Patients with intracranial aneurysms present for surgery electively or emergently following SAH.
Preoperative evaluation of patients with SAH should include all components of a routine anesthetic preoperative evaluation (Chapter 1: Evaluating the Patient Before Anesthesia), with attention to known associated physiologic perturbations. These include the neurologic grade (Table 23.2), presence of vasospasm (and the hemodynamic parameters that have been effective in relieving clinical symptoms),
degree of hydrocephalus, ICP elevation, and concurrent drug therapy such as calcium channel blockade with nimodipine, which may moderately lower systemic blood pressures intraoperatively.| Grade | Characteristics |
|---|---|
| I | Asymptomatic or minimal headache and slight nuchal rigidity |
| II | Moderate to severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy |
| III | Drowsiness, confusion, mild focal deficit |
| IV | Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity, vegetative disturbances |
| V | Deep coma, decerebrate rigidity, moribund |
Electrocardiographic changes are common after SAH and include arrhythmias and fluctuating ST-segment, QT-interval, and T-wave changes. These are probably caused by subendocardial injury following the autonomic discharge that occurs in association with the initial SAH. Provided these are not associated with cardiac dysfunction, no modification of patient management is necessary, although recent data suggest that a heart rate of either less than 60 or greater than 80 or the presence of nonspecific ST/T wave abnormalities are independently associated with increased mortality in patients with SAH receiving aneurysm clipping. Cardiac biomarkers may be increased as well.
Current practice is to intervene early during the first 24 to 48 hours after SAH for patients with neurologic grades I to III, which decreases the risk of rebleeding and facilitates the hypertensive management of vasospasm.
Specific anesthetic considerations include the following:
Avoidance of hypertension, which may increase the risk of aneurysm rupture before aneurysm clipping. Prophylactic use of agents such as IV nicardipine, fentanyl, β-adrenergic blockers, lidocaine, or additional doses of propofol will often attenuate the blood pressure response to noxious stimuli such as laryngoscopy and intubation.
Avoidance of hypotension to maintain adequate CPP in the setting of altered autoregulation.
Providing adequate brain relaxation to optimize surgical exposure. Rapid reductions in ICP may affect transmural pressure and increase the risk of aneurysm rupture. This should be done cautiously before opening the dura.
Induced hypertension may be requested during temporary clipping to improve collateral blood flow to regions that were perfused by the clipped arteries. Often, IV phenylephrine is used for this purpose. It is critical that hypertension be induced only after the temporary clip has been placed, otherwise the risk of aneurysm rupture is markedly increased.
Intraoperative aneurysm rupture can produce rapid and massive blood loss requiring large-bore IV access for volume resuscitation. Accurate estimation of blood loss is essential to guide volume repletion. Induced hypotension, adenosine-mediated cardiac standstill, or, occasionally, manual pressure on the ipsilateral carotid artery may be helpful during the desperate situation of a large and uncontrolled premature rupture.
Mild hypothermia (34 °C) has previously been used as a protective strategy for the brain during periods of cerebral ischemia. Data from the Intraoperative Hypothermia for Aneurysm Surgery Trial, suggests that hypothermia does not improve either neurologic or neuropsychologic outcome in patients with good-grade (grade I to III) surgical SAH. Given the results of this trial, targeted temperature management during aneurysm surgery is now the standard of care.
Once the permanent clips have been placed on the aneurysm, prevention of postoperative vasospasm becomes important. Blood pressure is increased moderately.
When appropriate, the anesthetic should be designed for a prompt emergence from anesthesia to enable an immediate neurologic
examination to ensure that clip placement does not compromise the parent vessel.An arteriovenous malformation (AVM) is a direct communication between cerebral arteries and veins without an intervening capillary bed. Because an AVM is a high-flow, low-resistance system, surrounding brain regions may be hypoperfused by the diversion of blood through the AVM (steal phenomenon). The most common presentations of an AVM are SAH, seizures, headaches, and, rarely, progressive neurologic deficits due to steal phenomenon.
Patients with AVMs may require anesthetic care for embolization procedures or surgical resection.
Embolizations are usually done to decrease blood flow to the AVM prior to surgical resection. Embolization may decrease the risk of intraoperative bleeding and postoperative reperfusion hyperemia.
Embolizations can be done under general anesthesia or monitored anesthesia care, which has the advantage of permitting continuous neurologic evaluation.
The anesthetist should be prepared for adverse reactions to the contrast dye (eg, anaphylaxis and osmotic load that may cause congestive heart failure), vessel perforation (sudden and rapid blood loss requiring immediate craniotomy), and neurologic changes.
