Anesthesia & Craniotomy for Patients with Mass Lesions
Intracranial masses may be congenital, neoplastic (benign or malignant), infectious (abscess or cyst), or vascular (hematoma or arteriovenous malforma-tion). Craniotomy is commonly undertaken for neo-plasms of the brain. Primary tumors usually arise from glial cells (astrocytoma, oligodendroglioma, or glioblastoma), ependymal cells (ependymoma), or supporting tissues (meningioma, schwannoma, or choroidal papilloma). Childhood tumors include medulloblastoma, neuroblastoma, and astrocytoma.
Regardless of the cause, intracranial masses present according to growth rate, location, andICP. Slowly growing masses are frequently asymp-tomatic for long periods (despite relatively large size), whereas rapidly growing ones may present when the mass remains relatively small. Common presenta-tions include headache, seizures, a general decline in cognitive or specific neurological functions, and focal neurological deficits. Symptoms typical to supratentorial masses include seizures, hemiplegia, or aphasia, whereas symptoms typical of infraten-torial may include cerebellar dysfunction (ataxia, nystagmus, and dysarthria) or brainstem compres-sion (cranial nerve palsies, altered consciousness, or abnormal respiration). As ICP increases, signs of intracranial hypertension also develop (see above).
The preoperative evaluation for patients undergoing craniotomy should attempt to establish the presenceor absence of intracranial hypertension. Com-puted tomography (CT) and magnetic resonance imaging (MRI) scans should be reviewed for evidence of brain edema, a midline shift greater than 0.5 cm, and ventricular displacement or compres-sion. The neurological examination should docu-ment mental status and any sensory or motor deficits. Medications should be reviewed with spe-cial reference to corticosteroid, diuretic, and anti-convulsant therapy. Laboratory evaluation should rule out corticosteroid-induced hyperglycemia, electrolyte disturbances due to diuretics, or abnor-mal secretion of antidiuretic hormone. Anticonvul-sant blood concentrations may be measured, particularly when seizures are not well controlled.
Sedative or opioid premedication is best avoided if intracranial hypertension is suspected. Hypercapnia secondary to respiratory depression increases ICP. Corticosteroids and anticonvulsant therapy should be continued until the time of surgery.
In addition to standard monitors, direct intraarterial pressure monitoring and bladder catheterization are used for most patients undergoing craniotomy. Rapid changes in blood pressure during anesthetic procedures, positioning, and surgical manipulation are best managed with guidance from continuous invasive monitoring of blood pressure. Moreover, arterial blood gas analyses are necessary to closely regulate Paco2. Many neuroanesthesiologists zero the arterial pressure transducer at the level of the head (external auditory meatus)—instead of the right atrium—to facilitate calculation of cerebral perfusion pressure (CPP). End-tidal CO2 measure-ments alone cannot be relied upon for precise regu-lation of ventilation; the arterial to end-tidal CO2 gradient must be determined. Central venous access and pressure monitoring should be considered for patients requiring vasoactive drugs. Use of the internal jugular vein for access is theoretically prob-lematic because of concern that the catheter might interfere with venous drainage from the brain. Some clinicians avoid this issue by passing a long catheter into the central circulation from the median basilic vein. The external jugular, subclavian, and femo-ral veins may be suitable alternatives for intraop-erative use. A bladder catheter is necessary because of the use of diuretics, the long duration of most neurosurgical procedures, and its utility in guid-ing fluid therapy. Neuromuscular function should be monitored on the unaffected side in patients with hemiparesis because the twitch response is often abnormally resistant on the affected side. Monitoring visual evoked potentials may be useful in preventing optic nerve damage during resections of large pituitary tumors. Additional monitors for surgery in the posterior fossa are described below.
Management of patients with intracranial hypertension may be guided by monitoring ICP perioperatively. Various ventricular, intraparenchy-mal, and subdural devices can be placed by neu-rosurgeons to provide measurements of ICP. The transducer should be zeroed to the same reference level as the arterial pressure transducer (usually the external auditory meatus; see above). A ventric-ulostomy catheter provides the added advantage of allowing removal of CSF to decrease ICP.
Induction of anesthesia and tracheal intubation are critical periods for patients with compromised intra-cranial pressure to volume relationships, particularly if there is an elevated ICP. Intracranial elastance can be improved by osmotic diuresis, dexamethasone, or removal of small volumes of CSF via a ventricu-lostomy drain. The goal of any technique should be to induce anesthesia and intubate the trachea with-out increasing ICP or compromising CBF. Arterial hypertension during induction increases CBV and promotes cerebral edema. Sustained hypertension can lead to marked increases in ICP, decreasing CPP and risking herniation. Excessive decreases in arte-rial blood pressure can be equally detrimental by compromising CPP.
