIAs) even if HTN is not controlled.

  iv) Intraoperative anesthetic considerations

(1) Choice of anesthesia

   (a) A recent multicenter study found no difference in outcome between general and local anesthesia for CEA (26).

(2) BP Control

   (a) Maintain BP high normal (MAP 20% over baseline, especially if a shunt is used) with phenylephrine infusion.

   (b) Patient should be hydrated to avoid labile BP.

(3) Maintain normocarbia

(4) Clamping of the carotid artery

   (a) Give heparin 70 U/kg just before clamping; reversal of heparin is not usually necessary but choice can be based on ACT results.

   (b) A neuroprotective agent may be infused for burst suppression before clamping if the surgeon requests.

(5) The EEG reflects only cortical events and not ischemia of deeper structures.

  v) Postoperative considerations

(1) Patients with carotid artery disease are often hypertensive preoperatively; higher than normal perfusion pressures may be desirable.

   (a) Postoperative BP control can be difficult; aim for a postoperative systolic pressure of 140 to 160 if appropriate.

   (b) Nicardipine infusion started just before emergence may help prevent BP swings.

(2) Coughing should be treated with small doses of lidocaine or narcotics.

  vi) Potential complications

(1) CVA

(2) MI

(3) Nerve injuries (most commonly hypoglossal, sublingual, or recurrent laryngeal)

(4) Wound hematoma

   (a) If there is any stridor or tracheal deviation, the best course of action may be to bring airway cart into OR, prep the neck and evacuate the hematoma with the patient awake, then perform rapid sequence induction and intubation.

    c) Craniotomy

  i) Tumors

(1) Limit preoperative sedation if ICP is high, there is midline shift, or the patient has signs of impending herniation, and take care to not increase ICP during induction (do not hypoventilate).

(2) Mannitol (0.25 to 1 gm/kg) infused slowly prior to opening the dura.

(3) Moderate hyperventilation (PaCO₂ 25 to 28) will decrease brain swelling in supratentorial tumors (27). Normalize CO₂ once dura is closed to minimize space available for accumulation of blood, fluid, or air.

(4) Acoustic neuromas and tumors of the cerebellopontine angle may compress the brain stem and affect cardiovascular status.

(5) During orbitozygomatic approach the surgeon may exert pressure on the globe, activating the oculocardiac reflex. Treat with anticholinergic agent.

(6) Anticipate extensive blood loss in the resection of large, highly vascular tumors (e.g., hemangiomas, some glioblastomas).

  ii) Vascular lesions

(1) Aneurysm

   (a) Use moderate hyperventilation (ETCO₂) (28–30) until aneurysm is clipped or wrapped.

   (b) Keep BP lower than normal to prevent intraoperative rupture or rerupture.

   (c) A temporary clip may be applied proximally to stop blood flow through the aneurysm, thus easing placement of the permanent titanium clip.

     (i) A temporary clip may be on a vessel that supplies a larger area, which will be at risk for ischemia until the clip is removed.

   (d) Once the permanent clip has been applied, minimize potential for vasospasm.

     (i) Resume normal ETCO₂.

     (ii) Allow BP to rise to normal-to-increased levels (MAP of 90 to 100); maintain this higher BP postoperatively.

   (e) Adenosine administration to cause hypotension or even momentary asystole acts as a “pharmacologic temporary clip.”

     (i) May be used if temporary clip placement is not practicable in large or difficult-to-isolate aneurysms.

     (ii) Defibrillator pads should be placed on the patient during positioning if adenosine may be used.

     (iii) Most commonly recommended initial dose is 12–18 mg followed by up to two more doses.

   (f) If clip location causes occlusion of a perforator artery to the brain stem, thalamus, or other structures, cardiovascular instability or loss of neurologic function may follow.

     (i) An intraoperative angiogram may be performed to confirm exclusion of the aneurysm.

   (g) If intraoperative aneurysm rupture occurs, ensure burst suppression and immediately control BP at MAP 40 to 60 until the surgeon regains control of the vessel. Use shorter-acting agents such as esmolol, nicardipine, sevoflurane, thiopental, and propofol.

(2) Arteriovenous malformation

   (a) Mass of thin-walled blood vessels with direct arterial-to-venous connection without intervening capillaries

     (i) Acts as low resistance circuit (shunt), causing chronic vasodilation with loss of autoregulation in surrounding normal tissue (in order to maintain flow)

     (ii) Up to 10% have an associated aneurysm

   (b) The arterial inflow vessels will be resected first, venous outflow after.

   (c) After AVM resection, the surrounding area that may have been hypoperfused due to the shunt is now exposed to higher CBF.

     (i) This higher CBF in normal tissue may lead to edema or hemorrhage, a situation called normal pressure perfusion breakthrough (NPPB), which can occur intra-or postoperatively.

     (ii) Preoperative embolization decreases the chance of intraoperative hemorrhage and NPPB, and potentially shortens the duration of resection.

     (iii) Treatment of NPPB includes scrupulous control of BP to keep systolic under 110 mm Hg (dexmedetomidine may be a good choice), hyperventilation, increased depth of anesthesia or sedation, mannitol, and diuretics.

   (d) Slow, calm wakeup of these patients will be helpful but must be balanced against the surgeon’s desire for neurologic exam at end of case.

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