Anesthetic management for surgical resection of an AVM is similar to that for cerebral aneurysms.
The primary focus is on tight blood pressure control because hypotension can lead to ischemia of hypoperfused regions. Hypertension can exacerbate perfusion pressure breakthrough, a poorly understood phenomenon that is thought to be caused by abrupt diversion of the AVM’s blood flow to adjacent, previously marginally perfused brain, which produces sudden cerebral engorgement and hemorrhage. Should perfusion pressure breakthrough and brain swelling occur, they are commonly treated with propofol and modest lowering of blood pressure.
Potential for large blood loss occurs in cases in which the AVM is large and has arterial feeders from more than one part of the cerebral arterial vasculature or when the preoperative embolization has been unsuccessful.
Postoperative angiography to confirm complete AVM resection is usually done immediately after surgery. Should any residual AVM be detected, further resection is indicated.
Posterior fossa surgery
Posterior fossa tumors may cause cranial nerve palsies, cerebellar dysfunction, and hydrocephalus due to obstruction of the fourth ventricle. Tumors or surgery around the glossopharyngeal and vagus nerves may impair the gag reflex and increase the risk of postoperative aspiration. Tumor resection that results in edema in the floor of the fourth ventricle may damage respiratory centers and necessitate postoperative mechanical ventilation.
Cardiovascular instability resulting from surgical manipulation is common. Sudden severe bradycardia and hypertension or hypotension occur if the trigeminal nerve is stimulated. Bradycardia, asystole, or hypotension may follow stimulation of the glossopharyngeal or vagus nerve. In such cases, the surgeon should be notified immediately because the instability usually resolves with cessation of the stimulus. Pharmacologic treatment (eg, atropine, glycopyrrolate, ephedrine) is rarely necessary.
A sitting position is occasionally used for posterior fossa surgery. The advantages include better surgical exposure, improved venous and CSF drainage, and diminished bleeding due to lower venous pressures. The sitting position is also associated with a higher incidence of venous air embolism and cardiovascular instability. Modified supine, prone, and three-quarter prone positioning may be substituted for the sitting position because of these concerns.
Venous air embolism is a risk whenever the operative site is above the level of the heart and there is an open vein. Under these circumstances, an open venous sinus can entrain air and produce hypoxia, hypercarbia, bronchoconstriction, hypotension, and ultimately, cardiovascular collapse. Systemic arterial air embolism is a risk whenever right-to-left shunts exist and can cause myocardial and cerebral ischemia. Monitoring devices for the detection of air embolism and central venous catheters for aspiration of air are often placed when there is risk for venous air embolism.
Methods used to monitor for venous air embolism include Doppler ultrasound (which reveals a characteristic “mill wheel” murmur when air is entrained), capnography (which may reveal a sudden decrease in end-tidal CO2), and TEE. Of these, TEE is the most sensitive of the invasive monitors, and Doppler ultrasound the most sensitive of noninvasive monitors.
If air is detected, the focus is to prevent further air entrainment and treatment of the adverse consequences. First, the surgeons are notified so they can eliminate the source of air (close the dural opening, place bone wax, or flood the surgical field), and the air is aspirated from the central venous pressure catheter. If possible, patient positioning should be modified to place the surgical site below the level of the heart to reverse the pressure gradient facilitating air entry. If the patient remains stable, the prevention of further air entry may be all that is needed. If hypotension develops, Trendelenburg positioning, fluid administration, and inotropic support may be required. If being used, nitrous oxide should be discontinued.
At the end of surgery, the adequacy of the airway and respiration should be verified before extubation. Surgical manipulation may damage the cranial nerves or respiratory centers in the brainstem with resulting pharyngeal or respiratory dysfunction. Postoperative infarction, edema, or hematoma formation in the posterior fossa can cause rapid clinical deterioration. Close observation and prompt support including intubation, mechanical ventilation, and circulatory management may be required.
Awake craniotomy
Recommended for removal of tumors involving or adjacent to speech centers and for epileptogenic focus resection. Intraoperative cortical mapping allows maximal resection with minimal postoperative neurologic dysfunction.
The goals are to provide adequate analgesia and sedation as well as to ensure hemodynamic stability, a patent airway, and patient cooperation with neurologic testing during cortical stimulation. Adequate local anesthesia is required. Conscious sedation with propofol, dexmedetomidine, remifentanil, or other agents may be used. Alternatively, an “asleep-awake-asleep” technique may be used as long as the patient is fully cooperative during testing. A laryngeal mask airway (LMA) may be necessary for airway patency during the “asleep” portions of the case.