The most common induction technique employs propofol together with modest hyperventi-lation to reduce ICP and blunt the noxious effects of laryngoscopy and intubation. Cooperative patients can be asked to hyperventilate during preoxygen-ation. All patients receive controlled ventilation once the propofol has been injected. A neuromuscular blocker (NMB) is given to facilitate ventilation and prevent straining or coughing, both of which can abruptly increase ICP. An intravenous opioid given with propofol blunts the sympathetic response, par-ticularly in young patients. Esmolol, 0.5–1.0 mcg/ kg, is effective in preventing tachycardia associated with intubation in lightly anesthetized patients.
The actual induction technique can be var-ied according to individual patient responses and coexisting diseases). Succinylcholine may theo-retically increase ICP, particularly if intubation is attempted prior to the establishment of deep anes-thesia. Succinylcholine, however, remains the agent of choice for rapid sequence induction or when there are concerns about a potentially difficult air-way, as hypoxemia and hypercarbia are much more detrimental than any effect of succinylcholine to the patient with intracranial hypertension.
Hypertension during induction can be treated with β1-blockers or by deepening the anesthetic with additional propofol. Modest concentrations of vola-tile agents (eg, sevoflurane) may also be used, pro-vided that hyperventilation is also used. Sevoflurane best preserves autoregulation of CBF and produces limited vasodilatation; it may be the preferred vol-atile agent in patients with elevated ICP. Because of their potentially deleterious effect on CBV and ICP, vasodilators (eg, nicardipine, nitroprus-side, nitroglycerin, and hydralazine) are avoided until the dura is opened. Hypotension is generally treated with incremental doses of vasopressors (eg, phenylephrine).
Frontal, temporal, and parietooccipital craniotomies are performed in the supine position. The head is elevated 15–30° to facilitate venous and CSF drain-age of CSF. The head may also be turned to the side to facilitate exposure. Excessive flexion or rotation of the neck impedes jugular venous drainage and can increase ICP. Before and after positioning, the tracheal tube should be secured, and all breathing circuit connections checked. The risk of unrecog-nized disconnections may be increased because the patient’s airway will not be easily assessed after surgi-cal draping; moreover, the operating table is usually turned 90° or 180° away from the anesthesiologist.
Anesthesia can be maintained with inhalation anesthesia, total intravenous anesthesia techniques (TIVA), or a combination of an opioid and intrave-nous hypnotic (most often propofol) and a low-dose inhalation agent. Even though periods of stimulation are few, neuromuscular blockade is recommended— unless neurophysiological monitoring contradicts its use—to prevent straining, bucking, or movement. Increased anesthetic requirements can be expected during the most stimulating periods: laryngoscopy– intubation, skin incision, dural opening, periosteal manipulations, including Mayfied pin placement and closure. TIVA with remifentanil and propofol facilitates rapid emergence and immediate neuro-logical assessment. Likewise, the α2-agonist dexme-detomidine can be employed during both asleep and awake craniotomies to similar effect.
Hyperventilation should be continued intraop-eratively to maintain Paco2 at roughly 30–35 mm Hg. Lower Paco2 tensions provide little additional benefit and may be associated with cerebral isch-emia and impaired oxygen dissociation from hemo-globin. Positive end-expiratory pressure (PEEP) and ventilatory patterns resulting in high mean air-way pressures (a low rate with large tidal volumes) should be avoided because of a potentially adverse effect on ICP by increasing central venous pressure and the potential for lung injury. Hypoxic patients may require PEEP and increased mean airway pres-sures; in such patients, the effect of PEEP on ICP is variable.
Intravenous fluid replacement should be limited to glucose-free isotonic crystalloid or colloid solu-tions. Hyperglycemia is common in neurosurgical patients (corticosteroid effect) and has been impli-cated in increasing ischemic brain injury. Colloid solutions can be used to restore intravascular vol-ume deficits, whereas isotonic crystalloid solu-tions are used for maintenance fluid requirements. Neurosurgical procedures are often associated with “occult” blood loss (underneath surgical drapes or on the floor).
Most patients undergoing elective craniotomy can be extubated at the end of the procedure, provided that neurological function is intact. Patients who will remain intubated should be sedated to prevent agitation. Extubation in the operating room requires special handling during emergence. Straining or bucking on the tracheal tube may precipitate intra-cranial hemorrhage or worsen cerebral edema. As the skin is being closed, the patient should resume breathing spontaneously. Should the patient’s head be secured in a Mayfield pin apparatus, care must be taken to avoid any patient motions (eg, “bucking on the tube”), which could promote neck or cra-nial injuries. After the head dressing is applied and full access to the patient is regained (the table is turned back to its original position as at induc-tion), any anesthetic gases are completely discontin-ued, and the neuromuscular blockade is reversed. Rapid awakening facilitates immediate neurological assessment and can generally be expected follow-ing an appropriate anesthetic. Delayed awakening may be seen following opioid or sedative overdose, when the end-tidal concentration of the volatile agent remains >.2 minimum alveolar concentration (MAC), because of various metabolic derangements, or when there is a perioperative neurological injury. Patients may need to be transported to the CT scan-ner directly from the operating room for evaluation when they do not respond as predicted. Immediate reexploration may be required. Most patients are taken to the intensive care unit postoperatively for close monitoring of neurological function.
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