Neurologic system
A Arteriovenous malformation neurosurgery
Arteriovenous malformations (AVMs) are congenital, intracerebral networks in which arteries flow directly into veins. Patients with these malformations generally are younger than those with aneurysms. Patients may have bleeding or seizures or, less commonly, ischemia resulting from “steal” from normal areas or occurring with high-output congestive heart failure.
The anesthetic problems parallel those associated with patients undergoing aneurysm surgery. Notably, AVMs do not autoregulate their blood flow. The operation is likely to be longer and bloodier than that of aneurysm clipping. Surgery may be preceded by an attempt at embolization by the neuroradiologist to diminish the risk of surgery. The neurologic examination should be repeated after embolization to document new deficits that otherwise might be attributed to anesthesia and surgery.
B Awake craniotomy
In a small percentage of patients (those in whom a seizure focus may be suppressed during general anesthesia or may be adjacent to an area of eloquent cortical function), awake craniotomy may be necessary. Awake craniotomy is the most reliable method to ensure neurologic integrity in cerebral gliomas that infiltrate or come close to the eloquent areas of the brain. It allows for the localization of eloquent cortical areas by electrical stimulation and epileptic foci through cortical recordings. Continuous monitoring of the functional integrity of the brain in awake patients is inherently protective while surgical removal of the gliomatous tissue is performed.
a) Patient selection: To minimize the risk of intraoperative complications, contraindications for awake craniotomy include developmental delay, lack of maturity, an exaggerated or unacceptable response to pain, a significant communication barrier, and a failure to obtain patient consent. Only patients who have the ability to clearly understand risks and benefits and, in the opinion of the neurosurgeon, will cooperate during surgery should be considered as candidates for an awake craniotomy. Seizure management should be optimized with acceptable levels of antiepileptic medications verified.
b) Patient teaching: The single most important element in successful awake craniotomy is a highly motivated, well-informed patient. Each step of the procedure is discussed with the patient and family. Special emphasis is paid to prolonged surgical procedure, positioning, head immobility, pain anxiety, monitoring, noise, seizure management, and any individual considerations.
a) Upon arrival to the holding area, an intravenous (IV) line is established.
b) Preanesthesia medications (antibiotics, steroids, antiemetic prophylaxis, and anticonvulsants as indicated) are administered.
c) In the operating room suite, the application of noninvasive monitoring is completed.
d) The patient is induced with propofol. Some sources use either dexmedetomidine singly or in combination with propofol.
e) After satisfactory general anesthesia is established, a laryngeal mask airway (LMA) is placed with patient ventilation controlled using a continuous propofol infusion.
f) Invasive monitoring is established (arterial line, central line), and a urinary catheter is placed.
g) The scalp is anesthetized with 0.5% bupivacaine, and the head is placed in a pinion head holder.
h) The patient is carefully positioned with all bony surfaces padded.
i) The patient is carefully secured to the table to minimize a sense of falling when the table is moved during the awake phase of the surgery. Frameless stereotaxis registration is accomplished.
j) Depending on the preoperative radiographic edema findings, hypertonic saline or mannitol is given.
k) During the draping, an area is constructed around the patient’s face such that the face may be clearly seen and accessed.
l) A light is introduced under the drapes to keep the patient from darkness.
m) During the scalp opening, spontaneous ventilation is established. Before bone flap removal, the LMA is removed and verbal contact established.
(1) All sedation is stopped. All issues regarding patient comfort and concerns are addressed before the incision of the dura.
(2) Conversation with the patient is confined to the surgeon and one member of the anesthesia team.
(3) Stimulation of eloquent areas is carried out with results noted.
(4) Any seizures are controlled with propofol. After the stimulation and mapping, volumetric surgical removal of the tumor or seizure focus is accomplished with interval monitoring.
(5) Upon completion of the surgical removal and requisite monitoring, propofol sedation may be restarted and titrated to patient preference. Sedation is discontinued upon conclusion of surgery.
(6) The most common complications associated with awake craniotomy are pain, seizures, nausea, and confusion.
C Cerebral aneurysm
Cerebral aneurysms are abnormal, localized dilations of the intracranial arteries. They are classified as berry or saccular, mycotic, traumatic, fusiform, neoplastic, or atherosclerotic. Rupture of a saccular aneurysm is a leading cause of subarachnoid hemorrhage (SAH).