Be prepared to treat a cortical stimulation–induced seizure. If one occurs, ask the neurosurgeons to irrigate the cortex with iced saline. Next, the seizure may be aborted with either midazolam or propofol. Small doses may stop the seizure and not overly sedate the patient so that testing may continue. It is important that the IV catheter is not placed across a joint, which may be flexed and ineffective during a grand mal seizure. Before the procedure, the patient’s anticonvulsant level should be checked to ensure that it is therapeutic.
Allow adequate access to the patient’s airway. This should include sufficient room to provide mask ventilation and LMA insertion should the circumstances require these interventions.
Transsphenoidal resection of the pituitary gland is performed through a nasal, transsphenoidal approach.
Although nonfunctioning pituitary adenomas are the most common tumor type, some patients have endocrine deficiencies due to hypothalamopituitary compression. Various hyperpituitarism syndromes may accompany functioning adenomas, including Cushing syndrome, acromegaly (with associated airway difficulties), and amenorrhea–galactorrhea.
ICP is not a concern as these tumors are usually small and unlikely to compromise intracranial compliance.
Uncontrollable bleeding is rare but can be massive and catastrophic due to lack of exposure. Frontal craniotomy ultimately may be required to achieve hemostasis.
Monitoring. The endotracheal tube must be firmly secured to the lower lip to keep it out of the surgical field. Continuous monitoring of ventilation is essential. Arterial monitors are usually not indicated unless indicated by other medical comorbidities.
Throat packs will prevent blood from accumulating in the stomach and may reduce postoperative vomiting. The throat pack must be removed before extubation.
At the conclusion of surgery, nasal breathing will be obstructed by packs. Patients should be prepared for this preoperatively.
Diabetes insipidus may occur after transsphenoidal hypophysectomy (usually 4 to 12 hours postoperatively). Treatment with IV fluids or desmopressin may be necessary (Section V.E.8). Some patients may develop postoperative adrenal insufficiency and require corticosteroids postoperatively.
Stereotactic surgery is usually performed through a burr hole, using a three-dimensional reference grid attached to the head with pins placed in the outer table of the skull. This approach allows localization of a discrete area of brain for biopsy or ablation. In most cases, the procedure is done under general anesthesia. However, when intraoperative testing is required, the procedure can be done under monitored anesthetic care. Because the stereotactic apparatus precludes full access to the airway, sedation must be given with caution. The stereotactic frame can be removed in an emergency; newer models can be quickly removed to provide more rapid access to the airway.
Deep brain stimulators are inserted in patients with movement disorders (mostly Parkinson disease) who have failed medical therapy. Microelectrodes are inserted through burr holes to a precise location in the subthalamic nuclei, globus pallidum, or thalamus. A stereotactic headframe with image-guided navigation is required to identify and locate the electrode target.
Patients often do not receive their morning dose of either dopaminergic or anticholinergic medications to improve electrode recordings that guide electrode placement to a specific cell layer.
Patients are awake and often not sedated during the electrode placement, since most sedatives can alter the electrode recordings. Once the electrodes are secure, appropriate sedation is implemented.
Epilepsy surgery is performed in patients with epilepsy of focal origin who are refractory to medical therapy or intolerant of the side effects of anticonvulsants.
Excision of a seizure focus. Electrophysiologic mapping of the epileptic focus and other cortical areas (eg, language, memory, sensorimotor) is often performed to maximize the resection of the epileptogenic lesion while minimizing the neurologic deficits. This procedure is often done with general anesthesia and electrocorticography. It offers the advantages of patient comfort, immobility, a secure airway, and the ability to control Paco2 and other variables. The anesthetic technique is chosen for its ability to augment (eg, methohexital, etomidate, ketamine) or attenuate (eg, benzodiazepines, isoflurane) the seizure focus and its compatibility with intraoperative monitoring (Section III). Because there is often an initial increase in seizure activity postoperatively, anticonvulsants should be resumed promptly.
Vagal nerve stimulators (VNS) may be placed for medically refractory epilepsy. The electrodes are typically placed through an incision in the left neck and then tunneled to a generator located above the left pectoralis fascia. VNS are typically placed under general anesthesia with endotracheal intubation. Patients frequently are taking multiple antiepileptic drugs, which may cause resistance to neuromuscular-blocking drugs. Additionally, medications that may trigger seizure activity (e.g., ketamine) should be avoided. Postoperatively, monitoring for peritracheal hematoma and vocal cord paralysis should be performed.
Head trauma. Anesthetic management of the patient with head trauma is complicated by the challenging combination of a “tight” head, full stomach, and potentially unstable cervical spine. While following the “ABCs” of resuscitation, the anesthesiologist should ascertain the mechanism and extent of injury. Cervical spinal cord injury must be suspected, and the neck stabilized until cervical injury is excluded.
Patients who are responsive and ventilating adequately should receive supplemental oxygen and be observed closely for evidence of neurologic deterioration.
Comatose patients require immediate endotracheal intubation for airway protection and to avoid hypercarbia and hypoxia, which can exacerbate increases in ICP and contribute to secondary brain injury.
Endotracheal intubation should be accomplished rapidly, with blood pressure stability and without coughing or straining.
A rapid sequence induction is usually performed. If a cervical spine injury has not been excluded, the neck should be immobilized with manual in-line stabilization (MILS). The anterior part of the cervical collar may be removed to apply gentle cricoid pressure (excessive pressure may displace a fracture) and obtain sufficient mouth opening. A short-acting induction agent such as propofol or etomidate is used to induce anesthesia, which is immediately followed by an intubating dose of muscle relaxant. Succinylcholine can be used safely unless contraindicated for other reasons (Section II.C and Chapter 14: Neuromuscular Blockade). Nondepolarizing relaxants also may
be used. When MILS is used, the laryngoscopist should anticipate an increased likelihood of poor glottic visualization during direct laryngoscopy due to limited extension of the occiput, C1, and C2.Awake intubation may be advocated because of full-stomach considerations, the potential for worsening neck injuries during manipulation of the airway, and anticipation of a difficult airway due to associated facial injuries. Awake approaches are often impractical or unwise in head-injured patients because of lack of cooperation, airway bleeding, and increases in ICP that can be induced by hypertension, coughing, and straining.
Nasal intubation and nasogastric tube placement are contraindicated in the presence of a basilar skull fracture (eg, CSF rhinorrhea, otorrhea, Le Fort III facial fracture).
Hypertension in head-injured patients may be the body’s compensatory effort to maintain CPP in the face of increased ICP. CPP should be maintained at 60 mm Hg. Hypotension can be detrimental in patients with elevated ICP and, when combined with tachycardia, should lead one to suspect bleeding from other injuries. Interventions to stop bleeding and restore intravascular volume should occur in concert with surgical treatment of the head injury.
Hypoxia should be aggressively treated as its presence dramatically worsens neurologic outcome in head-injured patients.
Hyperglycemia should be treated to improve neurologic outcome.
ICP monitoring can be performed if severe or progressive intracranial hypertension is suspected.
Seizures may accompany direct cerebral injury or signal the expansion of an intracranial hematoma.
Brain contusion is the most common type of head injury. Surgery is usually reserved for acute epidural hematomas and acute subdural hematomas. Subdural hematomas are much more common than epidural hematomas and carry a worse prognosis. Intracranial hypertension is frequently seen even after evacuation of hematomas because of severe brain swelling.
Penetrating brain injuries require early debridement of injured tissue, removal of bone fragments, and evacuation of hematoma. Skull fractures may require debridement, cranioplasty, and repair of dural lacerations.
Anesthetic management follows the general rules of maintaining CPP and ICP, and reducing cerebral edema. Postoperative intubation and ventilatory support are frequently required for ICP control and airway protection in patients with prolonged loss of consciousness or an inadequate gag reflex. Preoperative alteration in the level of consciousness is helpful in predicting the need for postoperative intubation.
Disseminated intravascular coagulation is a frequent complication of an acute head injury, particularly those associated with a subdural hematoma. Frequent monitoring of the patient’s coagulation status is recommended throughout the procedure and early postoperative period.
Corticosteroids are not indicated for head trauma and may increase morbidity and mortality.
CSF shunts are inserted in patients with hydrocephalus. A ventriculoperitoneal (VP) shunt is the most common treatment for hydrocephalus. A ventricular catheter is placed through a frontal burr hole and is attached to a valve. These are then attached to the draining catheter that is tunneled subcutaneously to the upper abdomen, where laparoscopy is performed to insert the catheter under direct visualization.
The anesthetic management of these patients is determined primarily by the acuity of their disease. Acute hydrocephalus is a neurosurgical emergency where rapidly rising ICP could cause ischemic neurologic damage. Management should focus on measures that will reduce the patient’s ICP, maintain a CPP of at least 60 mm Hg, and enable rapid neurosurgical decompression. Anesthetic management of elective VP shunt insertion or revision employs a standard, well-managed, and safe anesthetic where factors that cause extreme ICP elevation are avoided.