Approximately 5 million people in North America have cerebral aneurysms, with approximately 30,000 new cases of SAH occurring annually. The peak age for rupture of a cerebral aneurysm is 55 to 60 years. Aneurysmal ruptures are more common in women, occurring in three women for every two men.
More than one-third of patients with SAH die or develop significant and lasting neurologic disabilities before they receive any treatment. A small bleed occurs in approximately 50% of patients and is often tragically ignored or misdiagnosed. Even in patients who receive prompt care, only half remain functional survivors; the other half of patients die or develop serious neurologic deficits.
Aneurysms may arise at any point in the circle of Willis. The most common locations of aneurysms are shown in the following table. Most aneurysms are broad based and located in the middle cerebral system. Traumatic aneurysms develop as a result of direct trauma to an artery with injury to the wall.
Mirror aneurysms of the internal carotid system are common, and other combinations of locations occur (see table below). The site of the bleeding aneurysm is best located by computed tomography (CT) studies, evidence of vasospasm in the immediate vicinity, and lobulation of the aneurysm wall on angiographic studies.
Location and Occurrence of Cerebral Aneurysms
| Location | Occurrence (%) |
| Internal carotid | 38 |
| Anterior cerebral system | 36 |
| Anterior communicating junction | 30 |
| Internal carotid at posterior communicating junction | 25 |
| Middle cerebral system | 21 |
| Vertebrobasilar system | 5 |
From Frost AEM: Management of neurosurgical anesthesia: aneurysms. Curr Rev Clin Anesth 1991; 11:125-132.
b) Diagnosis of subarachnoid hemorrhage: Subarachnoid hemorrhage produces an abrupt intense headache in 85% of patients, and transient loss of consciousness may be seen in up to 45% of patients. Nausea and vomiting, photophobia, fever, meningismus, and focal neurologic deficits are common. The severity of an SAH can be graded clinically with the use of classifications listed in the table on pg. 372. Although surgical mortality rates vary somewhat among institutions, patients with a neurologic grade I SAH generally undergo surgical clipping with a low mortality rate (less than 5%), but grade V patients generally do not survive.
Hunt’s Classification of Patients with Intracranial Aneurysms According to Surgical Risk
| Grade | Perioperative Criterion | Mortality Rate (%) |
| I | Asymptomatic or minimal headache and slight nuchal rigidity | 0-5 |
| II | Moderate to severe headache, nuchal rigidity, no neurologic deficit, possible cranial nerve palsy | 2-10 |
| III | Drowsiness, confusion, or mild focal deficit | 10-15 |
| IV | Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances | 60-70 |
| V | Deep coma, decerebrate rigidity, moribund appearance | 70-100 |
From Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28:14.
Hypertension often accompanies acute SAH and is postulated to develop secondary to autonomic hyperactivity, which may increase transmural pressure in the aneurysmal sac. Transmural pressure is defined as the differential pressure between mean arterial pressure (MAP) and intracranial pressure (ICP) and represents the stress applied to the aneurysm’s wall.
Increases in blood pressure directly increase the transmural pressure and the likelihood of bleeding; conversely, reductions in blood pressure reduce transmural pressure. Caution should be exercised when purposefully reducing transmural pressure because cerebral autoregulation may be impaired after SAH, and a reduction in blood pressure may induce or aggravate cerebral ischemia, particularly if vasospasm is present. To balance these opposing concerns, many neurosurgeons attempt to maintain systolic blood pressure between 120 and 150 mmHg before clipping the aneurysm.
Electrocardiographic (ECG) changes are common after SAH and have been reported to occur in 50% to 80% of patients. The most common changes involve the T wave or the ST segment, but other changes such as the presence of a U wave, QTc-interval prolongation, and dysrhythmias may be present. Whether such changes in the ECG represent myocardial injury has long been debated. In the majority of patients, these changes do not appear to be associated with adverse neurologic or cardiac outcomes.
Rebleeding from a previously ruptured aneurysm is a life-threatening complication. The incidence of rebleeding is approximately 50% in the first days after SAH, and rebleeding is associated with an 80% mortality rate. The chance of rebleeding from an unsecured aneurysm declines over time, and by 6 months, the risk stabilizes at approximately 3% per year. Approaches used to decrease the risk of rebleeding include early surgical clipping, the use of antifibrinolytic agents, and blood pressure control.
(a) Vasospasm is reactive narrowing of cerebral arteries after SAH. Although arterial narrowing may be detected with angiography in 60% of patients, only half of these patients develop clinical symptoms. The accompanying neurologic deterioration, arising from impaired cerebral perfusion, ischemia, and secondary infarction of the brain, peaks between the fourth and ninth days after SAH and resolves over the following 2 to 3 weeks.
(b) Successful treatment of vasospasm depends on the maintenance of adequate cerebral perfusion pressure (CPP). This is accomplished with expansion of the intravascular volume, which augments blood pressure and cardiac output, avoidance of hyponatremia, and preservation of relative hemodilution (hematocrit approximately 32%). Because of the risk of rebleeding, both hypertension and hypervolemia are used with caution in the period preceding surgical correction.
(c) Pharmacologic vasodilatation of spastic vessels has been ineffective because vasospasm involves a structural alteration in the vessel wall rather than just a spastic contracture or failure of relaxation of the smooth muscle cells in the media of the vessels. Nimodipine and nicardipine (calcium channel blockers) are currently in wide use for prevention of delayed neurologic deficit after SAH. They diminish the level of myoplastic calcium in smooth muscle cells and impede the entry of extracellular calcium necessary for the contraction of the smooth muscle. Recent literature supports a role for magnesium as possible vasospasm prophylaxis.
The presence or absence of vasospasm on angiographic studies has frequently determined the timing of aneurysmal surgery. Current neurosurgical practice suggests that a good outcome is achieved with early operation (within 24 to 48 hours) in patients who are neurologically intact (grade I or II) regardless of whether vasospasm has been demonstrated. Such emergency intervention decreases the likelihood of rebleeding. Only 53% of grade III patients achieve a good outcome after early surgery; this indicates that the gross neurologic condition preoperatively is the best prognostic indicator of intact survival. In the first few days after hemorrhage, the brain is swollen, soft, hyperemic, and prone to contusion and laceration. Impaired autoregulation may decrease cerebral tolerance to brain retraction. Although removal of a subarachnoid clot probably decreases the incidence and severity of delayed arterial narrowing, operative management may be hazardous. In more severely injured patients (grades III through V), surgery is often delayed in anticipation of resolution of vasospasm and improvement in neurologic status.
Endovascular coiling has been used increasingly as an alternative to neurosurgical clipping for treating SAH secondary to aneurysm rupture. The risk of late rebleeding is low. However, there is an increased risk of bleeding after endovascular coiling than after neurosurgical clipping.
a) The baseline neurologic status must be ascertained. The level of consciousness may vary from perfect alertness to deep coma and is an important prognostic factor for the postoperative state. Evidence of increased ICP should be elicited preoperatively so that it can be managed appropriately intraoperatively. Focal motor and sensory signs may indicate intracerebral extension of SAH, vasospasm, or cerebral edema.
b) Pulmonary complications, such as pneumonia, neurogenic pulmonary edema, and atelectasis, are not uncommon and are potentially treatable. Patients often have an increased risk of aspiration because of their depressed level of consciousness, and measures should be taken to reduce gastric acidity and volume preoperatively. The use of prophylactic hypervolemia also increases the likelihood of pulmonary edema.
c) The hemodynamic status of the patient should be assessed, with particular attention paid to the relationship between neurologic deterioration and blood pressure changes. Continuous arterial blood pressure monitoring is essential. Serious dysrhythmias or evidence of ventricular dysfunction should be diagnosed preoperatively so that appropriate monitoring and management can be instituted.
d) The syndrome of inappropriate antidiuretic hormone (SIADH) and diabetes insipidus (DI) can occur in patients with SAH. Preoperative electrolyte studies should be examined to facilitate intraoperative management.
e) The presence of blood in the subarachnoid space may produce a 1° C to 2° C elevation of body temperature. Temperature elevation increases cerebral oxygen requirements and therefore should be treated to prevent an increase of cerebral ischemia.
f) Preoperative sedation is rarely necessary in these patients. Depression of ventilation associated with opioids, barbiturates, and benzodiazepines may result in hypercapnia with resultant increases in cerebral blood flow (CBF) and ICP. Additionally, the reduced level of consciousness preoperatively and postoperatively may make clinical assessment difficult. If preoperative sedation is considered necessary, a small dose of a benzodiazepine (midazolam) with continued observation after its administration is probably the best choice.
g) A type and cross with blood readily available to administer is necessary.
a) The maintenance of adequate intravascular volume requires two large-bore IV cannulas.
b) Intraoperative monitoring includes continuous ECG (V5), arterial pressure monitoring, peripheral nerve stimulator, central venous pressure (CVP) monitoring, electroencephalogram (EEG), end-tidal CO2 (etco2) monitoring, pulse oximetry, and monitoring of temperature and fluid balance.
c) The anesthetic induction should be slow and deliberate. The anesthetic depth should be sufficient to avoid the hypertensive responses that accompany laryngoscopy and endotracheal intubation.
d) Anesthesia is induced with titrated doses of either thiopental or propofol. The addition of an opioid (5 to 10 mcg/kg of fentanyl or 1 to 2 mcg/kg of sufentanil) and IV lidocaine (1.5 mg/kg) further blunts the patient’s response to sympathetic stimulation of laryngoscopy and intubation.
e) An additional dose of opioid or propofol is required for the placement of the three-point pin head holder.
f) Prior injection of local anesthetic minimizes the associated sympathetic stimulation. Isoflurane may be introduced after hyperventilation before laryngoscopy to increase the depth of anesthesia.
g) Ventilation is controlled with administration of 100% oxygen to achieve a Paco2 of 35 to 40 mmHg with normal intracranial compliance.
h) Mild hyperventilation (Paco2 of 25 to 30) is instituted when intracranial compliance is decreased and ICP is increased. Long-term maintenance of hypocarbia results in poor neurologic outcomes in patients with increased ICP.
i) Intubation can be accomplished with 1 mg/kg of rocuronium.
j) The patient is placed in one of several positions, depending on the site of the aneurysm.
(1) Aneurysms that arise from the anterior part of the circle of Willis require that the patient be supine for a frontotemporal approach.
(2) The lateral position for a temporal approach is required for aneurysms that arise from the posterior aspect of the basilar artery. Aneurysms that arise from the vertebral artery or from the lower basilar artery require a sitting or prone position for a suboccipital approach.
(3) Aneurysms that arise from the anterior communicating artery are usually approached from the right; those from the middle cerebral and posterior communicating arteries are approached from the side on which the aneurysm is located.
k) Anesthesia is maintained with air and oxygen or N2O and oxygen, with incremental titrated dosages of an opioid (fentanyl, alfentanil, or sufentanil) or an infusion of remifentanil and a muscle relaxant. Isoflurane may also be added in inspired concentrations not to exceed 1%.
l) Controlled hypotension is commonly used intraoperatively to make aneurysms softer and more pliable at the time of clipping, as well as to minimize blood loss should aneurysmal rupture occur at this time. Sodium nitroprusside and an inhalation anesthetic agent are the drugs most widely used for induction of hypotension.
m) The safe limit of controlled hypotension has not been definitively established. Because autoregulation is maintained to a MAP of 50 to 60 mmHg, some argue that this limit should not be exceeded. In addition, because patients with poor-grade aneurysms may not have intact autoregulation, some argue that a lower limit of 60 mmHg should be adopted. Limits of autoregulation are shifted to higher pressures in patients with preexisting hypertension, so MAP should probably be kept within 40% of baseline. Higher blood pressure maintenance is necessary to avoid cerebral hypoxia if the patients head is elevated.
n) Many neurosurgeons now routinely use temporary proximal occlusion of the parent vessel rather than induce hypotension to facilitate clip ligation of the neck of the aneurysm.
o) The use of mild intraoperative hypothermia has been advocated for cerebral protection during periods of temporary occlusion.
p) At the conclusion of the anesthetic procedure, patients with low-grade aneurysms may be extubated in the operating room, although care must be exercised so that coughing, straining, hypercarbia, and hypertension are avoided. Propofol, lidocaine, or small doses of fentanyl may be used for short-term anesthesia as the procedure is being finished and for reducing the hemodynamic responses to extubation.
q) Although the residual depressant effects of opioids may be reversed with judicious titrated dosages of naloxone, larger doses of naloxone can be hazardous because they may cause sudden, violent awakening of the patient and marked increases in systemic blood pressure.
r) Endotracheal tubes (ETTs) should be retained in patients with high-grade aneurysms and in those who have had intraoperative complications because these patients will probably require postoperative ventilation.
a) Postoperative care is directed at the prevention of vasospasm via the maintenance of intravascular volume expansion and moderate hypertension (MAP of 80 to 120 mm Hg).
b) Changes in the level of consciousness and development of focal neurologic deficits are usually early signs of vasospasm. These clinical signs should be aggressively managed with hypertension, hypervolemia, and hemodilution. Dopamine may be used for blood pressure support. CT should be used for ruling out other causes of neurologic deterioration, including rebleeding, infarction, and hydrocephalus.
Intraoperative aneurysmal rupture can be catastrophic. An abrupt increase in blood pressure during or after induction of anesthesia may indicate that an aneurysm has bled.
a) The use of propofol or 0.5 to 1 mcg/kg of sodium nitroprusside decreases the transmural pressure of the aneurysm, although hypotension can be detrimental at this juncture.
b) Intraoperative aneurysmal rupture necessitates maintenance of the MAP between 40 to 50 mm Hg or lower to facilitate surgical control of the neck of the aneurysm or the parent vessel.
c) Alternatively, one or both carotid arteries may be compressed for up to 3 minutes to produce a bloodless field.
d) Blood that is lost should be continuously replaced with blood, blood products, or colloid solution so that intravascular volume is maintained.
e) A propofol drip or small bolus may be administered immediately before the aneurysm clipping to decrease the cerebral metabolic rate of oxygen consumption.
D Cranioplasty
Cranioplasty can be performed for a bony tumor resulting from traumatic injury (e.g., depressed skull fracture) or, more rarely, from a condition resulting from a congenital malformation (e.g., fused suture lines). These defects may occur anywhere on the head, so the surgical procedure may take place with the patient in varying positions such as supine, sitting, prone, or supine with the head turned. Patients range widely in age from newborn to elderly.
These are individualized according to the patient’s need.
Complete blood count (CBC), electrolytes, blood urea nitrogen, creatinine, glucose, prothrombin time, and partial thromboplastin time (D-dimer or fibrin split products if disseminated intravascular coagulation needs to be ruled out) are used. Type and crossmatch (for at least 2 units). Arterial blood gases are measured if the patient is being ventilated.
a) Monitoring equipment: Standard. An arterial line and central line are used if suggested by the patient’s history. Foley catheter is indicated if surgery is scheduled for more than 2 hours. Some patients may have an ICP monitor in place, and ICP monitoring should be continued intraoperatively.
b) Additional equipment: Determine the patient’s position during surgery. If the patient is supine or supine with the head turned, a foam support aids in positioning the head. Longer ventilation tubing is often needed because the table will be rotated 90 to 180 degrees. When the patient is in the sitting position, a Doppler device and a central line (with a 60-mL syringe attached) are needed to assess and treat venous air embolism (VAE). With the prone position, use prone foam rest shoulder rolls and multiple pads. In all cases, a nasal ETT assists in clearing the surgical field and in stabilizing the ETT. However, if traumatic injury to the facial structures or sinus has occurred, nasal instrumentation should be avoided.
c) Drugs and tabletop: Thiopental and etomidate are useful in cranioplasty because of their cerebral protective properties. Propofol is known to decrease ICP. Most surgeons desire to administer antibiotics during surgery, and they may be helpful.
d) Blood and fluid requirements: Glucose-containing solutions are best avoided in neurologic surgery. It is better to err on the side of underhydration. Fluid is usually replaced with normal saline or lactated Ringer solution at 2 to 4 mL/kg/hr. Blood loss may be substantial, and blood should be immediately available to avoid hypotension or crystalloid overload.
a) Induction is IV, with one of the agents known to decrease ICP. In severe trauma, one may wish to use only oxygen, narcotic, and muscle relaxant.
b) For maintenance, keep the patient’s mean arterial blood pressure slightly below the baseline and maintain normocarbia to slight hypocarbia.
c) A constant infusion of thiopental, etomidate, or propofol with or without inhalation of isoflurane will help to maintain cerebral perfusion and will minimize the cerebral oxygen consumption.
d) Muscle relaxation is not necessary if the procedure is confined to the skull, and the head is immobilized with tongs or some other type of fixator.
e) Most practitioners leave the ETT in place until the neurologic status is certain to allow for regular respiration. Lidocaine is useful in minimizing cough.
Assess postoperative neurologic functions. Pain in patients with altered neurologic status is usually controlled with parenteral agents. Avoid hypercarbia in neurologic patients receiving opiates because it increases CBF and ICP.
E Craniotomy
Intracranial masses may be congenital, neoplastic (benign, malignant, or metastatic), infectious (abscess or cyst), or vascular (hematoma or malformation). Most, but not all, anesthetics can be used safely in patients with cerebral lesions. The effects of the agent on ICP, CPP, CBF, CMRo2 (cerebral metabolic rate of oxygen), promptness of return of consciousness, drug-related protection from cerebral ischemia or edema, blood pressure control, and compatibility with neurophysiologic monitoring techniques are important considerations.
Most craniotomy surgery in the United States today is performed after a propofol induction of anesthesia with intubation of the trachea after a nondepolarizing relaxant. Maintenance of anesthesia is commonly accomplished with a combination of an inhalation agent (usually isoflurane) and narcotic such as fentanyl, sufentanil, or alfentanil in various combinations during maintenance of low normocarbia.
a) The clinical signs of a supratentorial mass include seizures, hemiplegia, and aphasia. The clinical signs of infratentorial masses include cerebellar dysfunction (ataxia, nystagmus, dysarthria) and brainstem compression (cranial nerve palsies, altered consciousness, abnormal respiration). When ICP increases, frank signs of intracranial hypertension can also develop.
b) Preanesthetic evaluation should attempt to establish the presence or absence of intracranial hypertension. CT or magnetic resonance imaging (MRI) data should be reviewed for evidence of brain edema, midline shift greater than 0.5 cm, and ventricular size. A neurologic assessment should evaluate the current mental status and any existing neurologic deficits.
c) Medications prescribed for the control of ICP (corticosteroids, diuretics) and anticonvulsant therapy should be reviewed. Laboratory evaluation should rule out corticosteroid-induced hyperglycemia and electrolyte disturbances (such as SIADH or DI) that may develop secondary to diuretic therapy. Anticonvulsants, dosage time of last dose, and blood levels should be noted.
d) The decision regarding the amount and timing of the premedication administration should be made only after a thorough patient evaluation. Benzodiazepines produce respiratory depression and hypercapnia. Premedication should be omitted in patients with a large mass lesion, a midline shift, and abnormal ventricular size. Opioids are universally avoided in the preoperative period. If premedication is desired in patients deemed appropriate, careful titration of IV midazolam may begin when the patient has been delivered to the preoperative holding area. In an attempt to help control ICP in patients with mass lesions, the head of the bed should be elevated 15 to 30 degrees during transport to the preoperative holding area and the operating room.
e) Due diligence to all existing hospital recommendations for prophylactic antibiotics given at the appropriate time and in the appropriate amount should be performed.
(1) Routine monitors for supratentorial procedures include continuous ECG, cuff measurement of blood pressure, precordial stethoscope, monitoring of the fraction of inspired oxygen, pulse oximetry, temperature, peripheral nerve stimulation, etco2 monitoring, and indwelling urinary catheterization.
(2) For patients with ischemic heart disease, use of a modified V5 ECG lead is recommended. An arterial line placed either before or immediately after anesthetic induction provides for uninterrupted blood pressure monitoring and easy access for blood sampling for laboratory analysis.
(3) Somatosensory evoked potentials (SSEPs) may be assessed and may warrant the need for half an alternative anesthetic of 0.5 minimum alveolar concentration (MAC) and propofol infusion.
